Oral Medicine H Umarji

Concise
Oral Medicine
This Page is Intentionally Left Blank
Concise
Oral Medicine
HR Umarji MDS
Professor and Head
Department of Oral Medicine and Radiology
Government Dental College and Hospital
Mumbai
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to
my wife, Vasu
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Medha and Anagha
Preface
A fter Concise Oral Radiology was well-received by the undergraduate students, I had the
temptation of compiling a similar text on oral medicine and for this endeavor I was
encouraged and even goaded by many PG students and lecturers.
The basic motive behind this venture is to present important aspects of oral medicine readily
available in various textbooks in a nutshell, to help the exam-going students too hard pressed
for time to refer to various books.
Again I would make no claim regarding the originality of the text in Concise Oral Medicine,
on the other hand I may be guilty of ruthlessly cutting down on a lot of information with the
primary aim of keeping the text short and simple.
During my tenure as a student and a teacher, I had the privilege of learning this subject
under the erudite guidance of stalwarts of oral medicine in India namely Dr Girish Merchant,
Dr Aspi Surveyor, Dr Jakhi, Dr Ani John, Dr Bharati Parekh and Dr RN Mody. I will forever
remain indebted to these dedicated teachers. In fact this text has its roots in the notes made
during their lectures.
Compilation of this book, however, concise, was a challenge to my lazy nature and sceptical
attitude and without the active participation of many individuals, it would have been
impossible to accomplish this task. Dr Eswaran Ramaswamy and Dr Akshay Chaturmohatta
spearheaded the venture by compiling the first few chapters. Dr Harsha Puri, Dr Amruta
Bandal and Dr Ashish Talanje were lecturers in the department and of great help in this venture.
I relied heavily on the selfless efforts provided by lecturers Dr Suvarna Sawant,
Dr Hasan Ali, Dr Prashant Salve, Dr Kavita Amale and postgraduate students Dr Manasi
Kajale, Dr Minakshi Hivarkar, Dr Priyanka Verma, Dr Pooja Jain, Dr Ajas Gogri, Dr Deepika
Khurana, Dr Sunita Kakade and I express my heartfelt gratitude to all of them and many
others whom I might have failed to mention.
I owe a debt of gratitude to Dr Smriti Khanna, Lecturer, Oral Pathology, for diligent proof
reading of a few chapters and Dr Nitin with artistic talent for the line diagrams and also to
Mr Ashish Jalamkar and Mr Vikas Jadhav for converting old departmental slides into good
quality pictures.
Dr Shruti Shah was ever helpful and efficiently completed the laborious task of adding the
color pictures with legend and overall preparation of the manuscript.
I am extremely grateful to Dr Nandita Gupta for the preparation of index and Dr Varun
Manek for providing constructive criticism which helped in improving the content of the
book.
I consider myself blessed, that I am associated with Government Dental College and Hospital,
Mumbai, a great institution which has always encouraged me and almost all the cases presented
in this text belong to the patients attending the heavy OPD of GDCH and obtained with courtesy
from the ever helpful staff and PG students.
viii Concise Oral Medicine
Dr Sonali Kadam, Associate Professor, has always been co-operative and supportive and
I express my gratitude to her for all the help.
With Dr Jagdish V Tupkari, HOD, Oral Pathology, I have always enjoyed good rapport and
benefited immensely by his knowledge, wisdom and wit and willingness to offer a helping
hand.
I will always remain indebted to Dr Mansing G Pawar, Dean, GDCH, for constant support
and I always felt encouraged in this institution because of him.
Mr YN Arjuna and Mr Ramesh Krishnammachari of CBS Publishers always provided all
the assistance and it was their enthusiasm which made this text a possibility. I also wish to
express my gratitude to CBS Publishers & Distributors as without their efforts this book would
not have been published.
HR Umarji
Contents
Preface vii
1. Definition and Introduction 1
2. Ulcerative and Vesiculobullous Lesions 17
3. Red and White Lesions 49
4. Gingival Enlargement 76
5. Tongue Lesions 86
6. Pigmentations 101
7. Granulomatous Diseases and STDs 113
8. Cross-Infection Control 133
9. Bleeding and Clotting Disorders and Hematological Diseases 138
10. Temporomandibular Joint Disorders 163
11. Diseases of Maxillary Sinus 176
12. Salivary Gland Disorders 185
13. Orofacial Pain 199
14. Oral Cancer and Precancerous Lesions 211
15. Immunological Diseases 222
16. Endocrine Disease and Dysfunction 231
17. Management of Medically Compromised Patients and Drug Interactions 244
18. Differential Diagnosis of Miscellaneous Diseases 249
19. Forensic Odontology 256
20. Evidence-Based Dentistry 264
21. Orofacial Syndromes 269
22. Routine Blood Investigations 275
Index 281
1
Definition and Introduction
ORAL MEDICINE The case history includes the following parts:

Oral medicine may be defined as the branch 1. Patient’s personal data
of dentistry that deals with the diagnosis and 2. Chief complaint
management of diseases that are nonsurgical 3. Medical history
in nature, that may occur only in the oral 4. Past dental history
cavity or may be oral manifestations of
5. Personal history
systemic disease.
6. General examination
Scope of oral medicine: It is a clinical discipline
that encompasses the following: 7. Extraoral examination
1. Diagnosis and medical management of 8. Intraoral examination
diseases of oral mucosa, jaws and the 9. Detailed examination of the area of chief
salivary glands. complaint
2. Diagnosis and medical management of oro- 10. Provisional diagnosis and investigations
facial pain and TMJ disorders. 11. Final diagnosis
3. Dental management of patients with 12. Treatment plan
complicated medical diseases. As an alternative to the above mentioned
conventional method of history taking which
CASE HISTORY involves compiling the extensive list of normal
and abnormal data, a problem-oriented record
The first and the most important step in
(POR) can be maintained that emphasizes the
evaluating a patient is obtaining a detailed
evaluation and recording of pertinent abnormal
case history. Case history means gathering
findings. The POR has four components that
relevant information from the patient for the
can be described under the acronym SOAP in
purpose of establishing the diagnosis and
which,
providing oral health care needs to them. It
involves listening patiently to the patient’s S—Subjective is recording the patient’s
complaints and obtaining the necessary details chief complaint, symptoms and a brief
by asking him appropriate questions. This is review of his medical history.
followed by a thorough physical examination O—Objective involves a brief physical
with special attention to the area of chief com- examination followed by detailed examina-
plaint so as to arrive at a provisional diagnosis. tion of the area of chief complaint.
1
2 Concise Oral Medicine
A—Assessment, which involves arriving at health status. The possibility of drug

the diagnosis. interactions must also be considered as
P—Plan, where the required treatment is many senior individuals are under
planned and executed. medications for co-existing medical
diseases.
iii. Gender: Diseases are known to have pre-
THE IMPORTANCE OF CASE HISTORY
dilection to certain genders, e.g. diseases
As already mentioned above, case history is such as recurrent aphthous stomatitis,
the most integral part of patient assessment. lichen planus, MPDS, iron deficiency
Every detail recorded can be of enormous anemia, AOT, etc. are more common in the
importance and the time spent in obtaining females, while conditions such as leuko-
this vital information is worthwhile. plakia, squamous cell carcinoma, amelo-
blastoma, hemophilia, etc. are common in
1. Patient’s Personal Data the males.
This part of the history includes recording the iv. Address: Knowing the patient’s complete
patient’s name, age, gender, address, etc. residential address facilitates communi-
i. Name: Apart from identification, address- cation. With the advent of modern techno-
ing the patient by his name when he enters logies, it is advisable to record the patient’s
the office and during the appointments mobile numbers and e-mail address also
makes the patient feel important and at so that information regarding appoint-
home and helps in establishing a good ments and follow ups can be done very
rapport with the patient. easily!
ii. Age: The patient’s age is a vital information Apart from that, the knowledge of the
as it helps in diagnosis as well as treatment patient’s place of residence can give a clue
planning. Certain diseases have predilec- about his social and cultural background and
tion to affect certain age groups, e.g. prevalence of certain habits and diseases in
developmental anomalies, rampant caries that geographic location. For example, the
and lesions such as primary herpetic habit of reverse smoking is common in the
gingivostomatitis, measles, chickenpox, state of Goa and coastal area of Kerala, where
etc. are more common in children, while palatal changes could result in a premalignant
diseases such as root surface caries, change. Similarly enamel fluorosis is endemic
osteomyelitis, herpes zoster infection, in areas where fluoride content in drinking
pemphigus, etc. are common in the older water is high.
age group. Another important matter that
requires consideration of the patient’s age 2. Chief Complaint
is dosage of drugs in prescriptions. Chief complaint is the problem for which the
Dosages should be reduced appropriately patient approaches the doctor to seek
for children. Drugs such as tetracycline are treatment. “Listen to the patient, he is telling you
contraindicated in small children where the diagnosis” is an age old adage that still holds
it can cause permanent discoloration of the value. The complaints mentioned by the
developing dentition. Similarly aspirin is patients are called as symptoms and must be
contraindicated during viral infections in therefore listened to attentively. Carefully
the pediatric age group as this can result framed questions should be asked that would
in anicteric liver dysfunction called Reye’s encourage the patient to reveal some vital
syndrome. Drug dosage must be adjusted piece of information which otherwise the
for the elderly considering their general patient may not have expressed. These
Definition and Introduction 3
questions may be of two types, open-ended fulminating infections such as Ludwig’s

questions and close questions. Open questions angina spread fast and increase suddenly in
are those that will encourage the patient to size, while pain associated with TMJ disease,
narrate in detail the information asked to him, MPDS, etc. progress slowly in severity.
e.g. ‘what kind of pain do you experience?’ Lesions such as aphthous stomatitis, benign
Questions like these will make the patient migratory glossitis, herpes labialis, etc. charac-
think and give a reply in a descriptive manner. teristically show periods of remissions and
Closed questions on the other hand are more exacerbations and recur periodically.
objective in nature for which the patient has Aggravating factors are those that cause the
to choose just the right type of option given by symptoms to grow more severe. For example,
the doctor, e.g. ‘is the pain continuous or pain of acute pulpitis aggravates on lying
intermittent?’ down while neuralgic pain is aggravated
The common chief complaints that can lead by smiling or even touching specific parts of
the patient to a dentist are pain, swelling, the face lightly. Many oral lesions such as
bleeding from the gums, difficulty in opening lichen planus, aphthous stomatitis, herpes
the mouth, pain in the TMJ region, ulceration infection, etc. are known to be aggravated by
or burning sensation in the mouth, etc. Each stress.
of the symptoms must be recorded in the Relieving factors are those that help the
decreasing order of their severity. The chief patient to get relief from the symptoms. For
complaint must be recorded in the patient’s example, pain of dental diseases is usually
own words and technical terms must be best relieved on taking some anti-inflammatory/
avoided. The onset, duration, progress, analgesic drugs while that due to neuralgia is
aggravating and relieving factors must also be refractory to analgesics. Similarly muscular
recorded which are very useful in leading to pain due to MPDS may be relieved by applica-
the correct diagnosis. tion of hot fomentation.
Onset indicates the manner in which the
disease began. It denotes the acute or chronic 3. Medical History
nature of the disease, e.g. lesions such as It is very important to know about the patient’s
erythema multiforme, allergic reactions, etc. general medical health status prior to
have a sudden or acute onset. On the other beginning any sort of dental treatment. The
hand, chronic lesions and conditions such as objectives of knowing the medical history are
pemphigus, lichen planus, MPDS, OSMF and twofold. First it helps us to understand the
others have a gradual onset. compromised health status of the patient so
Duration indicates the time for which the that necessary precautions can be taken to
symptoms last, e.g. pain due to dental diseases avoid any untoward complications. Thus as
usually lasts for a longer period of time, while it is rightly said, ‘When you prepare for an emer-
pain in trigeminal neuralgia typically occurs gency, the emergency ceases to exist.’ A sound
in episodes and lasts for just a few seconds. knowledge of management of medically com-
Similarly lesions such as lichen planus, promised patient is important so as to avoid
pemphigus, aphthous major, etc. have a long undesirable complications and embarrass-
duration of history while conditions such as ment that accompanies it. Secondly, the
aphthous minor, herpes labialis, etc. have a patient may have certain oral lesions that may
short duration. be manifestation of systemic disease as oral
Progress indicates the manner in which the physicians it is our responsibility to manage
disease process has advanced. Rapid these lesions effectively.
A variety of medical problems are of impor- iv. Benzodiazepines and sedatives must be
tance to be considered by a dentist during avoided as they too can precipitate an
treatment planning. This list can be easily attack.
remembered by following the pnemonic v. Drugs such as aspirin and NSAIDs like
mentioned as below. mefenamic acid may induce an attack.
A — Asthma, allergy, anemia Nimesulide is safer in these patients.
B — Bleeding disorders Similarly morphine, thiopentone and
C — Cardiovascular disorders other opioids can stimulate histamine
release and so should be avoided.
D — Diabetes
vi. Severely asthmatic patients may be under
E — Endocrine disorders such as hyper- steroid therapy and hence necessary
hypothydroidism, etc. adjustments of steroid dose may be requi-
F — Fits and faints (epilepsy) red to prevent adrenal crisis. Long-term
G — Gastroinestinal disorders such as and frequent use of steroid inhalers pre-
peptic ulcer, hyperacidity, etc. disposes these patients to oral candidiasis.
H — Hospitalization and blood trans- vii. Emergency medications such as adrena-
fusion line and hydrocortisone must be available
I — Infections such as HIV, hepatitis, in the clinic to be used, should any sudden
tuberculosis, etc. attack be precipitated.
J — Jaundice Anemia is a disorder characterized by
K — Kidney disorders reduction in the hemoglobin levels in the
blood. Based on the cause, anemia may be
L — Lactation and pregnancy
categorized into iron deficiency anemia,
A—Asthma, Anemia hemolytic anemia, pernicious anemia, etc.
Some of the common clinical presentations
Asthma is a respiratory disorder characterized
include general lassitude, pallor of nails, con-
by hyper-responsiveness of the bronchi to
junctiva and oral mucosa, bald depapillated
stimuli resulting in wheezing and dyspnea.
tongue, glossitis, angular chelitis, etc.
Asthma may be extrinsic or intrinsic. Extrinsic
asthma is essentially allergic disorder seen Dental considerations:
commonly in children, while intrinsic asthma i. The patient’s hemoglobin level and RBC
is nonallergic and caused due to mast cell count must be ascertained prior to any
instability. surgical procedures. It is advisable to
Dental considerations: postpone any surgical procedures if the
i. Anxiety due to dental treatment can hemoglobin levels are below 10 mg/dl
precipitate an asthma attack. Hence these and the patient needs to be referred to a
patients must be reassured and handled hematologist/physician for opinion. GA
gently during treatment procedures. may not be safe in severe anemics.
ii. Local anesthesia is safe. However, LA con- ii. Oral manifestations of anemia include
taining adrenaline must be avoided as frequent aphthous ulcerations, glossitis,
sodium metabisulphite which is used to angular chelitis, Plummer-Vinson syn-
preserve adrenaline from being oxidized drome, candidiasis, etc. Patients presenting
can trigger an allergic reaction in asthmatics. with burning mouth or bald tongue must
iii. Patients should not forget to take their be investigated for anemia when there
medication and carry their inhaler pump is no other notable cause for these
with them. symptoms.
B—Bleeding Disorders vii. It is ideal to carry out surgical procedures

Disorders of hemostasis can cause manage- in a hospital setting so that emergencies
ment problems mainly due to excessive post- can be immediately handled.
operative bleeding. The causes for prolonged
C—Cardiovascular Diseases
bleeding may be due to platelet disorders like
thrombocytopenia, idiopathic thrombo- Cardiovascular diseases such as hypertension,
cytopenic purpura, drug such as aspirin, etc. ischemic heart diseases, etc. are becoming
Coagulation defects such as hemophilia, increasingly common in the modern days.
von Willebrand’s disease, Bernard-Soulier Hypertension may be defined as a persistent
syndrome, etc. can also result in abnormal rise in the arterial blood pressure. Ischemic
excessive bleeding. heart disease such as angina pectoris, myo-
cardial infarction, etc. result in a compromised
Dental considerations: state of health that these patients require
i. The coagulation profile must be obtained special care during dental treatment proce-
for these patients before beginning dental dures.
procedure. These include assessment of the
Dental considerations:
bleeding time (BT), clotting time (CT),
prothrombin time (PT), activated partial i. As most dental procedures are stressful
thromboplastin time (aPTT), etc. and stress can precipitate cardiac disease,
it is important that adequate stress reduc-
ii. Adequate factor replacements such as
tion protocols be initiated before beginning
factor VII for hemophilia A, factor IX for
extensive dental treatment. Short morning
hemophilia B, etc. must be given and their
appointments are preferable and the
levels must be maintained during and after
patient may be pre medicated with anti-
the surgery to prevent excessive bleeding.
anxiety drugs such as diazepam 5 mg.
iii. Preventive dental care must be empha-
sized for these patients so that serious ii. It is advisable to check the patient’s blood
consequences of dental neglect that result pressure before any surgical procedure is
in the need for surgeries can be avoided. attempted. In patients who have suffered
iv. Endodontics is safer than exodontia. from myocardial infarction, dental treat-
ment may be postponed until complete
v. Nerve block anesthesia such as pterygo-
recovery has taken place, i.e. for a period
mandibular block, etc. must be avoided as
of 6 months after the attack.
these techniques are blind procedures and
can result in extensive bleeding into the iii. Many patients with cardiac disease take a
deeper planes of the tissues. Infiltration low dose of aspirin daily. As aspirin has
anesthesia may be given but with caution antiplatelet effects, it may result in
for they too can lead to extensive bleeding. prolonged bleeding after extractions or
However, lingual infiltrations must be other surgical procedures. Hence, it is
avoided as the bleeding may track down recommended that aspirin be stopped at
and posteriorly into the parapharyngeal least 7 days before the surgery with the
spaces causing air space compression and physicians consent. However, recent
respiratory distress. Intraligamentary studies indicate that patients may be
injections are safer in these patients. allowed to continue aspirin if the bleeding
vi. Surgical procedures must be carried out time and clotting time are within normal
with minimal trauma and antifibrinolytic limits.
drugs such as tranexamic acid can be used iv. Antihypertensive agents such as nifedi-
to arrest uncontrolled bleeding. pine can induce gingival hyperplasia.
v. Local anesthesia can be used safely. iii. Children between 5 and 10 years who are not
Adrenaline containing solutions may be allergic to penicillin: 500 mg amoxycillin
avoided as adrenaline being a vaso- 1 hour prior to the procedure.
constrictor can raise the blood pressure. iv. Children between 5 and 10 years who are
However, the low concentration of allergic to penicillin: 300 mg clindamycin
adrenaline (1:80000) that is used in LA 1 hour prior to the procedure.
solutions is considered safe, and advisable v. Children less than 5 years who are not allergic
as anesthetic effect is longer lasting, but to penicillin: 250 mg amoxycillin 1 hour
not more than 4 ml of such LA solution prior to the procedure.
must be used. It is more likely that the vi. Children less than 5 years who are allergic to
release of endogenous catecholamines penicillin: 150 mg clindamycin 1 hour prior
[associated with stress in HT patients] can to the procedure.
suddenly shoot up the blood pressure. Procedures such as radiography, routine
Patients on antihypertensive beta blockers, dental examination, endodontics (confined to
for example, propranolol—if these the apex), exfoliation of primary teeth, suture
patients are given adrenaline there will be removal, etc. do not require antibiotic coverage.
an un-opposed action of alpha receptors D—Diabetes
which leads to exaggerated vasoconstric- Diabetes is a condition in which there is
tion and will precipitate anginal attack. impaired carbohydrate metabolism caused by
vi. Emergency drugs including nifedipine, insulin resistance or deficiency. The common
isosorbitrate, etc. must be readily available symptoms of diabetes are polyphagia
while treating unstable hypertensive and (increased appetite), polyuria (increased
angina patients. urination) and polydipsia (increased thirst).
vii. Referral to the physician is an essential Diabetic patients are under antidiabetic
prerequisite for reassurance and also therapy and sometimes pose difficulty in
immediate hospital support if warranted. management. They may frequently slip into
hypoglycemic coma and fall unconscious
Rheumatic heart disease is another condi-
during treatment. Further as dental treatment
tion affecting the CVS that requires special
can impose restrictions on their dietary intake,
considerations. These patients require anti-
this may affect their glycemic balance that is
biotic prophylaxis prior to dental treatment
critically maintained by drug therapy.
procedures such as extraction, scaling, curett-
age or even deep periodontal probing and
placement of wedges or rubber dam. Bacte- i. Routine dental therapy can be carried out
remia caused due to these procedures can affect without any special considerations.
However, when major therapy or surgeries
the heart valves and result in subacute bacterial
such as even extractions are planned, the
endocarditis. Antibiotic prophylaxis is also
patient’s blood sugar level must be
required for patients with valvular heart disease
evaluated before beginning the treatment
or prosthetic heart valves. The recommended
as hyperglycemia may predispose to
antibiotic prophylaxis is as follows:
infection and delayed wound healing.
i. Adults who are not allergic to penicillin: 2 gm Changes in the vessel wall such as micro-
amoxycillin to be taken 1 hour before the angiopathy leading to luminal narrowing
procedure. also causes delayed wound healing. Treat-
ii. Adults who are allergic to penicillin: 600 mg ment is best carried out in the morning
clindamycin to be taken 1 hour before the after the patient has had his breakfast and
procedure. a regular dose of antidiabetic medicines.
ii. Infections must be treated aggressively everyday. Pigmentation of oral tissues

with suitable antibiotics as they may may also be seen in Addison’s disease.
precipitate ketosis. ii. Aspirin and other NSAID must be used
iii. Local anesthesia is safe and the low dose cautiously in patients receiving steroid
and concentration of adrenaline does not therapy as this can cause peptic ulcera-
seem to affect much. tions. Long-term steroid therapy can cause
immunosuppression. Lesions such as
iv. Diabetic patients may also present with
candidiasis, hairy leukoplakia, Kaposi’s
oral manifestations such as burning
sarcoma, etc. may then begin to appear.
mouth, multiple periodontal abscesses,
iii. During an event of acute adrenal insuffi-
aggressive periodontal disease, non-
ciency, the patient must be laid flat with
healing wound, candidiasis, etc. These
his legs raised and intravenous steroids
conditions must me recognized early and
(hydrocortisone 200 mg) along with
managed effectively. Antidiabetic drugs
electrolytes must be administered.
can cause oral side effects such as lichenoid
reaction or even xerostomia. iv. Hypothyroid patients may precipitate
myxedema when drugs such as opioids,
v. Emergency medicines such as iv dextrose, diazepam or GA are given to them. LA is
glucose, glucagon, etc. must be readily avai- safer in these patients.
lable to manage unexpected complications.
v. Similarly, pain, anxiety or trauma can pre-
cipitate thyroid crisis in hyperthyroidism
E—Endocrine Disorders
that is untreated.
The term endocrine disorders encompass
vi. Hyperparathyroidism may cause genera-
various diseases such as hyperthyroidism,
lized rarefaction of the jaw bone and
hypothyroidism, Addison’s disease, Cushing’s
occasionally cause giant cell lesions called
syndrome, etc. Although these conditions are
Brown’s tumor.
rare in practice, the clinicians must have a brief
knowledge of these conditions as they may
F—Fits and Faints
alter the dental treatment plan.
Epilepsy is a central nervous system disorder
Dental considerations: which causes episodic disturbances of
i. Patient’s with adrenal insufficiency consciousness and is often accompanied by
(Addison’s disease) often receive exo- seizures. Sometimes these patients may suffer
genous steroids for treatment. This further from prolonged uncontrolled seizures that are
suppresses the hypophyseal axis and referred to as status epilepticus.
inhibits the release of endogenous steroids
that is required during periods of stress.
This can precipitate hypotensive collapse i. Epileptic patients have a greater chance
during stressful dental procedures. Hence of injuring their tongue, lip or buccal
high doses of corticosteroids were advo- mucosa during the attacks. Occasionally,
cated in the past before and after dental they may also sustain dental or jaw
procedures or during events like trauma fractures.
or infection. However, according to the ii. Antiepileptic drugs such as phenytoin
recent literature, the patient’s steroid dose sodium can cause gingival enlargement,
may be increased prior to the treatment folate deficiency and hence aphthous
only if patient is taking more than 50 mg stomatitis. Sodium valproate can result in
of hydrocortisone (12.5 mg of prednisolone) increased bleeding tendencies.
iii. The clinician should be ready to manage absorbed from the intestine causing defi-
an emergency situation created by the ciency and consequent chances of bleeding.
onset of epileptic attack. All procedures Drug dosage must be reduced and hepato-
must be stopped immediately and the toxic drugs must be avoided in these
patient must be put in a lateral position patients. Patients with hepatitis B infec-
with a soft mouth gag inserted between tion have to be managed more cautiously
the teeth to prevent the tongue from being [universal precautions to prevent cross-
bitten. If the seizures do not stop, diazepam infection].
injections may be given intramuscularly iv. Patients with history of gastroesophageal
and medical help must be sought. reflux disease suffer from frequent regurgi-
tation of stomach acids that can lead to
G—Gastrointestinal Disorders
erosion of the lingual surfaces of their
Gastrointestinal disorders include an array of teeth.
diseases affecting any part of the system from
the mouth to the rectum. Of particular interest H—Hospitalization and Blood Transfusion
to the dentist are, however, common conditions Patients having a frequent history of hospitali-
such as peptic ulceration, liver disorders, etc. zation usually have some of the medical
Dental considerations: problems mentioned above. Causes of hospitali-
zation and medication must be ascertained
i. Drugs such as aspirin and other NSAIDs
and necessary precautions must be taken to
must be used cautiously in patients with
avoid complications. Similarly patients who
history of peptic ulcerations as they can
have received frequent blood transfusion may
aggravate the existing condition. Selective
run a high risk of contracting blood-borne
COX2 inhibitors like nimesulide, pofecoxib,
infections such as HIV or hepatitis B, etc. Also
etc. are less harmful to the gastric mucosa.
they may be suffering from conditions such
The patients must be instructed to have
as thalassemia or hemophilia for which they
the medications with a glass of milk or
have received many transfusions.
plenty of water. If required tablets of
ranitidine (150 mg BD) or omeprazole I—Infections
(20 mg BD) can be added to the patient’s Such as tuberculosis, HIV, hepatitis, etc. are
prescription. These drugs help to reduce highly communicable and the dentist must
the acidity in the stomach. Also use of take adequate precautions to protect himself
systemic steroids is contraindicated for from getting infected as well as spreading the
they too can inhibit prostaglandin synthe- disease to other patients visiting his clinic.
sis and thus aggravate peptic ulceration. Proper cross-infection control protocol and
ii. Use of broad-spectrum antibiotics such as aseptic precautions must be followed and
amoxycillin can lead to diarrhea as they instruments used for these patients must be
suppress the normal intestinal microflora. sterilized thoroughly before they are used for
Combinations with lactobacillus spores are the next patients. Also patients with HIV may
available which prevent such complications. have many oral manifestations which shall be
iii. Severe liver disease can inhibit the produc- discussed in the appropriate sections. The
tion of clotting factors and hence these dentist must also be immunized against
patients are at a greater risk of bleeding hepatitis B virus.
during or after dental surgeries. Patients
with hepatitis have reduced secretion of J—Jaundice
Bile so that fats are not emulsified and fat- Jaundice refers to the rise in the serum bili-
soluble vitamins such as vitamin K is not rubin level which in turn results in yellowish
discoloration of the sclera, skin and the mucous ii. Patients with severe uremia may present
membrane. Jaundice may be categorized into with oral ulceration due to uremic
three main types, i.e. hemolytic, infective and stomatitis.
obstructive jaundice. The liver functions are iii. Dental treatment for patients undergoing
affected in jaundice and the patients must be hemodialysis may be carried out on the
tested for blood levels of bilirubin, SGOT, next day after the dialysis when there is
SGPT, HbS antigen, etc. maximum benefit of the dialysis and the
Dental treatment procedures may be post- effect of heparin which is given during
poned until the patient completely recovers hemodialysis has also worn off.
and drug prescription should be kept at mini- iv. Patients who require dental extractions,
mum. Patients with advanced liver diseases scaling or periodontal surgeries must be
may exhibit a greater tendency of bleeding provided antibiotic prophylaxis as
after surgical procedures as vitamin K bacteremia can result in peritonitis in
absorption is low and coagulation factors patients undergoing peritoneal dialysis.
production which takes place in the liver is
affected. L—Lactation and Pregnancy
Patients who are HbsAg positive, i.e. with i. Dental treatment during pregnancy
hepatitis B infection are a potential source of requires special consideration. Pregnancy
cross-infection and need to be handled may predispose to gingivitis and localized
cautiously in addition to following the gingival enlargements called as pregnancy
universal precautions. All dental clinicians tumor.
including the paramedical staff should be ii. Injudicious prescription of drugs must be
vaccinated against the hepatitis B virus. avoided as there is a risk of fetal damage.
Tetracyclines must be avoided as they can
K—Kidney Disorders cause irreversible staining of teeth in the
Kidney disorders such as renal failure, child. Drugs such as thalidomide, aspirin,
nephrotic syndrome, etc. are commonly etc. must not be prescribed due to their
encountered in practice. Some of these patients teratogenic side effects.
may be receiving dialysis or may have even iii. Penicillins, erythromycin and paracetamol
undergone renal transplants. Many of these are safe during pregnancy, but drug
patients thus require modifications in their prescription should be kept to minimum
dental treatment plan. especially during the first trimester. Local
i. Nephrotoxic drugs such as tetracycline, anesthetic lignocaine is safe but must be
aminoglycosides must be avoided. Anti- used only when necessary.
biotics like cloxacillin, doxycycline, iv. Extensive dental treatment should be
metronidazole are safe and can be prescri- avoided during the first and last trimester.
bed in their usual doses. Ampicillin, The second trimester is comparatively safe
amoxicillin, benzylpenicillin, erythro- for treatment.
mycin are fairly safe, but their dosages v. Exposure to X-rays must be strictly
must be reduced in severe renal disease. avoided in the first trimester. If radio-
NSAIDs including aspirin are less safe and graphs are unavoidable during pregnancy,
their doses need to be reduced even in the patient must be adequately protected
patient’s with mild renal disease. Safer with a lead apron, as otherwise, X-rays are
analgesics include paracetamol and potentially dangerous to the fetus.
codeine. Lignocaine and diazepam are 10-day rule: The basis of this rule was
safe for use. to do X-ray examinations only during the
10 days following the onset of menstrua- such as aphthous stomatitis, MPDS, etc.
tion as ovulation and fertilization of the Stoppage of such habits plays a crucial role in
ovum is least likely during this period and the treatment of these conditions. Patients
hence no chances of radiation hazard to with the habit of bruxism and/or of clenching
the foetus. have increased chances of attrition of teeth and
Now it is understood that the organo- tenderness of masseter.
genesis starts 3–5 weeks after conception A history of exposure to commercial sex
and the focus is now shifted to missed workers or multiple partners may be asked in
period and possibility of pregnancy. certain cases where oral lesions associated
vi. If a pregnant patient develops syncope with sexually transmitted diseases such as
which is more common in the third tri- HIV, syphilis, etc. are suspected.
mester, the patient must not be put in a
head low position as this may result in 6. General Examination
compression of the inferior vena cava by General examination should include examina-
the gravid uterus thereby reducing venous tion of the patient’s general health and vital
return to the heart and consequent supine signs. ‘A good clinical examination begins
hypotensive failure. Instead the patient from the moment the patient enters the clinic.’
must be made to remain supine in the left The patient’s general body composition, built,
lateral position. gait, etc. must be observed as he walks into
vii. A lactating mother should be prescribed the clinic. While evaluating cases of trauma,
drugs with caution as some of the drugs it is imperative to assess the patient’s level of
can be transferred to the child through consciousness and orientation to space and
breast milk. time. Partial or complete loss of consciousness
after trauma may be sign of CNS involvement
4. Past Dental History and should immediately receive the attention
A brief record of the patient’s past dental visits of neurosurgeon. Vital statistics such as the
must be noted including the frequency of need patient’s blood pressure, pulse, etc. must be
for dental treatment, nature of any treatment recorded, particularly if the patient has any
received. Particular attention must be given medical history or signs of an underlying
to any untoward reactions that the patient may systemic disease.
have experienced such as drug allergy or any The exposed parts of the skin should be
complications such as excessive bleeding, etc. examined for any lesions, scars or pigmen-
so that such events can be safely avoided. The tation. Many oral lesions such as lichen planus,
information obtained can also provide an erythema multiforme, etc. may also show skin
insight towards the patient’s level of aware- involvement. Pigmentation of the skin may be
ness about dental procedures and expectations observed in lichen planus, Addison’s disease,
from the dentist. Peutz-Jegher’s syndrome, Albright’s syn-
5. Personal History drome, neurofibromatosis, etc. Occasionally,
sinus tract opening may be seen on the skin
Personal history includes information about
in chronic infections such as osteomyelitis,
habits such as paan, supari (areca nut), tobacco
chewing or smoking, clenching, bruxism, teeth tuberculosis, chronic periapical infection, etc.
cleaning habits, etc. Lesions such as leuko- Nails should be checked for pallor, clubbing
plakia, OSMF, oral squamous cell carcinoma or other deformities. Pallor of nails means
are found with higher frequency in people paleness or lack of the normal pink color of
with tobacco-related habits. Stress and anxiety the nails and could indicate anemia. Spoon-
may be a contributing factor for conditions shaped nails (koilonychias) and cracking of
nails may be also seen in anemia. Such must be checked thoroughly. Tender, firm
patient’s should be referred for suitable lymph nodes are usually seen in infections,
investigations such as complete blood count, while hard, fixed lymph nodes may be due to
hemoglobin level estimation, etc. Clubbing metastasis from malignant tumor. Multiple
indicates alteration in the shape of the nails. lymph nodes may be present in tuberculosis,
The nail bed swells up and the nails become lymphomas, HIV, etc. For examining the
convex. Clubbing may be of varying grades submandibular nodes, the operator must
and is seen in conditions such as alcoholic liver stand behind the patient. The patient is asked
disease, cardiac ailments, bronchiectasis, lung to look slightly downwards and the operator
abscess, etc. Grooving or ridging of nails may must palpate the nodes with the tip of his first
be a feature in lichen planus. two fingers placing them medial to the body
Conjunctiva which is the mucosal lining of of the mandible. Similarly the cervical group
the eyeball (bulbar conjunctiva) and the eyelid of lymph nodes must be palpated anterior and
(palpebral conjunctiva) should be examined posterior to the sternocleidomastoid muscle.
for ecchymosis, ulceration and pallor. The The common causes of lymphadenopathy
normal colour of the palpebral conjunctiva is include, dental infections, metastatic malig-
pink. Pallor of palpebral conjunctiva may be nancies, lymphomas, tuberculosis, etc.
sign of anemia. Ecchymosis of the conjunctiva The TMJ must be examined for any tender-
may indicate fracture of the zygoma or the ness, restricted mouth opening, deviation,
infraorbital bone. Ulcerations of the conjunc- clicking, etc. which indicate pathology. In
tiva may be noted in Stevens-Johnson order to check for tenderness and clicking, the
syndrome, herpes zoster, etc. Symblepharon operator must stand behind the patient and
refers to the fusion of the palpebral and bulbar place a finger over the joint bilaterally and
conjunctiva that is a complication of cicatricial instruct the patient to open and close the
pemphigoid. mouth. The joint may be auscultated with a
The sclera which is the white portion of the stethoscope to detect clicking sound which
eye should be examined for icterus, yellowish may indicate disc derangement. Suitable
discoloration that is seen in jaundice. Appro- investigations may be then ordered to confirm
priate investigations may be ordered and the diagnosis after clinical examination.
the patient must be sent to a physician for
complete evaluation if needed. 8. Intraoral Examination
Intraoral examination may be divided into soft
7. Extraoral Examination tissue and hard tissue examination.
Extraoral examination includes the examina- a. Soft tissue examination includes, checking
tion of the face, jaws, neck and the TMJ. the labial mucosa, buccal mucosa, hard and
Observe keenly for any swellings or facial soft palate, gingiva, tongue, pharyngeal
asymmetry. If a swelling is present, its loca- and tonsillar areas. Normal anatomical
tion, size, shape, margins must be inspected. variations such as Fordyce’s spots and linea
The swelling must be palpated to study its alba should not be mistaken for any
consistency, and presence of tenderness. pathology. The papillae on the tongue must
Presence of any ulcer or draining sinus tract be examined carefully depapillation of
must be noted. tongue may be noted in geographic tongue,
Lymph nodes must be palpated to study median rhomboid glossitis, anemia, OSMF,
their location, number, consistency and fixity etc. The gingiva should be examined to
to the underlying tissues. The submandibular, indentify the presence of inflammation,
submental and cervical group of lymph nodes enlargements or pocket formation. The
floor of the mouth should also be inspected 11. Final Diagnosis

carefully. If any growth or ulceration or Once the reports of the investigations are
white lesion is present, it must be thoroughly available, the case should be reviewed to
checked. Openings of Wharton’s duct in the correlate the clinical and investigatory
floor of mouth and of Stensen’s duct in findings to arrive at a final diagnosis. When a
cheek mucosa opposite the upper molars tumor or cyst is suspected, biopsy may be
should be checked for normal secretions, required to arrive at the final diagnosis.
inflammation, etc.
12. Treatment Plan
b. Hard tissue examination includes inspecting
the overall status of the patient’s dentition. Once a case has been diagnosed, the next
crucial step is to chalk out a treatment plan
The teeth should be examined for their total
for the patient. If the patient is suffering from
number, presence of any developmental
pain or has signs of infection, antibiotic and
anomalies, hypoplasia, caries, discolora-
anti-inflammatory drugs must be prescribed
tion, wasting diseases such as attrition,
as an emergency measure. Appropriate
abrasion, erosion and abfraction.
treatment must then be planned for the patient
after obtaining necessary consultation from
9. Examination of the Area
the other specialists. While treating patients
of Chief Complaint
who are medically compromised, the nece-
The area of chief complaint must be examined ssary precautions and treatment modification
in detail. Presence of any soft tissue swelling, must be incorporated in the treatment plan.
pus discharge, bony expansion must be noted.
The teeth in the area must be evaluated for TERMINOLOGIES USED IN CLINICAL
dental caries and periodontal disease. The EXAMINATION OF LESIONS
teeth may be gently percussed by tapping the Clinical examination is by far the most impor-
occlusal surface lightly with the blunt end of tant step in the Diagnostic sequence. It is
the probe. Pain elicited on percussion indicates essential to identify various lesions which can
tenderness which may be a sign of periapical be manifested clinically and further analyze
disease. The teeth should be checked for and correlate their significance.
abnormal mobility and vitality.
Terminologies
10. Provisional Diagnosis and Investigations • Lesion may be described as a visible change
After taking a good history and performing in the normal anatomical structure caused
the clinical examination, the clinician must by a pathological process.
• Primary lesion is the first pathological
arrive at a provisional diagnosis. Also the
change manifested clinically, e.g. vesicle in
possible differential diagnosis should be
herpes simplex.
charted so that appropriate investigations can
• Secondary lesion is the altered primary
be advised to the patient. Commonly advised lesion, e.g. ulceration caused by the rupture
investigations are an IOPA radiograph, of the vesicle in herpes simplex.
occlusal or extraoral radiographs, blood Lesions may be flat such as a macule, raised
investigations such as CBC, etc. Advanced such as vesicle or depressed such as an
investigations such as CT, MRI, scintigraphy ulcer.
may be required in certain cases. Tests which • Vesicle is a circumscribed elevated serous
are not likely to yield any diagnostic fluid filled blister not more than 1 cm in
information for that particular case must not diameter with a thin covering of epithelium,
be advised to the patient. e.g. HSV infection, herpes zoster (Fig. 1.1).
• Bullae are circumscribed elevated serous • Pustule is a circumscribed elevated lesion

fluid filled blister more than 1 cm in which is filled with purulent fluid or pus,
diameter. The epithelial covering may be e.g. chickenpox (Fig. 1.3).
thin if the lesion is intraepithelial as in • Papule is a circumscribed elevated solid
pemphigus and thick if the lesion is (not fluid filled) lesion less than 1 cm in
subepithelial as in cicatricial pemphigoid diameter, e.g. primary lesion of aphthous,
(Fig. 1.2). lichen planus (Fig. 1.4).
A B
Fig 1.1: Line diagram and picture of vesicle
A B
Fig. 1.2: Line diagram and picture of bullous lesion
Fig. 1.3: Pustule

A B
Fig. 1.4: Line diagram and picture of papules
A B
Fig. 1.5: Line diagram and picture of plaque
A B
Fig. 1.6: Line diagram and picture of macule
• Plaque is a slightly raised clearly demar- • Petechiae are pin head size (1–2 mm)
cated area of gray or white discoloration, discolored spots caused by extravasation of
surface of which may be smooth, cracked blood, e.g. scurvy, thrombocytopenic
or fissured, e.g. leukoplakia, plaque type of
purpura (Fig. 1.7).
lichen planus (Fig. 1.5).
• Macule is a circumscribed flat (nonraised) • Ecchymoses refer to larger areas of dis-
area of altered coloration varying in size coloration caused by extravasation of
from a pin head to several cms, e.g. ephelis blood, e.g. subconjunctival ecchymoses in
(freckles) (Fig. 1.6). zygomatic arch fracture (Fig. 1.8).
Fig. 1.7: Petechial spots on the palate Fig. 1.8: Subconjunctival and periorbital ecchymosis
A B
Fig. 1.9: Line diagram and picture of erosive lesion (lichen planus)
A B
Fig. 1.10: Line diagram and picture of ulcer
• Erosion is a shallow defect in the mucosa tissue, e.g. tuberculous ulcer, aphthous ulcer
representing a loss of epithelial coverage, (Fig. 1.10).
e.g. erosive lichen planus (Fig. 1.9). • Wound is a breach in the continuity of skin
• Ulcer is a breach in the continuity of the skin or mucous membrane caused by trauma.
or mucous membrane caused by pathological • Nodule is a well-circumscribed condensa-
processes resulting in molecular death of tion of tissue that may project from the
surface as a polyp. It may be present in the

epidermis or dermis, e.g. small fibroma,
irritational fibroma (Fig. 1.11).
Suggested Reading
1. Burket’s Oral Medicine 9th, 10th and 11th
editions.
2. Medical problems in Dentistry, Scully and
Cawson.
3. Oral and Maxillofacial Pathology, by
Neville, 3rd edition.
4. Shafer’s Textbook of Oral Pathology, 6th
Fig. 1.11: An example of nodule—fibroma edition.
2
Ulcerative and Vesiculobullous Lesions
Ulcerative and vesiculobullous lesions are by • Patients with chronic multiple lesions:
far the most commonly manifested oral 1. Pemphigus vulgaris
mucosal lesions. It is very important to 2. Pemphigus vegetans:
differentially diagnose these lesions which i. Newman
closely resemble each other as the treatment ii. Hallopeau
for these lesions will be different and at times 3. Bullous pemphigoid
wrong diagnosis and treatment can lead to un-
4. Cicatricial pemphigoid
desirable consequences.
5. Erosive and bullous lichen planus
Whenever a patient presents with ulcerative
lesion as a routine 3 questions are asked: • Patients with single ulcers:
1. How many lesions are present—single/ 1. Trauma
multiple? 2. Tuberculosis
2. How long are these lesions present—acute/ 3. Malignancy
chronic? 4. Histoplasmosis
3. Has the patient suffered from similar 5. Blastomycosis
lesions in the past, i.e. history of recurrence? 6. Mucormycosis
Depending on the answers received, the 7. Chronic HSV infection
patients are classified as follows:
• Patients with acute multiple lesions: ACUTE MULTIPLE ULCERS
1. Acute viral stomatitis (HSV, Coxsackie, Herpes Simplex Virus (HSV)
VZV)
Nine types of HSV have been reported to be
2. Erythema multiforme—Stevens-Johnson
pathogenic in human beings—HSV1, HSV 2,
syndrome, TEN
VZV, EBV, CMV, HHV6, HHV7, HHV8,
3. Allergic stomatitis
Simian herpes virus B.
4. Ulcers secondary to cancer chemo-
therapy treatment Primary Herpetic Gingivostomatitis
5. ANUG Clinical Features
• Patients with recurring oral ulcers: 1. Age—6 months to 6 yrs (as till 6 months
1. Recurrent aphthous stomatitis (RAS) maternal antibodies are present)
2. Behçet’s disease, Reiter’s syndrome 2. Adult form also exists. Incubation period—
3. RHL and RIOH 5 to 7 days (2–12 days)
17
Type of virus 5. Each ulcer is surrounded by an inflamma-

HSV 1 Stomatitis, pharyngitis,
tory halo and is slightly raised. At margins
meningitis, encephalitis and of the ulcer ‘tissue tags’ are seen as a
dermatitis (above the waist) result of rupture of the vesicle. The appea-
HSV 2 Genital infection may be rance of the ulcer has been described as
transmitted from mother to ‘moon crater’ (Fig. 2.1).
newborn infant or may be 6. There is generalized acute marginal gingi-
of close personal contact vitis and the color of gingiva is dark red.
(venereal origin)
Several small gingival ulcers often present
HSV 1 and HSV 2 Carcinoma cervix with inflammation and edema of the entire
HSV Bell’s palsy gingiva.
HHV 6 HHV 6—infects T lymphocytes 7. Herpetic involvement of the tongue shows
and is considered a possible
multiple vesicles and ulcers on the dorsal
factor in HIV infection
surface and has been described as geometric
HHV 6A—Causes Roseola
infantum (exanthema subitum),
glossitis by Neville (Fig. 2.2).
manifested as fever and rash 8. Lymphadenopathy (submandibular and
(mononucleosis like syndrome) cervical) and pharyngitis present. Primary
HHV 6B—immunocompro- HSV may have labial and facial skin lesions
mised patient, interstitial without intraoral lesions.
pneumonitis and bone 9. It is considered important to differentiate
marrow suppression herpetic lesions from those of erythema
HHV 7 Found in saliva, no disease multiforme as these lesions resemble each
HHV 8 Kaposi’s sarcoma in HIV other and corticosteroids which are consi-
patients, lymphoma and dered drug of choice in EM is contra-
Castleman’s disease indicated in primary HSV. In HSV infection,
the ulcerative lesions are small, round,
3. To begin with there are prodromal
symptoms—headache, bodyache, nausea, symmetrical and shallow and those of
vomiting, malaise. After 1–2 days, multiple erythema multiforme are large, irregular,
vesicles appear within the oral cavity. They deep and bleeding. The vesicles and
resemble ‘drops of dew’. consequently the ulcers in HSV are intra-
4. These vesicles (circular, dome-shaped, epithelial, i.e. superficial and in EM the
2–3 mm) rupture immediately giving rise to vesicles and consequently the ulcers are
small shallow discrete round ulcers. These deeper and involve subepithelial capillaries
may coalesce to form a large ulcer. They are leading to bleeding and crustations.
sharply defined, shallow with yellowish Corticosteroids are contraindicated in viral
grey floor and red margin. infections as they suppress antibody
A B C
Fig. 2.1: Multiple vesicles and ulcerations in primary HSV infection

Ulcerative and Vesiculobullous Lesions 19
A B
Fig. 2.2: Primary HSV infection—geometric glossitis and palatal lesions
formation and there is always a danger of serum is diagnostic in primary. HSV

viral infections spreading rapidly when the isolation can be done on chorioallantoid
immune reaction is suppressed. Currently membrane of chick embryo or kidney of
HSV associated erythema multiforme cases rabbit.
have been reported and in such cases 4. Antibody titre is raised. To differentiate
suppression of erythema multiforme can be between recurrent and primary attack,
achieved with the help of acyclovir and acute and convalescent serum is collected.
steroids will be contraindicated in such In primary attack, only the convalescent
cases. serum shows raised titre, as during the
Diagnosis active stage antibodies are not formed. In
the recurrent attack, both the active and
1. Clinical picture—classically a young patient convalescent serums show raised titre, as
presenting with H/o fever, malaise the defense mechanism has been previously
multiple vesicles, acute marginal gingivitis exposed to the virus and produces large
and lymphadenopathy gives a clue. number of antibodies.
• Cytologic smear from the base of freshly
opened vesicle stained with Giemsa stain Differential Diagnosis
(also Wright and Papanicolau’s stain) Other conditions presenting as acute multiple
shows multinucleated giant cells or ulcers are included in the d/d. The ulcers
intranuclear inclusion bodies (Lipschultz
associated with primary HSV are seen in
bodies) with ballooning degeneration
younger patients and are small round
of nuclei and syncytium formation.
symmetrical and shallow with associated
(Syncytium—multinucleated proto-
marginal gingivitis and H/o prodromal
plasmic aggregation of cells without
symptoms.
apparent cell outlines). Ballooning
degeneration is absent in RAS, EM and 1. ANUG older patients, punched out necrotic
allergic stomatitis. ulcers on interdental papilla and marginal
2. Fluorescent staining of cytological smear. gingiva, tender submandibular lymph
3. Conclusive evidence of primary HSV nodes and H/o fever.
includes testing for complement fixing or 2. Erythema multiforme older patients with
neutralizing antibody in acute and convale- allergic background, acute explosive onset
scent sera—4 fold increase in convalescent with no H/o prodromal symptoms and
fever and no lymph nodes, bloody crusta- Coxsackie B4 virus is believed to cause
tions present on the lips, marginal gingivitis aseptic meningitis and encephalitis and has a
absent. role to play in the pathogenesis of IDDM and
3. Herpangina occurs in epidemics and pre- primary Sjögren’s syndrome.
sents milder symptoms, smaller lesions
involving posterior part of oral cavity, no Herpangina
gingivitis. Patient gives history of fever with rigors,
4. Varicella zoster unilateral distribution of anorexia, followed by dysphagia and sore
multiple vesicles/ulcers, lesions abruptly throat.
stop at midline, severe pain, symptoms of Intraoral examination shows multiple small
pre- and post-herpetic neuralgia. vesicular eruptions in the posterior half of oral
cavity.
Treatment
June to October: Increased incidence
1. Primary HSV in otherwise healthy children
Incubation period: 2–10 days
is self-limiting. Lesions heal in 7–10 days.
Age: 3–10 yrs but not uncommon in adole-
2. Tab. Acyclovir 200 mg five times a day
scents and adults.
(inhibits viral replication in HSV infected
cells without any effect on normal cells), Lesions start as punctate macules, which
IUDR—idoxuridine, cytosine arabinoside, quickly change to papules and vesicles
adinide arabinoside. These are antivirals involving posterior pharynx, tonsils, faucial
and known to cause hepatotoxicity and pillars and soft palate. Vesicles rupture within
renal toxicity. 24–48 hrs to form 1–2 mm ulcers (Fig. 2.3). The
disease is mild and heals without treatment
3. Corticosteroids contraindicated.
in one week.
4. Antibiotics given to prevent secondary
Treatment: Control of fever and mouth pain,
infection.
isolation. Effective antiviral agent against
5. Dyclonine hydrochloride 0.5% and Benadryl Coxsackie virus is not available.
with milk of magnesia—topical rinse before It is self-limiting. Treatment is just
meal. supportive—analgesics, anesthetic mouth-
6. Paracetamol for fever (avoid aspirin wash and lots of fluids.
because of possibility of Reye’s syndrome).
7. Fluids to maintain hydration and electrolyte
balance.
COXSACKIE VIRUS INFECTION

It is named after town in New York where the
virus was found. It is an RNA enterovirus and
can cause:
i. Herpangina (Coxsackie A4),
ii. Hand, foot and mouth disease,
iii. Acute lymphonodular pharyngitis and
mumps-like parotitis (rare). Fig. 2.3: Multiple vesicles on soft palate—herpangina
HSV Herpangina
Does not occur in epi- Occurs in epidemics
demics
Affects anterior part of Affects posterior part of
the oral cavity the oral cavity—pharynx,
tonsil, soft palate, faucial
area
Generalized marginal Absent
gingivitis is present
Lesions are larger in Lesions are smaller in
size, i.e. vesicles and size
ulcers
May not be self-limiting Self-limiting
Shows ballooning de- Giemsa stain does not
generation of nucleus show ballooning degenera-
tion of the nucleus
Caused by herpes virus Caused by Coxsackie Fig. 2.4: Lymphonodular pharyngitis
virus
Treatment: Self-limiting Treatment: Effective anti- 4. Histologically lesions are composed of
disease viral against Coxsackie densely packed lymphocytes.
virus not available 5. Disease is self-limiting and patient recovers
after 1–2 weeks.
Hand, Foot and Mouth Disease
6. Treatment is symptomatic.
Coxsackie A16
1. Fever, non-pruritic rashes of papular and VARICELLA ZOSTER VIRUS (VZV)
vesicular type on hands and feet.
2. Oral lesions are more extensive than VZV is a DNA virus and the infection is
herpangina. first manifested as chickenpox, which is an
3. Patient has fever and stomatitis. exanthematous fever [term exanthematous
4. Treatment same as herpangina when implies skin eruptions] commonly seen in
patients present with an acute stomatitis children.
and fever. After an attack of chickenpox, the VZV
5. Because of more frequent oral involvement, which has an affinity for the nervous tissue
dentists are more likely to see patients with remains latent in the dorsal root ganglion of
this disease than herpangina and they spinal nerves and extramedullary ganglion of
should remember to check hands and feet
cranial nerves V1, C3, T5, L1, L2 are the nerves
for macules and vesicles.
commonly affected by VZV. Herpes zoster
Acute Lymphonodular Pharyngitis affecting the spinal nerves is called as
‘Shingles’ meaning ‘belt like’ because of its
Coxsackie A10
distribution. V1 15–20 times more common
1. Common in children. than V2 and V3.
2. History of fever, anorexia, sore throat,
V1 (ophthalmic division of trigeminal
lymphadenopathy.
nerve) lesions appear on upper eyelid, fore-
3. Raised yellowish white nodules on an
head, and scalp.
erythematous base (do not progress to
vesicles and ulcers) are seen on posterior V2 (maxillary division) lesions appear on
wall of pharynx (Fig. 2.4). midface, upper lip and palate (Fig. 2.5).
HZ infection may be deep seated and get

disseminated causing pneumonia, meningo-
encephalitis and hepatitis.
Clinical Features
1. Prodromal phase—shooting pain, pares-
thesia, burning and tenderness along the
course of nerve. Lasts for 2–4 days.
2. Unilateral multiple vesicles appear on an
erythematous base showing single
dermatome involvement. [Some lesions
spread by viremia and may appear
beyond dermatome.]
Fig. 2.5: Herpes zoster involving the maxillary division 3. Vesicles weep serum, scab and heal within
of trigeminal nerve 2–4 weeks.
V3 (mandibular division) lesions appear on 4. Intraoral lesions are seen as unilaterally
lower face, lower lip, mandibular gingiva and distributed multiple ulcerative lesions
tongue (Fig. 2.6). which are extremely painful. Cases of
The VZV can be reactivated in some indivi- severe odontalgia, exfoliation of teeth and
duals causing lesions of localized herpes osteonecrosis have been reported.
zoster, pathogenesis of which is similar to RHL. 5. Herpes zoster of geniculate ganglion is
Patients with HIV infection, leukemia, known as Ramsay Hunt syndrome. It is
lymphoma and on immunosuppressant drugs rare and causes Bell’s palsy, unilateral
and cancer chemotherapy are more suscep- vesicles of external ear and intraorally on
tible to severe form of herpes zoster. palate, uvula and anterior tongue.
A B
Fig. 2.6: Herpes zoster involving mandibular division of trigeminal nerve

6. Healing of HZ lesions occurs with scarring ii. Fluorescent antibody stained smears using
and depigmentation of the skin. fluorescein conjugated monoclonal anti-
Serious and occasional side effect in bodies is more reliable.
ophthalmic division involvement—acute iii. Antibody titre rarely necessary except in
retinal necrosis, corneal scarring leading cases of herpes sine eruption.
to blindness in the affected eye. It is impor-
Treatment
tant to refer the patient to ophthalmologist
as soon as HZ lesions of V1 is spotted. Adequate and timely treatment [ideally within
7. After healing of ulcers, patients may suffer 72 hours of onset of disease] is essential to
from the agonising complication of post- reduce the pain, duration of lesions and
herpetic neuralgia, which is due to avoiding the postherpetic neuralgia in older
inflammation and fibrosis of the affected patients and preventing dissemination in
nerve. This condition is severe in old age, immunocompromised patients.
immunocompromised patients and can 1. Acyclovir—decreases pain, accelerates
involve motor nerves also. healing, minimizes ocular complication of
8. HZ can be associated with dental ano- corneal scarring and blindness. Dose is
malies, scarring of facial skin if HZ occurs 800 mg 5 times a day for 7 days (400 mg
in formative years. It can lead to pulpal three times a day for HSV).
necrosis and internal root resorption. 2. Valacyclovir—1000 mg tds, famiclovir-
9. Diagnosis is difficult during prodromal 500 mg tds for 7 days is effective in treat-
stage when pain is present without lesions. ment of HZ and should be started within
Unnecessary surgeries have been reportedly 72 hours of onset of disease. These drugs
done with mistaken diagnosis of acute also reduce the incidence of postherpetic
appendicitis, cholecystitis, pulpitis, etc. neuralgia when compared to acyclovir.
10. Herpes sine herpes: Zoster sine eruption— 3. In the past, corticosteroids [tab prednisolone,
[sine = without] peculiar condition diffi- 40–60 mg for 1–2 weeks] were prescribed
cult to diagnose because patients present to prevent postherpetic neuralgia in older
with severe unilateral burning pain individuals, however, presently it is consi-
without clinically visible lesions. Should dered controversial.
be considered in the differential diagnosis 4. Treatment of postherpetic neuralgia:
of orofacial pain.
1. Carbamazepine
Besides the clinical symptom of severe pain
2. Dilantin
only evidence is the increased antibody
titre. 3. Gabapentin 300–1200 mg and lidocaine
11. Of special importance is the fact that 1st patch
division trigeminal zoster may involve 4. Tricyclic antidepressants and opioid
nasociliary branches resulting in herpetic analgesics
keratitis and ciliary ganglion involvement 5. Steroid injection
may cause an Argyll Robertson pupil. 6. Alcohol block—sympathetic nerve block
[Prabhu Daftary]
7. Topical capsaicin (hot pepper) depletes the
Lab Findings substance P formed in the nerve endings
i. Multinucleated giant cells with ballooning 8. Live attenuated vaccine—decreases the
degeneration of nucleus, intranuclear severity of post herpetic neuralgia
eosinophilic inclusion bodies, virus 9. Chemical/surgical neurolysis may be
isolation. necessary in refractory cases.
Chickenpox Large atypical lymphocytes 20–80% of

a. Mild systemic symptoms. differential WBC count with pseudopodia that
project from the cell outline in 3–4 directions.
b. Generalized intensely pruritic eruption of
maculopapular lesions that rapidly develop Mono-spot test—detects the heterophile
antibody if the test is positive, it is most likely
into vesicles on an erythematous base.
that the patient is suffering from infectious
c. The vesicles turn cloudy and pustular. They mononucleosis, however, false positive test is
burst and scar. The crusts then fall off after seen in hepatitis, SLE and other conditions.
1–2 weeks.
Treatment
d. Lesions are present on trunk and face and
spread centrifugally. Oral lesions are ulcers. It is self-limiting
1. Alpha-interferon—reduces EBV replication
Infectious mononucleosis: Caused by epstein
and shedding in organ transplant
barr virus which may be transmitted due to
2. Acyclovir
close personal contact, direct salivary transfer
3. Ganciclovir
during intimate oral kissing hence also known
as kissing disease. Incubation period is 33–49 Cytomegalovirus (CMV)
days. CMV infection mostly in immunocompro-
mised patients causes infectious mononucleosis-
Clinical Features like symptoms. Unlike the more common EBV
i. Fever, fatigue, malaise sometimes morbili- associated infectious mononucleosis, there is
form rash. fever but little lymphadenopathy or spleno-
ii. Some cases have circumscribed mucosal megaly. In these (AIDS) patients, there is CMV
petechiae symmetrically distributed at the retinitis and blindness, if untreated. CMV
junction of hard and soft palate seen enteritis, perianal and perigenital involvement
between 5th and 17th day of sickness. are seen.
Ulcerative lesions may also be seen— Oral Manifestations
could represent immune induced reaction
In immunocompromised patients—single
to virus rather than direct effect of viral
large necrotic ulcer seen, less often multiple
infection.
ulcers which are painful and lasting for weeks
iii. Sore throat, enlarged tonsils with copious or months are also seen. Patients of CMV
amount of cheesy yellow exudates filling and VZV infection have occasional reports
the tonsillar crypts, cervical lymphadeno- of mandibular osteomyelitis and tooth
pathy also evident, hence called glandular exfoliation. Both viruses are associated with
fever. vasculopathy and thrombosis which may be
iv. Hepatosplenomegaly. the underlying pathogenesis.
v. Transient atypical lymphocytosis. CMV has feature of latency within connec-
tive tissue cells such as endothelium and
Clinical diagnosis is difficult. within endothelial cells, it contributes to
Lab Diagnosis vascular inflammation, vascular occlusion and
end organ damage.
Positive Paul-Bunnell reaction which detects
the heterophile antibody that agglutinates Laboratory Tests
sheep RBC. The test is also positive in • Systemic infection identified by blood
leukemia, serum sickness and reticulosis. culture by using shell vials of cultured cells
Therefore, Paul-Bunnell-Davidson test is more in which CMV antigens are detected
specific. through the use of monoclonal antibodies.
• DNA hybrid capture. acyclovir prevented recurrent EM in HSV

• Biopsy for microscopic examination and/or positive patients
to obtain for tissue culture. CMV produces 5. BT, MT, leiomyoma of stomach, ovary
large intranuclear inclusions within endo- 6. Crohn’s disease, sarcoidosis, histoplasmosis
thelial cells and monocytes within CT with and infectious mononucleosis
associated nonspecific inflammation. 7. Radiotherapy
Management 8. Idiopathic—unknown etiology
9. Stress or emotional factors.
Topical anesthetics and systemic analgesics for
pain control. Clinical Features
Antiviral agents ganciclovir, valganciclovir 1. Acute explosive onset, i.e. no prodromal
(tenfold bioavailability of ganciclovir), symptoms (unless associated with viral
cidofovir. respiratory tract infection in which case
fever, sore throat, rhinorrhea, malaise will
Erythema Multiforme
be the prodromal symptoms)
Erythema multiforme—is a hypersensitivity 2. Adults (between 20 and 40 years age) and
reaction. It is an acute self-limiting disease of children are usually affected and commonly
unknown etiology affecting skin and mucous give history of drug or food allergy.
membrane. As the name “multiforme” suggests 3. In EM simplex which is the least severe
the lesions present multiple forms, viz. form, symmetric maculopapular rash 0.5
macules, papules, vesicles, etc. to 2 cm in diameter is seen on the skin.
Various clinical types have been recognized: Skin and mucous membrane involvement
1. Simplex is seen in severe form.
2. Severe form: (a) Stevens-Johnson syndrome, 4. Skin lesions appear classically on hands,
(b) TEN (toxic epidermal necrolysis/Lyell feet, extensor surfaces of elbows and
disease) knees, face and neck rarely involved.
The lesions are nonspecific and can occur
3. Also rare chronic form
as macules, papules or vesicles with
4. Herpes associated erythema multiforme. petechiae in the centre of the lesion. These
Etiology/Predisposing Factors lesions spread centripetally towards the
trunk in a symmetric distribution
1. Drugs allergy: Sulpha drugs, trimethoprim,
phenobarbitone, nitrofurantoin 5. Typical skin lesions has been described as
iris, target or bulls eye lesions characterized
Food allergy: Benzoic acid, food preserva-
by central bulla/blister with concentric
tives
rings of erythema and are considered
2. Deposition of immune complex-IgM C3: pathognomonic for EM (Fig. 2.7).
Deposition of immune complexes in super- 6. Oral lesions appear in anterior part of
ficial microvasculature of skin and mucosa mouth, especially vermilion border of lips,
can be considered as a cause tongue, buccal mucosa, labial mucosa.
3. Cell-mediated immunity/vaccination 7. Formation of bullae and vesicles which
4. Micro-organisms: Mycoplasma pneumoniae, rupture and coalesce to form ulcers
HSV characterised by deep, irregular bleeding
Association between HSV and EM has been lesions. Typical presentation is bloody
reported, as cases once thought to be idio- crustations on the lips. Tissue tags present
pathic are infact cell-mediated immunologic peripheral to the ulcers (Fig. 2.8).
reaction to HSV infection and prophylactic 8. Increased salivation (may be blood-tinged).
A B
Fig. 2.7: Erythema multiforme—lip lesions and target lesions on the palms
A B
Fig. 2.8: Erythema multiforme showing bloody crustations on lip and ulcerations on tongue
9. Gingiva rarely affected. involvement of lungs, liver or kidneys.

10. Stevens-Johnson syndrome [SJS]—Severe Patients are best managed in burn centers
form of EM affecting skin, oral mucous where necrotic skin is removed and
membrane, eyes (keratoconjunctivitis, healing takes place under sheets of porcine
corneal ulcerations) (Fig. 2.9), genitalia xenografts.
(balanitis, urethritis, vaginitis). In the 12. Recent concept: SJS is less severe form of
severe form, Nikolsky’s sign may be TEN and both are separate from EM. Skin
positive. This condition, if untreated, may lesions of SJS and TEN are more severe
lead to infection, electrolyte imbalance and and arise on chest, called atypical targets
death. (erythematous, purpuric macules). SJS
11. TEN is the most severe form of EM, associated with drug allergy and myco-
secondary to drug reaction, it results in plasma and EM with HSV infection.
sloughing of skin and mucosa in large Diagnosis is based on—history, clinical
sheets. Death may be due to secondary characteristics, histopathology and biopsy of
infection; fluid, electrolyte imbalance or intact bulla.
A B
Fig. 2.9: Stevens-Johnson syndrome
Histopathology: Shows intraepithelial lesions Treatment

which may form subepithelial lesions, 1. In severe cases, it is best to hospitalize the
liquefactive degeneration of upper layers of patient to maintain electrolyte balance and
epithelium, thinning or absence of basement to prevent secondary infection. Drug of
membrane and inflammation of coreum. It is choice is corticosteroids (prednisonolone—
not specific. 30–50 mg, metamethasone or dexametha-
sone—2–5 mg more potent) which is given
D/D in tapering dose.
1. Allergic stomatitis: Difficult to differentiate, 2. Topical steroids in orabase—Betamethasone
erythema, vesiculations, ulcerations with a with neomycin, fluocinolone N, triamcino-
positive history of allergy helps, however, lone acetonide.
both these conditions are similar patho-
3. Cases suspected to be HSV associated are
logically and clinically.
treated with 400 mg acyclovir bid which
2. HSV: Primary HSV with prodromal prevents the development of EM.
symptoms, small round symmetrical
4. For non-HSV related EM—Azathioprine
shallow ulcers as opposed to EM with acute
(100–150 mg/day), Dapsone (100–150 mg/
explosive onset and large irregular deep
day), antimalarials are partially successful
bleeding ulcers. HSV associated with
in preventing recurrent outbreaks.
marginal gingivitis, lymphadenopathy
which is not seen in EM. 5. Local anesthetic mouthwashes prior to
3. Herpes zoster: Unilateral distribution is meals as lesions are painful.
pathognomonic of HZ with the lesions 6. Local as well as systemic effect by use of
abruptly stopping in the midline, severe 0.5 mg tab Betamethasone (tab Betnesol) –
pain, EM bloody crustations on both the crush the tablet + water and hold in mouth
sides of the lip. for 5–10 mins swish and swallow. This
4. Herpangina: Lymphadenopathy, lesions regimen lasting 20 days includes giving
affecting posterior part of oral cavity. Betamethasone 0.5 mg 1 tab 4 times a day
5. Pemphigus vulgaris: Patient gives history of for 5 days
chronic lesions (H/o 2–3 months), EM is of 3 times a day for next 5 days
acute duration, i.e. very short duration 2 times a day for next 5 days
history of few days. Once a day for next 5 days
In patients with diabetes or acidity or peptic

ulcer, systemic steroids are contraindicated
and patients can be asked to Swish and Spit
the medication.
7. Treatment: In severe cases, high dose of
steroid, I.V. immunoglobulins and thalido-
mide are given.
Allergy is antibody–antigen reaction in
which mast cells release histamine, bradykinin
and SRSA.
Anaphylaxis a patient previously exposed to
a drug or other antigen has antibody
(primarily IgE), fixed to basophils and mast
cells. When the antigen in the form of a drug,
food or air borne substance is re-introduced
into the body it will react with the fixed
antibody, bind complement and open mast
cell releasing active mediators such as
histamine and slow reacting substance of Fig. 2.10: Patient presenting with diffuse erythema
anaphylaxis (SRSA). These substances cause and vesiculations after self-medication with indigenous
preparation
vasodilation, increased capillary permeability,
emigration of leukocytes in the tissues. All as a white lesion and ulcer it is more likely to
these lead to edema. Constriction of bronchial be lichenoid reaction. Separation of these
smooth muscles also may result when IgE is entities leads to confusion.
bound in pulmonary region. Anaphylactic reac-
Causes: Penicillin, barbiturates, phenyl
tion can be localized (angioneurotic edema,
butazone, analgesics.
urticaria) or generalized (anaphylactic shock).
Characterized by edema along with vesicle
Allergy is of two basic types: Immediate
formation and ulceration. Oral vesicles and
reaction and delayed hypersensitivity.
ulcers of allergic etiology that should be
Immediate reaction:
distinguished from EM or lichenplanus are
1. Anaphylaxis (generalised) fixed drug eruptions and contact allergy.
2. Angioneurotic edema Contact allergy: On skin is dermatitis
3. Serum sickness venenata and that on oral mucous membrane
Delayed hypersensitivity: is stomatitis venenata. Here due to contact,
1. Allergic stomatitis there is antigen—antibody reaction. It can be
2. Fixed drug eruption due to contact with leather, nickel-chrome,
3. Contact allergy—stomatitis venenata, cosmetics and synthetic material.
dermatitis In mouth, amalgam restoration (due to
Delayed hypersensitivity reaction: Antigen release of mercury), chrome cobalt, gold
antibody reaction caused by systemic intake crowns, denture base, acrylic dentures (due to
of any allergen is called as stomatitis release of free monomer), toothpastes, chewing
medicamentosa. This term should be gums, lipstick can cause contact allergy.
discarded. Lesions when present as erythema, Another oral manifestation of contact
ulcers, vesicles and edema it is more likely to allergy is plasma cell gingivitis which is
be EM (Fig. 2.10) while lesions when present characterized by generalized erythematous,
edematous attached gingiva occasionally

accompanied by cheilitis and glossitis.
Histopathology shows sheets of plasma cells
that replace normal connective tissue.
Causes for the relative infrequency of
A
contact allergy of oral mucosa:
a. Relatively low number of Langerhans cell.
b. Saliva dilutes antigen and physically
washes them away. Increased vascularity
of the oral mucosa (compared to skin)
allows rapid removal of potential antigens. B
c. Lesser keratin than skin thus decreases the
possibility of hapten formation. Fig. 2.11: Patch test
Fixed Drug Eruption Diagnosis: For contact allergy—patch test

1. Definition: Characterized by localized area (Fig. 2.11). The suspected allergen is taped to
of involvement due to intake of allergen, the relatively non hairy skin of the back or the
presenting with erythema, edema and forearm and left for 48 hrs, the patch is removed
vesicle formation. and the area is examined for persistent
2. Clinical features: Multiple vesicles which erythema (test positive).
may rupture and form ulcers and further Localized anaphylaxis: When a localized
coalesce to form large ulcers. Its chara- reaction involving superficial blood vessels
cteristic is the acute nature, recurrence of results in urticarial (hives).
similar lesion at the same fixed location Urticaria begins with pruritis in the area of
after contact with the same allergen (hence release of histamine and other active sub-
called fixed drug eruption). stances. Wheal appears as an area of localized
edema over an erythematous base. Lesions can
3. Diagnosis: History to identify allergen.
occur on skin or mucous membrane.
Family history of allergy/asthma. Previous
Angioneurotic edema: When the blood vessels
history of similar lesion. History of allergy
deeper in the connective tissue are attacked,
to food, drugs. Systemic administration of
large diffuse area of subcutaneous swelling
any drugs. Change in cosmetics or dental
under normal overlying skin (Fig. 2.12).
treatment.
Swelling around eyes.
4. Treatment: Identifying and removing
the allergen. Antihistaminics like tab Avil
(25–50 mg), Incidal, Cosavil, Benadryl
(50 mg – 4 times). In severe cases 0.2 ml s.c.
epinephrine 1:1000 dilution
Corticosteroids: 5–10 mg of prednisolone or
1–2 mg of betamethasone (in local or
systemic form, given in tapering dose).
Increased fluid intake.
Local anesthetic mouthwash—xylocaine
viscous mouthwash, diclonine hydro- Fig. 2.12: Angioneurotic edema showing diffuse
chloride (half an hour before meals). swelling of lower lip
It can be idiopathic or after contact with it can lead to fatal cardiac arrhythmias.
the allergen. It can also be classified as— Inhalation of sympathomimetics. Oxygen
hereditary, non-hereditary, or allergic. to prevent or manage hypoxia.
Angioedema of larynx and posterior tongue 2. For laryngeal edema: Establish airway by
causes asphyxia which can be life-threatening. endotracheal intubation. Cricothyroido-
There is respiratory distress. tomy may be necessary.
Generalized anaphylaxis: Ulcers Secondary to Chemotherapy
• Allergic emergency
Cancer chemotherapeutic drugs are classified
• No time to call a consultant into 4 groups:
• Mechanism—reaction of IgE antibodies 1. Alkylating agents: Cyclophosphamide,
with an allergen to cause release of Chlorambucil
histamine, bradykinin and SRSA. These 2. Alkaloids: Vincristine, Vinblastine
chemical mediators cause contraction of
3. Antibiotics: Adriamycin, Actinomycin D,
smooth muscles of respiratory and
Bleomycin
intestinal tract as well as increased
4. Antimetabolites: 6 Mercaptopurine, Metho-
vascular permeability.
trexate
• Factors for increased risk of anaphylaxis:
These are either used singly or in combina-
1. History of allergy to food and drug tion. As these are potent drugs expected to kill
2. History of asthma the cancer cells, some damage to healthy cells
3. Family history of allergy also is unavoidable. One of the side effects is
4. Parenteral administration of drug multiple oral ulcers. Mechanism of ulcer
5. High-risk drug like penicillin formation:
Generalized anaphylaxis involves 4 systems: 1. Indirect: Depression of bone marrow and
1. CVS 2. GIT immune response caused, e.g. by vinblas-
tine leading to invasive infection of the
3. Respiratory system 4. Skin
oral mucosa which can be bacterial, viral
First signs seen on the skin are—localized
or fungal.
anaphylaxis, erythema, angioedema, urticaria,
2. Direct: Methotrexate causes oral ulcers by
pruritus.
direct effect on replication and growth of
Pulmonary—dyspnoea, wheezing, asthma. epithelial cells by interfering with nucleic
Gastrointestinal—vomitting, cramps, diarr- acids and protein synthesis leading to
hoea. thinning and ulceration of oral mucosa.
If these are untreated, there is hypotension
due to loss of intravascular fluid. If untreated, Clinical Features
shock occurs. Patients with generalized ana- 1. History of chemotherapy.
phylactic reaction may die from respiratory 2. Deep, large, necrotic ulcers without erythe-
failure, hypotensive shock or laryngeal edema. matous halo and without tissue tags.
Most important treatment is administration of
epinephrine—aqueous epinephrine 1:1000 in Differential Diagnosis
sterile easily accessible syringe 0.5 ml im or sc. 1. HSV: H/o chemotherapy is absent, ulcers
Epinephrine will usually reverse all severe are small, shallow round and show tissue
signs of generalized anaphylaxis. If no improve- tags, erythematous halo.
ment in 10 mins re-administer epinephrine. 2. EM: No H/o chemotherapy, bleeding ulcers
1. For bronchospasm: Slow iv aminophylline involving lips (bloody crustation), tissue
250 mg over 10 mins. If given too rapidly, tags present, skin lesions present.
3. Recurrent aphthous ulcers: No H/o chemo- of RAS. Evidence for inherited nature of this
therapy, H/o recurrence and healing after condition—genetically specific HLA Ag
7–10 days, ulcers are small and symmetrical. have been identified.
3. Hematologic deficiency—serum folate, iron or
Treatment
vitamin B 12 . Many such deficiency are
Oral ulcers may be an early sign to drug secondary to malabsorption syndrome such
toxicity—may warrant reduction of drug as celiac disease.
dosage or cessation of chemotherapy. 4. Autoimmune response.
Stopping the chemotherapy is often not
5. Immunologic—firstly altered immune
possible and oral ulcerations, alopecia and
response to Streptococcus sanguis 2A, now
myelosuppression must be faced by the
a role of lymphocytotoxicity, antibody
patient as unavoidable side effects while
dependent cell-mediated cytotoxicity,
achieving successful tumor remission.
defects in lymphocyte cell subpopulation.
1. Adjust the dose of drug or change the drug
6. Nutritional deficiencies—iron, vitamin B
with consent of the physician
complex and zinc.
2. Local application of xylocaine viscous
7. Psychological factors—tension, worry, anxiety.
mouthrinse
Patients are rigid, striving and inflexible.
3. Benadryl with milk of magnesia
8. Precipitated by trauma, menstruation,
4. Tetracycline mouthrinse (250 mg in 50 ml
upper respiratory tract infections, or contact
water) or 0.5 % povidone iodine solution
with certain foods.
(betadine).
Clinical Feature
Recurring Oral Ulcers
Minor RAS:
Recurrent Aphthous Ulcers 1. First episode occurs in 2nd decade.
Recurrent aphthous stomatitis (RAS) is a 2. Prodromal burning and itching sensation
disorder characterized by recurring ulcers 2–48 hrs before appearance of papule at
confined to the oral mucosa in patients with this stage erythema visible at site.
no other signs of the disease and is probably 3. Within a few hours, a small white papule
the most common ulcerative lesion encoun- appears which ulcerates in centre.
tered by the dental surgeon. 4. Within next 72 hours ulcer enlarges in its
Patients are classified into 3 categories: size, up to 0.3 to 1 cm in diameter.
1. Mild RAS: Crops of small ulcers which 5. Ulcers described as symmetrical, round or
heal within 2 weeks without scarring (size: oval without tissue tags (D/D – EM and
0.3–1 cm in diameter). HSV) with an erythematous halo (Fig. 2.13).
2. Major RAS: PMNR—Sutton’s disease— 6. Most patients have 2–6 lesions per episode
ulcers larger than 1 cm and take more than and suffer several such episodes in a year.
1 month to heal and heal with scarring. Number of ulcers vary at each episode.
(size: 1–5 cm in diameter). These are deeper.
7. Affects mobile mucosa which is less
3. Herpetiform ulcers: Recurrent episodes of
keratinized, e.g. tongue, lip, and cheek.
minute ulcers affecting large areas of oral
mucosa. 8. Aphthous ulcers are very painful and
affect patient’s speech and eating.
Etiology 9. Minor RAS ulcers heal within 10–14 days
1. It is not viral (HSV). without scarring.
2. Hereditary: Patients withs RAS positive 10. Ulcers of RAS are flat unlike HSV ulcers
parents had 90% chances of development which appear to be raised (moon crater).
A B
Fig. 2.13: Examples of minor aphthous ulcers
A B
Fig. 2.14: Examples of major aphthous ulcers
Major aphthae (PMNR, Sutton’s disease)

1. They are extremely painful, disabling ulcers
that interfere with speech and eating. Ulcers
are deep and larger (1–4 cm in diameter)
(Fig. 2.14)
2. Take more than 1 month to heal and heal
with scarring.
3. As these lesions take longer time to heal
they generate anxiety in the patients and
clinicians mind and sometimes biopsy is
needed to differentiate PMNR from SCC or
pemphigus.
Herpetiform Aphthous Ulcers
1. Small, punctate ulcers
2. Number more than 10–20 scattered over
erythematous mucosa (Fig. 2.15) Fig. 2.15: Herpetiform aphthous ulcers on upper lip
3. Resemble herpetic ulcers as they are small Behcet’s Syndrome

and shallow but unlike primary HSV H/o Hulusi Behcet was a Turkish dermatologist
recurrence is a characteristic feature. who described this condition with recurrent
Lab investigations: Level of serum iron, oral, genital and ocular ulcerations.
folate, vitamin B12 and ferritin and rule out
malabsorption syndrome. Etiology
1. Circulating immune complexes deposited
Treatment in small and medium-sized blood vessels
1. Local application of betamethasone with leading to vasculitis.
neomycin ointment helps to reduce the 2. Epithelial inflammation caused by immuno-
healing time. Fluocinolone gel, clobetasol competant T cells and plasma cells.
cream, beclomethasone spray have been
3. Environmental pollutants like DDT, chlor-
tried.
phenothane, polychlorinated biphenyls
2. Dissolve 250 mg of tetracycline in 50 ml
(PCBs).
of water and rinse mouth 4 times a day
for 5–6 days. 4. PPLO—pleura pneumonia like organisms.
3. Levamisole tablet (anthelminthic) 150 mg Clinical Features
1 tablet twice a day for 2 days has been Triad of signs or symptoms:
tried. Levamisole is an immune-potentiating
1. Recurring oral ulcers
drug that restores deficient phagocytic
function and cutaneous delayed hyper- 2. Recurring genital ulcers—in males scrotum
sensitivity reaction and increases absolute and penis while in females labia is involved
and relative T cell count 3. Inflammation of eye—uveitis, kerato-
4. Tab Rebamipide 100 mg BD for 7 days conjunctivitis, retinal vasculitis, optic atrophy
5. PMNR—intralesional injection of steroids 4. Oral ulcers of Behcet’s are small in size and
6. Since ulcers are extremely painful, topical cannot be differentiated from RAS
protective orabase can be used 5. Skin lesions: Patient shows reaction called
7. Lactobacillus therapy as pathergy, i.e. cutaneous reactivity to
8. Vitamin B complex tablets minor trauma
9. Iron replacement 6. Patient may also have arthritis and venous
10. In severe cases tranquilizers; chemical thrombosis
cautery with phenol has been used 7. Arthritis may involve 1 or 2 large joints,
11. Gentian violet joints are red and swollen. Involvement of
12. Fermented milk small joints does not occur.
In severe cases of RAS not responsive to Pathergy test: Placing 20 gauge needle 5 mm
steroids and tetracycline, try out dapsone or into the skin of forearm. Indurated papule or
thalidomide, if severity of disease warrants the pustule more than 2 mm in diameter is formed
risk of potential severe side effects. Thalidomide within 48 hrs which indicates a positive reaction.
is helpful in HIV-associated RAS. Thalido-
mide is not approved in USA due to its terato- Treatment
genic property and peripheral neuropathy. 1. Patients with life-threatening or sight-
Other therapies showing potential but threatening vasculitis are given steroids and
requiring further investigations are: immunosuppressant either prednisone +
1. Recombinant interferon alpha azathioprine, steroid + cholchicin or
2. Nicotine tablets cyclosporine, cholchicin or cyclosporine +
3. Colchicines thalidomide, plasmapheresis.
2. Steroids are mainstay and particularly Clinical Features

useful in controlling the disease until 1. Prodromal burning, itching and tingling
immunosuppressant drugs begin to work. sensation followed by erythema and edema
Recurrent Herpes Labialis/ Cold Sores/ Fever of lip
Blisters 2. Within this erythematous zone, cluster of
It is not a re-infection but reactivation of a vesicles appear (Fig. 2.16)
latent virus in nerve tissue. The virus travels 3. Size of cluster is 1–2 cm
down the nerve trunk to infect epithelial cells 4. Size of each vesicle is 1–3 mm
spreading from cell to cell to cause a lesion. 5. These vesicles rupture, weep serum and
RHL is precipitated by depression of cell- crustate
mediated immunity and commonly seen 6. Healing occurs within 2 weeks
during fever, menstruation, stress and Recurrent intraoral herpes (RIOH) lesions
exposure to UV light, trauma, sunburn, dental also appear as a cluster of vesicles affecting
treatment the highly keratinized and firmly adherent
Large chronic lesions of HSV in T cell mucosa such as palatal mucosa. Vesicles
deficiency due to: AIDS, transplant, chemo- rupture to form a cluster of multiple shallow
therapy and cancer. tender ulcers with tissue tags (Fig. 2.17).
A B
Fig. 2.16: Examples of recurrent herpes labialis
A B
Fig. 2.17: Examples of recurrent intraoral herpes

Diagnosis of RIOH • Herpetic whitlow is very debilitating to

1. Cytological smear—ballooning degeneration dentist. Minor vibration from dental
2. Detection of fluorescein labeled Ag handpiece may trigger recurrence.
3. Viral culture to differentiate VZV from HSV. • Spread from infected dentist to unprotected
patient has been reported.
Treatment Treatment preferred is tab acyclovir 200 mg
Symptomatic; antiviral drugs are recommended: 5 times a day for 7 to 10 days.
1. Diet low in arginine (an amino acid
essential for synthesis of herpes virions) Dental Considerations
2. Sunscreen to protect from harmful effect of 1. Not to treat patients with active HSV
UV rays, sunblock during intense sun lesions.
exposure 2. Application of rubber dam or emollient on
3. L-lysine and water soluble bioflavinoids— a herpetic vesicle can result in spread of
ascorbic acid helpful in wound healing. infectious fluid to adjacent dermal tissues.
L-lysine decreases viral replication 3. Treatment of infected patient can lead to
4. Topical agent zinc camphor solution and herpetic whitlow to the dentist.
ether 4. Use of airotor, 3 way syringe, ultrasonic
5. Iodoxuridine in DMSO (dimethyl sulph- scaler can cause inadvertent aerosolization
oxide) of the virus, leading to infection of eyes or
nasal mucosa.
6. Acyclovir—decreases viral replication,
decreases viral shedding, hastens lesion 5. HSV survives for at least 2–4 hrs on skin
resolution, reduces duration of pain and environmental surfaces but susceptible
to decontamination procedures.
7. Topical application of acyclovir cream for
RHL is preferred as it is a self-limiting 6. Therefore use: Barriers, disinfect the opera-
disease (unless the patient is immuno- tories surfaces between patients, disposal
of contaminated gloves and wash hands
compromised)
after handling items that have been exposed
8. Some clinicians recommend tab acyclovir
to infectious aerosols.
200 mg 5 times a day till lesions heal.
Differences between RHL and Chancre, RAS
Herpetic Whitlow and RIOH:
• Seen in children, thumb suckers and doctors
RHL Chancre
who put unprotected fingers in patients
mouth. 1. Cluster of vesicles Raised hard nodular
mass
• Begins as redness, inflammation and
swelling. 2. Painful Painless
• Vesicles within days accompanied by 3. Prodromal symptoms No prodromal symptoms
axillary lymphadenopathy and moderate to 4. Healing within 2 weeks Healing more than 2 weeks
severe pain. 5. No history of exposure History of exposure pre-
• The vesicles breakdown, exude infectious may be present sent
fluid and become pustular. 6. Lymphadenopathy Lymphadenopathy pre-
• Clinical appearance may mimic bacterial, absent sent
fungal or mycobacterial infection. 7. Causative organism: Treponema pallidum
• Lesions heal within 7–10 days. Herpes simplex virus (bacterium)
• Misdiagnosis and performance of invasive
procedure may delay healing. (contd.)
RAS RIOH Clinical Features

1. Occurs on freely Firmly adherent or fixed Classical lesion of pemphigus vulgaris is thin
movable and less mucosa which is hyper- walled bulla over the skin and mucous
keratinized mucosa keratinized membrane (Figs 2.18 and 2.19). Bulla rapidly
2. Initially erythematous Cluster of vesicles breaks but continues to extend peripherally
macule or papule seen eventually leaving large areas of denuded
which ulcerates
skin.
3. Mature lesion 0.5–1 cm A group of ulcers. Each
ulcer with yellow necro- one smaller than 5 mm i. Oral manifestations: 80–90% develops oral
tic base and erythe- lesions and in 60% it is the first sign.
matous halo • It begins as a classic thin-walled bulla
4. Number of lesions: 2–6 10–15 ulcers in a group on a non-inflamed base.
separate ulcers
• Shallow irregular ulcer because the
5. Histologically absence Presence of inclusion
of intranuclear inclusion bodies with ballooning
bullae rapidly break.
bodies degeneration of nuclei • Thin layer of epithelium peels away in
6. Absence of tissue tags Presence of tissue tags an irregular pattern leaving a denuded
base.
CHRONIC MULTIPLE ULCERS • The edges of the lesion continue to
extend peripherally.
Pemphigus Vulgaris ii. Transient vesicle and bullae which rupture
Pemphigus is an autoimmune, potentially life- and collapse leaving symmetrical ulcers,
threatening disease characterized by loss of such bullous lesion has been described as
epithelial cell adhesion (acantholysis) leading flaccid as it spreads laterally due to
to blisters and erosions of the skin and mucous suprabasilar clefting unlike the tense
membranes. localized bullous lesion in pemphigoid (as
it is located deeper to basement membrane
Etiology and cannot spread easily)
Desmoglein 1(DSG 1) is a transmembrane iii. Lesions are usually widespread involving
glycoprotein adhesion molecule present on many oral mucosal surfaces (Figs 2.20
desmosomes in the skin and Desmoglein 3 and 2.21)
(DSG 3) in the mucosal epithelium. The
immune reaction against these glycoproteins
causes loss of cell to cell adhesions leading to
separation of cells and formation of intra-
epithelial bullae.
i. Pemphigus vulgaris (PV) is noted more
frequently in Ashkenazi Jews , who have
strong association with HLA-DR4 and
DQ8 haplotypes
ii. PV is reported to coexist with other auto-
immune diseases, viz. myasthenia gravis,
thymoma, neoplasms like lymphoma.
iii. PV is also known to be associated with
intake of certain drugs such as penicilla-
mine [given in Wilson’s disease], captopril,
phenobarbitone, penicillin. Fig. 2.18: Picture of an intact bullous lesion
A B
Fig. 2.19: Pemphigus vulgaris—skin showing ruptured bullae
A B
Fig. 2.20: Patient with pemphigus vulgaris showing extensive erosions
A B
Fig. 2.21: Pemphigus vulgaris showing extensive erosions on right and left buccal mucosa (same patient as
in Fig. 2.20)
iv. A Nikolsky’s sign usually can be elicited Treatment and Prognosis

because of the underlying acantholysis i. Systemic steroids remains mainstay of
(also seen in severe EM and epidermolysis treatment, however, topical steroids may
bullosa), i.e. application of pressure on the be given in milder cases. And in patients
apparently normal skin or mucosal surface in whom systemic steroids are contra-
(or rubbing) results into formation of a indicated.
fresh bullous lesions. • Topical steroids clobetasol oint
Asboe-Hansen sign—also known as • Fluocinolone gel—0.05%
‘Indirect Nikolsky’s sign’. Applying light • Betamethasone valerate ointment—0.1%
pressure the intact bulla can be made to
• Triamcinolone acetonide
extend peripherally.
• Dexamethasone elixir 0.5 mg/5 ml—
v. The denuded areas may persist for months
rinse with 1 table spoon for 2 minutes
because the ongoing disease constantly
and then spit out
forms new lesions because of acantholysis.
• Systemic steroids and immuno-
vi. Secondary candidal infection is very
suppressants
common and at times the condition may
Betamethasone 0.5 mg 1 tab qid for 5 days,
be mistaken for chronic candidiasis.
1 tab tid for next 5 days, 1 tab bd for next
Microscopic Picture 5 days and 1 tab od for next 5 days. Tablet
i. Separation of the surface of epithelium to be dissolved in mouth and swish and
above the basal layer of epithelial cells swallow.
ii. The basal cells remain attached to the Very severe cases: Prednisolone 10 mg 5 tab
basement membrane and have been stat in the morning, then decrease by 1 tab
likened to a ‘row of tombstones’. each successive day.
ii. Immunosuppressant: Azathioprine cyclo-
iii. The resulting intraepithelial space contains
phosphamide, cyclosporine to decrease
neutrophils, eosinophils and free-floating
the harmful effects of steroids. Azathio-
epithelial cells which are characteristically
prine tab 50 mg BD for 15 days used to
ovoid in shape due to loss of desmosomal
reduce the side effects of steroids [steroid
attachments and reaction of tonofilaments.
sparing drug]
iv. The nuclei can be enlarged, these loose
iii. Methotrexate
epithelial cells are called as Tzanck cells.
iv. New immunosuppressant drug: Mycopheno-
Investigations late mofetil
i. Direct immunofluorescence test detects v. Plasmapheresis is done in patients refrac-
antibodies bound to surface of keratino- tory to steroids-removal of plasma from
cytes. [Biopsy specimen obtained from withdrawn blood with retransfusion of the
normal appearing perilesional skin or formed elements into donor. Generally
mucosa.] type specific fresh frozen plasma or
ii. Indirect immunofluorescence test: Patients albumin is used to replace the withdrawn
serum is placed over the prepared slide of plasma. The procedure is done for purpose
mucosal structure [monkey’s esophagus]. of removing the autoantibodies, i.e. for
Autoantibodies in the serum bind to the therapeutic purposes or to collect plasma
target antigen in the mucosa, e.g. in PV components.
the antikeratinocyte antibodies against Paraneoplastic pemphigus (PNPP): Associated
intercellular substance show up under with NHL, thymoma, Castleman’s disease,
fluorescent microscope. Waldenström’s macroglobulinemia.
1. The patient develops severe blistering and Bullous Pemphigoid

erosions of skin and mucous membrane. Clinical Features
2. Oral and conjunctival lesions are severe and i. Presents mainly as subepithelial blisters
common and may resemble EM or TEN but which rupture to form erosions.
the lesions are of much longer duration and
ii. Disease occurs chiefly in elderly patients
progressive respiratory involvement is seen
above 60 years of age and lasts from
in 40% of cases.
6 months to 5 years.
3. Combination of prednisolone and immuno- iii. Skin lesions predominate and involve
suppressive drug therapy may help control scalp, arms, legs, axilla, groin. Initial
the severity of these lesions. lesions may be papules or macules leading
4. It is important to consider possibility of to blister on inflamed base. Pruritus is a
PNPP in patients with clinical evidence of common symptom of the skin lesion.
chronic erosions of the oral cavity sugges- iv. Mucosal lesions in 30% patients and occur
tive of pemphigus. after the skin lesions.
v. Oral lesions are erythematous and vesicles
Pemphigus Vegetans are similar to cicatrical pemphigoid. They
1. A relatively benign variant of pemphigus are smaller and form more slowly as
as the denuded areas tend to heal. compared to PV. Bullous lesion in BP lasts
2. Two forms are recognized: longer without rupturing as it is sub-
epithelial and does not spread peri-
a. Newmann type has early lesions similar
pherally like the lesions of PV (Fig. 2.22).
to PV with large bullae and denuded
areas which heal with hyperplastic Desquamative gingivitis is the most
granulation tissue. common oral finding of BP. Gingival
lesions present as generalized edema,
b. Hallopeau type has pustules as initial inflammation, desquamation with discrete
lesions, which are followed by verrucous intact vesicles.
hyperkeratotic vegetations.
vi. Repeated ulcers seldom result in scar
3. Oral lesions: Lace-like ulcers with purulent formation which is characteristic of CP.
surface on a red base, or have a granular vii. CP could be distinguished from BP as CP
cobblestone appearance. Oral lesions that lesions predominantly involve oral
are associated with inflammatory bowel mucosa.
disease and resemble pemphigus vegetans
clinically and histologically are referred to
as pyostomatitis vegetans.
Subepithelial Bullous Dermatoses

These conditions have bullous lesions which
unlike PV are subepithelial.
a. Bullous pemphigoid
b. Benign mucous membrane pemphigoid or
cicatricial pemphigoid
c. Linear IgA disease
d. Epidermolysis bullosa acquisita Fig. 2.22: Bullous pemphigoid showing multiple bullae
e. Chronic bullous disease of childhood (Source: Internet)
Microscopic Features Clinical Features

i. Separation of the surface epithelium from i. Adults past middle ages above 50
underlying connective tissue via cleavage ii. Females > males
of the basement membrane.
iii. Oral features—chronic mucosal erythema,
ii. Unlike CP circulating antibasement mem- vesicles/bullae and ulcers
brane antibodies can be usually demons-
trated via indirect immunofluorescence. In iv. Vesicles are transient—forming and
addition the target or “bullous pemphi- rupturing within hours, ulcers may take
goid antigen” has been identified. several weeks to heal
v. Lesions may involve any surface but
Treatment and Prognosis gingival lesions are common along with
i. Topical and systemic steroids the attached alveolar mucosa, thereby
ii. Immunosuppressants presenting as ‘desquamative gingivitis’
(Fig. 2.23).
Cicatricial Pemphigoid
(Mucous Membrane Pemphigoid) vi. Nikolsky’s sign can be elicited by directing
It is a disease in which autoantibodies are stream of air with an air syringe at the
formed against components of basement margin of the ulcer.
membrane. This results in bullae and ulcers vii. Healing of ulcers with scar formation
primarily on mucosal surfaces that sometimes (Fig. 2.24) and this is evident orally if
heal with scarring. buccal mucosa is involved repeatedly.
A B
Fig. 2.23: Cicatricial pemphigoid—bullous lesion (arrow) and desquamative gingivitis
A B
Fig. 2.24: Example of palatal lesion of cicatricial pemphigoid healing with scarring
viii. Cicatricial pemphigoid can involve iii. Hansen et al recommended dapsone

conjunctival, nasal, pharyngeal, tracheal, 25–50 mg daily slowly increasing to
laryngeal, esophageal and vaginal mucosa 125–150 mg daily for 6 weeks. Then once
and skin. Esophageal involvement causes the patient is under control a lower
difficulty in swallowing and laryngeal maintenance dose is needed. Since
involvement can cause hoarseness of voice dapsone causes hemolysis and methemo-
and difficulty in breathing. Strictures may globinemia, G6PD deficiency should be
occur, thus requiring surgery. ruled out.
ix. Conjunctival involvement causes scarring
Linear IgA Disease (LAD)
and adhesion between bulbar and
palpebral conjunctiva (symblepharon) i. Characterized by deposition of IgA rather
(Fig. 2.25) and visual impairment. It may than IgG in the basement membrane.
lead to corneal damage and blindness is ii. Pruritic papules and blisters at the site of
seen in 15% cases. trauma such as knees and elbows, similar
to dermatitis herpetiformis.
Microscopic Picture iii. Oral lesions similar to CP, i.e. blisters and
i. Lesions of CP are caused by autoantibody erosions, desquamative gingivitis quite
reactivity against an antigen in the lamina common.
lucida of the epithelial basement mem- iv. Histopathologically subepithelial lesion in
brane. the basement membrane region similar to
ii. Antigen–antibody interaction sets off a CP but DIF shows IgA and not IgG.
chain of events and results in detachment v. Steroids given topically and systemically
of epithelium from the underlying connec- as in the treatment of CP.
tive tissue. Dapsone is often effective.
iii. DIF carried out in CP biopsy specimens In severe cases, immunosuppressive
demonstrate positive fluorescence for IgG drugs are given with systemic steroids.
and complement C3 in the basement
Epidermolysis Bullosa Acquisita (EBA)
membrane zone.
Clinically resembles cicatricial pemphigoid
Treatment and Prognosis and bullous pemphigoid. Widespread skin
i. Topical and systemic steroids. and oral mucosal lesions. Genital mucosa,
ii. Sulfones, azathioprine and cyclophospha- conjunctiva and larynx also involved.
mides azathioprine 50 mg bd for 15 days. Treatment is similar to CP and LAD.
A B
Fig. 2.25: Symblepharon (Source: Internet)

A B
Fig. 2.26: Traumatic ulcer associated with sharp edges of tooth
Chronic Bullous Disease of Childhood (CBDC)

i. Age below 5 years.
ii. Deposition of IgA antibodies in basement
membrane zone, detected by DIF
iii. Onset precipitated by respiratory infection
or drug therapy.
iv. Cluster of vesicles or bullae on inflamed
base on genitalia, conjunctiva, rectal and
oral mucosa.
v. Oral lesions resemble MMP but perioral
skin involvement common in CBDC.
vi. Management similar to MMP and LAD,
i.e. steroids and dapsone.
Fig. 2.27: Thermal burn—accidental ingestion of hot
Patients with Single Ulcers fluid
Traumatic Ulcer: Acute

of microwave oven to reheat the food causes
i. Traumatic ulcers are the most common differential heating so that cheese gets over-
single ulcers and the patients normally heated compared with other part of foods
give a history of mechanical, chemical, leading to burns.
thermal and on rare occasions electrical
injury. Iatrogenic cause of thermal injury is due to
Mechanical trauma can be due to direct inadvertent touching of overheated instru-
physical injury, acute bite injuries especially ment to the oral mucosa. Injury is more severe
if the patient is anesthetized for a dental if mucosa is anesthetized.
procedure. Injuries may also result from Chemical trauma is caused by patient
malocclusion, ill-fitting dentures, sharp tooth applying locally a caustic substance like clove
(Fig. 2.26). oil, aspirin tablet to cure toothache (Fig. 2.28).
Thermal injuries include accidental ingestion Accidentally certain noxious or caustic
of hot food, beverages (such as hot tea, pizza) chemicals might injure the mucosa during
leading to blistering of mucosa (Fig. 2.27). Use dental treatment.
Fig. 2.28: Aspirin burn Fig. 2.29: Chronic traumatic ulcer—Riga-Fede disease
Oral Findings 3. In the adult age group (50–60 years), chronic

Acute ulcerations or necrosis of mucosa with traumatic ulcers often present as painless
a clear history of injury. Burn injuries present clearly demarcated deep lesions with peri-
as blisters which rupture to form erosions pheral erythema or in some cases whiteness.
mainly on palate and lips. Ulcer margins are There may be induration surrounding the
irregular with sloping edges. Lesions are tender lesion. Such a lesion especially on the
and heal within 7–10 days unless if the trauma tongue justifiably raises the doubt of
continues or there is secondary infection. malignancy and biopsy becomes manda-
tory if the lesion persists even after
Management
eliminating the cause.
Removal of traumatic agent. Antibiotics to 4. In patients with tardive dyskinesia conti-
prevent secondary infections. Due care by nuous involuntary movement of the tongue
patients and dentists to prevent injury is can result in traumatic lesions of the tongue.
essential. In certain patients, there is a congenital
Electrical burn is deeper and might heal incapacity to sense pain (Lesch-Nyhan
with scarring. Artificial devices to prevent syndrome, Riley-Day syndrome) and they
microstomia in patients with injury to the can develop similar traumatic ulcers
commissure help. However, plastic surgeons without being aware of the self-inflicted
opinion should be sought to provide best care injury.
to the patients. 5. Management involves eliminating the
cause.
Traumatic Ulcerative Granuloma: Chronic
• Prevent trauma during sleep by giving
Traumatic Ulcer
nightguard for the lower arch.
1. Acute or chronic ulcerative conditions, if • Intralesional steroids
left untreated can become deep and • Wound debridement
penetrating.
• Excision and biopsy
2. Riga-Fede disease in infants caused by
newly erupted teeth traumatizing the Tuberculous Ulcer
tongue. Such lesions are located on the 1. The patients give a history of tuberculosis,
anterior border of the tongue. These lesions i.e. fever, persistent cough, lymphadeno-
occur within first 2 years of life (Fig. 2.29). pathy, etc.
2. Ulcer is generally solitary, extremely

painful, deep, with undermined edges
involving the tongue more often than other
areas (Fig. 2.30).
3. The ulcerative lesions generally develop
after seeding of the tubercle bacilli in
traumatic lesions which occur as a result of
violent bouts of coughing.
4. The lesion may be mistaken for malignancy
and if undiagnosed by history and clinical
Fig 2.31: Malignant ulcer
examination may warrant biopsy.
5. Treatment with antituberculosis drugs Chronic Herpetic Ulcer
resolves such lesions. 1. In immunocompromised individuals such
Malignant Ulcer as HIV/AIDS and patients on immuno-
1. The patient gives history of tobacco habit, suppressive drugs, chronic herpetic ulcers
either smoking or chewing. can develop.
2. The lesion presents as a solitary, painless 2. They present as solitary large painful ulcers
ulcer with everted margins which is fixed with irregular periphery resulting from
to the underlying structure. Presence of the multiple small ulcers which coalesce.
lesion markedly diminishes the mobility of 3. These lesions are relatively superficial
the part involved, e.g. inability to protrude compared to other chronic ulcers and may
the tongue if ventral surface or floor of not respond to acyclovir and require
mouth is involved (Fig. 2.31). administration of foscarnet.
3. The size and depth of the ulcer varies and Chronic Ulcer of Fungal Etiology
pain can be a feature if there is secondary
infection. 1. Mucormycosis: The fungus is considered
non-pathogenic for healthy individuals,
4. Involvement of underlying bone can occur
acts as an opportunistic rather than patho-
in advanced cases. Regional lymph node
genic organism.
involvement can also be a feature.
5. Biopsy findings and TNM staging helps the 2. Principally seen in patients with uncon-
oncologist to formulate the treatment plan. trolled DM, leukemia and those undergoing
cancer chemotherapy or immunosuppressive
drug therapy.
3. The rhinomaxillary form is a subdivision
of rhinocerebral form and begins with the
inhalation of the fungus by the susceptible
individuals.
4. The fungus invades the arteries and causes
thrombosis, ischemia leading to necrosis,
the fungal infection may spread from the
oral and nasal cavity to involve the brain
leading to death in many cases.
Common symptoms include proptosis, loss
of vision, nasal discharge, sinusitis and
Fig. 2.30: Tubercular ulcer (Source: Internet) palatal necrosis.
5. Oral findings include palatal ulceration Incidence

which is large and deep causing denudation • Age—adolescent (young adults)
of bone and results from necrosis secondary • Male and female are equally affected
to palatal vessel involvement.
• Seen in poor oral hygiene.
Mucormycosis can also involve lips, gingiva
and alveolar ridge and initially may be con- Etiology
fused with dental pain or maxillary sinusitis. 1. Stress
Mucormycosis should be included in the 2. Smoking
D/D of large chronic ulcers especially if the
3. Inadequate nutrition, starving
patient is immunocompromised or having
uncontrolled DM. Etiology: Borrelia vincentii and Fusobacterium
dentium were originally considered as patho-
6. Biopsy specimen is split to send for culture
genic organism. Recently Treponema species,
and histopathology. Histopathology shows
Prevotella intermedia, fusobacteria gingivalis
necrosis and non-septate hyphae stained
are found to be the predominant organisms
with PAS stain or methenamine silver stain.
involved in the pathogenesis of the disease.
Necrosis and vessel occlusion are also
frequent. Predisposing Factors
7. Management includes surgical debride-
Table 2.1: Predisposing factors (ANUG)
ment and systemic administration of
amphotericin B. Local Systemic
Patients receiving amphotericin should be Pericoronitis Stress
monitored to rule out renal toxicity by Chronic marginal gingivitis Acute anxiety
repeated measurement of BUN and serum Poor oral hygiene Fatigue
creatinine. Overhanging restoration Blood disorders
Posaconazole a new oral antifungal has (leukemia)
shown promise as an alternative for the Smoking Malnutrition
toxic amphotericin B.
Treponema species and fusobacteria
FUSOSPIROCHETAL INFECTIONS gingivalis are not innocent bystanders but
Fusospirochetal organismas such as Borrelia being anaerobic organisms,thrive in the
vincentii, Fusobacteria, Prevotella are anaerobic favourable conditions of the gingival sulcus,
organisms which can infect the oral cavity and giving rise to erosions/ulcerations of the
give rise to: interdental papilla and marginal gingiva.
• NUG Signs and Symptoms
• Vincent’s angina Sudden onset:
• Cancrum oris • Pain and tenderness in gums
Necrotizing Ulcerative Gingivitis (NUG) • Profuse salivation
Formerly known as acute necrotizing ulcera- • Metallic taste
tive gingivitis. Also known as ‘Trench mouth’ • Patient c/o diminished pleasure from
and Vincent’s disease. Soldiers in combat were smoking
forced to stay in trenches and faced a lot of • Tooth appears to be extruded, patient
stress and used to develop NUG. As this condi- describes the teeth as ‘wooden pegs’
tion often involves oral mucosa also, G in • Blunting of interdental papilla with gingival
ANUG represents gingivostomatitis. bleeding
A B
Fig. 2.32: Necrotic punched out ulcerations of interdental papilla—NUG
• Necrotic punched out ulcerative lesions • Bloody crustations

involving the interdental papilla (Fig. 2.32), • Gingiva rarely involved
buccal mucosa, labial mucosa, tongue,
3. Blood dyscrasias: Leukemia—gingival
palate, etc.
enlargement is seen and constitutional
• In severe cases, deeper ulcer involves symptoms are more pronounced than oral
alveolar bone and cause mobility of teeth. finding.
• Bleeding from the gingiva giving rise to
stained teeth and foetid odor. Treatment
• Pseudomembranous slough is formed. Three stages:
1. Control of bacterial phase:
• Patient gives history of fever and presents • Local debridement
with lymphadenopathy. • Antibiotics: Phenoxymethyl penicillin
250 mg four times a day for 5 days
Diagnosis • Metronidazole 400 mgs three times a day
From clinical features of fever and lympha- for 5 days
denopathy, necrotic ulcers on the gingiva, • Paracetamol 500 mg three times a day for
severe pain and gingival bleeding. 5 days
• 2% H2O2 mouthwash: This acts via three
Differential Diagnosis mechanisms:
1. Herpetic gingivostomatitis: Seen from a. It releases nascent O 2 which kills
6 months to 6 years of age: anaerobic bacteria.
• Fever and prodromal symptoms are seen. b. It produces effervescence which
dislodges the debris from the ulcers
• Vesicles are seen which ruptures to form
and helps in debridement.
ulcers with ragged borders, ulcers are
c. It helps in controlling the bleeding
small, round, shallow and symmetrical (Fig. 2.33).
with erythematous halo.
2. Elimination of local and systemic pre-
• Diffuse gingival inflammation
disposing factors:
• Lymphadenopathy • Vigorous rinsing and gentle brushing
While in NUG, ulcers are deep, irregular • Removal of local irritants, irrigation and
necrotic and punched out and involve inter- curettage
dental papillae. • Periodontal surgery.
2. Erythema multiforme: Acute onset 3. Patient education and counseling about
• Skin lesions are seen habits and proper oral hygiene.
A B
Fig. 2.33: Post-treatment improvement (phenoxymethyl penicillin, metronidazole and hydrogen peroxide
mouthwash)
Vincent’s Angina Differential Diagnosis

It is the fusobacterial infection of the tonsillar Vincent’s angina has to be differentiated from
and pharyngeal region. diphtheria.
Clinical Features Diphtheria Vincent’s angina

• Fever and malaise Bilateral extensive lesion Unilateral and localized
• Pain in the throat and dysphagia Pseudomembrane present Ulcerative lesion
when removed it is rapidly
• Lymphadenopathy replaced
• Necrotic ulcers are seen in the tonsillar and Toxemia symptoms like Milder symptoms, no
pharyngeal regions (Fig. 2.34). headache, bodyache and tachycardia
tachycardia
Complications are myo- No such complications
carditis, otitis media,
asphyxia and death
Treatment
• Procaine penicillin 6 lakh units per day for
8 days (after test dose) Or
• Phenoxymethyl penicillin 250–500 mg
6 hourly for 8 days.
Noma/Cancrum Oris
Rapidly spreading gangrene of mucocuta-
neous orifices of which oral cavity is the most
common. It is caused by Borrelia vincentii
and Fusobacterium dentium. Fusobacterium
necrophorum is likely to play an important role
in progression of NUP to cancrum oris because
it produces dermonecrotic toxin, hemolysin
leukotoxin and proteolytic enzymes all
Fig. 2.34: Vincent’s angina—necrotic ulcerations on leading to extensive tissue destruction. It may
palate and pharynx also stimulate Prevotella intermedia.
A B
Fig. 2.35: Cancrum oris with excessive destruction leading to perforation of cheek (Note: Blackish periphery)
Predisposing Factors Noma develops very fast within few days

• Measles, scarlet fever, typhoid, kala-azar and there is history of pre-existing ANUG,
• Syphilis, tuberculosis and blood dyscrasia malignancy on the other hand develops more
• Malnourished debilitated patients slowly, i.e. takes two to three months to reach
that size.
• Local factors—trauma, poor oral hygiene
and chronic irritation. Treatment
Clinical Features • Hospitalizing the patient and starting IV
• Offensive odor fluids and medications.
• Necrotic ulceration with extensive sloughing • Hyperbaric oxygen can be given, which
near the commissure giving rise to perfora- controls the anaerobic infections, gives rises
tion of the cheek. to angiogenesis, revascularization of the
• Blackish discoloration of the periphery of affected area and promotes healing.
the ulcer suggestive of gangrene (Fig. 2.35) • Procaine penicillin and metronidazole.
• Loosening and exfoliation of the teeth and • Plastic surgery for correction of defect
sequestration of bone caused by gangrene and esthetic rehabili-
• Excessive salivation tation.
• Compared to the size of the lesion pain is
not that severe. Suggested Reading
1. Burket’s Oral Medicine 9th, 10th and 11th
Differential Diagnosis
editions.
At times, noma may be mistaken for
malignancy because it presents as ulcerative
lesion, however, perforation associated with
noma is surrounded by blackish periphery 3. Oral diseases of the tropics—Prabhu and
and ulceration associated with carcinoma has Daftary.
everted margins and is fixed to underlying 4. Shafer’s Textbook of Oral Pathology, 6th
tissue and associated fixed lymph nodes. edition.
3
Red and White Lesions
WHITE LESIONS Whenever a patient presents with a white

lesion, it should first be determined whether
Normally oral mucosa appears pink in colour the lesion can be removed or dislodged by
because of transmission of light passing gentle rubbing. For this purpose a tongue
through translucent superficial mucosa blade or wet cotton plug held in a tweezer is
striking capillary bed and then being reflected used.
back again through the translucent layer.
Lesions which can be scraped off are
Changes within, below or above the mucosa
generally without hyperkeratosis, e.g.
which interfere with the passage of light will
chemical burn, pseudomembranous candi-
appear as white lesions.
diasis lesions.
Example Lesions which cannot be scraped off or
1. Simple thickening or oedema of cells— dislodged are usually hyperkeratotic, e.g.
leukoedema. leukoplakia, lichen planus.
2. Thickening of keratin layer—leukoplakia
Classification of White Lesions
3. Invasion of superficial layers of epithelium
by mycelia of candidiasis. A. Not Usually Associated with Hyperkeratosis
4. Caustic agents, thermal burns, chemical 1. Trauma:
burns produce coagulation of cytoplasm a. Mechanical—sudden
thereby resulting in a whitish appearing • Gradual
lesion. b. Thermal—hot—pizza burn or hot food
5. Abnormal changes within epithelium, e.g. • Cold—dry ice, cryoprobe
dysplastic changes associated with CA will c. Chemical—aspirin
also give rise to whitish lesion.
• Trichloroacetic acid
6. Changes in connective tissue—increased
• Phenol or clove oil
fibrosis and reduced vascularity as in
submucous fibrosis will also give rise to 2. Infection:
whitish blanched mucosa. a. Moniliasis—acute atrophic (antibiotic
7. The production of abnormal keratins which sore mouth)
imbibe fluid more readily than the normally • Acute pseudomembranous candidiasis
keratinised oral mucosa is a very important (thrush)
factor according to Payne. • Chronic atrophic (denture sore mouth)
49
• Chronic hyperplastic candidiasis 5. Infections—Koplik’s spot, syphilitic mucous

(candidal leukoplakia) patches, stomatitis, candidiasis.
• Angular cheilitis
C. Oral Candidiasis
• Median rhomboid glossitis
• ID reaction 1. Pseudomembranous candidiasis or thrush
• Systemic candidiasis 2. Atrophic candidiasis
b. Syphilis 3. Chronic atrophic candidiasis—DSM,
c. ANUG angular cheilitis and MRG
d. Koplik’s spot 4. ID reaction
e. Verruca—caused by papillomavirus 5. Chronic mucocutaneous candidiasis
3. Nutritional 6. Chronic hyperplastic candidiasis
4. Allergic 7. E/O candidiasis
5. Miscellaneous: Fordyce’s granules 8. Systemic candidiasis
• Leukoedema A. Keratotic Lesions with no Increased
• Uremic stomatitis Potential for Oral Cancer
• Psoriasis
1. Stomatitis nicotina palatini
• Radiation mucositis
2. Frictional or traumatic keratosis
B. Associated with Hyperkeratosis 3. Keratosis due to dental restorations
1. Leukoplakia 4. Intraoral skin grafts
a. With hyperkeratosis 5. Focal epithelial hyperplasia
b. With dysplastic changes 6. Psoriasis, Reiter’s syndrome, BMG
2. Speckled leukoplakia 7. Oral genodermatoses: White sponge nevus
3. Lichen planus 8. Lesions with chronic candidiasis, chronic
a. Erosive mucocutaneous candidiasis and with
b. Non-erosive endocrinopathy
• Annular 9. Acrodermatitis enteropathica
• Reticular 10. Epidermolysis bullosa, keratosis follicularis
• Linear 11. With abnormal deposits in submucosa:
• Plaque like Pseudoxanthoma elasticum, hyalinosis
4. Submucous fibrosis cutis
5. Carcinoma
B. Red and White Lesions with Defined
Classification of Red and White Lesions Precancerous Potential
A. Variation in Normal Appearance 1. Leukoplakia
and Structure of Oral Mucosa 2. Erythroplakia
1. Leukoedema 3. Oral submucous fibrosis
2. Fordyce’s granules 4. Lesions associated with alcohol and
3. Linea alba and normal frictional cornification tobacco
5. Carcinoma in situ
B. Non-keratotic 6. Lichen planus
1. Habitual cheek and lip biting 7. Discoid lupus erythematosus
2. Burns—chemical, thermal and iatrogenic 8. Dyskeratosis congenita
3. Uremic stomatitis 9. Lichenoid reactions: Drug induced and
4. Radiation mucositis GVHD
Red and White Lesions 51
Variations in Structure and Appearance Histologically parakeratosis, acanthosis,

of Oral Mucosa with intracellular edema in the epithelial
a. Leukoedema: Oral mucosa retains normal cells of stratum corneum.
softness and flexibility but exhibits greyish b. Fordyce’s granules are ectopic sebaceous
milky white slightly folded or wrinkled glands which appear on the vermilion
opalescent appearance which disappears on border of the lips and buccal mucosa as
stretching the mucosa. Underlying melanin small yellowish white spots apparent on
pigmentation enhances the opalescence. It closer inspection (Figs 3.2 and 3.3). Some-
is more common in dark skinned people. times they are large and confluent and can
Leukoedema is correlated to smoking. More be easily noticed. Can be disfiguring if
in pipe smokers than cigarette smokers and present on the vermilion border of the lips
snuff users (Fig. 3.1). (prolabial sebaceous glands) and may
warrant surgical treatment. Otherwise this
condition requires no treatment. Some
patients notice these spots and become
apprehensive and have to be reassured that
these are normal variants and hence benign
and require no treatment.
c. Linea alba and normal frictional keratosis: Linea
alba is a white line of keratinization on
cheek mucosa expanding to a triangular
area just inside each labial commissure. It
is at the level of occlusal plane and is related
to the keratosis caused by the occluding
teeth and hence increased in bruxism
(Fig. 3.4).
Mucosa over the hard palate, attached
gingiva is subjected to friction during masti-
cation and hence responds by depositing
more keratin and appears whitish while
Fig. 3.1: Milky white lesion of leukoedema other areas appears pinkish.
Fig. 3.2 Fig. 3.3
Figs 3.2 and 3.3: Yellowish spots of Fordyce’s granules

b. Thermal: Sudden intake of hot food will give

rise to transient nonkeratotic white lesion
due to precipitation of cytoplasmic proteins,
e.g. pizza burn (Fig. 3.7).
Accidental injury due to dry ice also gives
rise to a white lesion (dry ice, prolonged
contact of childs lips to frozen confections—
popsicle panniculitis)
c. Chemical: Most commonly manifested burn
is aspirin burn, (Fig. 3.8). This is seen as a
white pseudomembranous painful lesion
adjacent to a painful tooth.
Fig. 3.4: Linea alba d. Iatrogenic cause: As a result of inadvertent
or accidental exposure to formocresol,
White Lesions not Associated with
phenol, trichloroacetic acid (all used as
Hyperkeratosis
cauterising agents), glutaraldehyde
1. Trauma (antiseptic solution), alkaline ultrasonic
a. Mechanical: It can be sudden as a result of cleaning liquid, sodium hypochlorite used
inadvertent biting of cheek or tongue. This as root canal irrigant may cause chemical
gives rise to whitish tags of necrotic tissue injury followed by a white lesion.
commonly seen around traumatic ulcer. e. Cinnamon-flavored toothpaste and alcohol
Trauma can be gradual, e.g. habitual cheek containing mouthwash have been reported
biting (morsicatio buccarum, Figs 3.5 and to be associated with oral mucosal injuries
3.6), which can give rise to white lesions and ulcerations.
which are poorly outlined, macerated Treatment: Self-limiting condition. Mild
reddened areas with whitish patches of alkaline or bicarbonate mouthwash is given.
detached epithelium. These areas are rough f. Radiation mucositis: Develops secondary to
in texture, at times thicker and paler than therapeutic radiation of head and neck
adjacent mucosa. Habitual tongue biting cancer, manifested as large areas of mucosa
causes lesions which resembles hairy leuko- covered with greyish white slough alternat-
plakia, however, careful history can confirm ing with areas of more severe ulceration
the habit associated lesion. (Figs 3.9 and 3.10).
Fig. 3.5 Fig. 3.6
Figs 3.5 and 3.6: Morsicatio buccarum (habitual cheek biting)

Fig. 3.7: Thermal burn caused by hot fluid intake Fig. 3.8: Aspirin burn
Fig. 3.9 Fig. 3.10
Figs 3.9 and 3.10: Radiation-induced mucositis involving labial mucosa and tongue
Treatment urease which acts on salivary urea giving rise

Fractionization of radiation dose helps to to ammonia. Ammonia in turn acts as a
prevent mucositis. chemical irritant to oral mucosa and causes
Benzydamine hydrochloride (tantum oral burn injury (white lesion). However, this
rinse) mouthwash controls the mucositis, pathogenesis has now been questioned
reduces pain and inflammation. because
Normally heals without scarring. a. Patients with uremia/renal failure having
g. Uremic stomatitis: Relatively uncommon marked ammoniacal odor and increased
now because there is greater availability in BUN levels have presented with no clinical
treatment options for renal failure, viz. evidence of uremic stomatitis.
dialysis and renal transplant. b. Uremic stomatitis lesions often resolve
Extensive pseudomembranous white lesion despite persistently increased BUN levels.
that are sometimes seen in seriously ill patients It is, therefore, thought that other metabo-
with renal failure and excessive BUN level lites, xerostomia and secondary bacterial and
(blood urea-nitrogen level) in excess of fungal infections may account for the extensive
50 mg/dl. Salivary micro-organisms secrete white lesions of uremic stomatitis.
Koplik’s spot: (Measles) multiple yellowish Congenital: Endocrinal candidiasis

white spots on an erythematous base appear syndrome, thymoma, chronic familial
on the buccal mucosa and inner aspect of mucocutaneous candidiasis.
lower lip are pathognomonic of early measles Classification of Candidiasis
infection.
Acute—acute pseudomembranous candi-
Syphilitic mucous patch: It is a feature of
diasis—thrush
secondary stage of syphilis. Typically slightly
Acute erythematous candidiasis (atrophic)
raised, grayish white, glistening patches
antibiotic sore mouth
appear on the tongue, buccal mucosa, soft
Chronic:
palate. The whitish appearance is because of
exfoliation of fibrin and inflammatory cells 1. Chronic atrophic (erythematous)
that coagulate to form a pseudomembrane • Denture sore mouth
covering an area of erythema and inflamma- • Angular cheilitis
tion. Attempt to remove the pseudomembrane • Median rhomboid glossitis
or white patches reveal a reddened raw 2. Chronic hyperplastic candidiasis
mucosal surface underneath. In the revised classification the term
‘atrophic’ is replaced with ‘erythematous’ as
CANDIDIASIS these lesions are not actually atrophic but are
erythematous because of inflammation.
Candidiasis is known to be a disease of the
diseased and is said to affect the very young, Acute Pseudomembranous
the very old and the very sick. Candidiasis—Oral Thrush
Candida albicans is an opportunistic organism Thrush is a prototype of candidal infection
which can invade oral mucosa as a result of involving the superficial layers of oral
following predisposing factors: epithelium. The term ‘thrush’ is a name of the
1. Marked change in oral microbial flora bird having typical white spots on its chest
which resemble the candidal lesions.
2. Broad spectrum antibiotics—prolonged
use Clinical Features
3. Excessive use of antiseptics or oxygen • The lesions appear as “curd-like” bluish
liberating mouthwash white adherent plaques which can be easily
4. Xerostomia secondary to cholinergic scraped off leaving raw bleeding areas or
drugs and systemic diseases like Sjögren’s shallow ulcerations (Fig. 3.11).
syndrome and sarcoidosis • In infants, candida may be transferred
5. Denture stomatitis, orthodontic appliance from mothers genital tract and lesions
use seen as soft bluish white adherent lesions.
6. Smoking and consumption of alcohol • In adults, rapid onset of bad taste, loss of
7. Administration of corticosteroids—local, taste discrimination and burning of mouth
parenteral or aerosol form and throat are seen as prodromal symptoms.
• In adults, inflammation, erythema and pain-
8. Radiotherapy
ful eroded areas are observed and typical
9. Age is a predisposing factor—infancy and pearly white lesions are inconspicuous. It
oldage is a superficial infection of oral mucosa
10. Hospitalization and dehydration (upper layer results in formation of white
11. Immunodeficiency: patch, plaque or flecks on the mucosal
Acquired: HIV, AIDS, leukemia, lymphoma, surface that are composed of desquamated
bone marrow transplant, diabetes mellitus, epithelial cells, inflammatory cells , fibrin,
carcinoma, chemotherapy, etc. yeast and mycelia)
A B
Figs 3.11: Pre- and post-treatment pictures of pseudomembranous candidiasis involving the palate. Patient
treated with tab fluconazole 100 mg 1 od for 5 days
Diagnosis Management
From history of predisposing factors and Antifungal agents belong to 2 groups:
clinical features: • Polyenes: Mycostatin and amphotericin B
• Scrapings are stained with PAS stain, first line of treatment. Not absorbed
Sabouraud Agar media used for culture. through GI tract and do not develop
• To discriminate between different candida resistance
species Pagano–Levin agar is used. • Azoles: Miconazole, ketoconazole, itracona-
• Imprint culture—2.5 × 2.5 cm sterile plastic zole. Absorbed through GI tract. In patients
foam pads soaked in Sabouraud medium on warfarin, there is an increased propensity
are placed on the infected surface for 60 for bleeding. Candida also develop resis-
seconds. The pad is then firmly pressed on tance.
the Sabouraud agar medium and incubated Treatment
at 37°C. The result is expressed as colony
Infants: Nystatin syrup 1 ml 4 times/day for
forming units per cubic mm (CFU/cmm2).
10 days (1 ml = 1,00,000 IU)
Candidiasis patients have more than 400
CFU/cmm. This test is valuable in the Adult: Nystatin tablet (1 tab sucked in mouth)
diagnosis of erythematous candidiasis. 4 times/day for 7–10 days (1 tab = 5,00,000 IU)
• Antibody titre, i.e. salivary and serum. • Mycostatin tab, crushed and mixed with
glycerine and applied to the lesion.
• Special media for studying of spores—
OR
Rabbit coagulase plasma (EDTA).
• Clotrimazole solution (candid mouth paint)
Differential Diagnosis applied thrice daily for 7–10 days.
(Similar Appearing Lesions) OR
• ‘Interns thrush’—food debris and milk • Amphotericin B lozenges 4 tab/day for
remnants in children, antacid remaining 7–10 days.
attached to oral mucosa in very sick, OR
hospitalised patients may be mistaken for • Ketoconazole 200 mg or fluconazole 100 mg
candidal lesions by young interns. – 1 tab twice a day for the first day and once
• Chemical burns. a day for 5–7 days or till the lesions subside.
Ketoconazole and fluconazole are preferred Chronic Atrophic (Erythematous) Candidiasis

because: These lesions may be a sequelae to the pseudo-
1. These drugs reach the bloodstream and membranous candidiasis. Mainly includes:
genital lesions are also treated 1. Denture sore mouth
2. Less likelihood of reinfection 2. Angular cheilitis
3. Cheaper compared to mycostatin 3. Median rhomboid glossitis
4. Good for short-term use, i.e. no pruritus, Denture sore mouth is seen in patients wearing
abdominal pain or excessive liver enzymes. complete or partial denture, more common
Should not be given with antacids since it under the maxillary dentures. The maxillary
requires acidic medium for absorption. dentures have better retention compared to
mandibular dentures. This prevents the
Fluconazole interacts with anticoagulants,
salivary antibodies from reaching the palate
phenytoin, cyclosporin, oral hypoglycemics,
leading to greater candidial growth. Closer
antihistaminics and must be used with
adaptation of the denture to the palatal
caution. Ketoconazole when administered in
mucosa also helps the fungi on the impression
patients taking cisapride and antihistamines
surface to invade the mucosa (Fig. 3.13).
like terfenadine, astemizole can cause ventri-
cular arrhythmia and CVS complications and DSM presents three types of lesions:
hence should be avoided. i. Localised simple inflammation with
Butter milk/yogurt consumption 2–3 times pinpoint hyperemia.
a day is also found to be useful. ii. More diffuse erythema involving entire
denture bearing area.
Acute Atrophic (Erythematous)
Candidiasis/Antibiotic Sore Mouth iii. Granular or nodular type (palatal papillary
hyperplasia).
It is manifested after a long administration of
antibiotics. Patients start complaining of PPH: Multiple nodules on erythematous
severe burning sensation of oral mucosa, background gives an ‘over ripe strawberry
change of taste and also sore throat. It is seen appearance’ (Fig. 3.14). Antifungal therapy
as raw and reddish painful areas of mucosa modifies slight red inflammatory appearance
with or without angular cheilitis or thrush. but the basic nodular or papillomatous lesion
Patients taking inhalation steroids also still persists. Therefore, has to be surgically
develop erythematous lesions on the palate removed. But antifungal treatment is indicated
and tongue dorsum. Patients with chronic iron
deficiency may also develop erythematous
candidiasis (Fig. 3.12).
Treatment
Discontinue or change antibiotics (with
physicians consent)
Give neutrolin B (resets oral flora)
Local application of clotrimazole (candid
mouth paint)
OR
Mycostatin tablet crushed and applied with
glycerin. Fig. 3.12: Erythematous candidiasis
A B
Fig. 3.13: Denture sore mouth
d. Systemic administration of fluconazole in

patients with more severe candidiasis not
responding to above treatment.
Angular cheilitis is the term used to describe
infection involving the oral commissures
which presents as fissures with erythema. It
frequently coexists with DSM (Fig. 3.15).
Etiology
a. Coinfection with Candida and Staphylococcus
Fig. 3.14: Palatal papillary hyperplasia aureus
b. Coexists with DSM and uncommon in
as elimination of inflammation leaves a firmer patients with natural dentition
tissue for surgery and often decreases the c. Diminished vertical dimension and salivary
amount of tissue to be excised. stagnation
d. Nutritional deficiency, iron deficiency
Treatment of DSM anemia, vitamin B or folic acid deficiency
a. Dentures should be scrupulously cleaned, e. Diabetes mellitus
immersing the dentures overnight and
rinsing with dilute hypochlorite/chlorhexi-
dine solution helps. However, repeated
use of chlorhexidine can stain the acrylic
dentures.
b. Refabrication of CD using zinc oxide
eugenol impression paste as it gives
smoother and easily cleanable surface as
opposed to alginate which results in rough
surface.
c. Application of clotrimazole mouth paint/
nystatin solution to the edentulous ridge
and impression surface of the denture Fig. 3.15: Angular cheilitis due to reduced vertical
before their insertion. dimensions
Cheilo-candidiasis is an extensive, des- However, MRG is not detected until late

quamative lesions affecting full width of the in life and candidal organisms has been
lip and extending to the adjacent skin caused commonly isolated from these lesions and
by—habitual lip sucking and chronic candidal hence it is considered as a candidal infection.
infection. Smokers, denture wearers and patients on
inhalation steroids are more prone to develop
Treatment
MRG. In some patients, concurrent erythe-
• Fabrication of new CD with correct vertical matous lesion may be observed on the palatal
dimension mucosa. Such coexisting lesions are termed as
• Vitamin B complex kissing lesions.
• Local application of antifungals like Coexistence of MRG, angular cheilitis and
clotrimazole (candid mouth paint) DSM has also been observed signifying fungal
• Miconazole is effective against both candida etiology.
and Staphylococcus aureus and hence Diabetes mellitus which predisposes
preferred in angular cheilitis. patients to candidiasis is another factor.
Median Rhomboid Glossitis (MRG) Impaired local blood supply, as a result of
MRG is an erythematous lesion, rhomboid or atherosclerotic changes.
oval in shape which appears in the center of Impaired immune mechanisms as evidenced
the posterior part of tongue dorsum. The by diminished concentration of Langerhans
lesion appears erythemtous because of the cells in these lesions.
absence of filiform papillae. MRG may also Management includes reduction of pre-
present a tufted, lobulated or fissured appea- disposing factors and topical antifungal
rance (Fig. 3.16). agents. Biopsy is not warranted, MRG is not
Etiology
known to have increased risk for malignant
transformation.
It was first believed that MRG is a develop-
mental anomaly in which there is persistence Chronic Hyperplastic Candidiasis
of tuberculum impar when anterior lingual Also called as candidal leukoplakia, however
swellings and hypobranchial eminence fail to now the term is replaced by ‘chronic plaque-
completely fuse. type or nodular candidiasis’.With some
efforts, lesion can be scraped off as opposed
to pseudomembranous type where the lesions
can be dislodged with ease (Fig. 3.17).
Fig. 3.16: Median rhomboid glossitis Fig. 3.17: Chronic hyperplastic candidiasis
These lesions are more often associated Following are the categories of chronic
with speckled leukoplakia. mucocutaneous candidiasis:
Epithelial dysplasia is found to be more a. Familial CMC
common in candidal leukoplakia (Fig. 3.18). b. Diffuse CMC
c. Candidiasis endocrinopathy syndrome
Carcinomatous changes are reported to
(CES)
occur more frequently in candidal leukoplakia.
d. CMC with late onset
Such lesions respond to antifungal treat-
ment. Infact, some clinicians advocate routine ID Reaction (Monilid Reaction)
use of antifungal agents in all chronic oral Patients with chronic candidiasis may develop
white lesions and it is surprising to see that secondary skin response in the form of sterile
many lesions become less extensive, leathery vesiculopapular rash (no organisms are
and satellite plaques disappear. Therefore, present), i.e. believed to be an allergic reaction
long-term treatment of oral white lesions to Candida antigen. This occurs in perioral
with antifungal agents is justified along with area and hence important to dental clinician
and these usually resolve with treatment of
retinoids, even though the relationship
Candida infection.
between Candida and epithelial hyperplasia
and risk of future malignancy remains Keratotic White Lesions with no increased
unsolved. Potential for Oral Cancer
Smokers Palate (Stomatitis Nicotina Palati)
Extraoral Candidiasis
1. Specific lesion which develops on the
Most common sites are orificial areas palatal mucosa of heavy cigarette, bidi or
(anogenital), moist folds around groin, pipe smokers.
armpits, submammary folds, nail folds, etc. 2. Palatal mucosa shows diffuse hyperkeratosis
Candidiasis can also afflict organs such as and appears greyish white and thickened.
lungs, liver, kidney, heart valves, etc. 3. The minor salivary gland ducts get blocked
by the hyperkeratosis and metaplasia of the
Chronic Mucocutaneous Candidiasis ductal epithelium occurs.
Persistent infection with candidiasis can result 4. There is retention of the secretions leading
from defect in cell mediated immunity or to multiple small nodular swellings on the
structure in epidermis palate. Ductal orifices get inflamed as a
result of retention of secretions and they
appear as red umbilicated dots in the centre
of the nodular swellings (Fig. 3.19).
5. Not a premalignant lesion unless associated
with reverse smoking commonly seen in
coastal areas of Kerala and Karnataka. The
fishermen out at sea prefer reverse smoking
as the spray of the seawater extinguishes
the bidi/cigarette repeatedly. Women folk
tend to do reverse smoking as they want to
prevent the ash falling on the baby they
have in their arms or in the food they are
cooking! Lesions associated with reverse
smoking have an increased incidence of
Fig. 3.18: Candidal leukoplakia carcinoma.
heavy metals and polonium 210 which are

potentially carcinogenic.
3. These habits lead to lesions with a malig-
nant potential. However, in early stages
tobacco pouch keratosis is more easily
reversible (Fig. 3.20).
4. Patients present with a wrinkled white
lesion, in the area where the tobacco is
placed, the teeth in this region show more
stains than the adjacent teeth and there is
marked gingival recession. In heavy users
of smokeless tobacco white and leathery
lesions develop with occasional erythro-
plasia component within the white lesion
Fig. 3.19: Smokers palate 5. Discontinuing the habit and local applica-
tion of clotrimazole (candid mouth paint)
6. Dentures are not contraindicated, in fact and vit A chewable tablets twice daily helps
they protect the palatal mucosa. to resolve the lesion.
However, if it persists biopsy must be
Smokeless Tobacco-induced Keratosis
carried out to rule out dysplastic changes.
Also called as smokeless tobacco keratosis or
snuff dippers keratosis or tobacco pouch Frictional Keratosis
keratosis. Describes an isolated area of thickened white
1. Most common smokeless tobacco habit in mucosa that is clearly related to an identifiable
India is paan chewing (betel leaf, areca nut local irritant and that resolves after the
pieces, slaked lime and tobacco), gutka removal of irritant (denture clasp, sharp teeth).
chewing and tobacco quid habit. Snuff The lesion is observed in the areas of the
dipping habit is at times observed in elderly oral mucosa subjected to increased friction,
female patients. e.g. edentulous ridge in patients not wearing
2. Smokeless tobacco contains N-nitrosonor- dentures. The lesion is asymptomatic but can
nicotine, polycyclic hydrocarbons, aldehydes, cause anxiety to the patient.
A B
Fig. 3.20: Pre- and post-treatment pictures of tobacco pouch keratosis

Treatment • Intraorally white scaly lesions affecting

Removal of the irritant and give antifungal palate and buccal mucosa appear with the
agent topically for 1–2 weeks, if lesion persists, exacerbation of skin psoriasis. Another type
advise biopsy. of lesion is well demarcated, flat and erythe-
matous lesions with raised white annular
White Sponge Nevus or serpenginous border similar to BMG.
• It is a rare disorder also called as Cannon’s • Auspitz sign is positive, i.e. removal of the
disease, white folded gingivostomatitis. scaly lesion leaves a raw bleeding area
• This condition is grouped under oral geno- behind.
dermatoses (inherited diseases affecting • Histopathologically intraepithelial micro-
oral mucosa). abscesses (Monro’s abscess) are found
• The condition may be detected in infancy within the epithelium.
but not recognised till adolescence or even Clinically and histopathologically psoriasis,
adulthood. BMG, erythema circinata migrans, Reiter’s
• The affected mucosa appears white/gray, syndrome resemble each other.
thickened, folded and spongy with irregular
Leukoplakia—Premalignant White Condition
surface (Fig. 3.21). Mostly involving the
buccal mucosa, and also extraoral sites such Def by WHO: It is a clinical descriptive term
as esophagus and anogenital mucosa. which refers to grayish white raised patch on
• This condition may be mistaken for leuko- oral mucosa which is more than 1 cm, cannot
plakia or candidiasis. History, clinical be scraped off and cannot be attributed to any
examination and histopathology can help other diagnosable disease.
to pinpoint the diagnosis. New def: Whitish patch that cannot be
• White sponge nevus is a benign and characterised clinically or pathologically as
asymptomatic condition and does not any other disease and is not associated with
require any treatment. any physical or chemical causative agent
except the use of tobacco.
Psoriasis
• Is a common dermatological condition Etiology
characterized by white, scaly papules or Traditionally ‘6Ss’ were named as etiological
plaques on erythematous base primarily factors for leukoplakia and consequently oral
affecting the extremities and scalp. cancer.
• Occasionally associated with non- Smoking, sharp tooth, spirit (alcohol),
rheumatoid arthritis affecting many joints syphilis, sepsis and spices appear to be
including TMJ. directly and indirectly relevant even today!
A B
Fig. 3.21: Thickened and folded lesions of white sponge nevus

Systemic Factors a wrinkled ‘cracked mud’ appearance on

1. Hypovitaminosis: Vit A and B complex, vit the buccal mucosa (Fig. 3.22). On the ventral
A is responsible for keratinization and its surface of the tongue leukoplakia presents
absence may give rise to leukoplakia. a corrugated ‘like a beach at ebbing tide’
2. Siderophenic dysphagia or Plummer- appearance with a pattern of fine lines
Vinson syndrome. (cristae).
3. Nutritional deficiency: Atrophic glossitis 2. Lack of painful symptoms.
(more prone to leukoplakia). 3. Loss of pliability and flexibility. Feels rough
4. Co-existence of leukoplakia with tertiary and leathery on palpation.
syphilis. 4. Lesion is well defined with no inflamma-
Local Factors tory reaction adjacent to it.
1. Trauma: Chronic irritation to sharp edges 5. Cheek mucosa, tongue, floor of mouth,
of malposed tooth, denture clasp causes mandibular alveolar ridge are the common
frictional keratosis sites.
2. Chemical/thermal: Tobacco and its combus- Speckled Leukoplakia (Nodular or Fissured)
tion products—tobacco induced keratosis
1. Appears as a white plaque within which red
3. Poor oral hygiene
areas (with missing keratinization) are
4. Electro-galvanic reaction present or small hyperkeratotic nodules
5. Alcohol scattered over an erythroplakic patch of
Clinical Features mucosa (Fig. 3.23).
Three times more common in males as com- 2. Red areas devoid of keratin are more likely
pared to females, age 40–50 years, leukoplakia to transform into malignancy, as the basal
can manifest as homogenous, speckled/ cell layer which have more rapidly
fissured and verrucous forms. multiplying cells come closer to the surface
and interact with the carcinogens present
Homogenous Leukoplakia in the oral cavity.
1. Raised, white, well demarcated plaque Also speckled appearance is because of
having identical pattern throughout the candidiasis thereby suggesting immuno-
lesion. The surface texture varies from logical factors active in that area which could
smooth to leathery with fissures which give predispose to dysplastic changes.
A B
Fig. 3.22: Examples of cracked mud appearance in homogenous leukoplakia

A B
Fig. 2.23: Examples of speckled leukoplakia
In short a combination of red and white is

considered more dangerous as far as the dys-
plastic changes in leukoplakia are concerned.
Verrucous Leukoplakia
• The oral white lesion in which the surface
is thrown into multiple papillary projec-
tions the surface resembles turkish or
sponge towel (Fig. 3.24).
Proliferative Verrucous Leukoplakia
• Suspected to have a viral etiology because
it clinically resembles papilloma.
• PVL is usually encountered in older women
and lower gingiva is a predilection site. Fig. 3.24: Verrucous leukoplakia
• As the name suggests this leukoplakia is
extensive and involves a large area and thin epithelium and are non-keratinized,
presents typical papillary projections on the thereby bringing the rapidly dividing basal
surface (Fig. 3.25). cell layer closer to the carcinogens.
• Known to have a high malignant potential. The floor of mouth is called as the ‘sump of
Leukoplakias on the ventral surface of the the oral cavity’ which leads to pooling of saliva
tongue and floor of the mouth have high (with carcinogens) due to gravity leading to
malignant potential because these areas have greater action of the carcinogens.
A B
Fig. 3.25: Examples of proliferative verrucous leukoplakia

staining glycogen. When 2% Lugol’s iodine is

applied to the normal oral mucosa it takes up
a deep mahogany brown stain. During this test
the stain is applied to the lesion and adjacent
uninvolved mucosa. If the lesion takes up
same stain as the adjacent mucosa it is lichen
planus, if the lesion takes up no stain it is
leukoplakia and if the lesion takes up a deeper
stain than the adjacent mucosa it is considered
traumatic lesion (Fig. 3.27).
Fig. 3.26: Smokers patch 3. Toluidine Blue Test

This test is carried out before biopsy as it helps
If leukoplakia affects the tongue, it gives to select the site. Mechanism of increased up-
rise to depapillation. take of the dye by the dysplastic or malignant
On the lip smokers patch is observed as a lesions can be explained as follows:
diffuse white lesion with red dots of minor a. Toluidine blue is a basic dye, having an
salivary glands (Fig. 3.26). At the commissures, affinity for acidic DNA content present in
leukoplakia can either be homogenous or the rapidly multiplying dysplastic cells.
speckled.
b. There is a greater diffusion of the dye
Diagnosis through the haphazardly arranged tumour
cells.
1. Clinical Features
c. There are channels in the tumour cells
Presence of a non-scraple and hyperkeratotic through which diffusion takes place.
white lesion as described above especially in
Toluidine blue test is helpful as there a
patients with tobacco habit easily helps in
greater dye uptake and retention in dysplastic
suspecting or diagnosing leukoplakia. But
areas of leukoplakia, erythroplakia which
clinical appearance is a poor indicator of its
helps to select the site for biopsy (Fig. 3.28).
behaviour and histological features.
Toluidine blue helps the surgeon to deter-
2. Lugol’s Iodine Test mine the boundaries of the lesion to be excised.
Has been useful to differentiate between It also helps to differentiate between chronic
leukoplakia, lichen planus and traumatic non-healing ulcer seen after radiotherapy and
lesion. Lugol’s iodine has a property of persistent or recurrent lesion of malignancy.
A B
Fig. 3.27: Lugol’s iodine test. (A) Leukoplakia does not take up stain; (B) Lichen planus stains as much as
adjacent uninvolved mucosa
A B
Fig. 3.28: Toluidine blue stain—positive uptake in speckled leukoplakia
The drawback of toluidine blue is that it Punch or scalpel biopsy followed by histo-
may also stain traumatic/inflammatory lesions pathology is the gold standard in the diagnosis
(false positive reaction). In such cases, sympto- of leukoplakia, and the oral pathologist has
matic treatment is given and the test repeated the last word!
after 14 days if the lesion persists.
Exfoliative Cytology 1. Erythroplakia—red in color
Indicative of the true nature of the lesion but 2. Benign inflammatory lesion—toluidine blue
not very reliable as only superficial cells are helps in diagnosis
screened. Papanicolaou stain is used. 3. Early CA
4. Linea alba—disappears on stretching the
Biopsy mucosa.
Cytobrush, brush with firm bristles that pierce 5. Leukoedema—whitish opalescent wrinkled
the mucosa and obtain individual cells from water logged appearance of cheek mucosa
its entire thickness, i.e. transepithelial sample seen in dark individuals and smokers,
unlike exfoliative cytology which collects only lesion disappears on stretching the cheek
superficial cells. Oral CDX system also uses and is generalised.
computer software to locate and detect the 6. Lichen planus—no tobacco habit, bluish
abnormal cells which makes the task of the white lesion, lace like pattern, mucosa is
oral pathologist less laborious (Fig. 3.29). pliable dendritic processes and Wickham
A B
Fig. 3.29: Brush biopsy

striae are seen. Iodine test shows uptake • Clotrimazole mouth paint (candid) local
in equal amount. Irregular lesion. No application thrice daily
depapillation of tongue. • Antioxidants such as antoxid twice a day
7. White sponge nevus present since early age for a month (to start with) continued as once
appears whitish and spongy. a day thereafter.
8. Candidiasis—predisposing factors present
Mode of Action of Vitamin A
it is scrapable and treated with antifungal
agents. • Interferes with pathological keratinization
• Stimulates cellular mitotic activity of the
Classification and Staging of Oral Leukoplakia epithelial mucosa
Provisional or clinical diagnosis: • Its absence causes cell changes and keratini-
zation.
L—extent S—site C—clinical
of leukoplakia aspect Side Effects
L0—no e/o S1—all sites C1—homogenous Alopecia, weight loss, increased liver enzymes,
lesion excluding floor C2—non liver damage, dependent edema. Vitamin A
L1—less than of mouth and homogenous
2 cm tongue Cx—not specified
is avoided in pregnancy because of possible
L2—2–4 cm S2—floor of teratogenic effects.
L3—more than mouth and/or Mode of Action of Antioxidants
4 cm tongue
Lx—not specified Sx—not specified Quenches free radicals.
Note: When Not to follow prescribe, ‘wait and
Definitive (Histopathological Diagnosis) watch’ policy
P—histopathological features 1. If lesion is on the floor of mouth or ventral
P1—no dysplasia surface of tongue.
P2—mild dysplasia 2. If the lesion is red and white, i.e. speckled
P3—moderate dysplasia or erythroplakic and coexists with SMF.
P4—severe dyspalsia 3. If leukoplakia is generalised like PVL or is
Px—no specification associated with other mucosal disorders.
Staging 4. In patients susceptible to oral CA, e.g. heavy
smokers, alcoholic, presence of dysplastic
Stage 1: Any L, S1, C1, P1 or P2 oral lesions.
Stage 2: Any L, S1 or S2, C2, P1 or P2
5. If there is doubt about association between
Stage 3: Any L, S2, C2, P1 or P2
suspected irritant and the lesion.
Stage 4: Any L, any S, any C, P3 or P4
6. If lesion is observed in patients without
Treatment tobacco habit as it is likely to be of viral
• Vit A, tretinoin, retinoids, antifungals (HPV) etiology and more aggressive.
• Patients with homogenous leukoplakia are If leukoplakia is speckled or on the ventral
instructed to Stop Habit and prescribed anti- surface of tongue or floor of mouth biopsy is
fungals and vit A and recalled after 10 days carried out and depending on the histopatho-
• Vit A chewable (50,000 IU): Twice a day for logical findings the patient is given vitamin A
30 days (to start with) continued as once a supplements or if dysplastic changes are
day thereafter, patients are instructed to present, refer to oncosurgeon.
chew/dissolve the tablet in mouth—swish Surgical excision of leukoplakia with laser
and swallow or cryosurgery is preferred by some clinicians.
ERYTHROPLAKIA Wickham’s striae. Oral lesions are commonly

seen either with skin lesions or can occur
It comprises eroded red lesion with clear independently.
demarcation from adjacent normal mucosa
(Fig. 3.30). Etiology—Unknown
Unlike lichen planus, erythroplakia patients There is cell-mediated immunologically
are asymptomatic. Erythroplakia may be induced degeneration of basal cell layer of
overlooked as on cursory examination it epithelium.
resembles traumatic lesion. History and closer T-lymphocyte cytotoxicity directed against
scrutiny makes the real nature of this lesion antigens expressed by the basal cell layer. This
apparent. gives rise to liquefaction degeneration of basal
Reverse smoking, i.e. chutta smoking cells and there is T-lymphocyte dominated
practiced in India is associated with a special infiltrate in the subepithelial region.
form of erythroplakia—well demarcated red Seen in patients with tension, anxiety,
areas, along with ulcerations and pigmenta- worry, excessive physical and emotional stress
tions. Patient’s holding post of a great responsi-
Biopsy is essential to rule out malignant bility and facing inescapable and stressful
changes. Treatment is similar to that of situations.
leukoplakia. Two forms of lichen planus:
a. Non-erosive
Malignant transformation of leukoplakia
6.9% according to Warnakulasuriya (2011). b. Erosive
Non-erosive Lichen Planus Types
LICHEN PLANUS 1. Linear: Seen on buccal mucosa, lips as a thin
Term lichen planus is derived from similarity linear lace like bluish white lesion at
which exists between lichen planus and periphery of which are flame-shaped
pattern mode by fungi and algae on certain dendritic processes (Fig. 3.31).
rocks where they symbiotically exist. It is an 2. Papular seen as multiple raised small bluish
immunologically mediated skin condition white papules (Fig. 3.32).
wherein purplish blue coloured papules 3. Reticular: Seen more commonly on buccal
appear on the skin with severe itching sensa- mucosa as bluish white striae arranged in
tion. When studied closely lesion shows a network pattern (Fig. 3.33).
A B
Fig. 3.30: Erythroplakia showing positive uptake with toluidine blue

Fig. 3.31: Linear variant of lichen planus Fig. 3.32: Papular variant of lichen planus
Fig. 3.33: Reticular variant of lichen planus
4. Annular: Bluish white lace-like lesions

arranged in a circular or ring-like pattern
(Fig. 3.34).
5. Plaque-like: A bluish white lesion like a
plaque, i.e. with an oval or rounded geo-
metric shape more commonly seen on the
tongue dorsum and sometimes buccal
mucosa. Plaque-like lesion of lichen planus
on the tongue can be differentiated from
leukoplakia as in leukoplakia the lingual
papillae disappear within the lesion
whereas in lichen planus they persist and
also careful examination mostly shows the
striae of lichen planus elsewhere in the oral
cavity (Fig. 3.35). Fig. 3.34: Annular variant of lichen planus
A B
Fig. 3.35: Plaque type lichen planus
A B
Fig. 3.36: Erosive variant of lichen planus
Erosive Lichen Planus Significance of diagnosing and suspecting

• As the name suggests the patient presents this syndrome is that erosive lichen planus
with red erosive lesions accompanied with is treated by corticosteroids while diabetes
severe burning sensation, causing intole- is aggravated by steroids as it causes hyper-
rance to spicy food. At the periphery of glycemia and also increases the hypertension.
these erosive lesions invariably there is So once erosive LP is diagnosed DM and
typical bluish white lace-like striae of lichen HT should be ruled out before starting with
planus (Fig. 3.36). steroids.
• Erosive lichen planus can show extensive
involvement of buccal mucosa, tongue,
ventral surface, floor of mouth, palate, lips,
gingiva making the patient quite miserable.
• Lichen planus affecting gingiva leads to
desquamative gingivitis (Fig. 3.37) further
increasing the patient’s discomfort during
mastication.
• Grinspan syndrome was believed to be a
triad of—erosive lichen planus + diabetes Fig. 3.37: Desquamative gingivitis with peripheral
mellitus + vascular hypertension bluish striae
• It is now believed that erosive lichen planus • Topical steroids: Clobetasol propionate
in grinspans syndrome is actually a ointment (tenovate) local application thrice
lichenoid reaction to the antihypertensive daily 10–15 days and then tapered or
or hypoglycemic drugs. triamcinolone acetonide 1% oral paste
• Bullous lichen planus is rare and may (kenacort/tess) local application thrice
sometimes resemble linear IgA disease, daily for 15 days and then tapered.
presentation similar to erosive lichen Or
planus. Tab betamethasone 0.5 mg (betnesol)
• Skin lesions of lichen planus have been 1–1–1–1 × 5 days (to be dissolved in the
described with ‘5Ps’ as—purplish, pruritic, mouth)
polygonal, planar, papules.
1–1–1 × 5 days
• The skin lesions are seen as purplish papules
on the flexor surfaces of arms and legs with 1–1 × 5 days
severe itching sensation (Fig. 3.38). The 1 × 5 days
patients report relief after intense scratching Dissolve in the mouth, swish and swallow.
but the trauma involved aggravates the Swish and spit to avoid undesirable side-
disease this is called as Koebner’s pheno- effects of steroids in diabetes mellitus,
menon. Genital mucosa is a common hypertension, acidity, peptic ulcer cases.
extraoral site for lichen planus. • In desquamative gingivitis prefabricated
• Nail involvement with lichen planus gives plastic/soft acrylic trays are used to carry
rise to fissuring and ridging and at times the steroid ointment or solution for longer
described as pup tent appearance. and better effect. Removal of local factors
like supra- and subgingival calculus is
Treatment essential to improve the response of the
Initiated only if patients are symptomatic: gingiva to therapy.
• Patients are asked to stop tobacco habit if • If erosive LP lesion is localized and not
any. responding to topical steroids, intralesional
• Assurance to patient that lesions are less injection of triamcinolone acetonide (10 or
likely to turn malignant (0.2%) compared 40 mg) + local anesthetic is given, usually
to leukoplakia (6.9%) and emphasizing the healing takes place after 2–3 injections.
need for regular follow-up. • Vit A chewable tablets 50,000 IU twice a day
for 30 days or more can be given after the
erosive lesions show improvement with
steroids. Topical retinoids, tretinoin,
systemic etretinate are found to be useful.
• Topical application of cyclosporin tried as
2nd line of therapy OR topical application
of 1% tacrolimus (tacroz cream) has also
been tried with success, however, has been
associated with risk of developing CA or
lymphoma and hence to be used with
caution.
• PUVA therapy, i.e. psoralen and ultraviolet
Fig. 3.38: Dermatological manifestation of cutaneous light has also been tried.
lichen planus • Other therapies: Griseofulvin , and dapsone.
Lichen planus does not have a complete Drugs

cure and can recur. This fact should be made Antimicrobials Streptomycin, PAS, tetra-
clear to the patients before starting the therapy cycline, dapsone
to avoid disappointments. As the LP lesions Antihypertensives ACE inhibitors
persist or recurs patients become anxious and Antiparasitic Chloroquine, quinacrine
develop cancerophobia, hence require Anti-arthritic Colloidal gold, aurothio-
counselling and reassurance. glucose
Anxiolytic Lorazepam
Differential Diagnosis NSAID Ibuprofen
1. Lichenoid reaction: H/o taking certain medi- Oral hypoglycemic Tolbutamide, chlorpropa-
mide
cation, lesion disappears after stopping the
Uricosuric Allopurinol
medication.
2. Leukoplakia: Tobacco habit, typical plaque Lichenoid Contact Reactions (LCR)
with cracked mud appearance, no peripheral • Considered as a delayed hypersensitivity
striae, lesion rough and leathery to feel, reaction to dental restorative materials
speckled variety shows red areas without (Fig. 3.39).
the peripheral striae and are asymptomatic • Mercury is considered as an etiologic factor.
unlike the erosive LP. Amalgam, casting metals, composites can
3. Leukoedema: White, opalescent, wrinkled, also cause LCR.
water logged appearance, disappears on • Both DILR and LCR lesions resemble
stretching. reticular/erosive LP lesions. LCR lesions
4. Pemphigus: Pemphigus shows positive appear in proximity to the offending mate-
Nikolsky’s sign and loosely attached rial. These lesions disappear on removal of
epithelial tissue at periphery while LP the restorative material. Similarly the DILR
shows bluish white dendritic processes at lesions disappear once the drug in question
the periphery. On biopsy—pemphigus will is replaced.
show acantholysis. LP shows juxta- Lichenoid Reactions of Graft-Versus-Host
epithelial band of inflammatory cells, saw Disease (GVHD)
tooth appearance of rete ridges and
• These lesions are seen in patients who have
indistinct basement membrane. Cicatricial undergone allogenic bone marrow trans-
pemphigoid and LP present as desquama- plantation for the treatment of leukemia.
tive gingivitis but CP shows no striae
peripherally and there is history of bulla
formation.
5. DLE lesions have white striae giving a
brush border appearance surrounded by
red telangiectatic halo, lichen planus on the
other hand has red central lesion surroun-
ded by bluish white striae.
Lichenoid Reactions
Associated with drugs called as drug-induced
lichenoid reactions (DILR). The list of drugs Fig. 3.39: Lichenoid reaction secondary to amalgam
causing LR is quite exhaustive. restoration
• In GVHD, it is the transplanted immuno- • The oral lesions of SLE and DLE are similar
competent tissue that attempts to reject the and the typical lesion comprises white striae
tissues of the host. The donor T cells with radiating orientation, these terminate
recognise the host cells as foreign and react sharply towards the centre of the lesions
against them. which has a more erythematous appea-
• The mouth is a sensitive reflector of rance. At the periphery the striae appear
reactions associated with bone marrow diffusely distributed and hence called as
transplantation. The oral changes in such brush border, surrounding this there is a
cases could be due to: red telangiectatic halo.
1. Chemotherapy induced ulcerations • LE lesions can occur on palate, gingiva,
2. Opportunistic infections like candidiasis buccal mucosa, tongue. The palatal lesions
as immunity is suppressed are dominated by red lesions without the
3. Unusual viral infections like chronic white brush border.
herpes, CMV • The classic skin lesions are described as
4. Drug induced lichenoid reactions (DILR) butterfly rash or malar rash—well-
5. GVHD associated lichenoid reactions demarcated cutaneous lesions which are
In GVHD, the lichenoid reactions are similar round or oval erythematous plaques with
to the skin and oral lesions of lichen planus. scales and follicular plugging on the cheeks
There is a history of leukemia requiring the and nose.
bone marrow transplant.
The management of oral lesions is similar Management
to that of lichen planus. Potent topical steroids like clobetasol propionate
gel, betamethasone solution can be topically
LUPUS ERYTHEMATOSUS applied. Steroids and immunosuppressive
• Represents the classic prototype of auto- drugs used to treat SLE may cause candidiasis
immune disease. It has a genetic predisposi- and antifungal treatment is necessary. Patients
tion with elevated risk of siblings to develop with SLE undergoing dental treatment may
LE. require monitoring, physicians consent and
• SLE more common in females than males increased dose of steroids to prevent adrenal
(10:1) crisis.
Lupus erythematosus is associated with
following clinical manifestations: ORAL SUBMUCOUS FIBROSIS
• Multisystem autoimmune inflammatory According to Pindborg, SMF may be defined
disease (that may be fatal), which includes as an insidious chronic disease affecting any
renal disorder, arthritis, hematologic part of oral cavity and sometimes pharynx
disorders such as hemolytic anemia, leuko- although occasionally preceded by and/or
penia, TCP. associated with vesicle formation, it is always
• Neurologic disorder: seizures, psychosis associated with juxta-epithelial inflammatory
• Higher titre of antinuclear antibody reaction followed by a fibroelastic change of
• Onset associated with drugs such as: the lamina propria with epithelial atrophy
– Hydralazine, methyldopa, chlorproma- leading to stiffness of the oral mucosa and
zine, quinidine causing trismus and inability to eat. It is
– Anti-arrhythmic—procainamide considered that the term SMF is incorrect since
– Antibacterial—isoniazid the deposition of fibrous bands is juxta-
– Anticonvulsant—phenytoin epithelial and not submucous.
Etiology is not known. Following factors are

considered:
• Autoimmune background
• Betel quid habit: With areca nut
• Chillies: Capsaicin
• Deficiency of vitamins and degeneration of
muscles
• Eosinophilia and ESR raised
• Fibrin producing factors
• Genetic predisposition
• HLA DR3
• Fe (iron) deficiency anemia
Fig. 3.40: Healing lichen planus with pigmentation
Conclusive evidence that areca nut—
containing arecoline, tannin and copper • Tongue appears depapillated and feels hard
contribute to collagen deposition in the sub- on palpation.
epithelial region leading to SMF. • Soft palate movement becomes restricted
Clinical Presentation associated with change in voice.
• Patients experience difficulty in self-
• Burning sensation with or without spicy
cleansing, brushing, etc. and dental sur-
food.
geons find difficulty in treating the patients.
• Progressive inability to open the mouth,
blow the cheeks, protrude the tongue. Grading of SMF [Warnakulasuriya, 2010]
• Blanching of oral mucosa which is due to Grade I: Burning sensation, blanching or
decreased vascularity, increased fibrosis leathery mucosa ID (interincisal distance)
(Fig. 3.40). Patches or spots of melanin >35 mm
pigment appear on the whitish blanched
Grade II: Moderate limitation of opening ID
mucosa giving a marble-like appearance.
20–35 mm
• Fibrous bands on palpation, involving the
orbicularis oris, buccal mucosa and poste- Grade III: Severe SMF limitation of opening
riorly soft palate, faucial pillars, uvula which <20 mm
looks shrunken and bud-like (Fig. 3.41). Grade IVA: OSMF coexisting with potentially
• Erosive lesions preceded by vesicles and malignant disorders, e.g. leukoplakia, erythro-
causing extreme intolerance to spicy food. plakia
A B
Fig. 3.41: Submucous fibrosis—fibrous bands and blanching of the palate and lower lip
A B
Fig. 3.42: Submucous fibrosis—blanching and fibrous bands of upper and lower lips
Fig. 3.43: Ulceroproliferative growth with SMF
Grade IVB: OSMF with oral epithelial dysplasia Injection Triamcinolone acetonide (kenacort
Grade V: OSMF coexisting with squamous cell 30 mg) (10 such inj, 1 inj biweekly for 5 weeks).
carcinoma (Fig. 3.43). OR
Malignant transformation in OSMF patients Inj Hyaluronidase 1500 IU mixed with
is high, i.e. 7–13% incidence at 10-year period LA – 1 injection biweekly for 5 weeks.
is approx 8%.
OR
Treatment Inj Plancentrex 1 inj biweekly for 5 weeks.
It is important to counsel the patient and
Vitamin E has been tried: It prevents oxida-
inform him of the incurable nature of this
tion of certain essential cellular constituents
condition and not to paint a rosy picture of its
and protects against various drugs and metals
prognosis.
and acts as scavenger of free radicals.
Stoppage of the habit.
Antioxidants are prescribed.
Intralesionl injections are preferably given
with the syringe and needle normally used for Surgical treatment: Reserved for more severe
administering insulin. The needle is pierced form of SMF and include surgical excision and
submucosally and the injection solution is laser ablation of the fibrous bands followed
deposited slowly with minimal pressure at by numerous reconstructive approaches such
multiple points. as split thickness skin grafting. Buccal pad of
fat, tongue flap, palatal island flap, nasolabial To summarize, the treatment of SMF
flap and temporal fascia. whether by medical or surgical options is far
Temporal myotomy and coronoidectomy from satisfactory and this dreadful disease
have been advocated. seems to have no cure at present.
Oral physiotherapy, jaw stretching exercises Suggested Reading
with special device, balloon blowing exercise.
Prognosis: Poor, intralesional injections 1. Burket’s Oral Medicine, 9th, 10th and 11th
control the burning sensation and improve the editions.
opening to a certain extent in milder SMF. 2. Oral and Maxillofacial Pathology by
Surgical method gives good improvement in Neville, 3rd edition.
opening initially but fibrosis during and after 3. Shafer’s Textbook of Oral Pathology, 6th
healing seems to reduce the beneficial effect. edition.
4
Gingival Enlargement
In healthy individuals the marginal gingiva c. Poor oral hygiene: Calculus, materia alba
is situated at the CEJ and the epithelial attach- d. Occlusal interferences
ment is well preserved, with no deepening of e. Habits: Mouthbreathing, misuse of toothpick
the gingival sulcus and the gingiva charac- Gingival enlargement caused only by local
teristically shows stippling. Absence of factors will be localised to that particular area
stippling is suggestive of edematous changes and involve either buccal or lingual side only.
associated with inflammation. Mouthbreathing is associated with class II
For the sake of clarity and simplicity the malocclusion or nasal obstruction or abnormal
terms hyperplasia/hypertrophy are avoided facial development and gives rise to alternate
here and if a patient presents with the evidence moistening and dehydration of gingiva which
of marginal gingiva present coronal to the CEJ, acts as an irritation to gingiva and leads to
we term it plainly as gingival enlargement. gingival enlargement.
Classification Treatment
I. Such patients are referred to ENT to rule out
and treat enlarged adenoids or other obstruc-
1. Inflammatory: Gingival tissue becomes fiery
tions. Protective ointment can be applied;
red, edematous, tender shiny (loss of
mouthguards can be prepared (provided the
stippling) and bleeds easily.
nasal obstruction is treated); orthodontic
2. Fibrotic: Gingiva is pale in color, surface is treatment can be done to correct malocclusion
coarse, granular fibrous and pink and does
not bleed easily. II. Systemic Factors
II.
a. Inflammatory
i. Nutritional—scurvy
According to etiological factors:
• B complex deficiency
I. Local factors
ii. Endocrinal cause—puberty
II. Systemic factors
• Pregnancy
I. Local Factors • Menstruation/menopause
a. Tooth: Malposition, fracture, malposed • Oral contraceptives
contacts iii. Diabetes
b. Restoration: overhanging, class II, cast iv. Blood dyscrasias—leukemia, polycythemia
partial denture vera
76
Gingival Enlargement 77
b. Fibrotic At times the gingival epulis appears as a

i. Drugs like dilantin, nifedipine, cyclosporin, reddish nodular growth and histologically
oral contraceptives may show dilated capillaries. This is
ii. Idiopathic diffuse fibromatosis termed as telangiectatic granuloma, and
c. Localized gingival growth: The term ‘epulis’ might present with associated bone loss
literally means ‘upon the gums’ and these (Figs 4.3 and 4.4).
are seen as exophytic pedunculated growths • Pregnancy appears similar to the vascular
attached to the gingiva. epulis and is known to resolve after
• Epulis types: Fibroid—appears as pale in parturition (Figs 4.5 and 4.6).
color and might show calcification on
radiograph (Fig. 4.1). • Neonatal: Is made up of embryonic cells
• Giant cell: May appear brownish in color and is rarely manifested.
due to the areas of hemorrhage within the If gingival enlargement is caused by
growth. Hyperparathyroidism should be systemic factors (not local factors) then the
suspected and ruled out in these cases. involvement is seen in all the four quadrants
• Vascular: Appears dark red or purplish in and both the buccal as well as lingual/palatal
color (Fig. 4.2). gingiva are involved.
Fig. 4.1: Fibroid epulis Fig. 4.2: Vascular epulis
Fig. 4.3: Telangiectatic granuloma Fig. 4.4: IOPA showing bone loss between 13 and 14
Fig. 4.5 Fig. 4.6
Figs 4.5 and 4.6: Pregnancy epulis
SCURVY Intraoral manifestations of scurvy are as

follows (Figs 4.7 to 4.9):
It is a manifestation of vit C deficiency. The
primary function of vit C is to produce and
maintain the health of collagen. Deficiency of
vit C results in defective collagen formation
between the endothelial cells leading to
increased capillary fragility and delayed
wound healing. It presents with weakness,
hemorrhage, anaemia. Hemorrhage may be
pinpoint, ecchymosis or hemarthrosis.
Perifollicular hemorrhages have also been Fig. 4.7: Purplish red gingival enlargement in
observed in some patients. Patients suffering scorbutic patient
from scurvy have extreme tenderness of the
lower limbs and of the knee joints which is
believed to be due to subperiosteal hemorr-
hage and hemarthrosis. As a result of severe
pain the scorbutic child assumes a ‘frog-like
position’ and is unable to stand up. Fatigue
and apathy is also noted.
Deficiency of vit C seriously affects cells like
osteoblasts, fibroblasts, odontoblasts, etc. Due
to defective cells their products are also Fig. 4.8: Improvement seen after vitamin C
administration
defective and ability of cells to form connective
tissue elements and vascular tissue is seriously
affected. This leads to increased tendency of
bleeding, osteoporosis, impaired wound
healing. Vit C also plays an important role in
absorption of iron.
Vit C or ascorbic acid is found abundantly
in citrus fruits and hence this condition has
become extremely rare as vit C is very much
part of day-to-day diet and deficiency is Fig. 4.9: Further improvement in same patient after
unlikely to manifest. prophylaxis
1. Enlarged, purple, spongy gingiva is seen. 3rd Trimester

2. Bleeding of gingiva on slightest pressure. Lasting from 7th month to 9th month.
3. Breakdown of PDL fibers and alveolar bone a. During this stage premature delivery
leading to mobility of teeth. becomes a hazard.
4. It increases the susceptibility to develop
fusospirochetal infection. b. Prolonged chair time should be avoided.
5. Delayed wound healing. Supine hypotensive syndrome may occur.
When the pregnant patient is in a semi-
Treatment reclining or supine position, the inferior vena
Vit C tab 500 mg TDS for 3 months cava is compressed by the uterus, thereby
Vit C is also necessary for: reducing venous return to the heart causing
• Formation of osteoid, bone, dentin hypotension and decreased cardiac output
• For healing of wound and eventual loss of consciousness. This can
• For Hb formation be reversed by turning the patient to the left
lateral position thereby relieving the pressure
Puberty and Menstruation on the inferior vena cava. During third
During puberty and menstruation, pain, trimester the diaphragm is pushed upwards
swelling and hyperplasia of gingiva is noticed. thereby compressing the lungs and hence the
There may be gingival bleeding. Other patients are prone to feel dyspnoeic or breath-
findings are: less.
Recurrent herpes labialis.
Oral changes in pregnancy are seen in 2nd
Recurrent aphthous stomatitis.
trimester onwards and are as follows:
Pregnancy 1. Pregnancy gingivitis: Diffuse inflammatory
Normally pregnancy lasts for 40 weeks in gingivitis with bleeding and hypertrophy
which many physiologic changes occur in of interdental papilla.
body, e.g. increased cardiac output, increased 2. Pregnancy epulis (see Figs 4.5 and 4.6)
blood pressure, increased plasma volume,
increased heart rate, mild hypertension, a. It is a purplish-red or deep-blue swelling
increased estrogen and progesterone. either sessile or pedunculated arising from
Pregnancy period is divided into 3 trimesters. interdental papilla.
b. Color depends on the vascularity of the
1st Trimester
lesion; degree of venous stasis and size of
a. Period of organogenesis the pedicle.
b. Approx. 75 to 80% spontaneous abortions
c. Hemorrhage is the most frequent and
occur before the 16th week
important symptom and pain is usually
c. The fetus is very sensitive to environmental absent.
influences.
d. The swelling may also show ulceration in
Due care has to be taken to protect the foetus
the area where it is traumatized by the
from any harm (developmental malformations)
opposing teeth.
during this period. (Avoid X-rays, unsafe
drugs, lengthy and stressful dental treatment.) These changes are believed to be due to
exaggerated response to local irritants due to
2nd Trimester increased levels of estrogen and progesterone.
Lasting from 3rd to 6th month is considered Majority of these lesions regress after parturi-
relatively safe for selective dental treatment. tion and rarely require surgical intervention.
Dental Treatment Subleukemic Leukemia

1. Give maximum protection to mother and Blood count is normal but WBCs are neo-
foetus. Avoid radiographs (remember to plastic and immature.
use lead apron to protect the fetus when Leukemia is also classified depending on
radiography is unavoidable) traumatic the cells of origin, i.e. primary hematopoietic
surgeries; unsafe drugs and tetracycline. cell line affected, i.e. myeloid or lymphoid.
Drugs considered safe: Penicillin, amoxicillin, The four principal types are:
cephalosporins, paracetamol, lidocaine. 1. Acute myelogenous leukemia (AML)
Drugs which must be avoided: Tetracyclin, 2. Acute lymphocytic leukemia (ALL)
aspirin, carbamazepine, diazepam, thalido- 3. Chronic myelogenous leukemia
mide. 4. Chronic lymphocytic leukemia
2. Stress on the importance of good oral
Etiology
hygiene.
1. Viruses: They are believed to trigger
3. Avoid treatment in 1st and 3rd trimesters.
unknown biochemical abnormality in
2nd trimester is preferred for treatment.
DNA.
However, stressful procedures like single
sitting root canal treatment, periodontal 2. Radiation: Leukemia is seen commonly
surgeries, disimpactions should be avoided. amongst radiologists and victims of atomic
explosion.
3. Chemicals: Such as benzene and its
LEUKEMIA
derivatives can cause leukemia.
It is a neoplastic proliferation of precursor cells 4. Philadelphia chromosome: 85% of cases of
of WBCs demonstrated in peripheral blood CML shows reciprocal translocation of long
smear or bone marrow or in organs such as arm of chromosome 22 to chromosome 9.
liver, spleen, lymph nodes.
Acute Leukemias
In leukemia, WBCs are immature and their
number is increased (>2 lacs). Signs and Symptoms
Leukemia is classified according to clinical a. Due to bone marrow suppression:
behaviour as acute or chronic. i. Anaemia: Causing pallor, dyspnea, fatigue
If leukemic cells are more anaplastic and ii. Thrombocytopenia: Causing hemorrhages
immature then the disease runs a rapid course (Figs 4.10 and 4.11): Purpura, ecchymosis,
leading to death. Such a type is called as acute epistaxis, gingival bleeding, melena, etc.
leukemia. Chronic leukemia on the other hand iii. Decreased functioning of WBCs: As WBCs
runs a slower course and shows comparatively are immature, phagocytosis and bacteri-
more mature WBCs. Acute leukemias are cidal functions are affected thereby
more common in children below 6 years and increasing susceptibility to infections like
in adults above 60 years. ALL more common URTI , UTI with accompanying fever.
in children and AML in adults. Chronic leuke- b. Due to leukocytic infiltration: Lympha-
mias more common in adults. denopathy, splenomegaly, hepatomegaly,
Chronic leukemia is found in the age group cranial nerve palsy, paresthesia, anesthesia
of 30–40. is seen
Chloromas are collection of leukemic cells
Aleukemic Leukemia having green color surface which turns blue
Bone marrow shows leukemic cells but on exposure to light due to presence of
peripheral smear does not show them. enzyme myeloperoxidase.
Fig 4.10 Fig 4.11
Figs 4.10 and 4.11: Showing ecchymosis and petechiae in aleukemic patient
Oral manifestations are commonly seen in hemorrhage and also necrosis. The gingi-
leukemic patients and indeed the dental val enlargement is caused by the leucocytic
clinician may be able to suspect the presence infiltration.
of this serious condition by careful observation • Necrotic ulceration of mouth without any
of clinical signs and symptoms. inflammatory halo.
Oral manifestations of leukemia are as follows: • Recurrent infections
• Persistent gingival bleeding: Oral problems • Pallor
are more common in patients with acute • Bald tongue
leukemia than in patients with chronic
leukemia and gingival bleeding is the most
common presenting symptom and is
mainly caused by thrombocytopenia.
• Gingival enlargement (Figs 4.12 to 4.14):
Inflammatory enlargement present in all the
four quadrants, involving both the buccal
and lingual gingiva. The gingiva which is
purplish red in color, covers more than half
or at times the entire clinical crown of the Fig. 4.12: Enlargement of labial gingiva upper and
teeth, in certain areas shows evidence of lower arches
Fig 4.13 Fig 4.14
Figs 4.13 and 4.14: Buccal and lingual gingival enlargement involving upper and lower arches
• Noncarious teeth suddenly become non- Prognosis is good for chronic leukemic
vital and develop pulpal abscess. patients in whom remission occurs in 2–3
years.
Radiographic Findings
• Destruction of alveolar bone Oral and Dental Considerations
• Loss of lamina dura, increased bone 1. Necessary to have high suspicion index,
marrow spaces leading to step ladder advisable to get blood examination done in
pattern of trabeculae. almost all patients showing gingival
enlargement.
Diagnosis
2. Avoid any kind of surgical treatment.
• Peripheral blood smear: Differential WBC
3. Root canal treatment is better than exo-
count in peripheral blood smear will show
dontia.
presence of highly immature WBCs
(abnormal hematopoietic cells). In certain 4. Alkaline and/or povidone iodine mouth-
cases, bone marrow biopsy is essential to wash should be used to maintain oral
arrive at the diagnosis (aleukemic leukemia) hygiene.
• Total WBC count more than 2–2.5 lacs. 5. Cytoprotective agents such as palifermin is
Further tests are: currently being used, as it is keratinocyte
– Cytochemical staining (myeloperoxidase, growth factor, which decreases the severity
sudan black B) and duration of mucositis.
– Immunophenotyping and cytogenic 6. Irrigation is better than scaling during the
analysis of chromosomal abnormalities. period of remission.
Physicians consent must be sought before
Treatment any dental treatment.
Since leukemia is a malignant condition
involving the WBCs, it is not restricted to a POLYCYTHEMIA
single organ hence chemotherapy is required.
The goal of chemotherapy (remission– It is an abnormal increase in the no. of RBCs
induction therapy) is to eradicate the leukemic accompanied by abnormal increase in
cells and to restore normal hematopoiesis. hemoglobin concentration.
Acute lymphocytic leukemia: Vincristine + Relative Polycythemia
prednisolone with 1-asparaginase or It is due to loss of body fluids due to diarrhea,
daunorubicin followed by methotrexate and vomiting, use of diuretics, post-surgical
6-mercaptopurine. complications, diabetic ketoacidosis, nil by
Acute myeoloid leukemia: Daunorubicin, mouth (NBM).
cytarabine. Real or primary/polycythemia vera: This is due
Chronic myelogenous leukemia; imatinib to neoplastic proliferation of RBCs.
mesylate, busulphan, cytarabine, cyclophospha- Secondary polycythemia: It is due to increased
mide combined with whole body radiation demand of oxygen to body like at high alti-
therapy followed by allogenic hematopoietic tudes, congestive cardiac failures, emphysema.
stem cell transplantation (HSCT).
To treat anemia: Packed RBCs, blood trans- Clinical Findings
fusion, and platelet transfusion to counter 1. Purplish red color of limbs
thrombocytopenia. 2. Distension of superficial veins
Infections are treated by using heavy dose 3. Tinnitus and headache
of antibiotics. 4. Enlargement of spleen
5. Cyanotic finger tips, ruddy cyanosis of the

face and extremities (because of deoxy-
genated blood in cutaneous vessels)
6. Systolic hypertension
7. Tendency for excessive hemorrhage due to
secondary thrombocytopenia.
Oral Manifestations
1. Purplish-red discoloration of oral mucosa
2. Gingival enlargement that bleeds profusely
Fig. 4.15: Phenytoin-induced gingival enlargement
3. Excessive hemorrhage after extraction,
petechiae Other effects of dilantin are hirsutism, coarse
4. Crystal violet tongue due to increased face, megaloblastic anemia; long-term therapy
varicosites can cause osteomalacia in elderly patients.
Diagnosis Other drugs causing gingival enlargement:
nifedipine, cyclosporin.
Clinical Features
Nifedipine is the drug commonly used to
Lab findings are RBCs more than 7 million/
manage hypertension and many patients
cu mm and Hb 18–24 mg%.
taking this drug presents with fibrotic gingival
Treatment enlargement with bulbous appearance of
1. Venesection interdental papillae and marginal gingiva. The
2. Radioactive phosphorus P32 degree of enlargement is more pronounced in
3. Triethylene melamine 30 mg satisfactory the region of excessive local deposits. Manage-
symptomatic and hematologic response ment in such cases involves scrupulous
4. Maintenance of good oral hygiene periodontal therapy and replacement of the
5. Avoiding trauma during treatment drug with another group of antihypertensive
agents with the consent of the physician
FIBROTIC GINGIVAL ENLARGEMENT (Figs 4.16 and 4.17).
Cyclosporin is the drug which is used as
Dilantin-induced Hyperplasia an immunosuppressant in transplant cases
Dilantin sodium is used in treatment of and gives rise to fibrotic gingival enlargement,
epileptic patients. It is believed to release more so in the vicinity of excessive local
heparin, histamine, hyaluronic acid from deposits. This will respond to periodontal
gingival mast cells giving rise to connective treatment and change of drugs (tacrolimus)
tissue proliferation.
with the consent of the physician (Figs 4.18
Gingival enlargement due to dilantin is
and 4.19). Resolution of cyclosporin-related
fibrotic type and on closer examination found
gingival enlargement with short course of
to be made-up of minute lobular swellings
(pebbled surface) and unlike inflammatory azithromycin has been documented.
gingival enlargement does not bleed easily. Dilantin, cyclosporin and nifedipine are
Enlargement is also related to local irritants chemically dissimilar drugs and have no
(Fig. 4.15). common metabolic breakdown products.
To treat dilantin induced hyperplasia one However, all the three influences Ca++/Na+
must discontinue the drug with physicians flux and this effect is proposed as a common
consent. Other drugs that can be given are mechanism for pathogenesis of gingival
carbamazepine, ethosuximide, primidone. hyperplasia.
Fig. 4.16: Nifedipine-induced gingival enlargement Fig. 4.17: Improvement after prophylaxis
Fig. 4.18: Cyclosporin-induced gingival enlargement Fig. 4.19: Improvement after prophylaxis
Diffuse Fibromatoses of the Gingiva • The treatment for gingival fibromatosis

• It is less common form of gingival hyper- is often unsatisfactory, gingivectomy is
plasia. In many cases, it is congenital or usually necessary although the tissue may
inherited (Figs 4.20 to 4.22). regrow.
• If well developed, the dense firm gingival
tissue results in increased diastema between
the teeth, changes the profile and general
facial appearance.
• The hyperplasia may be so excessive that it
can crowd the tongue and cause difficulty
in chewing and prevent normal closure of
lips.
• The surface of the hyperplastic tissue
usually has a nodular appearance. Detailed
medical history is necessary to rule out drug
induced gingival enlargement.
• Positive family history may provide
evidence for genetically determined Fig. 4.20: Showing sisters with excessive gingival
factor. fibromatosis
A B
Fig. 4.21: Gingival fibromatosis in upper and lower arches of elder sister
A B
Fig. 4.22: Gingival fibromatosis in upper and lower arches of younger sister
Syndromes Associated with Gingival Enlargement
Syndromes Features
Associated with gingival Rutherford syndrome Congenital gingival enlargement associated with
enlargement altered eruption pattern and corneal dystrophy
Cross syndrome Gingival enlargement associated with hypopigmen-
tation, micro-ophthalmus, oligophrenia (mental
retardation) and athetosis (ceaseless movements)
Robinow’s syndrome Foetal face syndrome
Papillon Lefevere Hyperkeratosis palmoplantaris and periodontoclasia
syndrome in childhood
Sturge-Weber syndrome Encephalofacial hemangiomatosis
Cowden’s syndrome Multiple hamartoma and neoplasia syndrome,
gingival papillomas as a part of widespread oral
pharyngeal and facial papillomatosis
Associated with gingival Zimmerman-Laband Gingival fibromatosis, ear, nose, nail defect and
fibromatosis syndrome hepatosplenomegaly
Murrey-Puretic-Drescher Gingival fibromatosis associated with multiple hyaline
syndrome fibromas
Suggested Reading
1. Burket’s Oral Medicine, 9th, 10th and 11th 3. Shafer’s Textbook of Oral Pathology, 6th
editions. edn.
2. Oral and Maxillofacial Pathology, by 4. Textbook of Periodontology, Carranza, 10th
Neville, 3rd edition. edn.
5
Tongue Lesions
DISEASES OF THE TONGUE d. Plummer-Vinson syndrome

e. Sprue (malabsorption syndrome)
The tongue is a complex muscular organ that
f. Chronic alcoholism
is anchored to hyoid bone, styloid process, and
genial tubercles of mandible by the hyo- g. Circulatory disturbances
glossus, styloglossus and genioglossus h. Endocrinal dysfunction—diabetes mellitus,
muscles. It is the most important organ of the chronic candidiasis
oral cavity with very important functions. i. Long-standing lichen planus, SMF, sclero-
derma, tertiary syphilis, SLE
I. Examination j. Long-standing xerostomia (drugs, radio-
a. Shape, color and size therapy, Sjögren’s syndrome)
b. Papillae and taste buds
B. Increased Coating on Tongue
c. Coating
a. Black hairy tongue (true or pseudo)
d. Tone (palpation)
b. Altered oral physiology
e. Lesions c. Chronic illness, liquid diet, stomatitis, etc.
II. Developmental Anomalies d. Xerostomia
a. Ankyloglossia e. Mouth breathing
b. Bifid tongue f. Constipation
c. Macroglossia g. O2 liberating mouth washes
d. Fissured tongue/scrotal tongue h. Persistent vomiting of pyloric stenosis
e. Median rhomboid glossitis C. Glossodynia
f. Thyroglossal duct cyst Painful burning tongue
g. Microglossia a. With clinical observable changes
h. Aglossia Local—dental irritants
• Food
III. Lesion Typical of Tongue
• Habits
A. Changes in Coating (Atrophic) • Allergy
a. Benign migratory glossitis or geographic Systemic—vit B complex deficiency
tongue • Anemia
b. Nutritional deficiency—riboflavin, niacin • Endocrinal disorders
c. Iron deficiency anemia, pernicious anemia b. Without clinical changes—psychogenic
86
Tongue Lesions 87
D. Indentation on Tongue alcoholism or parkinsonism. If tongue is

a. Nutritional deviated, it is suggestive of paralysis. If patient
b. Vit B complex deficiency cannot protrude the tongue, SMF, ankylo-
c. Endocrinal—hypothyroidism (cretinism) glossia or carcinoma may be suspected.
d. Blood dyscrasias—anemia Tongue Movement Variations
e. ANUG, HSV, EM, etc. Trefoil tongue: Ability to voluntarily deform
E. Traumatic Injuries tongue tip into clover leaf pattern
Unusual extensibility of tongue forward to
Falls, fight, epileptic attacks, dental treatment
touch the nose, backward to touch the palate
(iatrogenic).
and pharynx—Gorlin’s sign which is positive
F. Other Lesions in Ehlers-Danlos syndrome.
a. Moeller’s glossitis Tuberous sclerosis: Long and narrow tongue
b. Painful circumvallate and foliate papilla as a consequence of hyperostosis and
c. Lingual varicosities—senility thickening of mandible.
Sublingual administration of drugs, hyper- Reduced mobility due to scar formation
tension. secondary to blisters in epidermolysis bullosa,
healing of burn injury and SMF.
G. Atypical Lesions
Specialized Examination Procedure
These lesions are not typical of the tongue and
of Tongue
can also affect other areas of the oral cavity.
These are covered under relevant headings: 1. Cine radiographic study of oral cavity and
pharynx is done during drinking, chewing,
a. Erythema multiforme
suckling and phonation. It helps to better
b. Lichen planus understand the position and shape of the
c. Leukoplakia tongue in motion, especially in congenital
d. Carcinoma and surgically induced defects. However,
e. Haemangioma due to the high radiation exposure involved
its use is limited.
Functions of the Tongue
2. CT scan causes increased radiation exposure
a. Prehension and ingestion of food and but still is used to identify
assists in mastication a. Space occupying lesions
b. Swallowing, sucking b. Muscular atrophy following hypoglossal
c. Perception—taste, pain, temperature nerve damage (deep lesions)
assessment, general sensation c. Tongue size may be estimated—allow
d. Jaw development D/D of macroglossia from muscular
e. Respiration—hyoglossus and genioglossus disturbance.
f. Phonation However, streak artifacts caused by metallic
g. Symbolic dental restorations lead to diminished
image clarity and is an unavoidable
Examination of Tongue
drawback of CT scan.
Color of tongue is examined when tongue is 3. Pulse Doppler ultrasound: Has been used to
lying passively in the floor of the mouth. Dark- study characteristics of arterial blood flow
red in polycythemia and alcoholism and pale in tongue. Abnormal pulse waves noted in
in anemia and SMF. lingual arteries of individual with evidence
Patient is asked to protrude the tongue. If of compromised blood supply or flow in
tremors are seen, it may be suggestive of other branches of carotid arterial tree.
Real time ultrasound (gray scale B mode ) 8. Scanning electron microscopy (SEM) to
with probes of small cross sectional study surface topography of tongue
diameter can be used to explore ventral dorsum and the character and morpho-
surface of tongue. This method can be used logy of tongue papillae.
to differentiate fluid filled cavity (cyst/ 9. Videomicroscopy and stereomicroscopy
abscess) from solid or vascular lesion. to visualize tongue papillae, capillary
4. Isotopic (radionuclide) scanning techniques networks and taste pores.
are used in lingual thyroid cases wherein
10. Psychophysical evaluation of lingual
radioactive iodine 131I is used.
sensory function.
Tc pertechnetate (Tc99m), gallium ( Ga67) and
tumor labeling with radioactive indium and Taste test—for evaluation of sweet, bitter,
cobalt-bleomycin chelates have been used sour and salty taste
to outline the extent of lingual and other Electrogustometry and tongue mapping
oral tumors with varying success. for localized taste dysfunction.
5. Electromyography: To understand lingual Tactile sensation testing by means of von
and masticatory muscle function. For this Frey fibers or a series of objects of graded
purpose, non-invasive technique with texture and testing for stereotactic activity
surface electrodes can be used as opposed by means of set of objects of different
to thin needle electrodes introduced in the shapes and other 3D objects. The latter
muscles in the past. approach is helpful in evaluating lingual
6. MRI function in speech disorders.
a. Excellent details of soft tissue such as
tongue and pharynx. Papilla and Taste Buds (Fig. 5.1)
b. CT scan has drawbacks of artifacts Filiform Papillae
caused by metallic restorations and also 500 cm2 in anterior two-thirds of the tongue.
the beam hardening effect because of
They have a small connective tissue core and
absorption of X-rays by the mandible.
elongated hair-like projections. They have
These drawbacks are minimized in MRI.
c. Direct coronal and sagittal sections are
seen—accurate delineation of lingual
muscles and extent of tumor infiltration.
d. Enhanced contrast of carcinoma, sarcoma,
inflamed salivary glandand normal
oropharyngeal structures can be observed
with gadolinium—diethylene triamine
penta-acetic acid (DTPA) enhancement
of MRI signed intensity.
e. Differentiation of fluid-filled and/or solid
lesions is possible as fluid appears hyper-
intense (bright) on T2-weighted images.
7. Direct microscopic examination of tongue
papilla and capillary blood flow in
fungiform papilla with IV fluorescein dye.
Similar to ophthalmic study of retinal blood
vessels. Helps in studying localized areas
of decreased blood flow secondary to
diabetic angiopathy. Fig. 5.1: Schematic diagram of tongue dorsum
Tongue Lesions 89
arterial and venous supply and nerve endings von Ebner glands are strategically situated
like the conical papillae but carry no taste at a point where the milk is expressed
buds. Heavily concentrated in the centre of the during suckling.
dorsum. Function is to help in licking and
propagating the food distally. Foliate Papillae
Seen on the lateral border of the tongue
Fungiform Papillae posteriorly. They are conical in shape and
• Mushroom shaped, present on the anterior elongated resembling small leaves and hence
two-thirds of tongue. They are 200/cm2. called foliate (Fig. 5.3). Arranged in 2 to 3 rows.
They have vascular supply and nerve They get traumatized and inflamed often and
endings. They are identifiable as reddish the patients suddenly become conscious of
dots against a carpet of filiform and conical tender red areas with irregular surface and
papillae (Fig. 5.2). Sometimes the fungiform become apprehensive that it may be
papillae show small spots of melanin malignant. These patients become habitual
pigment. Taste pores of the papillae can be mirror watchers and keep on pulling out the
demonstrated in vivo on videomicroscopy tongue which gets traumatized by the lingual
by application of methylene blue stain. Each cusps of lower molars. This further aggravates
papilla has 0–20 taste buds. the problem.
• Both the filiform and fungiform papillae Such patients should be counselled and
take part in the atrophy of tongue. reassured that this is a normal feature of the
tongue and unlikely to turn malignant. Soft
Circumvallate Papillae acrylic tray for lower arch to be used as mouth-
• 10 to 20 in number arranged in the form of guard.
inverted V at the junction of anterior two- They do not take part in atrophic changes.
thirds and posterior one-third of the tongue. Taste buds are present.
• Do not take part in atrophic changes. Coating of the tongue is made of fungiform,
• These papillae are surrounded by a valley- filiform papilla enmeshed food debris,
like depression and hence called ‘circum- desquamated epithelial cells, bacteria and
vallate’ walls of the papilla contain von salivary proteins.
Ebner’s serous glands which secrete Posterior one-third of the tongue may be
lipoprotein lipase in neonates. This enzyme folded because of collected lymphoid tissue
is important for digestion of fat in milk. The called lingual tonsil.
Fig. 5.2: Tongue dorsum showing bulbous red

fungiform papillae with whitish filiform papillae Fig. 5.3: Foliate papillae
Tone of the Tongue

It is palpated bidigitally and is reduced in
pernicious anaemia and increased in SMF.
Anterior two-thirds of tongue: Devoid of
mucous or serous glands except directly under
the tip where small mucous glands of Blandin
and Nuhn are present.
Developmental Anomalies
a. Ankyloglossia
Absent or shortened lingual frenum (Fig. 5.4).
Tongue tie or ankyloglossia is a relatively
unimportant cause of defective speech. It Fig. 5.4: Partial ankyloglossia
causes difficulty in sucking and swallowing,
Macroglossia is feature of EMG (exophthalmos-
also recurrent traumatic ulcers. Also reduced
macroglossia-gigantism) syndrome also
self-cleansing capacity and inability to wet
known as Beckwith-Wiedeman syndrome.
lips.
If tongue tie is too severe and restricts the True macroglossia is rare, however, it is
mobility of tongue then it can be corrected by seen in:
frenectomy. Frenectomy is done only if there 1. Cretinism
is defective pronunciation of T, D, L, N. 2. Mongolism
3. Amyloidosis
b. Bifid Tongue
4. Hemangioma (Fig. 5.6)
It is a rare anomaly due to failure of union of
5. Lymphangioma (Fig. 5.7)
lateral halves of lingual swelling. It is of no
clinical significance (Fig. 5.5). 6. Long-term edentulous area
7. In mature adults acromegaly and in adole-
c. Macroglossia scent group dermoid–epidermoid cysts can
It is a component of numerous syndromes. In cause macroglossia.
these syndromes, the tongue enlargement is If tongue is large, slurred speech and defec-
caused by abnormal lysosomal storage of tive development of maxilla and mandible
carbohydrate macromolecules. with diastema will be present.
A B
Fig. 5.5: Examples of bifid tongue

Tongue Lesions 91
A B
Fig. 5.6. Examples of macroglossia due to hemangioma
Congenital lingual hemangiomas or

lymphangiomas
Neurofibromatosis
Cowden’s syndrome
Epidermal nevus (ichthyosis hystrix
associated with papillomatosis) syndrome
Similar appearance of the tongue may be
seen in leprosy, Melkersson-Rosenthal
syndrome also.
d. Abnormally Fissured Tongue
It is a developmental variation in which no. of
Fig. 5.7: Lymphangioma deep fissures are seen on the dorsal surface of
tongue (Fig. 5.8). It normally goes un noticed
Lymphangioma of tongue with cystic unless patient gets traumatized its described
hygroma is the most common of congenital as scrotal, plicated or cerebriform tongue. It
macroglossia. Surface of tongue is nodular and may be associated with mild burning sensa-
irregular. Altered pattern of blood and lymph tion.
flow also can be responsible for recurrent Factors which can contribute to increased
tongue enlargement. Macroglossia associated prevalence of fissured tongue with age include
with storage disease—happy puppet (Angel-
man) syndrome and cretinism. Increased total
bulk of tongue. Often considered problem of
muscular control rather than true macroglossia.
Treatment
Surgery to reduce the tongue bulk may be
needed if congenital or acquired macroglossia
interferes with oropharyngeal function or is a
major cosmetic deformity.
In certain congenital disorders the tongue
dorsum becomes papillomatous or exhibits
localised enlargements, described as cobble
stone, pebbled or lumpy. Fig. 5.8: Fissured tongue
salivary hypofunction, vit B deficiency, Treatment

candidiasis and chronic lichenoid reactions. • Give reassurance to the patient.
Treatment • Antifungal ointment, nystatin or clotrima-
Clean fissures with H2O2 swab. zole.
Melkersson-Rosenthal syndrome: Fissured Thyroglossal Duct Cyst
tongue + psychosis (mental retardation) facial Seen as a round swelling at foramen cecum
palsy and hypoplasia of salivary gland. level, at times lingual thyroid is seen. Such a
Median Rhomboid Glossitis diagnosis can be made with radionuclide
Shows presence of rhomboidal or diamond- scanning-131I and Tc pertechnetate 99m and
shaped area in midline of tongue just anterior confirmed with biopsy.
to inverted V formed by circumvallate papilla Changes in the Coating of the Tongue
(Fig. 5.9). More common in males than in Coating of the tongue is made of fungiform,
females after the age of 30. filiform papillae, enmeshed food debris,
It may have: desquamated epithelial cells, bacteria and
1. Depapillated surface salivary proteins.
2. Tufted surface The changes in the coating of the tongue
3. Fissured surface are seen as the mirror of general health status
4. Lobulated surface in Western and Chinese medical traditions.
It was believed to be caused by failure of According to Brightman (Burket IXth Edn.)
tuberculum impar to retract before fusion of while depapillation of the tongue may be a
lateral halves and hypobranchial eminence so result of metabolic abnormality, there is no
that area devoid of papillae is present in the evidence that elongated filiform papillae and
midline. the halitosis that often accompanies it is
Recently, it is believed to have fungal origin, anything other than the result of local environ-
i.e. chronic candidiasis (coexistence of angular mental changes.
cheilitis, MRG and palatal erythematous The tongue coating is normally removed by
candidiasis), diabetes mellitus , impaired local salivary flow, mastication, deglutition and
blood supply due to atherosclerosis, impaired speech. Any condition interfering with salivary
local immune mechanism and reduced flow, mastication and deglutition will cause
concentration of Langerhans’ cells are the disturbance in tongue coating. Therefore,
other possible causative factors. tongue coating is increased in hospitalised,
dehydrated (nil by mouth) patients and those
with persistent vomiting. Patients using H2O2
mouthwash shows elongated filiform papillae
and subsequent increased coating of the
tongue.
Black hairy tongue (lingua nigra) is
characterized by elongation of the filiform
papillae and growth of black pigment
producing bacteria or other organism. Filiform
papillae may be 3 cm or longer which brush
against palate causing gagging. They appear
A B
as black hair as a result of pigment produced
Fig. 5.9: Examples of median rhomboid glossitis by fungi or micro-organisms (Fig. 5.10).
Tongue Lesions 93
ded by a whitish margin of regenerating

filiform papillae overall resembling a map.
Etiology
Remains obscure it is suggested that it is
related to:
• Reduced activity of keratinase enzyme
system
• Immunological reaction
• Psychosomatic background
• Personality type: Patients who are “more
Fig. 5.10: Elongated and pigmented filiform papillae prone to complain or verbalise discomfort”
of black hairy tongue • Allergic reaction
Pseudo Black Hairy Tongue • BMG associated with increased frequency
of human leukocyte antigen (HLA) allele
When tongue appears black as a result of
B15
certain black-colored medications, food debris
and does not have pigment producing Clinical Features
organisms, it is called as pseudo black hairy 1. In early stage no symptoms are present and
tongue. Also seen after extensive oral surgery the lesion may not be noticed by patient.
when tongue is coated with blood pigments. But sometimes burning sensation may be
Treatment present and patient becomes conscious of
this condition.
Maintenance of proper oral hygiene and
cleaning tongue with brush and tongue blade 2. Lesions are multiple and appear as reddish
(podophyllin resin which is keratolytic). depapillated areas, irregular in shape
surrounded by erythematous halo which is
Benign Migratory Glossitis/ Geographic in turn surrounded by a raised whitish
Tongue/ Erythema Circinata Migrans/ margin of regenerating filiform papilla
Wandering Rash (Fig. 5.11).
As the name suggests typical BMG lesions are 3. These change their location within 3–7 days
reddish, irregular depapillated areas surroun- and hence called migratory.
A B
Fig. 5.11: Examples of benign migratory glossitis

4. Irregular lesions give a map-like appea- Depapillation of Tongue Caused

rance hence called geographic tongue. by Nutritional Deficiency and Anaemia
5. Persistence of an everchanging painful Redness, loss of papillae and painful swelling
(apparently) lesions on the dorsum of of tongue are characteristically found in
tongue is frightening to the patient and he deficiencies of several B vitamins.
may develop cancerophobia. • Niacin—pellagra
6. Ectopic geographic tongue is seen on • Riboflavin
ventral surface of tongue, lips, buccal • Pyridoxine
mucosa, palate and are called as erythema • Folic acid and vit B12—pernicious anemia
circinata migrans (Fig. 5.12).
Similar changes are associated with iron
Differential Diagnosis—Median Rhomboid deficiency anaemia and malabsorption syn-
Glossitis drome sprue.
Histologically: Papilla of variable height with Each of these factors involved in the
some submucosal round cell infiltrate and production of epithelial cells and RBCs and
areas of spongitic epithelium with localised manifestation of their deficiency affects other
intraepithelial infiltrates of polymorpho- mucosal surfaces, skin, RBCs, bone marrow,
nuclear leukocytes, so-called spongiotic and tongue papillae. Various changes occur
pustules or Monro’s abscesses. Clinically and in other organs also. Deficiency of one factor
histologically similar lesions also occur in rarely occurs alone because of dietary
Reiter’s syndrome, dermatitis herpetiformis, deficiency.
pustular psoriatic dermatitis. Specific deficiency may result from mal-
absorption syndrome causing pernicious
Treatment anaemia and sprue or drug induced defi-
The term ‘benign’ in BMG has therapeutic ciency, i.e. isoniazid leading to pyridoxine
value (since patient is worried that it is deficiency.
malignant). Various terms were used to describe—
Give assurance to the patient about the atrophic glossitis, e.g. raw, beefy tongue,
benign nature of the lesion. magenta, bright red, hunters glossitis and in
Xylocaine viscous mouth wash if burning the past the appearance was considered to be
is present. specific for a particular vitamin deficiency.
Cautious topical application of salicylic acid However, the atrophic appearance of the
and tretinoin recommended by some as an tongue depends on various factors such as
effective remedy. secondary candidiasis and in the absence of
A B
Fig. 5.12: Examples of erythema circinata migrans

Tongue Lesions 95
hematologic evidence of anemia or vitamin

deficiency it is difficult to pinpoint the diag-
nosis.
Iron Deficiency Anemia
Patient will have pallor, dyspnea, fatigue, bald
tongue, angular cheilitis and koilonychia. First
oral symptom is that tip and sides of the A B
tongue become sore and sensitive to changes

in temperature.
O/E: Reddish, inflamed depapillated areas
seen. In advanced cases, entire tongue will be
involved and papilla totally disappear giving
a bald tongue (Fig. 5.13).
Plummer-Vinson syndrome: Paterson-Kelly
syndrome
1. Seen in middle aged patients with
anaemia caused by poor diet or blood loss.
2. Females more commonly affected than
males.
3. Thin narrow lips with narrow orifice. C D
4. Patient complains of dysphagia and pre-
sents with angular cheilitis and stomatitis Fig. 5.14: (A) Bald tongue and angular cheilitis;
and bald tongue (Fig. 5.14A). (B) conjunctival palor; (C) spoon-shaped nails;
5. Mucosa becomes pale dry, inelastic and (D) esophageal web—in barium swallow examination.
glazed. Plummer-Vinson syndrome
6. Brittle spoon-shaped nails (koilonychia),
dry skin with pallor (Fig. 5.14C). 9. This is a premalignant condition and may
7. Patient develops esophageal strictures and lead to oesophageal CA or post-cricoid
webs therefore barium swallow X-ray is CA, pharyngeal CA or oral CA (in
indicated (Fig. 5.14D). descending order).
8. Possibly dryness and atrophic changes in 10. Patients complain of spasm or food
conjunctiva (Fig. 5.14B), vaginal and anal sticking in throat, and may present with
mucosa. pagophagia (compulsive consumption of
cold drinks and ice).
11. Loss of teeth in early age.
Thin narrow lips with narrow orifice may
also be observed in Sjögren, scleroderma,
SMF.
Sjögren’s syndrome associated with ophthalmic
signs, rheumatoid arthritis, Hb may be normal.
A B
(SJS more predisposed to lymphoma,
Fig. 5.13: Examples of bald tongue carcinoma more common in PV syndrome).
Pernicious Anemia absorbed therefore less than 3% B12 excreted

It is caused by deficiency of intrinsic factor in urine.
secreted by the parietal cells of the fundus of After this the patient is given the intrinsic
stomach. In normal course this intrinsic factor factor along with radioactive B12, if patient still
combines with extrinsic factor, i.e. vit B12 and excretes less than 3% radioactive B 12 then
helps in iron synthesis after getting absorbed patient is having problem with absorption
through the ileum. In pernicious anaemia (malabsorption syndrome). Patients with
there is an autoantibody to the parietal cells/ pernicious anemia may also have achlor-
intrinsic factor. It is also seen in connection hydria.
with other autoimmune disorders such as Antibody test—Schilling’s test is now replaced
Graves’ disease and in patients with history by tests to check the presence of anti-parietal
of surgery of fundus of stomach. cell antibodies and antibodies to the intrinsic
Clinical Features factor. With both these tests results are more
accurate.
1. Patient complains of epigastric discomfort,
diarrhea and constipation Treatment
2. Pallor, dyspnea and fatigue Parenteral vit B12 throughout life.
3. Tingling, numbness and lack of co- Note: Since the hematologic changes in
ordination in movement of extremities, i.e pernicious anemia may be reversed by oral
neurological symptoms (if present with folic acid administration without the arrest of
anaemia), should raise the suspicion of neurological changes, one should not give
pernicious anemia multivitamins with folic acid to patients with
4. Tongue is bald or depapillated glossitis and pernicious anemia as anemia improves in
glossodynia these patients but serious neurological symp-
toms may worsen.
5. Red beefy tongue due to loss of filiform
papilla
PERIPHERAL VASCULAR DISEASES
6. Severe burning sensation
7. Loss of taste a. Decreased nutritional status of the lingual
papillae in diabetes mellitus could be due
Laboratory Findings to:
• RBCs show variation in size, macrocytic and • Vascular changes in the subpapillary
normochromic dorsal capillary plexus or lingual vessels
• Platelets are large supplying it.
• WBCs are hypersegmented • Chronic candidiasis and this could lead
Schillings test: Patient is given a measured to atrophic glossitis.
amount of radioactive B12 orally. After that a b. Fibrosis of submucosal tissue secondary to
flushing dose of parenteral Vit B12 (normal) is obliteration of small vessels suggestive of
given. Since the total dose of B12 exceeds renal autoimmune process which is responsible
threshold, excess B12 will appear in urine. for the scarred shunken atrophic appea-
Normal patient who has intrinsic factor will rance of tongue in scleroderma, mixed
show greater absorption of radioactive B12 connective tissue diseases and in lupus
through GI tract and therefore excrete 7 to 30% erythematosus.
radioactive B 12 in urine. In patients with c. Infarcts of the tongue may be associated
pernicious anemia, however, intrinsic factor with shrunken tongue with atrophic
is missing therefore radioactive B 12 not mucosal changes.
Tongue Lesions 97
Tertiary Syphilis and Interstitial Glossitis 3. The ulcerative lesions affecting the tongue
Non-ulcerating irregular indurations with an and the oral mucosa are elaborated in the
asymmetric pattern of alternating grooves ulcerative lesion chapter.
with leukoplakia and smooth (atrophic) fields
covering entire dorsum of the tongue. The Diseases Affecting Body of Tongue
tongue has been described as upholstered The following diseases can cause swelling of
tongue because of the scarring of the healed the body of tongue:
gummata. 1. Amyloidosis
Carcinoma of the dorsum of tongue asso-
2. Infections: Lingual abscess, Ludwig’s
ciated with interstitial glossitis is an exception
to the general finding that carcinoma of the angina, actinomycosis, cysticercosis and
tongue is rare on the dorsum. trichinosis.
Pigmentation of Tongue Amyloidosis

1. Racial a. Miscellaneous group of conditions in which
2. Exogenous an amorphous material (amyloid) is
• Microbial growth—pigment producing deposited extracellularly in a single organ
pathogens (localized) or many organs (systemic).
• Food debris b. Nephrotic syndrome is the most common
• Candy dyes clinical manifestation.
• Beverages c. Macroglossia is the most common oral
• Mouth rinses manifestation. The enlarged tongue
• Amalgam tattoo protrudes between the teeth and presents
3. Drugs: Doxorubicin hydrochloride (cancer with indentations. Patients complain of
therapy) large, firm and immobile tongue which
• Alpha methyl dopa (antihypertensive) interferes with speech, mastication,
• Nortryptyline (tricyclic antidepressant) swallowing and affects the dentition.
• Zidovudine (antiretroviral) d. Amyloidosis should be suspected in
4. Endocrinal: Addison’s disease—primary patients with tongue enlargement, having
adrenal insufficiency a history of multiple myeloma, long
5. Peutz-Jeghers syndrome standing tuberculosis, rheumatoid arthritis,
6. Albright syndrome severe anemia.
7. Acanthosis nigricans e. Salivary gland involvement: Periductal and
8. Neurofibromatosis periacinar deposition of amyloid leads to
9. Hemochromatosis acinar atrophy.
Ulcerations of the tongue can result from f. Amyloid has characteristic staining pro-
traumatic injuries, and infectious diseases: perties, polarized light microscopy shows
1. Fine striated folds (fimbriae) and apple green birefringence in the tissue
Wharton’s duct opening on either sides stained with Congo red.
of lingual frenum is likely to be trauma-
tized during dental procedures because Infections
of aspiration causing ulceration and 1. Lingual abscess caused by contaminated
ecchymosis. injuries and streptococci and anaerobic
2. Ulcers on tongue are seen in infectious organisms are responsible. Drainage,
diseases and in riga fede disease in debridement under proper antibiotic cover
neonates. is essential.
2. Ludwig’s angina is actually not a lingual understands what he/she hears and has no
infection but elevates the tongue and difficulty in writing, if literate.
underlying spaces are involved, this very Dystonia refers to abnormally increased
dangerous rapidly spreading infection was muscular tone results in fixed abnormal
considered fatal in the preantibiotic era. posture. These are due to anatomic or bio-
Lingual cellulitis associated with Haemo- chemical lesions involving the basal ganglia
philus influenzae bacteremia can be fatal. and referred to as extra-pyramidal disorders;
3. Actinomycosis: Induration and multiple lingual and palatal muscular dystonia are seen
discharging sinuses, so called wooden patients with parkinsonism, athetoses, drug-
tongue of cattle is very rare. induced basal ganglia dysfunctions. Focal dys-
4. Larval stage of pork tapeworm taenia tonia of tongue and oropharyngeal muscles
solium (cysticercosis), roundworm and may occur with levodopa, prochlorperazine
gnathostomiasis infestation may affect the and other phenothiazines and antipsychotics.
tongue and is accompanied by other skeletal Spasmodic torticollis (wry neck syndrome):
muscle involvement leading to fever, Involuntary spasm of sternocleidomastoid,
generalized muscle tenderness and marked trapezius causing involuntary turning or
eosinophilia. Radiographically larvae of dipping of head.
cysticercosis are visualized as multiple Dyskinesia: Repetitive uncontrolled muscular
small oval opaque shadows in the soft activity related to long-term administration of
tissue. phenothiazine, reserpine and other anti-
Neuromuscular Disorders
psychotic drugs. Symptoms include:
• Rapid and repetitive movements of the
Neuromuscular disorders of central, peri- tongue, jaw and lips
pheral or muscular origin may produce • Fine tremors and fasciculation of tongue—
symptoms of dysphagia and choking and vermicular movements
speech and masticatory problems. • Rapid darting movements—fly catchers
Dysphagia caused by the weakness of the tongue, bon-bon sign
tongue musculature is referred to as oro- • Rabbit syndrome—involuntary mouthing,
pharyngeal dysphagia and symptoms include: chewing, smacking movements of lips with
• Aspiration while swallowing constant tremors
• Nasal regurgitation • Senile tremor associated with senile de-
• Pain on swallowing mentia has buccal-lingual-facial dyskinesia.
Newer drugs like clozapine have fewer
• Inability of the tongue to move the bolus of
complications of this type.
food into pharynx.
Myasthenia gravis is characterized by weak-
Other causes of dysphagia are SJS, PV ness and easy fatiguability affecting facial,
syndrome, acute pharyngitis, Vincent’s oculomotor, laryngeal, pharyngeal, respira-
angina, glossitis, and retropharyngeal abscess. tory muscles rather than lingual muscles.
Dysarthria is the speech problem caused by the This disorder is caused by decrease in the
neuromuscular disorders involving the number of available acetylcholinesterase
tongue, in which defect is there in accurate receptors at the myoneural junctions due to
articulation and phrasing. This condition is to antibody mediated autoimmune damage.
be distinguished from aphasia or dysphasia The defect is reversed by anticholinesterase
which are cerebral disorders in which the medications such as pyridostigmine. Improve-
ability to produce or comprehend spoken ment with thymectomy and immuno-
language is limited. The dysarthric patient suppression.
Tongue Lesions 99
Amyotrophic Lateral Sclerosis (ALS) On EMG study of genioglossus, diaphragm

Steadily progressive disorder of motor neurons and other respiratory muscles, it was found
with clinical manifestation of muscle weakness, that genioglossus pulls the tongue forward
atrophy, spasticity with exaggerated reflexes. and opposes the tendency of pharynx to
The muscles supplied by the brainstem are collapse due to negative pressure during
affected resulting in weakness atrophy and inspiration. In OSAS, there is a weakness of
obvious fasciculation (persistent muscle genioglossus which fails to pull the tongue
twitches) in the tongue and facial muscles. forward leading to posterior and inferior
After the diagnosis of ALS is made, some positioning leading to interference in breathing.
patients develop an attitude of denial and seek Management of mild cases includes weight
opinions of many consultants. Such patients reduction, alcohol avoidance, increasing nasal
vainly hope that a new denture or tooth patency, altering sleep posture.
extraction or treatment of burning tongue Severe cases may require continuous nasal
will cure their symptoms. It is important that positive pressure, supplemental oxygen.
the dentist, through medical history and Surgical enlargement or tightening of
communication with the physician, become pharyngeal lumen, i.e. uvulopalatopharyngo-
aware of the diagnosis and undertake dental plasty.
treatment with the complete understanding of Surgical repositioning of mandible and
the reality of patients condition. occlusal splints, night guardin cases where
Obstructive Sleep Apnea Syndrome (OSAS) there is mandibular retrognathism.
1. Group of disorders characterized by Angioneurotic Edema
episodes of apnea (intermittent cessation of • It is a manifestation of allergy or anaphylaxis.
respiration) associated with regular sleep • Leads to transient painless swelling of
or hypersomnolence. tongue, lips.
2. Underventilation of pulmonary alveoli— • Angioedema of larynx in anaphylaxis can
alveolar hypoxemia and hypercapnia be life-threatening.
3. Primary disorder of alveolar hypoventila- • Angioedema of the lips and tongue can
tion or secondary to alcohol or barbiturate be managed by avoiding the allergen,
intoxication or respiratory centre damage antihistaminics, steroids. Treatment of
(from bulbar poliomyelitis or brainstem anaphylaxis is covered in Chapter 2—
infarcts) Ulcerative Vesiculobullous Lesions.
4. Obstructive sleep apnea results from the Various Appearances of the Tongue
blockage of the pharyngeal airway by the • Pellagra: Niacin (vit. B3) deficiency ‘5Ds’
tongue: (dark-red tongue, diarrhea, dermatitis,
a. Congenital deformity Pierre Robin dementia, and death)
syndrome and severe retrognathism of • Riboflavin deficiency: Magenta red tongue
other causes. • Strawberry tongue: Scarlet fever—prominent
b. Adenotonsillar hypertrophy, macro- red fungiform papillae against pinkish
glossia white tongue coating
c. Pickwickian syndrome/fat boy • Baked tongue: Dry/brown-typhoid fever
syndrome—morbid obesity, hyper- • Parrot tongue: Dry/horny/immobile—
somnolescence, periodic breathing with chronic low grade fever
hypoventilation, weakness or altered • Fly catchers tongue: Dyskinesia tarda—rabbit
tonus of genioglossus muscles. syndrome
• Wooden tongue of cattle: Actinomycosis— inflammatory changes, if the symptom persists

induration and multiple draining sinuses. then deep seated/neurological/psychological
causes are suspected. Subsequent and
Glossodynia/Glossopyrosis
adequate treatment of the etiological factor.
The term glossodynia is used to denote painful
b. Glossodynia without observable clinical
tongue and glossopyrosis for burning sensation
changes –75% of cases
of the tongue. This symptom is most annoying
to the patient, the physician and the dentist. 1. Common in postmenopausal women
Unfortunately for the patients, quite often 2. Patients also complain of disturbed taste,
(75% of cases) there are no clinically observ- insomnia
able changes. In the remaining patients 3. Anxious and worried
observable clinical changes are seen and are 4. Clinical examination fails to show any cause
related to either local or systemic factors. for burning.
a. Glossodynia with observable clinical Before labelling their symptoms as psychogenic, it
changes –25% of cases is important to rule out
i. Local factors • Diabetes mellitus (fasting and postprandial
• Traumatic lesions associated with sharp blood sugar)
tooth, restorations, etc. • Anemia
• Allergy to dentifrices, lipsticks, mouth- • Lymphoid tissue infection at the base of the
wash tongue
• Poor oral hygiene, candidiasis • Glossopharyngeal neuralgia
• Chronic edentulous condition with
• Painful red erosive lesions with inflamed
decreased vertical intermaxillary space
papillae
compressing the tongue.
ii. Systemic factors
Treatment
• Extensive generalised atrophy of
lingual papillae and erosive lesions— • Patients should be handled with diplomacy
vit B complex deficiency and care.
• Bald or depapillated tongue—iron • Never tell the patients that the pain is
deficiency anemia imaginary.
• Reddish inflamed tongue—diabetes • Assurance to the patient that there is no
mellitus evidence of malignancy.
• Depapillated tongue with dry shiny • Diazepam 5 mg 1 bedtime for 10–15 days
lobulated surface—Sjögren’s syndrome (or tricyclic antidepressant).
• Pernicious anemia tip and lateral • Patients who are hysterical are referred to
borders bright and fiery red. psychiatrist.
The above appearances are characteristically Suggested Reading
indicative but not pathognomonic
Management: Identification of the causative 1. Burket’s Oral Medicine, 8th, 9th editions.
factor. 2. Oral and Maxillofacial Pathology by
The patients are prescribed local anesthetic Neville, 3rd edition.
gel/mouth wash—if the symptom disappears 3. Shafer’s Textbook of Oral Pathology, 6th
then the cause is related to local erosive/ edition.
6
Pigmentations
Oral and perioral tissues can at times present 5. Carotenemia

a variety of discolorations. These could be 6. Antimalarial drugs
normal (racial) or associated with either 7. Suntan and drugs like chlorpromazine,
endogenous or exogenous pigmentations. tetracycline, sulphonamides, etc.
ENDOGENOUS PIGMENTATIONS—MELANIN EXOGENOUS PIGMENTATION
1. Racial Sources
2. Addison’s disease • Occupational
3. McCune-Albright syndrome • Therapeutic
4. Peutz-Jeghers syndrome • Accidental
5. Pituitary hyperfunction
• Suicidal
6. Pregnancy
• Habits
7. von Recklinghausen’s disease with neuro-
fibromatosis Causes
Others Pigments • Foreign body
1. Jaundice—bilirubin and biliverdin • Amalgam
2. Anemia • Bi, Pb, Hg, Ag
3. Hemochromatosis • Gold, Cu, chromium
4. Iron and melanin • Zn, P, arsenic, Fe
Clinical Classification of Oral Pigmentation
Focal Diffuse Multifocal
Blue, purple Varix Hemangioma Kaposi’s sarcoma
Red Hemangioma Hereditary hemorrhagic telangiectasia
Brown Melanocytic macule Ecchymosis Physiologic pigmentation
Nevus Melanoma Neurofibromatosis
Melanoma Hairy tongue Hemochromatosis
Drug induced Lichen planus
Addison’s disease
Peutz-Jeghers syndrome
Petechiae
Gray/black Amalgam Amalgam Heavy metal deposition
Graphite Melanoma
Nevus Hairy tongue
101
ENDOGENOUS PIGMENTATION pituitary adrenocorticotropic hormone, and

genetic factors.
It is most often explained by presence of
Melanocyte overpopulation occurs with
hemoglobin, hemosiderin and melanin.
benign nevi and in malignant melanomas.
Hemoglobin: Red or blue appearance to mucosa,
which is rendered by circulating erythrocytes BLUE/PURPLE VASCULAR LESIONS
coursing through patent vessels.
Hemosiderin: Brown appearance of blood extra- Hemangioma
vasation which may occur as a consequence Tumor-like hamartomas which are prolifera-
of trauma or defect in hemostatic mechanisms. tions of vascular channels occurring in
Hemochromatosis may occur as a variety of childhood. These spontaneously regress after
pathological states (generalized hemosiderin puberty (Fig. 6.1).
tissue deposits).
Clinical Features
Melanin: Pigment derivative of tyrosine
synthesized by melanocytes which sub- Site
sequently transfer melanin granules into • Skin—flat, macular and diffuse, particularly
adjacent basal cells in order to protect against on facial skin where they are referred as
effect of actinic radiation. portwine stains.
An increase in melanin pigment occurs • Portwine hemangioma of facial skin may
when melanocytes oversynthesize or over- also involve the oral mucosa, and may
populate. Overproduction (basilar melanosis) continue in a macular fashion or become
may be caused by sun exposure, drugs, tumefactive (Fig. 6.2).
A B
Fig. 6.1: Examples of hemangioma involving the tongue
A B
Fig. 6.2: Portwine hemangioma with palatal involvement

Pigmentations 103
• Intramuscular lesions may fail to show Histopathological Features

surface discoloration. • Large dilated vascular channels lined by
Oral Hemangiomas endothelial cells without muscular coat,
Site: Tongue, lip mucosa. referred to as cavernous hemangiomas.
• Capillary hemangiomas show small vas-
Presentation
cular channels with significant endothelial
• Multinodular, bluish red, localized,
proliferation.
blanching underpressure (diascopy test).
• Thrombi may form within hemangiomas Treatment
which may calcify with time, giving rise to • Since many hemangiomas spontaneously
phleboliths which are radiographically involute, treatment withheld in children up
evident. to puberty.
Syndromes associated • Conventional surgery, laser surgery or
1. Sturge-Weber syndrome: Portwine heman- cryosurgery for smaller lesions.
gioma with concurrent history of seizures • If the lesions are large and extending to
represents encephalo-trigeminal angio- muscles, and difficult to eradicate surgically,
matosis (vascular lesions seen in brain and
sclerosing agents like 1% sodium tetradecyl
skin). Skull radiographs show vessel wall
sulfate may be administered intralesionally.
calcifications called tram line calcifications.
Analgesics like oxycodone or asprin with
2. Osler-Weber-Rendu syndrome (hereditary
codeine are prescribed for postoperative
haemorrhagic telangiectasia): It represents
pain.
multiple microaneurysms owing to
weakening defect in adventitial coat of – Selective embolization
venules. More than hundred such purple
papules appear on the lips, buccal mucosa VARIX
and tongue. Facial skin may also be involved. Pathologic focal dilatation of veins or venules.
Nasal cavity involvement with epistaxis Site: Ventral surface of tongue
may be present. (Differential diagnosis should
include petechial hemorrhages associated Age: Elderly age group
with thrombocytopenia in which petechial Presentation: Serpentine, blue, red, purple,
hemorrhages will be macular, brown or red elevations, surface mucosa is often lobulated
in color and no blanching on pressure or nodular. Once formed, they do not regress.
noted. HHT has a genetic basis and may be Diascopy test presents blanching of the lesion
noticed in other family members.) (Fig. 6.3).
A B
Fig. 6.3: Purplish blue varix with diascopy test

Hemangioma: These occur in childhood and
regress with age, whereas varix occurs in
elderly patients and does not regress.
Histopathological features: Similar to cavernous
hemangioma.
Treatment
• Electrosurgery
• Cryosurgery
• Intralesional 1% sodium tetradecyl sulfate Fig. 6.4: Gingiva showing melanin deposits
injections injected directly into the lumina
with a tuberculin syringe depositing 0.05 Minimum Pigmentation
to 0.15 ml/cm3. Soles of feet and palms.
– Selective embolization In oral cavity, more pigmentation is seen in:
1. Gingiva (Fig. 6.4)
BROWN MELANOTIC LESIONS
2. Buccal mucosa
Endogenous Pigmentations 3. Tongue
Melanin serves as a protection against 4. Rarely fungiform papillae
prolonged exposure to sunlight and this 5. Hard palate
pigmentation is mainly due to melanin which
Ephelis and Oral Melanocytic Macule
is an insoluble polymer of high molecular
(Freckles)
weight, color of which varies from brown,
bluish-black and dark-black. It represents increase in melanin pigment
Development of melanin requires a pre- synthesis by basal layer, without an increase
cursor acid tyrosine which is provided by in the number of melanocytes in sun-exposed
tyrosine-tyrosinate system. areas. Ephelides are most commonly
In albinism, tyrosine is absent and in negroes encountered on vermilion border of lower lip
absence of inhibitory factors. which tend to receive more solar exposure.
Intraoral counterpart to the ephelis is the
Common Areas of Excessive Pigmentation oral melanocytic macule. These are oval or
1. Dorsal surface of hands and feet irregular in outline, brown to black in color,
2. Genitalia tend to occur on the gingiva, palate and buccal
3. Areola of nipples mucosa (Fig. 6.5).
A B
Fig. 6.5: Examples of oral melanotic macule

Pigmentations 105
Differential Diagnosis Treatment

Nevus, superficial spreading melanoma, Surgical excision.
amalgam tattoo, focal ecchymosis. Malignant Melanoma
Nevocellular Nevus and Blue Nevus It is the uncontrolled proliferation of melano-
It represents the benign proliferation of cytes.
melanocytes. Based on histology, two major Site: Malar region, sun-exposed areas of face.
types of nevi are present: Male predilection seen. Elderly patients are
i. Nevocellular nevus: Arise from basal layer more affected.
melanocytes early in life. Presentation: macular or nodular, varied
• Junctional nevi: Located at junctional coloration (ranging from brown to black to
epithelium and connective tissue and blue) with zones of depigmentation, irregular
appear as macular or flat nevi. outlines. Melanomas may exhibit radial or
• Compound nevi: Increased proliferation of vertical growth pattern (Fig. 6.7).
melanocytes in the underlying connec- A—assymetric (one half does not match
tive tissue give rise to dome-shaped other half)
appearance because of increase in the B—border irregularity with blurred,
number of cells. notched or ragged borders
• Intradermal nevi: In late puberty, melano- C—color irregularity (non-uniform
cytes loose connectivity with the surface pigmentation)
epithelium, and become localized in the D—diameter >6 mm
deeper connective tissue. They are then E—elevation (raised surface)
termed as intradermal nevi. On the skin Lentigo maligna melanoma/Hutchinson’s
they are elevated brown nodules that freckle: Skin lesions that exhibit atypical
have hair protruding from them. melanocytic hyperplasia or melanoma in situ.
ii. Blue nevus: The blue nevus is blue on skin Mucosal melanomas are extremely rare.
because the melanocytic cells reside deep They tend to occur on the anterior labial
in the connective tissue and overlying gingiva and anterior aspect of hard palate. In
vessels dampen the brown coloration of the the early stages, melanomas are macular,
melanin, yielding a blue tint (Fig. 6.6). brown or black plaques with irregular outline
Both nevocellular and blue nevi tend to be and eventually become diffuse, nodular and
brown, and may be macular or nodular. tumefactive.
Nevi, melanotic macules and amalgam tattoo.
Treatment
Excision with wide margins.
Endocrinopathic Pigmentation
Bronzing of the skin and patchy melanosis of
oral mucosa are signs of Addison’s disease and
pituitary based Cushing syndrome.
In both of these endocrine disorders, the
cause of hyperpigmentation is oversecretion
of ACTH a hormone with melanocyte stimula-
Fig. 6.6: Blue nevus on the palate ting properties.
A B
Fig. 6.7: Malignant melanoma
Addison’s Disease Replacement Therapy

It is caused by chronic insufficiency of adrenal In Addison’s disease, stress related release of
cortex which is believed to be due to: cortisone is not there, one has to give
a. Autoimmune disease additional steroids during stressful conditions
like surgery, trauma, dental treatment. Stress
b. Tuberculosis
can precipitate hypotensive collapse. 25–40 mg
c. Amyloidosis cortisone should be given before dental
d. Inflammation followed by necrosis treatment. Hence, patient should be given
e. Neoplasia 100 to 200 mg hydrocortisone hemisuccinate
preoperatively.
In this disease cortisone and aldosterone levels
are low and patient suffers from: McCune-Albright Syndrome
a. Extreme fatigue, weakness 1. Polyostotic fibrous dysplasia.
b. Hypotension, hypoglycaemia 2. Café au lait spots with irregular margins
resembling a map of coastline of maine
c. Weight loss
(Fig. 6.8). (Unlike the smooth margins of
d. Diuresis café au lait spots associated with neuro-
e. Nausea, vomiting, etc. fibromatosis resembling coast of California,
f. Increased pigmentation Fig. 6.9.)
Decreased cortisol level in blood stimulates 3. Precocious puberty.
anterior pituitary to release adrenocortico- Peutz-Jeghers Syndrome
trophic hormone (ACTH) and melanocyte
1. Intestinal polyposis (CA intestine, abdo-
stimulating hormone (MSH).
minal pain, blood in stools)
MSH gives rise to excessive pigmentation 2. Nasal and uterine polyposis may be seen.
in the form of bluish black areas on skin folds 3. Associated with excessive pigmentation
and scars. In oral cavity these lesions appear which is in the form of multiple focal
blotchy as if ‘ink is sprinkled on the mucosa’. melanotic macules in circumoral area
At a later stage, this disease gives rise to (Fig. 6.10), around eyes and nostrils, in
typical bronze appearance to the skin. interdigital areas of hands (1–10 mm),
anterior tongue, buccal mucosa and
Laboratory Diagnosis
mucosal surface of lips.
a. Decreased level of Na
b. Increased level of K Familial Colonic Polyposis
c. Level of 17 ketosteroids (which is an index Does not exhibit abnormal pigmentation but
of stress) is dimished in the urine has a very high malignancy transformation rate.
Pigmentations 107
A B
Fig. 6.8: McCune-Albright syndrome—café au lait pigmentation with irregular outline—coast of maine
(Source: Internet)
A B
Fig. 6.9: Pigmentation with smooth outline—coast of California (Source: Internet)
Carotenemia
Condition occurs due to excessive consump-
tion of carotene pigments like carrot, sweet
potato and yolk of egg. There is an orange to
yellow pigmentation of skin.
To differentiate from jaundice:
1. Sclera not affected
Fig. 6.10: Perioral pigmentations of Peutz-Jeghers
2. Serum bilirubin normal
syndrome (Source: Internet) 3. Serum carotene increased
4. Systemic signs and symptoms of jaundice
von Recklinghausen Disease/ absent—like fever, malaise and vomiting
Neurofibromatosis
5. Color intense on soles, palms and hard
• Multiple, small, painless, sessile nodular
palate
and pendulous enlargements seen on the
skin
Brown Heme Associated Pigment
• Excessive pigmentation and café au lait
(color of coffee with cream) spots may be Ecchymosis
seen. Pigmentation on lip, tongue, gingiva. It occurs due to erythrocyte extravasation
These lesions have regular borders and are into the submucosa following an episode of
termed as “Coast of California”. trauma. It resolves within 2 weeks.
Site: Lips, face and uncommon in oral mucosa. and melanin in body tissues. It is a primary
Presentation: Bright-red macule which pro- heritable disease with a prominent male pre-
gressively turns brown and later greenish with dilection.
progress of time (Fig. 6.11). • May be due to increased Fe intake
• Excessive transfusion
• Idiopathic
When multiple brown macules, hemorrhagic
Patient’s skin becomes bronzed color
diatheses should be considered.
similar to Addison’s disease. Brown to gray
Anticoagulant drugs, hereditary coagulo- diffuse macules tend to occur in the palate and
pathic disorders and chronic liver failure. gingiva.
Petechiae
Tetrad Associated with Hemochromatosis
These arise due to capillary hemorrhages. • Liver cirrhosis
Most commonly seen on soft palate after • CCF
an episode of viral or allergic pharyngitis due • Diabetes
to irritation from posterior part of the tongue • Bronze colored skin
(Fig. 6.12).
Intraorally: Brown to gray pigmentation of
Hemochromatosis (Bronze Diabetes) hard palate
This endogenous pigmentation of hard palate Age: 40–60 yrs
results from excessive amount of deposited Fe
Diagnosis: Special staining of biopsy specimen
with Prussian blue.
In laboratory findings, increased plasma
iron concentration.
Drug Induced Melanosis
Site: Localized on hard palate or multifocal
throughout the mouth.
Presentation: Flat without evidence of
nodularity or swelling.
Drugs implicated: Quinolone, hydroxy-
Fig. 6.11: Post-traumatic subconjunctival and peri- quinoline and amodiaquine antimalarials.
orbital ecchymosis
Quinacrine hydrochloride given for long
duration then bluish black pigmentation
evident on hard palate and sharply delineated
from soft palate (Fig. 6.13).
Minocycline for treatment of acne can give
rise to oral pigmentation.
Drugs causing pigmentations of the tongue:
• Chemotherapy with doxorubicin hydro-
chloride which also colours the urine, nail
bed and skin folds
• Alpha methyldopa
• Tricyclic antidepressants
Fig. 6.12: Palatal petechiae • Zidovudine—antiretroviral drug
Pigmentations 109
Fig. 6.13: Drug-induced melanosis on the palate Fig. 6.15: Smoker’s melanosis
Oral contraceptives and pregnancy are HIV Melanosis

associated with hyperpigmentation of AIDS patients may have adrenocortical
periorbital and perioral regions (melasma/ involvement by a variety of organisms which
chloasma). manifest as Addison’s disease (e.g. Myco-
Pigmentation slowly disappears on dis- bacterium avium intracellulare) leading to
continuation of drugs. melanosis (Fig. 6.16). Drug given in the treat-
ment of HIV/AIDS such as zidovudine is
Lichen Planus known to cause pigmentation.
Lesions are known to heal with pigmentation. However, the validity of the above two
However, lesions remain recognizable usually causes have been questioned and the etiology
in the buccal mucosa and vestibule as the remains undetermined.
reticular or linear pattern persists (Fig. 6.14).
GRAY-BLACK PIGMENTATIONS
Smokers Melanosis
Diffuse macular melanosis of buccal mucosa, Amalgam Tattoo
lateral border of tongue and palate (Fig. 6.15). Most common sources of solitary or focal
Lesions are brown, flat and macular. Some are pigmentation.
even geographic and map-like in configura- Site: Association with large amalgam restora-
tion. It is suggested that in certain individuals tions or crowned teeth, extraction sockets in
melanin deposition is stimulated by tobacco vicinity of large amalgam restorations seen in
smoke products. buccal mucosa, gingiva or palate (Fig. 6.17).
Fig. 6.14: Pigmented lichen planus Fig. 6.16: Melanosis in HIV/AIDS patient
line appears well demarcated to the eye but

when observed with a hand lens it appears to
be more diffusely distributed compared to
lead line.
Paper test: It will indicate whether the pig-
mentation is present in the gingival tissue or
on the surface of the tooth. Paper introduced
in the sulcus will accentuate the metallic black
line in the gingiva and if the black line is a
stain on the tooth it will disappear (Fig. 6.18).
Fig. 6.17: Amalgam tattoo Unlike lead intoxication, constitutional
symptoms are usually absent and the treat-
Presentation: Macular, bluish-gray to black. ment is directed to maintenance of good oral
Differential diagnosis: Nevi, melanoma. hygiene.
Graphite Tattoo Lead Poisoning

Traumatic implantation from lead pencils. Lead poisoning may result from ingestion of
Site: Palate lead in the pigments, paints, cooking vessels,
containers, batteries, automobile exhausts.
Presentation: Macular, focal, gray or black.
Ingested lead is taken up by circulating
Hairy Tongue RBCs. Lead has affinity for cells in central and
Site: Dorsum of tongue (middle and posterior peripheral nervous system. The classical
third of tongue). poisoning presents with:
A—anemia
Presentation: Elongated filliform papillae
which are hyperplastic and become pigmented B—blue line
by the colonization of chromogenic bacteria C—colicky pain
imparting green, brown or black color to D—drop foot/wrist drop suggestive of
tongue. neurological damage
E—encephalopathy
Heavy Metal Poisoning Oral aspects: Patients have metallic taste and
Bismuthism: Bismuth was used as a medicine oral symptoms are overshadowed by systemic
in the past for the treatment of syphilis and manifestations of the disease. The lead line
was associated with a few toxic effects, e.g. (burtonian line) is seen as gray-black line along
GIT disturbances and bloody diarrhea—
“Bismuth Grippe”. Bismuth lines could be
demonstrated radiographically in the growing
ends of the bones.
Bismuth line may exist at the marginal
gingiva and patient may complain of
annoying gingivostomatitis similar to ANUG.
The blue-black line is because of the action of
hydrogen sulphide on the bismuth salts in the
bloodstream precipitated as bismuth sulphide
in the marginal gingiva. Hydrogen sulphide
is produced by the bacteria in the gingival
sulcus in the area of poor oral hygiene. This Fig. 6.18: Paper test
Pigmentations 111
Fig. 6.19: Lower gingival margin showing burtonian line
gingival margin caused by the formation of Systemic Aspects

lead sulphide salt in the gingival crevice • Intestinal colic
(Fig. 6.19). If the periodontal health is good, a • Diarrhea
lead line will not be present. Lead lines may • Headache
be deposited in the bones of young children.
• Tremors of fingers and tongue
Diagnosis • Renal symptoms and neurological changes
• Measurement of whole blood lead Oral Aspects
• Basophilic stippling of RBC • Marked increase in the flow of ropy, viscid,
• Lead line in the long bones and skull and saliva accompanied by itching sensation
presence in the intestinal tract provides and metallic taste in the mouth—termed as
radiographic evidence “hot mouth”
• Abnormal neurological values for peri- • Lips are dry, cracked and swollen and
pheral and central nervous system diffuse grayish pigmentation of gingiva
• In adults hair lead concentrations can be • Oral mucosal ulcerations are more prone
used and in children tooth lead level can to occur than bismuth or lead intoxication
be used. • Ulcers occur on throat and palate
Treatment • Tongue is usually enlarged, painful and
ulcerated
• The patient should be moved away from
• Lymph nodes and salivary glands are
the source of the toxic element.
enlarged and painful.
• Chelating agents such as calcium edetate
or EDTA and penicillamine. Diagnosis
Usually oral symptoms overshadow systemic
Mercury Poisoning
complaints and patients give h/o occupa-
Mercury poisoning develops as a result of tional, therapeutic or accidental ingestion of
occupational contact, drug over dosage the metal.
(mercurial diuretic), suicide attempts or self- Mucosal or gingival ulceration in a patient
medication with mercury compounds. taking diuretic by injection should be sus-
Ingestion of mercurial compounds by children pected of having mercury poisoning.
is called as acrodynia. Cases of acrodynia have
been reported from inhalation of mercury Treatment
vapours arising from paints, especially in the • Similar to ANUG
poorly ventilated rooms. • Extractions contraindicated due to
The dermatitis and stomatitis associated extensive tissue necrosis
with amalgam fillings is considered as an • Atropine or belladonna to reduce salivary
allergic reaction rather than a true intoxication. flow
Argyria or Silver Poisoning Stomatitis due to Copper, Chromium,

It gives rise to permanent discoloration of skin Cadmium or Zinc
and mucosa resulting from local or systemic Copper compounds give rise to bluish-green
absorption of silver compounds. line of gingiva, and at times tooth discolora-
tion which is permanent due to etching of the
Signs and Symptoms enamel. It may be associated with anemia.
• Skin and nailbeds are deeply discolored Chrome platers are exposed to fine spray
• Patients appear to be extremely ill, although of chromic acid which is irritating and corro-
they experience a few subjective symptoms sive to mucous membrane of nose and the
throat. Some patients develop ulcerations of
• Skin appears slate gray, violate or cyanotic,
the nasal septum leading to perforation. Also
however, this is not due to heart disorder
causes burning, soreness and dryness of the
• Cyanosis due to cardiac or pulmonary mouth. Teeth may become etched and show
causes or due to administration of acetani- persistent deep orange stain. Similar symptoms
lide are more bluish-purple in color and and lesions are found in cadmium platers.
there is blanching of tissue when blood is
forced out by pressure. Zinc Intoxication
Occupational hazard in galvanizers, zinc oxide
Treatment and molten brass workers and at times electric
The source of contact should be eliminated. arc welders. Chronic zinc stomatitis is
characterized by congestion and suppuration
Auric Stomatitis of gingival tissue with a bluish-grey line
Gold salts were primarily used for treatment and metallic taste. Teeth may become loose
of rheumatoid arthritis, leprosy and lupus because of destruction of alveolar bone.
erythematosus.
Phosphorus Poisoning
Purpura and malignant neutropenia have
been reported occasionally following gold The outstanding symptom is phossy jaw—
therapy, but dermatitis and stomatitis are periostitis and osteomyelitis of the jaw—
more commonly observed toxic reactions and usually the mandible. Localized areas of
consist of vesiculation and ulceration. necrosis may develop at the site of injury
accompanied by pain and garlic-like odor.
Treatment Necrotic process spreads to involve large
• Discontinuation of gold therapy portion of the jaw. Rapid disintegration/
• Alkaline mouthwash. exfoliation of teeth has been noted. The oral
hygiene of all phosphorus workers should be
Arsenic Poisoning maintained in the best possible state. Surgical
This results from industrial exposure, removal of sequestrum with minimal trauma
accidental or intentional poisoning. Chronic to the adjacent tissue is the treatment advocated.
gastritis and colitis are the only symptoms. The
Suggested Reading
oral changes are similar to mercurial stomatitis,
and oral tissues are painful, and deep red in 1. Burket’s Oral Medicine, 9th, 10th and 11th
color. However, unlike mercury poisoning, editions.
mouth in the arsenic stomatitis is dry. 2. Oral and Maxillofacial Pathology by
Treatment is symptomatic and involves Neville, 3rd edition.
giving anesthetic mouthwash such as 3. Shafer’s Textbook of Oral Pathology, 6th
lidocaine mouthwash. edition.
7
Granulomatous Diseases and STDs
In the older pathology texts, ‘chronic granulo- leukocytes, principally lymphocytes and
matous diseases’ were described in great detail occasionally plasma cells.
and many important diseases, such as TB, i. Infections
syphilis, Hansen’s, Hodgkin’s, Wegener’s
a. Syphilis
granuloma were included, however, more
recent texts describe these under the heading b. Tuberculosis
of ‘specific infections’ or as per the etiopatho- c. Leprosy
genesis of each condition. It is important for d. Actinomycosis
the student and clinician to have a good e. Blastomycosis
working knowledge of these conditions f. Lymphogranuloma venereum
irrespective of the heading under which they
ii. Unknown etiology
are described.
a. Hodgkin’s disease
Granulomas are characterized by formation
b. Sarcoidosis
of aggregates of chronic inflammatory cells,
connective tissue and capillaries in an attempt c. Midline lethal granuloma
to contain a chronic infection. d. Wegener’s granuloma
SYPHILIS
DEFINITION
Syphilis has been described as “king of diseases
Granular Inflammation and disease of kings.” King of diseases because
Distinct pattern of chronic inflammation in it has such varied clinical presentations and
which predominant cell type is an active protean manifestations that Sir Osler stated
macrophage with a modified epithelial-like that if you study syphilis in all its forms you
(epitheloid) appearance, e.g. tuberculosis, can cover the entire medicine! It is called
lymphogranuloma venereum, leprosy and disease of kings because being men of power
syphilis. the kings enjoyed greater sexual favors and
syphilis is basically a sexually transmitted
Granulomatous Disease disease. The disease also gained the reputation
Focal area of granulomatous inflammation of being a ‘great imitator’.
consists of microscopic aggregates of macro- It is a chronic infectious systemic disease
phages that are transformed into epitheloid caused by Treponema pallidum and transmitted
cells surrounded by a collar of mononuclear by sexual contact. Oral lesions are present in
113
all three stages of the disease and these are as a slightly raised brown plaque or papule
second in frequency to genital lesions. The on genitalia or oral cavity (lips, soft palate,
dentist, therefore, has an unusual opportunity tongue). Size of chancre varies from 0.5 to 1
for detecting unsuspected syphilis. cm. It undergoes ulceration and brownish
crustations (Fig. 7.1). It heals within 2–3 weeks
Classification of Syphilis
giving false sense of security. Chancre is
Syphilis is classified as acquired and con- painless unless superinfected. The ulcerated
genital. Acquired syphilis presents in 3 stages: surface of chancre shows presence of
Primary: Treponema and hence considered infectious.
Chancre Differential diagnosis chancre is recurrent herpes
• Genital 95% labialis
• Extragenital 5% Chancre is painless, brownish nodule with
ulceration whereas RHL is a cluster of fluid
Secondary: filled vesicles which can be painful.
• General: Maculopapular rash, lymphadeno- Chancre is associated with non-tender
pathy shotty regional lymph nodes.
• Oral: Mucous patch, split papule, condyloma
There is history of exposure in chancre,
lata
h/o recurrence, cold or fever in RHL.
Tertiary: Smear obtained from chancre studied on
• General: Neurosyphilis—general paresis, dark ground illumination show treponemal
tabes dorsalis organisms whereas scrapings from freshly
• CVS: Aneurysm of aorta ruptured RHL vesicle when stained with
• Oral symptoms: Gumma of palate, tongue Giemsa, Wright’s stain shows multinucleated
• Neurological symptoms: Tingling, numbness giant cells with ballooning degeneration.
• Osteomyelitis
Secondary Stage
• Leukoplakia
• It appears 3–6 weeks after healing of
• Syphilitic glossitis
primary lesion.
Prenatal/congenital syphilis • Sometimes with fever, lymphadenopathy
• Skin cracked and scaly and laryngitis leading to hoarseness of
• Saddle nose voice.
• Frontal bossing
• Snuffles
• Oral-post rhagade scars
• Hutchinson’s triad
a. Interstitial keratitis
b. VIII nerve deafness
c. Mulberry molars and Hutchinson’s incisors
1. Acquired Syphilis
Acquired syphilis manifests in 3 stages:
Primary Stage
In this stage, a chancre appears 2–3 weeks after
exposure at the site of inoculation. It appears Fig. 7.1: Primary chancre on upper lip (Source: Internet)
Granulomatous Diseases and STDs 115
• Maculopapular rash or ham-colored

patches on skin may be associated with
alopecia. The rashes of secondary syphilis
are varied and pleomorphic and mis-
diagnosed as allergic lesions, viral (roseola,
infectious mononucleosis) or psoriasis.
• Mucous patch: Can occur in oral cavity
(tongue, buccal mucosa, tonsil, etc.). Seen
as greyish dirty white raised patch on an
erythematous base (Fig. 7.2). It can be
scrapped off and bleeds easily, compared
to the size of the lesion, there is little pain.
(If the same lesion was an aphthous ulcera- Fig. 7.4: Split papule (Source: Internet)
tion, there would have been considerable
pain.) • Condyloma lata: Slightly raised, silvery
• At times, linear serpenginous ulcers are gray, moist, flat topped or wart-like papule
seen on palate and tongue and are described occurring in oral cavity, axilla, groin, etc.
as ‘snail track’ ulcers (Fig. 7.3). (Fig. 7.5).
• Split papule: Seen at the commissures as a • The mucous patch, split papule are teeming
papular lesion divided into upper and lower with Treponema and can transmit infection.
half by means of a split or fissure (Fig. 7.4). Tertiary Stage
Lesion usually seen in gumma. It occurs after
5–10 years of secondary stage.
May affect CNS or CVS.
CNS-neurosyphilis: Tabes dorsalis, involve-
ment of posterior root ganglion.
i. Loss of positional sense of lower extremity
giving rise to slapping step.
ii. Burning, paresthesia, pricking of area
supplied by dorsal root ganglion.
iii. Positive Romberg sign: Patient is unable to
stand erect, unaided, with his eyes closed
Fig. 7.2: Mucous patch on ventral surface of the
tongue (Source: Internet)
and tends to loose balance and tilt/fall to
one side.
Fig. 7.3: Snail track ulcer (Source: Internet) Fig. 7.5: Condyloma lata (Source: Internet)
iv. Tabetic crises: Sharp shooting pain (knife-

like) in abdominal region often mis-
diagnosed and treated with unnecessary
surgeries, e.g. appendicectomy.
v. Trophic changes consist of deep perfo-
rating ulcers and painless destruction of
larger joints (Charcot’s joint).
vi. Ataxia: Loss of balance.
vii. General paresis due to cerebral tissue
involvement:
• Personality changes
• Increased irritability, fatigue Fig. 7.7: Gummatous lesions of tongue ( Source :
• Mental sluggishness Internet)
• Euphoric symptoms, feelings of
grandeur, and importance far beyond Syphilitic glossitis if accompanied with
one's station in life leukoplakia, then it is likely to turn malignant.
• Loss of muscle coordination, inability Bone involvement: Osteomyelitis may
to enunciate clearly to perform delicate manifest as periostitis and diffuse/localized
tasks with hands gummatous infiltration. Delayed healing of
viii. Argyll Robertson pupil reacting to fractures noted.
accommodation, but does not react to light 2. Congenital Syphilis
due to cranial nerve involvements. For first 16 weeks, fetus is unaffected, after this
Oral Manifestations fetus manifests disease
Gumma affects palate giving rise to perfo- 1. Child may be stillborn
ration of palate (Fig. 7.6). (D/d for perforation 2. Born with lesions
of palate include trauma, midline lethal 3. Born without lesions
granuloma, oroantral fistula, iatrogenic, cleft Lesions may manifest within 2 years of life:
palate, malignancy and deep fungal infection). 1. Maculopapular lesions on skin
Gumma of tongue: Syphilitic glossitis which 2. Scaling and dry and cracked skin giving the
after healing with scar formation gives a tufted child ‘wizened old man’ appearance
or upholstered appearance (Fig. 7.7). 3. Snuffles-persistent nasal discharge
4. Frontal bossing
5. Saddle nose (depressed nasal septum)
patients with congenital syphilis have an
abnormal facies: frontal bossing, saddle
nose, underdeveloped premaxilla, anterior
open bite described as one of the stigmata
(Fig. 7.8)
6. Sabre tibia (forward bending of tibial bone)
7. Oral cavity showing post-rhagadic scars
which are healed gummatous lesions, which
radiate peripherally from the commissure
(Fig. 7.9)
Fig. 7.6: Perforation of palate—tertiary syphilis 8. Hutchinson’s triad (Hutchinson’s teeth,
(Source: Internet) interstitial keratitis, VIII nerve deafness)
Fig. 7.11: Dwarfing of first molar compared to second

Fig. 7.8: Saddle nose—congenital syphilis (Source: molar
Internet)
• Mulberry molars (irregular droplets of
enamel) seen on occlusal surface and tooth
are hypoplastic. First molars are invariably
affected and crown and root are smaller
than second molar (normally 2nd molars
are smaller than 1st). Moon’s molar—the
crown is smooth rounded with less promi-
nent cusps. The cusps located closer to the
centre of crown. Differential diagnosis—in
rickets, the crown of the 1st molar is hypo-
plastic but roots are normal in congenital
syphilis, both crown and roots are dwarfed
(Fig. 7.11).
Fig. 7.9: Rhagadic scar
B. Interstitial Keratitis (Fig. 7.12)
A. Hutchinson’s Teeth [Incisors and 1st Molars]
Chronic variety of keratitis with deep deposits
• Notched incisors absence of central in the substance of cornea having a ground-
mamelons of incisors giving notched glass appearance.
appearance (Fig. 7.10).
• Barrel or screw driver shaped incisors: The C. Eighth Nerve Deafness
mesiodistal width is reduced at the incisal Lab Diagnosis
edge, so that the incisors appear broad in 1. In primary stage, serological testing may
the center and taper towards incisal edge. be negative
Fig. 7.10: Hutchinson’s incisors Fig. 7.12: Interstitial keratitis (Source: Internet)
2. Dark ground illumination test, hanging With the introduction of Streptomycin in1940s
drop preparation will show the Treponema there was reduction in transmission rates and
3. Staining with Fontana/Giemsa stains improvement in survival rates, however, in
4. Staining the tissue with Levaditi method, 1980s there was a resurgence in TB infection
silver impregnation caused by the spread of HIV infection and
AIDS.
5. Noguchi’s medium for isolation
6. VDRL and serological tests are positive Etiology
during second stage • Caused by Mycobacterium tuberculosis an
7. Wasserman and complement fixation test acid-fast bacillus (aerobic slender rods).
can also be done • Droplet infection is the main mode of
8. Staining with fluorescein-labeled anti- spread, i.e. there is inhalation of myco-
Treponema antibody test called FTA-ABS bacteria loaded respiratory microdroplets.
9. Treponema pallidum immobilization test • Prolonged close contact of a susceptible
10. Flocculation test host with a source of infection leads to
inhalation of aerosolized bacilli.
11. Histopathology
• M. tuberculosis reaches lung alveoli, if not
Treatment eliminated by the immune system they
1. Injection of benzathine penicillin 2.4 million grow into localized lesions called tubercles.
units IM as a single dose after test dose Cellular immunity comes into action in 4–6
weeks and most of the bacilli are eliminated
2. If patient is sensitive to pencillin, tetracycline
ending the primary infection. The Ghon’s
500 mg QDS for 10 days
complex is the remnant of this infection,
• Erythromycin 500 mg QDS for 10 days most often occurs in infants and children,
3. Jarisch-Herxheimer reaction: When a potent comprises small calcified lung nodules and
dose is given, no. of microorganisms are lymphadenopathy of the hilar nodes.
killed, giving rise to sudden aggravation of • In symptomatic TB, the organisms spread
symptoms due to liberation of toxins. via the lymphatics to cause the granulo-
4. Treatment of late neurosyphilis matous infection in both the lungs, hilar
• Inj benzathine penicillin 2.4 million units nodes and is accompanied by respiratory
IM (1 inj per week for 3 weeks) or symptoms.
• Erythromycin for 1 month • Progressive primary tuberculosis: In indivi-
duals who are less resistant to TB, micro-
To prolong action of penicillin tab
organisms spread throughout the body
probenecid 500 mg QDS for 10 days is given.
either:
It prevents renal excretion of penicillin.
– Through the blood leading to the
dangerous miliary TB
TUBERCULOSIS (KOCH DISEASE)
– Through the respiratory system causing
Tuberculosis is a widespread infectious bronchopneumonia
disease that has afflicted the mankind globally – Through GI tract as a result of bacilli
for many centuries and till date remains the which are swallowed.
most common cause of death from a single
Clinical Features
microbial agent.
WHO estimates that 30% of world popula- • Pulmonary TB is the most common type
tion is infected with TB. India has the largest • Chest pain
patient load compared to the rest of the world. • Fever—evening rise of temperature
• Persistent and productive cough of more

than 3 weeks duration. (Both the fever and
cough do not respond to normal anti-
pyretics and antitussives.) Sputum has
purulent exudate containing large number
of acid-fast bacilli (AFB).
• Hemoptysis is a feature in certain cases.
• Loss of appetite and extreme fatigue.
• Extrapulmonary TB involves lymph nodes
which are enlarged, nontender, matted and
do not respond to antibiotics. Scrofula is a
chronic tuberculous involvement of cervical
LN (believed to be caused by consumption
Fig. 7.13: Cold abscess
of raw milk from infected cows) associated
with persistent purulent discharge. Healing
• Skin lesion of TB is called lupus vulgaris,
of such LN swellings is associated with
caused by lymphatic and blood spread of
pigmentation and scarring.
tuberculous foci, affect the skin around
• Cold abscess: Chronic cutaneous abscess with
nose, eyelids, lips, ears. The ear and nose
persistent pus discharge, the abscess being
chronic is nontender and not warm to touch, cartilage may be destroyed. The lesions are
hence, termed as cold abscess (Fig. 7.13). painful well-demarcated papules that pro-
• TB meningitis causes fever, seizures, persis- gress to plaque, when pressed with glass
tent headache, muscle weakness. Tubercular slide yellowish nodules (tubercles) are seen.
abscess of the brain mimics a cerebral
Oral Manifestations
tumor.
• Tuberculous arthritis can affect any joint, • Tuberculous ulcer mostly seen on tongue,
but common in hip and knee joints. buccal mucosa , deep, severely painful ulcer
• TB spine in children is commonly called as with undermined edges and periulcer
Pott’s spine. swelling and erythema (Fig. 7.14). Gingival
• GI tract-persistent ulcers can occur from lesions are also common. Either these
oral cavity to the anus. Stomach and lesions are disseminated from pulmonary
intestinal TB ulcers are painful and can lead infection or develop because of seeding of
to persistent pain, diarrhea and mal- tubercle bacilli in traumatic lesions during
absorption. Intestinal TB can form a mass violent bouts of coughing. Extraction sockets
and be mistaken for cancer. may also be affected in similar manner.
A B
Fig. 7.14: Examples of tuberculous ulcers (Source: Internet)

A B C
Fig. 7.15: Matted tuberculous lymph nodes, clinical picture, USG and MRI
• Associated cervical lymphadenopathy

(matted, Fig. 7.15).
• Tuberculous osteomyelitis is seen commonly
in individuals with diminished resistance.
Diffuse swelling, pus discharge, pain
LN involvement are observed. Radio-
graphically osteolysis, sequestration,
pathological fracture, periosteal reaction is
evident.
• TB should be included in the differential
diagnosis of persistent ulcer with LN
enlargement especially if the patient is
immunocompromised. Fig. 7.16: Cervicofacial actinomycosis (Source: Internet)
Treatment
• Cervicofacial actinomycosis is chara-
Streptomycin, isoniazid, rifampicin, PAS, cterized by purplish-red swelling in the
ethambutol, pyrizinamide are the various perimandibular area which spreads deep
antibacterials given. The treatment should be into adjacent tissues forming multiple
carried out by the specialists experienced to abscesses, with discharge of purulent
manage this condition and patients should be material containing granules resembling
monitored and advised not to prematurely sulphur hence termed ‘sulphur granules‘
discontinue the treatment as it can lead to the (Fig. 7.16).
feared multidrug-resistant TB.
• A pus sample obtained from the discharg-
ing sinus or a needle aspirate when stained
ACTINOMYCOSIS shows presence of beaded, branched,
• Slowly progressing chronic infection with filamentous, gram-positive rods.
granulomatous and suppurative features. • Preliminary diagnosis can be made by
• Caused by filamentous, nonacid-fast, gram- crushing the sulphur granule between 2
positive bacteria—Actinomyces israelii with slides and staining with 1% methylene blue
Actinobacillus actinomycetem comitans called to show the typical features of actinomy-
as companion bacteria which enhances the coses described as ray fungus.
pathogenic potential of Actinomyces. • Treated with antibiotics like penicillin G or
• It usually affects soft tissues and can also V, tetracycline, amoxicillin with clavulanic
affect bone. acid (augmentin).
LEPROSY (HANSEN’S DISEASE) Borderline

Rare oral lesions appear as focal or diffuse
It is a chronic granulomatous disease pre-
valent in developing countries, mainly Asia exanthemas, or papules rarely forming ulcers.
and Africa. It is caused by Mycobacterium Lepromatous
leprae, which causes mild or subclinical • Multiple, erythematous, bilateral symme-
infection on initial entry to tissues. trical lesions on skin of face, arms and legs.
Mode of transmission: Droplet infection, • Lesions are anesthetic, i.e. exhibit a loss of
source being nasal discharge of patients with sensation/numbness in the area.
lepromatous leprosy. • Bone lesions lead to malformations of
Types of Leprosy hands, feet and skull.
It is of three types: • Lesions of skull may cause atrophy of the
1. Lepromatous: Here a cell-mediated response anterior nasasl spine, recession of the
does not occur, humoral response is marked alveolar process of premaxillary region, with
with the production of high titres of loosening of maxillary incisor teeth (Fig. 7.17).
antibodies. Infection is widespread, large • Inflammatory changes in the superior
number of bacilli present in lesions surface of hard palate.
(caseating granulomas), with negative • Pink discoloration of upper incisors due to
lepromin skin test. invasion of pulp by infected granulation
2. Tuberculoid: Cell-mediated response is tissue that can produce pulpitis and pulp
strong with little or no production of death.
antibodies. Disease is localized and positive • Intraoral nodules are yellowish-red, sessile,
lepromin test present. Bacilli are scanty. soft to hard, single or confluent lesions that
3. Borderline: Here patient progresses from a tend to ulcerate.
tuberculoid like form of the disease to a • Healing leads to scarring
more lepromatous presentation. • Premaxillary gingiva, hard and soft palate,
The potential for human to human trans- uvula and tongue are most affected
mission is low compared with tuberculosis. • Cobblestone appearance of anterior two-
thirds of tongue.
Clinical Features
Diagnosis
Tuberculoid • Signs and symptoms
• Rare presentation in oral cavity • Anesthetic skin lesions, thickened peri-
• Neurologic features associated with tuber- pheral nerves
culoid form may affect mouth and face—
hyperesthesis or paresthesia of face, lips,
tongue, palate, cheeks or gingiva may occur
in case of involvement of trigeminal nerve
• Facial paralysis with involvement of facial
nerve
• Tuberculoid leprosy presents as dry,
hairless, hypopigmented plaque with well
defined and raised border about 2.5 cm in
diameter. Patients complain that they feel
numbness in the lesional area and on testing
are anaesthetic to touch and pinprick
• Corneal and conjunctival sensory loss Fig. 7.17: Facial changes in leprosy
• Ziehl-Neelsen staining for demonstrating gland swelling, xerostomia, uveitis and

acid-, alcohol-fast bacilli facial nerve palsy
• Lepromin test is of a little diagnostic value. • Treatment: Steroids as long-term therapy,
Methotrexate, Azathioprine, and Chloro-
Treatment quine are currently used as steroid sparing
Dapsone (diphenyl sulphone) with rifampicin immune modulators.
plus clofazimine, ethionamide or prothiona-
mide. WEGENER’S GRANULOMATOSIS
Family contacts are given dapsone. No
vaccine is available. • Wegener’s granulomatosis is a rare necroti-
zing granulomatous disease affecting the
SARCOIDOSIS small to medium vessels.
• Etiology: Unknown, believed to be a
• Multisystem granulomatous disease mainly complex interaction of immune system with
affecting the lungs, and lymph nodes environmental triggers such as respiratory
• More common in males and in African infection or allergy.
population
• Anti-neutrophil cytoplasmic antibody
• Clinical features: Fever, anorexia, fatigue and
(ANCA) associated vasculitis leading to
cough
necrotizing granulomas.
• Lung involvement causes dyspnea, cough
and chest pain • Clinical features include fever, night sweats,
lethargy, arthralgia.
• Skin lesions: chronic indurated papules or
plaques on the ala of the nose. Erythema Sinusitis is very common, rhinitis, epistaxis,
nodosum and skin rash deformed shape of the nose by collapsed
• Greater risk of thyroid disorders in women nasal septum.
• Oral changes—multiple asymptomatic Conjunctivitis, scleritis, uveitis, otitis
submucosal nodules in the palate, buccal media—hearing loss, pulmonary symptoms,
mucosa, indurated swellings on the gingiva cough, hemoptysis, dyspnea, wheezing.
and tongue Glomerulonephritis with hematuria.
• Salivary gland involvement—bilateral • Oral manifestations: Granular enlargement
painless parotid swellings with reduced and erythema of the gingivae termed as
secretions. Minor salivary gland biopsy strawberry gingival hyperplasia or straw-
shows noncaseating granuloma berry gingivitis. Starts as red purple friable
• Sarcoidosis patients may develop Heerfordt’s papules on the interdental papillae and then
syndrome (uveoparotid fever)—parotid spreads to other sites (Fig. 7.18).
A B
Fig. 7.18: Wegener’s granulomatosis (Source: Internet)

• In WG, the palatal and oral ulceration is EOSINOPHILIC GRANULOMA

independent of nasal lesions, and in midline
lethal granuloma, the destruction of the The term is used to describe a lesion of bone
hard palate and alveolar bone is caused by which is primarily a histiocytic proliferation,
the spread of the lesions from the nasal with an abundance of eosinophilic leukocytes
cavity and maxillary sinus lesions to the but no intracellular lipid accumulation.
oral cavity. Clinical Features
• Treatment: Combination of corticosteroids • This disease occurs primarily in older
and cyclophosphamide. children and young adults.
Azathioprine to maintain remission, • Male to female ratio is 2 : 1.
methotrexate also effective.
• The lesion may present no physical signs
Surgery to repair damage caused by tissue or symptoms and may be revealed as
necrosis, fibrosis to the nose, trachea,
incidental radiographic finding.
bronchi.
• It may present with local pain, swelling or
Langerhans’ Cell Histiocytosis tenderness with or without generalized
• A group of disorders characterized by malaise or fever.
proliferation of Langerhans’ cells formerly • The lesions are destructive and well demar-
known as histiocytosis X is included under cated, roughly round or oval in shape.
granulomatous diseases as it is associated • The area destroyed is replaced by soft tissue
with lesions which can be considered as which at early stage is soft and brown and
granulomatous.
later becomes fibrous and grayish.
• It comprises a group of conditions that are
characterised histologically by monoclonal Radiographic Features
proliferation of large mononuclear cells • Radiolucent scooped out lesions usually
accompanied by a prominent eosinophilic involving superficial bone often seen
infiltrate. The mononuclear cells have been bilaterally in the mandible.
identified as Langerhans’ cells by their • Cortex is often destroyed and pathologic
immunologic staining characteristics and
fracture may occur.
the presence of a cytoplasmic inclusion
called the Birbeck granule. • Lesions in the jaw usually appear as single
or multiple areas of rarefaction which may
• Whether this condition represents a neo-
be well circumscribed resembling cyst of
plastic or non-neoplastic, immunologic or
reactive process remains controversial. jaw, periapical granuloma or periodontal
disease.
The clinical spectrum of Langerhans’ cell
histiocytosis includes: Treatment and Prognosis
1. Eosinophilic granuloma: Single or multiple The prognosis in majority of cases is excellent.
bone lesions with no visceral involvement. Treatment involves the curettage or radio-
2. Hand-Schüller-Christian disease: A chronic therapy. Chemotherapy is also given (CHOP).
disseminated form that includes classic Symptoms subside within two weeks of
triad of skin lesions, exophthalmos and treatment.
diabetes insipidus.
HAND-SCHÜLLER-CHRISTIAN DISEASE
3. Letterer-Siwe disease: An acute disseminated
form that affects multiple organs and has • Also known as multifocal eosinophlic
poor prognosis. granuloma
• Characterized by widespread skeletal and 3. Lymphogranuloma venereum

extra-skeletal lesions and a chronic clinical 4. Gonococcal stomatitis
course 5. Condyloma accuminatum
• Occurs usually before the age of five 6. Herpes simplex
Clinical Features 7. Molluscum contagiosum
8. Hepatitis B
The disease is characterized by classic triad:
9. Chancroid
• Single or multiple punched out bone
destruction in the skull 10. Gonorrhea
• Unilateral or bilateral exophthalmos
ACQUIRED IMMUNODEFICIENCY SYNDROME
• Diabetes insipidus with or without other (AIDS)
manifestations such as polyuria, dwarfism.
It is a term given to a group of disorders chara-
Oral Manifestations cterized by profound cell-mediated immune
• They are often non-specific and include sore deficiency (CMI); various opportunistic
mouth, with or without ulcerative lesions, infections, and neoplasms. AIDS is caused
halitosis, gingivitis and suppuration and by human immunodeficiency virus (HIV)
unpleasant taste. transmitted through blood or semen. The HIV
• Loose and sore teeth with premature has an affinity to glycoprotein molecules of
exfoliation of teeth and failure of healing T4 lymphocyte.
of sockets following extraction.
• Loss of supporting alveolar bone mimicking Pathogenesis
advance periodontal disease is chara- In AIDS patient, HIV enters cells and nucleus
cteristic and this finding in a child should of T4 cells. Within the nucleus, with the help
always be viewed with suspicion. of reverse transcriptase, it converts RNA to
DNA (hence the virus is called as retrovirus).
Treatment and Prognosis
This DNA gets integrated within host cell
The prognosis of Hand-Schüller-Christian gene. At this stage, virus known as Provirus
disease is good. Approximately half of the where it remains dormant. When T4 cells are
patients undergo spontaneous regression. The stimulated to multiply virus multiplies, so that
treatment of choice is curettage or excision of
T4 cell becomes a factory of virus. These viruses
lesions. Inaccessible lesions may be irradiated.
are given out of the T4 cells by causing holes in
Some patients benefit from chemotherapeutic
the cell membrane. The viruses thus given out
drugs, including prednisone, vinblastine and
will infect other T4 cells. The original infected
cyclophosphamide.
cells with holes undergoes death. Thereby giving
Letterer-Siwe Disease rise to lymphocytopenia. HIV also suppresses
It is an acute, fulminating disease with wide- the natural killer cells (Fig. 7.19).
spread lesions of skeletal and extra-skeletal High risk patients
tissues, including the skin affecting young 1. Homosexuals and bisexuals
infants. The multiple punched out lesions of 2. Commercial sex worker
the skull have been described as geographic
3. Drug addicts
skull.
4. Hemophiliacs
Sexually Transmitted Diseases 5. Repeated blood transfusion
1. Syphilis 6. Professional blood donors
2. AIDS or HIV infections 7. Medical personnel
Fig. 7.19: Pathogenesis of HIV infection
Transmission is mainly due to sexual inter- After approximately 5 years, patient may
course including anal intercourse, transfusion suffer from full blown AIDS manifesting as
of blood and blood products. follows:
After initial infection, there is an incubation 1. Opportunistic infections: Pneumonia by
period of 9–22 months during which time, Pneumocystis carinii
glandular fever type of reaction may be 2. Herpetic lesions: HSV, HZ
present. As the virus can remain latent and 3. Disseminated infection of cytomegalovirus
full blown symptoms can appear after a long and Epstein-Barr virus
time this virus is also called as lente virus. 4. Neoplasia
After this there is AIDS related complex • Kaposi’s sarcoma (tumor of endothelial
(ARC): blood vessels, very uncommon in normal
1. Fever persons caused due to cytomegalovirus)
2. Malaise • Lymphoma
• Squamous cell carcinoma
3. Persistent generalized lymphadenopathy
• Leukemia
4. Weight loss
Other complications
5. Night sweats • ITP: Idiopathic thrombocytopenic purpura
6. Diarrhea • Lupus erythematosus
7. Candidiasis • Encephalopathy
Oral Manifestations
Lesions strongly associated Less commonly associated Seen in HIV infection

with HIV infection with HIV infection
Candidiasis Bacterial infections Bacterial infections
Mycobacterium avium intracellulare • Actinomyces israelii
• Escherichia coli
Mycobacterium tuberculosis • Klebsiella pneumoniae
Hairy leukoplakia Melanotic hyperpigmentation Cat-scratch disease
Kaposi’s sarcoma Necrotising ulcerative stomatitis Epithelioid angiomatosis
Non-Hodgkin’s lymphoma Salivary gland diseases Drug reactions
• Dry mouth • Ulcerations
• Unilateral and bilateral swelling of • Erythema multiforme
major salivary gland • Lichenoid
• Toxic epidermolysis
Periodontal diseases Thrombocytopenic purpura Other fungal infections
• Linear gingival erythema • Cryptococcus neoformans
• NUG • Geotrichum candidum
• NUP • Histoplasma capsulatum
• Aspergillus flavus
Oral ulcerations Neurological disturbances
• Facial palsy
• Trigeminal neuralgia
Viral infections Viral infections
• Herpes simplex • Cytomegalovirus
• Human papilloma • Molluscum contagiosum
• Varicella zoster
1. Candidiasis also a common feature more so in full blown

By far the most common and predominant cases (Fig. 7.20).
clinical feature of HIV/AIDS. • Certain patients also present with eso-
• Affects the palate, tongue, buccal mucosa phageal candidiasis associated with
and presents more often as erythematous complaint of extreme burning sensation.
type of candidiasis. Combined lesions of • Extensive candidiasis involves all parts of
chronic pseudomembranous intermingled oral cavity and does not respond to anti-
with erythematous type of candidiasis is fungal agents hence termed recalcitrant.
A B C
Fig. 7.20: Examples of candidiasis in HIV-AIDS patients

• Treatment is based on severity and the Treatment

extent of the infection. Clotrimazole (10 mg OHL does not require any treatment because
as an oral troche), nystatin oral suspension, of its asymptomatic nature but it responds to
fluconazole (100 mg), ketoconazole (200 mg) acyclovir. Podophyllin and interferon are also
are the drugs usually tried. In severe used to treat OHL has no malignant potential.
candidiasis resistant to medication IV
amphotericin B can be given. 3. Kaposi’s Sarcoma
• Reddish-blue swelling arising from the
2. Hairy Leukoplakia vascular endothelium, however, not
• Occurs on lateral border of tongue associated with capillary engorgement and
hence unlike capillary hemangioma it will
• Raised white hairy lesions similar to
not blanch on pressure. In the early stages,
verrucous outgrowths with corrugated
certain cases start as a dark-pigmented
surface (Fig. 7.21)
areas more often on the palate, gingiva and
• Caused by human papillomavirus, or tongue (Fig. 7.22). At later stages, it may
Epstein-Barr virus. turn into a nodular swelling and become
In the past, this lesion was believed to be ulcerated and painful.
associated only with homosexual males having • Treatment is surgical excision with CO2
HIV infection, however, now it is also observed laser, radiotherapy for large lesions,
to be a feature of immunosuppression, e.g. intralesional injections of vincristine or
renal transplant patients on immuno- vinblastine or sodium tetradecyl sulfate (as
suppressive drugs. a sclerosing agent).
A B
Fig. 7.21: Examples of hairy leukoplakia
A B
Fig. 7.22: Kaposi’s sarcoma on gingiva and palate (Source: Internet)

A B
Fig. 7.23: Linear gingival erythema
4. HIV Gingivitis
Presents as linear gingival erythema (LGE)
which on closer inspection with a lens shows
translucent gingival margin with small
capillary loops (Fig. 7.23). Associated
erythema does not diminish after scaling and
may require antifungal agents and ART.
Necrotizing ulcerative gingivitis (NUG)
associated with AIDS resembles ANUG,
however, the ulcerative lesions are deeper and Fig. 7.25: Necrotizing ulcerative periodontitis
more severe and clinically found to extend
beyond the mucogingival junction (Fig. 7.24). Second form is less aggressive with less
Treatment includes debridement and use of necrosis affecting interproximal areas with
oxygenating mouthwash, broad-spectrum rapid bone destruction and deep interproximal
antibiotics. pockets. Treatment includes broad-spectrum
antibiotic, debridement, chlorhexidine mouth-
5. HIV Periodontitis wash and povidone iodine mouthwash.
Aggressive form also termed as necrotizing Extensive periodontal treatment and extrac-
ulcerative periodontitis (NUP) presents as tion of teeth if indicated.
extensive tissue ulceration, necrosis with expo-
6. Persistent Generalized Lymphadenopathy
sure of alveolar bone, loss of attachment and
formation of interproximal craters (Fig. 7.25). HIV infection should be considered in the
differential diagnosis of any chronic lympha-
denopathy more so if multiple site involvement
is present.
7. Herpetic Infections
In HIV/AIDS, the defence mechanism being
affected. Patients fall prey to primary HSV
infection (Fig. 7.26) and herpes zoster
infections. These infections are more severe
longer lasting and more resistant to treatment.
Herpes zoster observed in a younger indivi-
dual should alert the clinician about the
possibility of HIV infection (Fig. 7.27). Herpetic
Fig. 7.24: Necrotizing ulcerative gingivitis infections can be treated with acyclovir/
Fig. 7.26: Recurrent herpes labialis in HIV/AIDS patient
A B
Fig. 7.27: Herpes zoster of left mandibular division in a young HIV/AIDS patient
valacyclovir/famcyclovir. Patients not • Xerostomia may be present.

responding to routine anti-virals have to be • Diffuse infiltrative lymphocytosis syndrome
managed with foscarnet (40 mg/kg IV every (DILS) has been reported in these patients.
four hours for 3 weeks). This condition resembles Sjögren’s syndrome
but the lymphocytosis is characterized by
8. Non-Hodgkin’s Lymphoma
CD8 cells and not CD4 cells as seen in SS.
More common in males and presents as soft
• CT scan and MRI show multicystic enlarge-
tissue swelling with or without ulceration.
ment of the parotid gland.
Palate and gingiva are the common sites
affected (Fig. 7.28A and B). • FNAB is useful to ruleout lymphoma
• Diagnosis of NHL is made by biopsy and sarcoidosis and lymphadenitis.
histopathological examination.
10. Oral Tuberculosis
• Radiotherapy and systemic chemotherapy
In HIV/AIDS patient, tuberculosis may
are the preferred mode of treatment.
present as a persistent ulcer firm swelling or
9. HIV Associated Salivary Gland Disease a granulomatous growth. Oral involvement is
(HIV-SGD) secondary to pulmonary tuberculosis.
Presents as parotid gland enlargement manifested Biopsy and histological examination of oral
bilaterally as soft but non-fluctuant swellings. lesion stained with Ziehl-Neelsen stain.
Fig. 7.28A: NHL presenting as soft tissue growth in the right maxillary region
Fig. 7.28B: Axial and coronal CT scan showing soft tissue lesion causing osteolysis of the right maxilla
X-ray chest, skin tuberculin test (mantoux), azidothymidine and adrenal gland infection
culture studies are of diagnostic importance. caused by Mycobacterium avium intracellulare
leading to Addison’s disease.
11. Melanotic Hyperpigmentation
Patients with HIV infection may present with 11. Atypical Oral Ulcerations
excessive melanin pigmentation (Fig. 7.29), this Ulcers resembling aphthous may be mani-
could be attributed to side effects of the drug fested in HIV/AIDS patient, however, these
Fig. 7.29: Melanotic hyperpigmentation of the tongue

ulcers are larger in size, persistent, deep and lesion that mainly affects HIV-infected
crater-like extending through the epithelium patients. Oral lesions are seen as nodular
into connective tissue (Fig. 7.30). It may be growths on the palate and cutaneous and
associated with cytomegalovirus infections. systemic involvement is common. Erythro-
Treatment is topical steroids (clobetasol mycin (500 mg qid) is the drug of choice.
0.05%), intralesional steroids (triamicinolone/
betamethasone). Systemic steroids like 14. Human Papillomavirus Infection
prednisolone (40–60 mg single daily dose), It can present as oral warts (verruca vulgaris),
thalidomide (100–200 mg once daily) contra- condyloma acuminatum and focal epithelial
indicated in pregnant women. CMV ulcers hyperplasia.
respond to ganciclovir. Oral warts: These are asymptomatic
nodular cauliflower-like growths 1–3 mm
13. Bacillary Angiomatosis in diameter. They may be solitary or
It is an infectious disease caused by Bartonella multiple affecting non-keratinised mucosa
quintana. Presenting as proliferative vascular (Fig. 7.31).
A B
Fig. 7.30: Atypical oral ulcerations in HIV/AIDS patient
B C
Fig. 7.31: Oral warts in HIV/AIDS patient

A B
Fig. 7.32: Multiple pearly nodules—molluscum contagiosum
Condyloma acuminatum: Usually a single lesion Treatment

nodular in appearance seen in the floor of the • No effective treatment
mouth, labial mucosa and gingiva. • Symptomatic treatment with very little
Focal epithelial hyperplasia: Generally appears effect—zidovudine/azidothymidine (AZT)
as multiple flat pink-colored nodules usually is said to increase T4 cells and has shown
affecting the lips. some promise in treatment.
Treatment includes: Surgical removal with Dental considerations: T4 count should be
CO2 lasers, topical application of podophyllin. above 200 before carrying out any surgical
procedure otherwise post-surgical infection
15. Molluscum Contagiosum and delayed wound-healing might result.
It is a viral infection of the skin and mucous While Treating AIDS Patients
membrane called as water warts caused
by molluscum contagiosum virus (MCV). • Use disposable gloves, masks, syringes and
Appears as multiple dome shaped nodular needles (HIV kit)
swellings with pearly appearance affecting the • Glasses should be worn
skin (Fig. 7.32). It can be spread by person to • Contaminated material should be removed,
person contact by touching the affected skin. put in plastic bag, sealed and disposed by
Treatment includes salicylic acid topical incineration
tretinoin and astringent chemicals such as • Antiseptic against HIV-Glutaraldehyde
potassium hydrochloride. (Korosolex)
• Prevention is better than cure.
Diagnosis
• Clinical features Suggested Reading
• Lymphocytopenia—CD4 count 1. Burket’s Oral Medicine, 9th, 10th and 11th
• Inverted T4–T8 ratio editions.
• Positive sputum culture for Pneumocystic-
carinii
3. Oral manifestations of HIV, Michael Glick.
• ELISA (enzyme-linked immunosorbent assay) 4. Shafer’s Textbook of Oral Pathology, 6th
• Western blot test (confirmatory test) edition
• Radioimmunoassay 5. Triple O, 1991; 71:158–166.
8
Cross-Infection Control
TRANSMISSION OF INFECTIONS – Unknown carriers, that is those having

subclinical infection.
There are four factors essential for trans-
This is most dangerous group since it
mission of infection:
cannot be normally identified.
1. Source of infection can be from
• Patient Risk of infection following exposure is
• Member of dental team who is suffering influenced by:
from disease or is a carrier • Route: There is increased chances by
2. Means of transmission parenteral route
• Can be from contact with blood or saliva • Decreased host resistance
mixed with blood • Dose of virus
• Dose is more than minimum infection • Number of incidents/exposures (increased
dose. risk with increased number)
3. Route of transmission
• Inoculation with Risk to Dental Staff
– Abraded skin Dentists are at higher risks than general
– Needle stick injury, sharp instruments population to get the infections.
or flying debris Infections of concern in dentistry.
• Inhalation of contaminated aerosols. By inoculation are:
4. Susceptible host is one with
1. Hepatitis B, C and D
• Low resistance
2. HSV-1
• Heredity
• Poor nutritional status • Oral herpes
• Medications (steroids) • Herpetic whitlow
• Chemotherapy • Herpetic keratitis
• Diseases (like diabetes mellitus) 3. HIV/AIDS
Sources of Infection 4. Treponema pallidum: Syphilis
5. Staphylococcus aureus, Pseudomonas: Wound
• Patients with acute infections (do not come
abscess
to dentist)
• Patients in prodormal stage 6. Clostridium tetani
• Carrier: They can be: By inhalation are:
– Known and identified. 1. Varicella: Chickenpox
133
2. Measles: Mumps b. Inhalation of aerosols and splatter:

3. Rhinovirus, adenovirus: Common cold • Aerosol generated by:
4. Mycobacterium tuberculosis: Koch. – Air-rotor handpiece
– Three-way syringe
How Dental Staff Acquire Infections? – Ultrasonic scalers
a. Injury caused by contaminated instruments Aerosol is defined as small droplet about
which acts as the portal of entry: 5 μm or less in diameter which can remain
• Needle stick injury: suspended in air for some time. There is
– On an average one needle stick injury/ limited evidence that aerosol can transmit
year. infections.
– Volume of blood in needle stick injury But respiratory tract infections are seen
= 1.4 μl. more in dentist than the general population.
– Risk of seroconversion after needle Mycobacterium tuberculosis is detected in
stick injury with HIV is about 0.4%. aerosols.
– In case of HBV—0.1 μl may be suffi- • To reduce level of contaminated aerosol:
cient. a. A good quality mask should be used.
b. Good ventilation should be there.
– Risk of infection with HBV after
needle stick injury is 20–25%. c. Bactericidal mouthwash should be given
pretreatment
– To avoid needle stick injury never
d. High-speed vacuum aspiration.
recap the needle with the hands, use
needle disposal unit or recap the Splashes of Contaminated Sharp Material
needle without touching the plastic • Air-rotor handpiece can propel particles
cover (bayonet technique). more than 0.1 mm in diameter up to 6 m at
– In case of needle stick injury imme- a speed of 50 to 60 km/hr.
diately remove the gloves and press • Dentist may sustain microtrauma to face,
the finger and promote more bleeding eyes, hands, etc.
cover the injury with waterproof • HBV, HSV-1 causing herpetic keratitis.
bandage and reglove the hand. Ideally • So one must wear protective eye glasses and
patient’s HIV status should be found masks.
out, and if positive, postexposure
prophylaxis (PEP) with zidovudine is Risk to the Patients
indicated. A few reports describe the transmission of
– The sharp instrument should be diseases to the patients during dental treat-
handed over to the operator taking ment like:
care to keep the sharp end away. • HBV
• Lesions on operators hands: • HSV-1
– Blood remnants found under nails of • Koch
thumbs and index fingers seen in • Abscesses
about 80% of dentist (not wearing Majority of cases of transmission are via
gloves)—study by Allen and organ hands. It can be through:
– In 40% cases, blood was found after 1. Lesions on operators ungloved hands.
the weekend. 2. Contaminated gloves.
– Microlesions in the hand skin of 40% 3. Contaminated instruments and other dental
of dentist studied. equipment.
Cross-Infection Control 135
Surface Contamination b. Cirrhosis

During dental procedures flying debris like c. Primary hepatocellular CA
aerosols, droplet, splatter and contaminated • HBV results in 600 hospitalizations and 250
hands or instruments can cause widespread deaths in health care workers per year.
contamination. But possibility of transmission • HBV is a heat-resistant virus. Destroyed
is questioned as organisms like HIV die very after 5 min at 95°. It is found in blood, blood
fast. A few organism can survive, e.g. rota- products, saliva, sputum, breast milk,
virus, rhinovirus which can cause common semen, vaginal discharge.
cold. • Minimum quantity may be sufficient for
AIDS or HIV Infection parenteral transmission, e.g. 0.1 μl of blood.
Once HIV enters into body, the possible • Transmission of HBV:
sequelae that occur are: – Greater risk than HIV
a. There is increased antibody production. In – Transmission is by inoculation, inhala-
2–12 weeks, mild influenza type illness tion and contact with infected oral and
occurs, characterized by fever, sore throat nasal mucosa.
then patient becomes asymptomatic. • High-risk groups are:
b. HIV gets incorporated into the nucleo- – Drug addicts (IV)
proteins of the lymphocytes. Latent form – Homosexuals, bisexuals
which is about 90% of total number of – Patients with chronic liver diseases
infected persons. These patients are – Patients with history of recurrent blood
unaware of their condition. Unknown transfusions
carriers of HIV are infectious. Patients who
– Heath care personnel
are seropositive for HIV remain infected.
– Dialysis patients
c. The virus reproduces itself and infects more
lymphocytes. • HBV is a cause for concern because:
d. The virus depresses the number of T4 – There is widespread incidence of HBV
lymphocytes which reduces the immunity. – Chronic carrier state is common
Majority of clinical signs and symptoms of – Virus is hardly survives well outside
AIDS are a consequence of depressed body
immunity. HIV is found in blood, semen – Minute amounts of body fluid can
and body fluids. HIV does not survive in transmit infection. Therefore, vaccine is
saliva. HIV is killed easily outside body in mandatory.
dry atmosphere. Normal sterilization and
disinfection is sufficient. It can survive for Objectives of Cross-infection Control
7 days in blood at room temperature. 1. To protect the patient and dentist from
Risk of transmission during provision of contracting infection during dental proce-
health care is low. Scientific studies reported dure.
only 26 of HIV infected health care workers 2. To decrease number of pathogenic micro-
(including dentist) with no reported non- organisms to the lowest possible level.
occupational risk. 3. To exercise the universal precautionary
measures for all the patients.
Hepatitis B 4. To simplify cross-infection control to
• HBV is a major cause of: complete dental procedure with minimal
a. Acute and chronic hepatitis inconvenience.
Infection Control between patients but repeated use is not

The goal is to eliminate transfer of micro- advisable because:
organisms. This can be accomplished by: a. Exposure to disinfectant causes defects and
a. Use of barrier equipment. increased permeability.
b. Proper technique for handling sharp instru- b. Damage can occur to gloves by chemicals
ments. like eugenol, varnish, etc.
c. Vaccines for health care workers against c. Mechanical damage due to dental instru-
infectious diseases. Maintenance of good ments.
health to decrease susceptibility. d. Increased sweating causes skin irritation.
d. Correct cleaning and disinfection of sur- e. Bacteria multiply beneath glove material.
faces and equipment to remove infectious
Masks
agents.
To protect face from contaminated splatter
e. Sterilization of instruments.
and prevent inhalation of aerosols.
Handwashing Requirements for a good masks are:
Should have short and clean nails, no jewelry. 1. Good bacterial filtration efficiency
a. Rubbing removes microorganisms from 2. Does not touch nostrils and tips
skin. 3. Close fit around the periphery
b. Lathering holds them suspended away
4. Should not fog the eye glasses
from skin surface.
5. High filtration but tolerable breathability
c. Rinsing washes them off hands.
d. Cover hand injury with waterproof Eye Protection
dressing. 1. Aerosols and splatter can transmit HSV-1
e. Use alcohol-based disinfectant like Sterillium and even HBV.
which evaporates quickly. 2. Therefore, eye glasses must be worn.
Gloves To prevent fogging of glasses:
There are different types of gloves: 1. Well fitting mask adapted to the bridge of
1. Latex the nose.
a. Sterile 2. Use of antifogging liquid, e.g. antimist
b. Nonsterile marker.
2. Vinyl
a. Sterile Disposables
b. Nonsterile 1. Choose a disposable alternative when
3. Surgeons sterile gloves sterilization is not satisfactory.
4. General purpose utility gloves 2. If sterilization is simple, quick and efficient
The reasons to wear gloves are: Intact hand and does not damage the instrument
skin gives good protection. But 40% dentists disposable alternative may not be used.
have microlesions on hands which require Unless it is cheap and of similar quality.
added protection. 3. Common disposables used are:
1. To protect the patients. a. Anesthetic syringes and needles
2. To protect the dentist. b. Mouthwash cups
Gloves can be single use or reuse. Gloves can c. Saliva ejector tips
be satisfactorily cleaned of microorganisms d. Masks and gloves
Cross-Infection Control 137
Sterilization and Disinfection of Instruments 4. Organize instruments carefully. Either in

Sterilization is destruction of all micro- tray system or sterilizable pouches for
organisms whether vegetative or pathogenic instruments.
including highly resistant bacterial and 5. Sterilize or disinfect all the instruments and
mycotic spores. items used during dental procedures.
Disinfection is removal of or inactivation a. Remove the soft debris and blood
of most of the organisms but not all. Dis- remnants from the instruments by
infectants commonly used are glutraldehyde, scrubbing.
sodium hypochlorite, formaldehyde, etc. b. Place the instruments in the holding
Instruments are classified as: solutions, i.e. sodium hypochloride bath.
a. Critical: The instrument is used to penetrate c. Ultrasonic cleaner may be used to clean
the tissue or touch bone, it must be the instruments before sterilization.
sterilized, e.g. scissors, forceps, elevators, d. Sterilization using autoclave 121°C at
scalers, etc. pressure 15 psi for about 15 mins. Test
b. Semi-critical: Instrument which touches the strips can be used to confirm the steriliza-
mucous membrane but does not penetrate tion.
tissue, e.g. mirror, tweezer, amalgam e. There should be an area reserved for
carrier, etc. These instruments should be sterilization and disinfection procedures
sterilized or subjected to high level of dis- and a suitable cabinet for aseptic storage.
infection.
6. There should be minimal possible contami-
c. Noncritical: These instruments only contact
nation from dental equipment:
the skin surfaces, e.g. mixing slabs, spatula,
rubber bowl, etc. These should be a. Clean water supply.
decontaminated by intermediate level b. Anti-retraction valve for air-rotor control
disinfection. unit. This is to prevent salivary secretions
from getting aspirated in the air-rotor
Strategies for cross-infection control in a
handpiece when the foot control is
dental office:
deactivated.
1. Members of the dental team must stay
healthy c. Some units are provided with a special
Immunization, handwash, hand care, and bottle for asepsis containing hypochlorite
personal hygiene. solution and the handpiece is run for
2. Barriers for personal protection 30 sec using this solution to effectively
disinfect the handpiece between two
Gloves, mask, eye protection, clinical attire,
patients.
etc.
3. Practice careful aseptic techniques: d. Proper cleanliness of the three-way
a. Limit the spread of blood and saliva. syringe, ultrasonic scalers, etc.
b. Careful handling of the sharp instru- e. Dispose the contaminated waste safely.
ments. Sharp needles blades in puncture proof
c. Limiting surface contact. containers, blood contaminated waste
d. Surface disinfectant, drapes and covers properly treated and packed in red
to be used. covers.
e. Minimize the aerosol and splatter by f. Suction machine should be cleaned with
using high volume aspiration, pre- hypochlorite.
operative mouthwash, rubber dam, etc. g. Glass bead sterilizer in endodontics.
9
Bleeding and Clotting Disorders
and Hematological Diseases
BLEEDING AND CLOTTING DISORDERS
Whenever there is any injury to any part of • Factor V: Labile factor (proaccelerin,
body, bleeding starts but after some time this accelerator globulin)
stops and blood forms a jelly-like mass. This • Factor VI: Not present
process is extremely important as it avoids • Factor VII: Stable factor (proconvertin)
excessive blood loss. This process by which • Factor VIII: Antihemophilic factor (anti-
body maintains its blood volume is referred hemophilic globulin)
as process of hemostasis. • Factor IX: Christmas factor
Hemostasis: When a blood vessel is cut or • Factor X: Stuart-Prower factor
damaged, the injury initiates series of • Factor XI: Plasma thromboplastin anticedent
reactions, which prevent the further blood • Factor XII: Hegman factor (contact factor)
loss. This type of arrest of bleeding is called • Factor XIII: Fibrin stabilizing factor
as hemostasis. It is divided into 4 phases: (fibrinase)
1. Vascular phase
2. Platelet phase Sequence of Clotting Mechanism
3. Coagulation cascade Clotting occurs in three stages:
4. Fibrinolyitc phase 1. Formation of prothrombin activator
2. Conversion of prothrombin into thrombin
Blood clotting: When blood is shed out or
3. Conversion of fibrinogen into fibrin, these
collected in container, it loses its fluidity and
fibrin threads entangle with platelets and
becomes a jelly-like mass after a few minutes.
other blood cells to form a blood clot.
This process is called as “coagulation” or
“clotting” of blood. Blood clot is a mesh of thin Various reactions of blood clotting are explai-
fibrils of fibrin entangling the blood cells. This ned by “cascade” or “waterfall” theory. As every
process involves series of various factors step of these reactions initiates the next step it
which are referred as coagulation factors. is known as process of “bioamplification”.
Factors involved in blood clotting: Formation of Prothrombin Activator
• Factor I: Fibrinogen It is formed in two ways:
• Factor II: Prothrombin 1. Extrinsic pathway: In this, formation of
• Factor III: Thromboplastin prothrombin activator is initiated by tissue
• Factor IV: Calcium thromboplastin.
138
Bleeding and Clotting Disorders and Hematological Diseases 139
2. Intrinsic pathway: In this, formation of pro- Thrombin itself can accelerate this reaction
thrombin activator is initiated by platelets by positive feedback mechanism.
which are within the blood itself
3. Common pathway: In this, a sequence of
enzymic reactions takes place to form
prothrombin activator after activation of
factor X.
Extrinsic Pathway
After tissue injury takes place it releases tissue
thromboplastin (factor III) along with
phosphoproteins and glycolipids. These
phosphoproteins and glycolipids along with
factor X and factor number VII lead to
conversion of factor X into its active form F: factor
factor Xa. This factor Xa with phospholipids Conversion of fibrinogen into fibrin:
and factor V and calcium ions lead to • Thrombin converts fibrinogen into fibrin.
formation of prothrombin activator. • Fibrin stabilizing factor (F XIII) convert
loosely arranged fibrin aggregates into
dense tight aggregates in the presence of
calcium ions. These fibrin filaments get
entangled with blood cells to form blood clot.
Fibrinolytic phase: Process of fibrinolysis helps
in lysis of blood clot. This process is also as
essential as blood clotting since it helps to
reopen blood vessels which are blocked due
to intravascular clot formation. This involves
following steps:
• Clot retraction: It is contraction of clot after
Intrinsic Pathway
30–45 min. due to oozing out of serum.
In this pathway blood platelets trigger the Contractile proteins of platelets like actin,
formation of prothrombin activator. After myosin, and thrombosthenin are responsible
blood vessels rupture the endothelium of for it.
blood vessel comes in contact with factor XII • Lysis of blood clot: A few days after injury,
and it gets converted to its activated form XIIa. injured tissue enzymes and damaged
This XIIa converts factor XI to its active form endothelium release tissue plasminogen
(XIa). This XIa along with factor IX and activator. It converts plasminogen into
calcium ions converts factor IX into IXa plasmin. Plasmin dissolves clot by digesting
(activated form). This activator factor IXa fibrin threads.
converts factor X into Xa (activated form). This • Significance: In certain organs like heart,
activated form of factor X with factor V and formation of blood clot can lead to
phospholipids form prothrombin activator. obstruction of blood flow to a certain part
Conversion of prothrombin into thrombin: of heart leading to infarction. Lysis of the
• Prothrombin activator converts prothrombin blood clot reopens blood vessel and
into thrombin in presence of calcium ions. prevents infarction.
Lab Assessment for Bleeding 3. Deficiency of factors V, VII, X, pro-

and Clotting Disorders thrombin and fibrinogen
Platelet count: Normal = 1,50,000 to 4,50,00/mm3
Activated Partial Thromboplastin Time
• Surgical or traumatic hemorrhage can occur
• It is a screening test for intrinsic limb and
if it is below 50,000/mm3
common pathway of coagulation system.
• If it is below 10,000–20,000/mm 3 then
• Blood samples are collected in tubes with
spontaneous hemorrhage can occur.
oxalate or citrate to arrest coagulation by
Bleeding time: It is time interval between skin binding calcium. The specimen is then
puncture and arrest of bleeding. delivered to the laboratory. In order to
• Normal bleeding time: 3 to 6 min activate the intrinsic pathway, phospho-
• It is sensitive measure of platelet function lipids, an activator (such as silica, celite,
• Increased in: kaolin), and calcium (to reverse the anti-
coagulant effect of the oxalate) are mixed
– Thrombocytopenia, von Willebrand’s
into the plasma sample. The time is
disease, platelet dysfunction.
measured until a clot forms.
Clotting time (CT): Time taken by blood to clot • The test is termed “partial” due to the
after collection from body. Normal 3 to 8 min. absence of tissue factor from the reaction
• Physiologic variation: CT is decreased in mixture.
menstruation and before parturition. • Normal range below 45 sec. (Note: PTT is
• Pathologic variation: CT increased in: insensitive to large changes in intrinsic
1. Hemophilia coagulation pathway. A 70% decrease in
2. Liver damage factor levels may still provide normal PTT
3. Any clotting factor deficiency hence even a small change in PTT is of great
4. Vitamin K deficiency significance).
5. Anticoagulant treatment • It is increased in hemophilia.
6. Disseminated intravascular coagulation International Normalized Ratio
(DIC) • As prothrombin time estimated in different
Prothrombin Time laboratories is not comparable due to
difference in the source of thromboplastin
Blood is collected and oxalated so that pro-
used and difference in type of instrumen-
thrombin is not converted to thrombin; to
tation.
prevent blood clotting. Then a large quantity
of tissue thromboplastin and calcium ion is • Hence, an attempt to introduce standardiza-
added to this blood. Calcium nullifies the tion leads to development of INR.
effect of oxalate and tissue thromboplastin • It relates all thromboplastins to the stan-
activates prothrombin and blood coagulation dard of human brain thromboplastin with
occurs. During this, time taken by blood to clot the use of internal sensitivity index (ISI).
after adding tissue thromboplastin is called as • INR of normal patient is 1.
prothrombin time. ISI
⎧ prothrombin time of patient ⎫
It indicates quantity of prothrombin present • INR = ⎨ ⎬
in blood. Normal 12–14 sec. ⎩ prothrombin time of control ⎭
• It is increased in: • When INR is below 3.5 normal extraction
1. Warfarin therapy of tooth can be done without any change in
2. Vitamin K deficiency anticoagulant therapy.
Classification of Bleeding • Enhances platelet aggregation.

and Clotting Disorders • Has a carrier function for factor VIII in
• Vessel wall disorders: plasma and protects it from proteolytic
1. Vit. C deficiency degradation.
2. Cushing’s syndrome • Normal level of von Willebrand’s factor in
3. Hereditary hemorrhagic telangiectasia blood is 10 mg/L with half-life of 6–15 hrs.
4. Ehlers-Danlos syndrome Classification of von Willebrand’s Disease
• Platelet disorders: Can be congenital or
• Type I: Partial quantitative deficiency (85%
acquired and can be thrombocytopenic or
of all vWD)
nonthrombocytopenic in each category.
• Congenital coagulopathies: Hemophilia A and • Type II: Qualitative deficiency (seen in about
B, von Willebrand’s disease. 10–15% cases) has four sub-types:
• Anticoagulant-related coagulopathies: Heparin, 1. IIA: Decreased platelet adhesion due to
coumarin. deficiency of vWF
• Disease related coagulopathies: Liver diseases, 2. IIB: Increased affinity for platelet
vitamin K deficiency, DIC. glycoprotein Ib
Oral findings in any patient of bleeding and 3. IIM: Defective platelet adhesion despite
clotting disorder: of normal vWF
• Platelet deficiency and vascular wall 4. IIN: Decreased affinity for factor VIII
diseases will lead to formation of petechiae, • Type III: Complete deficiency of vWF
ecchymosis on face also intraorally (also on
• Pseudo or platelet type of vWD due to
abdomen, forearm, etc.).
primary platelet disorders that mimics
• Platelet dysfunction in leukemia leads to
vWD.
hyperplastic hyperemic gingival enlargement.
• Spontaneous and prolonged gingival Clinical Features
bleeding (or after minor trauma also other 1. Most patients are asymptomatic and
parts of oral mucous membrane can show diagnosed by positive family history.
this feature). 2. Excessive bleeding spontaneously or after
• Deposition of hemosiderin and other blood minor trauma.
pigments on surface of teeth leading to their 3. Most common bleeding sites are nose, skin,
brown discolouration. gingiva.
• Poor oral hygiene as patient is afraid of
4. Bleeding within GI tract, menorrhagia is
brushing for fear of gingival bleeding.
also observed.
von Willebrand’s Disease (vWD)
Oral Manifestations
• Most common inherited coagulopathy.
1. Excessive bleeding after tooth extraction
Also known as “pseudohemophilia”.
• Described by Erik Aldrich von Willebrand 2. Spontaneous bleeding of gingiva or
in 1926, which results from inherited defects gingival bleeding after even minor trauma.
in structure and function of von Willebrand Lab Findings
factor.
1. Increased bleeding time
• It is synthesized from endothelium of blood
vessels. 2. Normal clotting time
• Function of von Willebrand’s factor: Enables 3. Normal prothrombin time
attachment of platelets to the exposed 4. Increased activated partial thromboplastin
collagen of damaged vessel. time
5. Increased capillary fragility (positive Two types

tourniquet test) 1. Hemophilia A: Factor VIII deficiency
6. Normal clot retraction 2. Hemophilia B: Factor IX deficiency (also
known as Christmas disease)
Treatment
Hemophilia A
Mild cases respond to infusion of desmo-
pressin IV 0.3 μg/kg in 100 ml normal saline Seen more commonly than type B
over 30 min. This increases concentration of Classification
vWF by 2 to 10 folds and concentration of • Mild: Factor activity >5%
factor VIII by 3 folds which are maintained • Moderate: Factor activity 1–5%
for about 12 to 24 hrs. • Severe: Factor activity <1%
Generally individuals with baseline concen-
Clinical Features
tration of vWF 10 IU/dl respond favorably to
desmopressin infusion therapy. • Depend on severity of deficiency of clotting
• For any major surgeries, concentration of factor
VIII and vWF needs to be checked after • Persistent bleeding either spontaneous or
infusion of desmopressin. It should be following even minor trauma
given for at least 5 days postoperatively and • Hemorrhage in subcutaneous tissue,
internal organs resulting into massive
concentrations of factor VIII and vWF
hematomas
should be monitored daily.
• Hemarthrosis of weight-bearing joints is a
• Type IIB and type III patients do not
common feature of body due to hemorr-
respond to desmopressin. They can be hage.
managed by blood product replacement.
• Virally inactivated factor VIII concentrates Oral Findings
also provide good concentration of vWF 1. Gingival hemorrhage most common, may
that is required for hemostasis. be massive prolonged even physiologic
• If this is not available then fresh frozen tooth eruption and exfoliation can result
plasma (FFP) and cryoprecipitate can be into uncontrolled hemorrhage.
used. 2. “Pseudotumor” of mandible which is caused
• Local hemostatic measures and antifibrino- due to subperiosteal bleeding with reactive
lytic agents should be used as supplement new bone formation causing tumor-like
to these therapies. bone expansion is also seen.
• Avoid aspirin and other NSAIDS for their Treatment
antiplatelet action. • To have normal coagulation profile during
any treatment procedures, it is required that
Hemophilia
factor VIII activity should be at least 50%
• Characterized by prolonged coagulation of normal.
time and hemorrhagic tendencies. • This can be achieved by IV infusion of FFP
• Transmitted as X-linked recessive mende- or DDAVP or factor concentrate or cryo-
lian trend in humans precipitate.
• Affects males more often and females are • For pain control:
generally the carriers. The patients give the – Use intrapulpal or intraligamentary or
history of their maternal uncles suffering local infiltration
from Hemophilia. (Only homozygous – For nerve block, minimum level of factor
females may get affected.) required is 20–30%
– Avoid intramuscular injections as it may • Stainless steel crowns should be adjusted

cause hematoma. such that minimum enamel near gingiva
For surgery, oral endotracheal tube inser- needs to be removed.
tion is preferred over nasal intubation to avoid • Preventive treatments like topical fluoride
nasal bleed. application and pit and fissure sealants
should be used to minimize need of any
Preventive and Periodontal Treatment
complex treatment.
• Periodontal probing, supragingival scaling
and polishing can be done as routine proce- Orthodontic Treatment
dure. • Can be done normally such that mucosal
• Careful subgingival scaling with a sharp laceration by orthodontic bands, brackets
scaler rarely requires any factor replace- and wires will not occur.
ment
• Fixed therapy is preferred over removable
• For severely inflamed tissue gross debride- functional appliance therapy.
ment should be done with chlorhexidine
mouth rinses • Use of extraoral anchorage shortens the
duration of treatment hence reduces chances
• Any deep scaling and root planing should
of bleeding.
be done quadrantwise.
• Supplemental use of local hemostatic Dental Management of Patient
measures is essential. with Platelet Disorders
• For any dental surgical procedure, platelet
Restorative and Prosthetic Procedures
count should be more than 50,000 mm3.
• Rubber dam isolation to avoid soft tissue
laceration (carefully select a clamp that does • Aspirin should be stopped 1 week prior to
not hurt gingiva). surgical procedure.
• Caution: Use of matrices, wedges, hemo- • For chemotherapy associated thrombocyto-
static gingival retraction cord. penia, transfusion of FFP, HLA matched
platelets should be done.
• Denture trauma should be minimized by
prompt and careful denture adjustment. Patient on Anticoagulant Treatment
Endodontic Treatment • Generally anticoagulant therapy of any
patient is adjusted in such away that INR
• RCT treatment of choice without any contra-
indication. value will be between 1.5 and 2.
• Avoid overinstrumentation and overfilling • For any surgical dental procedure, physician
of canal. consultation is compulsory.
• When risk of thrombosis and embolism
Pedodontic Treatment is small and risk of hemorrhage is high,
• For extraction of mobile deciduous tooth. coumarin therapy is discontinued briefly at
• 2 days of vigorous oral hygiene procedures the time of surgery followed by prompt
to reduce inflammation followed by reinstitution postoperatively.
infiltration, or intraligamentary LA to • Whenever coumarin therapy needs to be
extract tooth without any factor replace- stopped prior to any surgical procedure, it
ment. should be stopped for 2 days, as half-life of
• Preferred procedure: Pulpotomy. coumarin is long, i.e. 42 hr.
• For moderate thromboembolic and hemorr- Low Molecular Weight Heparin (LMWH)
hagic risks, coumarin therapy can be • Selective inhibition of Xa NOT IIa also it
maintained in therapeutic range with use bring about conformational changes in
of local measures to control postoperative AT III.
oozing. • It has lesser effect on a PTT and CT hence
• High-risk patients can be managed with lab monitoring is not required.
combination of “unfractioned heparin- • Longer and more consistent results.
coumarin” method. It requires hospital • Better subcutaneous bioavailability 70–90%.
admission of patient.
Warfarin and Coumarin Anticoagulants
• Coumarin therapy is stopped 24 hr prior to
• They interfere with synthesis of vit. K
hospital admission. And it is substituted by
dependant clotting factors, i.e. factors VII,
unfractioned heparin IV that has half-life
IX, and X.
of 4 hr.
• Mechanism of action: Warfarin and coumarin
• Heparin therapy instituted on admission is are competitive antagonists of vit. K.
stopped 6–8 hr preoperatively. • They interfere with production of active
• Surgery is accomplished when PT/INR and metabolite of vit. K, i.e. hydroquinone.
aPTT are within normal range. • Hydroquinone is required for gamma
• Heparin therapy is reinstituted 6 to 8 hr. carboxylation of glutamate residues of
after surgery when adequate clot has prothrombin and factors VII, IX, X which
formed. Followed by gradual restart of is required for ability of clotting factors to
coumarin therapy. bind calcium for clotting.
• A less costly alternative to unfractioned Antiplatelet Drugs
heparin can be used which is “low mole- • During clotting, platelets stick to damaged
cular weight heparin”. vessel wall and release ADP, TXA2 which
Commonly used Medicinal Agents promote further aggregation of platelets to
Affecting Clotting Mechanism form platelet plug.
• Heparin: Natural anticoagulant of blood. • Intima of blood vessels synthesize prosta-
Also artificially synthesized form of drug cyclin (PGI 2) that is strong inhibitor of
can be used to treat hypercoagulative states. platelet aggregation.
• The release of TXA2 from platelets and PGI2
• Low molecular weight heparin (LMWH):
from endothelium controls intravascular
Heparin molecule can be fractioned into
thrombus formation.
low molecular weight derivatives that can
• Due to sluggishness of blood flow in veins
be used for anticoagulation.
to achieve anticoagulation effects in vein
use “anticoagulants”.
HEPARIN • In arteries, blood clot is mainly consisting
of platelets hence use antiplatelet drugs to
Unfractioned Heparin
avoid intra-arterial clot formation.
• MOA: Activates plasma antithrombin III • Aspirin: MOA—it acetylates and inhibits
(AT III) and inactivates clotting factors enzyme cyclo-oxygenase and thromboxane
involved in intrinsic and common pathway irreversibly.
of blood coagulation (mainly factors Xa • Inhibits PGI2
and IIa). • Inhibits release of ADP from platelets and
• Subcutaneous bioavailability 20–30%. prevent their aggregation.
• As low as 75–150 mg of aspirin can show • Postsurgical hemorrhage: After extraction of

these effects. teeth, biting of tongue
• As lifespan of platelets is about 8 days, • Congenital malformation: Hemangioma,
hence it is advised to stop aspirin one week hereditary hemorrhagic telangiectasiae.
prior to oral surgical procedures.
2. Hemorrhage due to
Fibrinolytic Agents Clotting Factor Deficiency
• Streptokinase: Obtained from beta hemolytic • Hereditary: Hemophilia A, hemophilia B,
streptococci group C. von Willebrand’s disease
• It combines with plasminogen and activates • Iatrogenic: Anticoagulant therapy
formation of plasmin. • Liver diseases: Factors II, VII, IX, X deficiency
• Other agents: Urokinase, alteplase. • Dysfunction: Multiple myeloma, SLE, macro-
globulinemia.
Antifibrinolytics
• Epsilon aminocaproic acid (EACA) 3. Hemorrhage due to Platelet
• Analogue of lysine which combines with Deficiency or Dysfunction
the lysine binding sites of plasminogen and • Deficiency: Idiopathic thrombocytopenic
plasmin so that plasmin will not be able to purpura
bind fibrin to lyses the blood clot. • Dysfunction: Defective adherence Bernard-
• Dose: 5% mouthwash or 5 g oral/IV stat Soulier syndrome
followed by 1 g hourly till bleeding stops. • Defective platelet release reaction: Storage pool
• Transexamic acid: Binds to lysine binding disease
sites on plasminogen and prevents its • Defective aggregation: Thrombasthenia
interaction with fibrin to cause blood clot • Defects of uncertain nature: Uremia, crypto-
lysis. globulinemia, macroglobulinemia,
• Dose: 10–15 mg/kg 2–3 times/day
4. Hemorrhage due to Systemic Diseases
1 to 1.5 g TDS oral
• Septic embolization in bacterial endo-
Causes of Intraoral Bleeding carditis
1. Hemorrhage due to Local Cause • Scurvy
• Infection: ANUG, erythema multiforme, • EM
primary HSV infection • Pemphigus
• Local irritants: Malposed tooth, prosthetic • Pemphigoid
appliance, calculus • Allergy
HEMATOLOGIC DISEASES
Hematologic diseases are broadly divided Hemoglobinopathies

into: • Sickle cell disease
• WBC disorders • Thalassemia
• RBC disorders • G6PD deficiency
• Platelet disorders
• Pernicious anemia
• Hemoglobinopathies
• Folic acid deficiency anemias
Dentist may be the first clinician approached • Aplastic anemias
by patients with hematologic disorders
(unaware of their systemic condition) with the Disorders of WBC
following complaints: The three types of granulocytes are neutro-
• Bleeding gums phils, eosinophils, and basophils. Peripheral
• Gingival enlargement blood contains approximately 4000 to 11,000
• Extensive ulcerative lesions WBCs per cubic millimeter.
• Lymphadenopathy Diseases of granulocytes are divided into
The dental clinician has the responsibility three major types:
of suspecting, recognising and aiding in the 1. Quantitative: Abnormal number of white
diagnosis of serious diseases like leukemia, cells
anemia, thrombocytopenia.
2. Qualitative: Poor functioning of white cells
WBC Disorders 3. Myeloproliferative: Acquired clonal abnor-
• Granulocytosis malities of hematopoietic stem cell.
• Agranulocytosis
• Neutropenia Granulocytosis
• Cyclic neutropenia Increase in the number of circulating white
• Leukemia blood cells. This occurs due to:
• Lymphoma: • Infection
– Hodgkin’s disease • Tissue necrosis
– Non-Hodgkin’s lymphoma • Allergic reactions
– Burkitt’s lymphoma • Neoplastic diseases
• Multiple myeloma
• Inflammatory diseases
• Infectious mononucleosis
• Stress or exercise
RBC Disorders Left shift and leukemoid reaction: A persistent
• Polycythemia elevation of the WBC count with the absolute
• Anemia neutrophil count remaining above 30,000/mm3
• Plummer-Vinson disease with a pronounced left shift and the presence
• Hemolytic anemia of myelocytes, metamyelocytes, and band
forms is called a leukemoid reaction. In
Diseases of Platelets response to an increased demand, an
• Thrombocytopenic purpura increased number of immature neutrophils
• Thrombocytosis called “bands” enter the circulation, a process
• Thrombasthenia called as “Left shift”.
GRANULOCYTOPENIA • Decreased number of neutrophils. Neutro-

penia secondary to cancer chemotherapy is
Decrease in granulocytes below 4000/cu mm. manifested between 7 and 14 days after
Increased risk of infections occurs if neutrophil starting the therapy.
count falls below 1000/mm3. Life-threatening
infections occurs if leukocyte count falls below • Antineutrophil antibodies may be detected
200/cu mm. by flow cytometry, agglutination assays for
The term “agranulocytosis” is used when diagnosis of immune-mediated neutro-
no neutrophils are seen on a peripheral blood penia and bone marrow study in severe and
smear. It is most often caused by a drug or persistent cases.
medication that interferes with cell formation Treatment
or enhances cell destruction.
Half-life of a neutrophil is 6–7 hrs. Neutro- • Identification and removal of cause
penia has a wide range of underlying causes: • Antibiotic prophylaxis with ciprofloxacin/
• Decreased production due to deficiency of levofloxacin reduces febrile episodes,
vit. B12 and folic acid bacterial infections and mortality. Hence,
• Increased destruction prophylaxis with fluoroquinolones is
• Increased utilization routinely recommended in patients with
leukemia, lymphoma, etc. who are
Etiology anticipated to receive drugs leading to
• Certain infections decrease the number of neutropenia.
neutrophils in circulating blood because of • Topical use of antibacterial mouthrinse.
increased migration of neutrophils in the
tissues • Combination of topical neomycin, bacitracin
and nystatin used with individualized soft
• Sequestration of neutrophils
splints to cover palatal lesions reduces risk
• Direct toxic effect of microorganisms and
of secondary ulcers.
its effect on blood marrow
• Toxic neutropenia secondary to cancer chemo- • Maintenance of good oral hygiene: Hydrogen
therapy, side effects to drugs antibiotics, peroxide mouth rinse combined with
anticonvulsants, diuretics, anti-inflamma- baking soda.
tories, phenothiazines, sulfonamides, • Solution containing 5% dyclonine and 5%
chloramphenicol. diphenhydramine hydrochloride mixed
Clinical Features with milk of magnesia or kaolin with pectin
helps reduce pain.
• Infections: Signs such as fever, malaise
• Mucosal ulcers, acute pharyngitis and
lymphadenopathy CYCLIC NEUTROPENIA
• Boils and carbuncles It is a rare disorder secondary to a periodic
• Ulcers that lack surrounding inflammation
failure of the stem cells in the bone marrow
and are characterized by necrosis
due to abnormality in the regulation of bone
• Ulcers become large, irregular, deep lesions
marrow precursor cells or an inhibitor of
that are painful and have foul odour
neutrophils released from monocytes. The
Diagnosis neutropenic episodes recur after a period of
• History of particular drug intake, severe 2–4 weeks, with 21 days being most common
infection presenting with fever, sore throat, and lasts for 3–5 days at each episode where
necrotic oral ulcers. neutrophil count falls below 500/mm3.
Clinical Features CHEDIAK-HIGASHI SYNDOME

• Infection, fever, stomatitis, pharyngitis, and
It is a congenital, autosomal recessive defect
skin abscess occurring during neutropenic
of granule containing cells like granulocytes
episodes.
and melanocytes. As a result of this,
• Oral mucosal lesions are large, irregular neutrophils show reduced chemotactic and
and scarring similar to major aphthae. bactericidal activity, although phagocytosis
• Periodontal involvement ranging from remains intact.
marginal gingivitis to advancing perio-
dontal bone loss. Clinical Features
• Patients with unusual periodontal destruc- • Oculocutaneous albinism milky white to
tion or severe oral ulcerations should be slate gray skin, light coloured eyes, hypo-
subjected to total and differential WBC pigmentation of hair (peculiar silver
count to rule out the possibility of cyclic colour). Presence of large but fewer melanin
neutropenia. granules produces pigment dilution.
Treatment • Bacterial infections of skin and respiratory
• Careful monitoring of patients for infection tract and enterocolitis
during neutropenic periods. • Easy bruisability and bleeding
• Hematopoietic growth factor such as G-CSF • Photophobia
(Neupogen {filgastrim}, amgen) reduces the • Nystagmus
number and severity of infectious episodes.
• Peripheral neuropathy and ataxia
• Maintenance of oral hygiene.
• Oral cavity shows gingival and periodontal
diseases, ulcerations, early loss of teeth.
LAZY LEUKOCYTE SYNDROME
• Sinus and oral infections caused by β
It is caused by a loss of chemotactic function hemolytic streptococci, S. aureus, gram-
of neutrophils. Severe neutropenia results due negative organisms.
to inability of cells to migrate from marrow to
peripheral blood. Phagocytic and bactericidal Diagnosis
functions remain intact. Presence of giant blue granules in cytoplasm
Clinical Features of granulocytes on peripheral blood smear,
bone marrow aspirate examination—myeloid
• Manifestation become apparent at 1 to 2
precursor cells, eosinophils.
years of age
• Common infections noted are gingivitis, Treatment
stomatitis, otitis media, and bronchitis. Symptomatic antibiotics for infection, child-
hood immunization. Bleeding can be avoided
Diagnosis by avoiding aspirin. For severe bleeding—
• Neutrophil migration tests showing lack of desmopressin, aminocaproic acid, or platelet
normal response to epinephrine and transfusion. Chemotherapy, corticosteroids,
piromen (Pseudomonas polysaccharide) IV immunogloboulins currently hematopoietic
• Inflammatory stimulation using skin stem cell transplant (HSCT).
windows will show a little neutrophil Oral surgical procedure can lead to
migration excessive blood loss hence better plan for
• Normal phagocytosis and bacteriocidal hemostasis, patients cannot tolerate bright
activity. operatory light advised sunglasses.
LEUKEMIA Diagnosis
Can be established with the lymph node
Gingival enlargements are commonly mani-
biopsy. Characteristic Reed-Sternberg cells
fested in Leukemia and hence this topic is
diagnostic, but the nature of these cells is
described in the chapter on gingival enlarge-
controversial.
ments.
CT scans can help to study the location size
LYMPHOMA and extent of LN enlargements.
Whole body radionuclide scans and PET
Lymphomas are a group of malignant solid scans to localize the LN
tumours involving the cells of lymphoreticular
Ann Arbor classification is currently used
or immune system such as B lymphocytes,
to stage lymphoma and guide the treatment
T lymphocytes and monocytes.
choice.
Two major categories:
Treatment
1. Hodgkin’s lymphoma (HL)
2. Non-Hodgkin’s lymphoma (NHL) Radiation: IFRT involved field radiation
therapy 35 Gy.
Hodgkin’s Lymphoma
Chemotherapy: ABVD adriamycin (doxorubicin)
• Was first described by a British pathologist bleomycin, vinblastine, dacarbazine.
Thomas Hodgkin in 1832.
• Etiology unknown, genetic and environ- Non-Hodgkin’s Lymphoma
mental factors and EBV play a role. • Arises from B or T lymphocytes.
Clinical Features • NHL is associated with immunosuppression:
HIV infection (100-fold more risk than
Painless enlargement of lymph nodes without
normal population), medication after organ
any other symptoms of the disease. Cervical
transplant, Sjögren’s syndrome, celiac
nodes involvement most common followed by
disease, rheumatoid arthritis.
axillary, inguinal, mediastinal. Waldeyer’s
• More common in patients above 40 years,
ring structures also involved.
however, can occur at any age.
• The involved nodes are non-tender and • Painless, persistent enlargement of LN, but
feel rubbery. Asymptomatic enlarged extranodal lesions more common than in
lymph nodes common in young patients HL.
(histologically lymphocyte predominant/ • NHL lesions appear in Waldeyer’s ring
nodular sclerosis).
GI tract: Large abdominal masses
• In older patients (increased chances of Spleen: Splenomegaly
lymphocyte depleted, mixed cellularity Bone marrow: Cytopenia
histologic pattern), symptoms such as fever,
• In the oral cavity, NHL presents as gingival
malaise, nightsweats may precede the
or mucosal tissue enlargements/swellings,
noticeable lymphadenopathy.
intrabony lesions may be mistaken for
• In advanced cases, signs and symptoms toothache associated with periodontal
are due to pressure from enlarging LN: infection and extraction of the tooth is
dysphagia—mediastinal LN, ureteral followed by rapid growth of NHL from the
obstruction—retroperitoneal LN unhealed socket.
• Cyclic spiking of high fever—Pel-Ebstein • If the clinical examination shows mobile
fever. Severe pruritus, more so in young tooth surrounded by suspicious growth
women. and radiograph shows irregular bone loss
(unlike the periodontal abscess with the • Radiographically alveolar bone resorption,
well demarcated bone loss), it is better to loss of lamina dura, enlargement of tooth
subject the patient to biopsy than to follicle, disappearance of cortex around
extraction. tooth crypts, displacement of teeth and
• In fact it is now important to include NHL tooth buds by the enlarging tumor giving
in the differential diagnosis of localized rise to ‘floating tooth appearance’ and
gingival swellings, more so if the patient is periosteal reactions—‘sunray spicules’ as
immunosuppressed. bone forms perpendicular to the mandible.
• Ann Arbor classification to stage and to • Histologically uniform, large, neoplastic
help select treatment plan. cells with abundant cytoplasm, high mitotic
• Treatment includes chemotherapy cyclo- rate and numerous macrophages scattered
phosphamide, doxorubicin, oncovin create a characteristic ‘starry sky’ appea-
(vincristine) and prednisolone (CHOP). rance.
Addition of rituximab to this regimen helps • BL has a dramatic response to chemo-
to improve response and prolongs event- therapy, specially cyclophosphamide.
free survival in elderly patients. Other agents used are vincristine, metho-
Radiotherapy IFRT trexate and corticosteroids. However,
(Involved Field Radiation Therapy) surgical debulking and palliative low dose
radiotherapy to local tumor site are also
Radioimmunotherapy: NHL cells are radio- considered in treatment planning.
sensitive and can be targeted by monoclonal
antibody. Radioimmuno conjugates (Yttrium
90, ibritumomab, tiuxetan and iodine 131 MULTIPLE MYELOMA
tositumomab) used as a novel therapy for Multiple myeloma (MM) is a malignant
relapse. neoplasm of plasma cells, that is characterized
If radiotherapy is delivered to the mandible by bone marrow plasmacytosis, production of
or maxilla during tooth formation phase there pathologic M protein (abnormal paraprotein),
is delayed and ectopic eruption, the roots bone lesions, kidney disease, hyperviscosity
show malformations and appear blunt, and hypercalcemia.
shortened, tapered, V-shaped. Third most common hematologic malig-
nancy after leukemia and lymphoma.
Burkitt’s Lymphoma
• Dennis Burkitt in 1950s described a rapidly Clinical Features
growing jaw and abdominal lymphoid • Fatigue, weakness, weight loss
tumor, in East African children in areas • Bone pain: Most common symptom resulting
where malaria was endemic. from osteolysis caused by the accumulating
• This tumor is the human cancer most closely tumor cells or indirectly from the osteoclast-
linked with a Epstein-Barr virus. activating factors secreted by the MM cells
• It is a rapidly growing extranodal jaw and or by osteoblast inhibition. Numbness or
abdominal tumor, which expands rapidly paresthesia can also occur.
and may double in size every 1–3 days, • Recurrent infection
making it the fastest growing human • Renal failure results from a combination of
cancer. amyloidosis, hypercalcemia and infiltration
• Clinically evident jaw tumor may result in of malignant cells.
mobility of teeth, pain, swelling of mandible • Bleeding in MM results from many causes:
and maxilla and anterior open bite. – Thrombocytopenia
– Abnormal platelet function Bisphosphonate-induced osteonecrosis is a

– Clotting defects result from abnormal serious complication affecting the jaw bones.
myeloma protein coating the platelets Multidisciplinary approach involving dental
and interfering the coagulation cascade. specialists, hematologist, physician and
surgeon necessary for the management of
– Paraprotein-induced factor VIII or
osteonecrosis.
X deficiency
Consultation with the hematologist is
– Hyperviscosity of blood and tissue
mandatory to avoid and arrest hemorrhage
fragility associated with amyloidosis
during and after dental surgery.
• Typical radiographic picture is that of
multiple separate punched out radio-
PLATELET DISORDERS
lucencies in the skull, resulting from the
focal proliferation of plasma cells in the Platelet disorders are divided into 2 categories
bone marrow and mandibular involvement by etiology: Congenital and acquired.
varying from clear cut osteolytic lesion to Into two additional categories by type:
pathologic fracture. Generalized osteo- Thrombocytopenias: Reduction in number of
porosis can also occur.
platelets caused by:
Diagnosis • Decreased production in the bone marrow
i. From clinical picture of pain, swelling and • Increased sequestration in the spleen
paresthesia of bone, unexplained mobility • Accelerated destruction
of teeth, epulis formation. Thrombocytopathies: Qualitative platelet
ii. Typical punched out radiolucent lesions disorders: defect in 3 platelet reaction
of skull vault, mandible. • Adhesion
iii. Monoclonal protein in plasma and urine. • Aggregation
Bence-Jones proteins in urine (also seen in • Granule release
polycythemia vera and leukemia)
Thrombocytopenic Purpura
iv. Bone marrow biopsy reveals atypical
Two of the most commonly encountered
plasma cells.
platelet disorders, idiopathic or immune
v. The tongue may be enlarged and studded thrombocytopenic purpura (ITP) and
with small garnet colored enlargements, thrombotic thrombocytopenic purpura (TTP),
biopsy in such cases will show evidence have clinical symptoms including petechiae
of amyloidosis. and purpura over the chest, neck, and limbs—
Treatment usually more severe on the lower extremities.
Mucosal bleeding may occur in the oral
Chemotherapy with vincristine, doxorubicin
cavity and gastrointestinal and genitourinary
and dexamethasone.
tracts.
Radiotherapy, surgery for focal lesions.
HSCT (usually autologous) improves Idiopathic Thrombocytopenic Purpura
response and overall disease-free survival. ITP may be acute and self-limiting (2 to 6
Bisphosphonates are specific inhibitors of weeks) in children.
osteoclastic activity and monthly IV infusion In adults slow onset, persistent, lasting for
of zoledronic acid/pamidronate have reduced years and has recurrent exacerbations.
the skeletal complications and are mainstay In severe cases of ITP, oral hematomas and
of myeloma therapy. hemorrhagic bullae may be the presenting
clinical sign. Most patients with chronic ITP ‘Dengue’ a parasitic infection common in
are young women. Intracerebral hemorrhage, mosquito infested area can also cause thrombo-
although rare, is the most common cause of cytopenia.
death. ITP is assumed to be caused by Medications can also reduce absolute num-
accelerated antibody-mediated platelet bers of platelets or interfere with their function,
consumption. ITP may be a component of resulting in postsurgical haemorrhage.
other systemic diseases. Drug-related platelet disorders are rever-
Autoimmune thrombocytopenia like that sible within 7 to 10 days of discontinuation of
associated with systemic lupus erythematosus the drug. Aspirin prevents platelet aggrega-
can be severe and require aggressive treat- tion, induces a functional defect in platelets
ment. Immune-mediated thrombocytopenia detectable as prolongation of BT. Aspirin is
associated with HIV disease. commonly used as an inexpensive and
Thrombotic thrombocytopenic purpura effective antiplatelet therapy for thrombo-
catastrophic disease considered fatal in the embolic protection to reduce the risk of
past. myocardial infarction and stroke.
Causes Management
• Metastatic malignancy Modality determined by the type of defect.
• Pregnancy Thrombocytopenias—platelet transfusion
• Mitomycin C ITP—corticosteroids
• High-dose chemotherapy Chronic ITP—splenectomy
Bone marrow transplantation
Clinical Features Plasmapheresis to remove circulating iso-
In addition to thrombocytopenia, clinical antibodies is held in reserve for cases of severe
features of TTP include: thrombasthenia and life-threatening bleeding.
• Microangiopathic hemolytic anemia
• Fluctuating neurologic abnormalities RBC DISEASES
• Renal dysfunction
Polycythemia
• Fever
• Microvascular infarcts occur in gingival and Polycythemia may be defined as an abnormal
other mucosal tissues and appear as platelet increase in the erythrocyte count in the
rich thrombi. peripheral blood, usually accompanied by an
Thrombocytopenia may be a component of increase in hemoglobin and hematocrit. It is
other hematologic disease such as myelo- divided into absolute erythrocytosis (a true
increase in red cell mass) and relative erythro-
dysplastic disorders, aplastic anemia, and
cytosis (the red cell mass is normal, but the
leukemia.
plasma volume is reduced).
Bone marrow suppression from cytotoxic
chemotherapy can result in severe thrombo- Relative Real/primary
cytopenia. polycythemia polycythemia vera
Thrombocytopenia and thrombocytopathy
Loss of tissue and intra- Actual neoplastic
in liver diseases are complicated by coagula- vascular fluid proliferation of
tion defects. Diabetic ketoacidosis erythrocytes
In renal disease the coagulopathy consists Postsurgical dehydration
of acquired platelet defect resulting from Prolonged vomiting or de-
uremia. hydration
Rapid diuresis (treatment of CCF)
Alcohol can also induce thrombocytopenia.
Secondary Polycythemia Oral Manifestations

It is due to an increase in erythropoietin pro- • A purplish-red discoloration of the oral
duction to compensate for hypoxia. mucosa is visible on the tongue, cheeks, and
• People who live in high altitudes lips.
• Chronic pulmonary disease • Purplish-red discolored tongue called as
• Congenital heart disease crystal violet tongue
• Renal disease (hydronephrosis) • The gingivae are red and may bleed
spontaneously.
• Tumours producing erythropoietin-like
substance • Petechiae and ecchymoses are observed in
patients with platelet abnormalities.
Apparent Polycythemia • Varicosities in the ventral tongue, a frequent
It is characterized by an increased hemoglobin normal finding, are exaggerated in cases of
concentration and packed cell volume but polycythemia.
normal RBC mass, due to reduction in plasma Treatment
volume.
• The major therapy for PV involves repeated
• Obese men with hypertension and signifi- phlebotomy.
cant social history of smoking and alcohol
• Myelosuppressive agents to reduce the
consumption
hematocrit to its upper limit of 50%.
• Diuretic therapy • Alkylating agents and radioactive phos-
Polycythemia Vera phorus (32P) have been shown to increase
Polycythemia vera (PV) is a myeloprolifera- the risk of leukemia and should be avoided.
tive disorder characterized by excessive • Chemotherapy with agents such as
proliferation of erythroid elements along with busulfan, chlorambucil, cyclophosphamide,
granulocytic and megakaryocytic cells. It and melphalan may also be beneficial.
usually begins after 50 years of age. • Treatment with hydroxyurea also decreases
the thrombotic complications.
Etiology
Oral and Dental Considerations
Acquired genetic changes in the stem cell lead-
ing to disturbances of normal cellular growth. • Dental treatment presents a risk because of
the possibility of bleeding or thrombosis.
Clinical Features • Patients should have a complete blood
• Patients with PV develop episodes of count prior to treatment.
thrombosis and hemorrhage in the later • To prevent complications, it is recommen-
stages of the disease. ded that the hemoglobin be reduced below
• A characteristic clinical picture of ruddy 16 g/dl and the hematocrit to below 47%.
cyanosis is seen on the face and extremities, • Patients with this disease require special
owing to the presence of deoxygenated attention to local hemostasis.
blood in cutaneous vessels. • Preoperative myelosuppressive treatment
• Patients complain of headache, dizziness, should be considered prior to dental
tinnitus, fullness of the head and face, and treatment when the blood counts are not
pruritus. controlled with phlebotomy alone.
• Splenomegaly Anemia
• Coronary thrombosis Anemia is present whenever there is a
• “Erythromelalgia” may manifest as decrease in the normal amount of circulating
paresthesias involving the cranial nerves. hemoglobin.
Anemia may result from: Clinical features include pallor, dyspnea

• Blood loss, as in common iron deficiency and fatigue and also palpitation, numbness and
anemia tingling in fingers, toes.
• Increased destruction of red blood cells as
Oral Manifestations
in the hemolytic anemias
• Decreased production of red cells, as in • The major oral sign of iron deficiency
pernicious and folic acid deficiency anemia is pallor of the mucosa.
anemias, or • In addition, the oral mucosa become
• Combinations of these three. atrophic, with loss of normal keratinization.
Anemias also may be classified according • The tongue may become smooth due to
to their pathophysiologic basis: atrophy of the filiform and fungiform
Size of RBCs: papillae, and glossodynia can be a
• Microcytic presenting or associated symptom. These
changes are associated with significant
• Normocytic
reduction of mean epithelial thickness.
• Macrocytic
• Dietary iron deficiency anemia should
On the basis of their hemoglobin concen- be suspected in every case of glossitis,
tration: glossodynia, angular cheilitis, erythe-
• Hypochromic matous mucositis, candidiasis and burning
• Normochromic. mouth when no other obvious causes are
The term “hyperchromic” is seldom used, identified.
but it refers to a macrocytic cell with normal • In long-standing cases, esophageal stric-
hemoglobin concentration that, because of its tures or webs can develop, resulting in
large size, has an increased hemoglobin dysphagia.
content.
Diagnosis
General symptoms of all anemias include:
• Pallor of the skin, palpebral conjunctiva, • Lowered hemoglobin in routine blood
and nailbeds counts.
• Dyspnea and easy fatigability, palpitation • RBCs microcytic and hypochromic on
• Cracked and splits in nails, spoon-shaped peripheral smear.
nails. • Mean corpuscular hemoglobin, the mean
corpuscular hemoglobin concentration, and
Iron Deficiency Anemia (Blood Loss Anemia, the mean corpuscular volume are decreased.
Hypochromic Microcytic Anemia)
• Serum ferritin levels are markedly reduced
It is the most common of all anemias. It may <30 μg/L—index of iron stores.
result from chronic blood loss, such as occurs Serum transferrin receptor—index of tissue
in: iron deficiency.
• Menstrual or menopausal bleeding
• Parturition, bleeding hemorrhoids, varices Dental Considerations
• Bleeding malignant lesion or ulcer in the Evaluation of complete blood count and
gastrointestinal tract referral to physician.
• Subtotal or complete gastrectomy, or a habit Increased bleeding and delayed wound-
of clay eating healing noted, hence surgeries should not be
• Malabsorption syndromes performed on patients with marked anaemia.
• Worm infestations like hookworm, tape- General anesthesia is contraindicated, if
worm, etc. hemoglobin is below 10 gm/dl.
Treatment carcinomas are more common in these patients.

Ferrous sulphate 325 mg three times daily Patients with symptoms of this syndrome
preferred because of low cost and high bio- should be followed up at short intervals and
availability. checked for the development of lesions that
Side effects: Nausea and epigastric pain raise the suspicion of malignancy.
relieved with food intake. Therapeutic response Hemolytic Anemias
in 4–8 weeks time.
The normal lifespan of RBCs is 90–120 days
Plummer-Vinson Syndrome in circulation. The hemolytic anemias result
This syndrome is characterized by dysphagia from decreased survival of erythrocytes, either
and a microcytic hypochromic anemia. episodically or continuously, resulting from
intracorpuscular defects in the erythrocytes
• Smooth, depapillated and sore tongue
(often hereditary) or from extracorpuscular
• Spoon-shaped nails factors.
• Angular cheilitis
Extracorpuscular Factors
• Atrophy of the tongue papillae
• Overwhelming infections and toxins
• Atrophic changes in the oral mucosa, the
• Cardiac valvular prostheses
pharynx, the upper esophagus, and the
vulva. These tissues are dry, inelastic, and • Hypersplenism
glazed in appearance. • Rh factor incompatibility (hemolytic disease
of newborn, erythroblastosis fetalis)
• Dry mouth
• Chronic liver disease
• Listlessness, pallor, ankle edema, and
• Autoimmune hemolytic disease (e.g. as in
dyspnea
systemic lupus erythematosus)
• Patients’ complaint of “spasm in the throat”
• Transfusion reactions
or of “food sticking in the throat.” Is indica-
tive of dysphagia,which represents an Intracorpuscular Defects
important feature of this condition, appears • Abnormal shape of the erythrocytes
to be the result of muscular degeneration – Hereditary spherocytosis
in the esophagus and stenoses or webs of – Hereditary elliptocytosis
the esophageal mucosa. • Paroxysmal nocturnal hemoglobinuria
Diagnosis • Erythrocyte enzyme deficiencies
• History and hematologic findings. – Glucose-6-phosphate dehydrogenase
deficiency
• The esophageal webs, strictures, stenoses – Pyruvate kinase deficiency
are demonstrable radiologically (barium
• Abnormal hemoglobins (hemoglobino-
swallow) or by endoscopy.
pathies)
• Relative degrees of achlorhydria are usually – Sickle cell anemia and sickle cell trait
present. – Thalassemia
• As many of the symptoms in this syndrome – Other hemoglobinopathies (e.g. hemo-
are similar to those observed in vitamin B globin C and F)
complex deficiency and simple hypo- • Erythrocyte defects associated with other
chromic anemias, these conditions should disease
be treated. – CGL
Plummer-Vinson syndrome is potentially – Folic acid and vitamin B 12 deficiency
serious because pharyngeal and intraoral anemias
Diagnosis Oral Manifestations

• Decreased hemoglobin • When sufficient hemolysis has taken place
• Increased reticulocytes (an indicator of to produce anemia, pallor results. This is
erythroid hyperplasia of the bone marrow most easily observed in the nail beds and
to compensate for the excessive hemolytic palpebral conjunctiva.
destruction) • Pallor of the oral mucosa, especially evident
• Raised serum bilirubin in the soft palate, tongue, and sublingual
tissues.
• To measure red cell survival time, a small
• The hemolytic anemias produce jaundice
amount of the patient’s red cells may be
caused by the hyperbilirubinemia secon-
tagged with radioactive chromium (51Cr)
dary to erythrocyte destruction—seen in the
and re-injected. If the hemolysis is caused
sclera, skin, soft palate, and tissues of the
by an extracorpuscular factor, a compatible
floor of the mouth as icterus.
donor’s red cells, similarly tagged and
• The erythroid elements of the bone marrow
injected into the patient, should disappear
are hyperplastic in an attempt to compen-
as quickly as the patient’s own red cells. If
sate for the anemia. This hyperplasia
the hemolysis is caused by intracorpuscular
produces a characteristic appearance on the
defects, the compatible donor’s red cells
dental radiograph.
should survive longer than do the patient’s
Because of the enlargement of the medullary
red cells.
spaces, the trabeculae become more promi-
• Decrease in the serum haptoglobins, which nent, creating increased bone radiolucency
are globulins with a marked affinity to bind with prominent lamellar striations—step
hemoglobin. ladder appearance.
• Although the hemolytic anemias are
usually characterized by normocytic Hemoglobinopathies
normochromic morphology on a blood The hemoglobinopathies, exemplified by
smear with normal RBC indices, the cells sickle cell disease and thalassemia, are caused
in hereditary spherocytosis and hereditary by defects in the globin portion of the hemo-
elliptocytosis may exhibit an abnormal globin molecule which render the erythrocyte
spherical or elliptical shape. containing the abnormal hemoglobin more
• The cells in hereditary spherocytosis show susceptible to hemolysis.
increased hemolysis (osmotic fragility) in A normal hemoglobin molecule consists of
hypotonic solutions. two pairs of amino acid chains, the α and β
• The direct Coombs’ test demonstrates chains—hemoglobin A, may be represented
incomplete antibodies attached to the by the formula α2Aβ2A.
erythrocytes, which require a substance In the hemoglobinopathies, abnormal
such as antihuman globulin to produce hemoglobins are produced either in the form
hemolysis. of abnormal chains (e.g. γ, δ) or of small
• The indirect Coombs’ test detects antibodies alterations in the α or β chain.
to the red cells, which are present in the Fetal hemoglobin, normal in the fetus but
patient’s serum, usually immunoglobulin abnormal if persisting into adult life, is
IgG1 and IgG3, both of which activate designated hemoglobin F and is represented
complement. by the formula α2Aγ2F, indicating that it
• Hemoglobin electrophoresis for the detec- differs from hemoglobin A in that the β chains
tion of pathologic hemoglobin proteins. are replaced by two γ chains.
Sickle Cell Disease • Aplastic crises sometimes develop from

In sickle cell disease, an autosomal recessive infection, hypersensitivity reactions, or
disorder, an abnormality in the β chain of unknown causes. In these aplastic crises, the
hemoglobin is present in which valine is patient becomes acutely ill, red cell
substituted for the normal glutamic acid production virtually stops, and the hemo-
residue on position 6. As a result the normal globin drops precipitously. It has been
discoid shape of RBC is changed to sickle suggested that folic acid deficiency may
shape. develop in these patients because of the
increased demand for folic acid as a result
This leads to: of increased erythropoiesis. The folic acid
• Stasis and hemolysis of the red cells, deficiency may play a part in the genesis of
especially in end-capillary circulation the aplastic crisis.
• Stasis then results in an even lower oxygen Oral Manifestations
tension, and increased pH, and further
• Jaundice and pallor of the oral mucosa
sickling.
• Delayed eruption and hypoplasia of the
• This reduces their plasticity and lifespan dentition
from 120 to 14 days.
• Because of the chronic increased erythro-
• This results in anemia and hypertrophic poietic activity and marrow hyperplasia,
bone marrow. which are attempts to compensate for the
hemolysis, increased radiolucency resulting
Clinical Manifestations
from the decreased number of trabeculae
• Patients show marked underdevelopment is seen on dental radiographs. This change
and often die before 40 years of age. is noted especially in the alveolar bone
• Clinical features are because of: between the roots of the teeth, where the
i. Anemia trabeculae may appear as horizontal rows,
creating a ladder-like effect. Some authors
ii. Hemolytic process (jaundice, pallor, and
have used the term ‘chicken net’ to describe
cardiac failure)
this appearance. By contrast, the lamina
iii. Necrosis following stasis of blood and dura appears dense and distinct. The teeth
vaso-occlusion leading to splenic do not present undue mobility.
infarction, chronic leg ulcers, retinitis • Interruption of the blood supply causes
leading to blindness, priapism, cerebral anesthesia of inf. alveolar nerve and pulpal
vascular thromboses (“strokes”) attacks necrosis of otherwise healthy premolar and
of abdominal and bone pain (pain crises), molar teeth.
renal failure.
• In skull films, the diploë is thickened, and
• Acute chest syndrome: Fever, cough, sputum the trabeculae are coarse and tend to run
production, dyspnea, hypoxia, X-ray chest perpendicular to the inner and outer tables,
showing new infiltrate—considered a major giving a radiographic appearance of “hair
cause of morbidity and mortality. on end”. Areas of sclerosis or increased
• The long bones may present radiodense radiopacity represent areas of past throm-
sclerotic areas as a residual of small infarcts. boses with subsequent bony infarction.
The femoral head, humerous head are • Patients with sickle cell anemia are parti-
prone to avascular necrosis in sickle cell cularly prone to developing osteomyelitis,
disease. Hip joint dysfunction is related to probably because of hypovascularity of the
femoral head destruction. bone marrow secondary to thromboses.
• Periodontal infection and mandibular • Elimination of oral sources of infection

osteomyelitis have been reported to be should be instituted since infection can
precipitating factors for sickle cell crisis. precipitate an aplastic crisis.
• General anesthesia should be used with
Diagnosis
caution in patients with sickle cell trait or
• Smear shows normochromic normocytic sickle cell anemia; when used, it is impera-
cells tive to avoid episodes of hypoxia because
• Sickling at low oxygen tension cerebral or myocardial thrombosis can result.
• Hemoglobin electrophoresis • Preoperative transfusion of SCA patients
• Radionuclide scan of mandible to detect the undergoing GA and LA for surgical
position and extent of infarcted area. procedures to maintain adequate level of
Treatment normal Hb A to prevent sickle cell crisis.
• Symptomatic treatment Thalassemia
• Antibiotics should be used early in the The thalassemias are a group of congenital
treatment of infection, and analgesic drugs disorders characterized by a deficient
should be used if necessary. synthesis of either the α or the β chains of
• Neither splenectomy nor antianemic drugs globin in the hemoglobin molecule. As a
(except possibly folic acid) are of any value. result, the red blood cells are microcytic and
• Transfusions are avoided unless the patient hypochromic with an aberrant morphology.
has an aplastic crisis with a resulting In α-thalassemia (deficient or reduced α
extremely low hemoglobin level. chain), intracellular inclusions Heinz bodies
• Many physicians routinely use folic acid are formed by the precipitation of the β chains
dietary supplements for patients with sickle that accumulate in excess following the
cell anaemia, increasing levels to therapeutic impaired chain production.
doses to treat an aplastic crisis. In the most severe form of this disease, the
• Cytotoxic agents such as hydroxyurea have fetus red blood cells contain hemoglobin
been shown to increase hemoglobin F and composed of γ chains only. This condition is
reduce the frequency of painful episodes; incompatible with life, due to the hemo-
they are indicated in patients whose quality globin’s lack of oxygen-carrying capacity. The
of life is disrupted by frequent painful heterozygous individual has the β-thalassemia
episodes. trait; the homozygous state is known as β-
• Allogeneic stem cell transplantation is being thalassemia major or Cooley’s anemia.
studied as a possible curative option for Reduced erythropoiesis and hemolysis are
severely affected young patients. characteristic of the disease as a result of an
• Preoperative transfusion of SCA patients imbalance in β chain production.
undergoing GA and LA for surgical In the major type, there is a relative excess
procedures to maintain adequate level of of β chains that eventually aggregate and form
normal Hb A to prevent sickle cell crisis. inclusion bodies. Due to this defect, RBCs
show abnormal membrane permeability, are
Dental Considerations entrapped and removed from the circulation
• Elective dental procedures involving the soft by phagocytosis or lysis.
tissues should not be performed in patients Clinical signs are minimal in β-thalassemia
with poorly controlled disease unless minor (β-thalassemia trait); most of the affec-
absolutely necessary because of increased ted individuals are never diagnosed and have
risk of complications secondary to chronic only a mild, clinically insignificant microcytic
anemia and delayed wound healing. anemia.
β-thalassemia major or Cooley’s anemia is • Hematopoietic stem cell transplantation

the most severe congenital hemolytic anemia. constitutes a future hope for the treatment
of thalassemia.
Clinical Features
• The hematocrit decreases to less than 20. Oral Manifestations
• Degree of anemia can reach a hemoglobin • Bimaxillary protrusion and other occlusal
level of 2 to 3 g/dl, and the hemolysis is abnormalities
extensive, as is the iron overload. • Poor spacing of teeth, spiky-shaped and
• Growth and development in children is short roots, taurodontism
slow. • Marked open bite
• In adolescence, secondary sex charac- • Prominent malar bones
teristics are delayed.
• Saddlenose.
• The skin color becomes ashen-gray due to
• Pneumatization of the maxillary sinuses is
the combination of pallor, jaundice,
delayed and appear small on X-rays
hemosiderosis, cardiomegaly, hepato-
megaly, and splenomegaly. • Class II skeletal base relationship with short
mandible, prominent anterior maxilla,
Diagnosis reduced posterior facial height, increased
• Hypochromic microcytic red blood cells. anterior facial proportions—due to these
• Increased amounts of fetal hemoglobin and skeletal changes, the upper lip is retracted,
variable amounts of normal adult hemo- giving the child a “chipmunk facies.”
globin. • The radiographic changes seen in the jaws
• Prenatal diagnosis of thalassemia is include generalized rarefaction of the
facilitated by deoxyribonucleic acid (DNA) alveolar bone, thinning of cortical bone,
analysis of amniotic fluid cells, and it plays absent inferior alveolar canal, enlarged
an important role in genetic counseling. marrow spaces, and coarse trabeculae,
which are similar to the changes observed
Treatment
in sickle cell disease patients.
• Patients with mild thalassemia (α trait or β
minor) are clinically normal and require no • In the parietal bones, the thin cortex
treatment. covering the coarse vertical trabeculae and
the enlarged diploë produce a “hair on end”
• In thalassemia major cases, the patient’s
appearance.
survival depends on blood transfusions.
• Prevention of a hemoglobin concentration • Cranial nerve palsies have been described
decrease to under 10 g/dl improves the in thalassemia due to the extramedullary
chances of normal development and hematopoiesis resulting in pressure on the
survival into adulthood. nerves.
• This hypertransfusion treatment results in • The skeletal retardation increases with age
iron overload with hemosiderosis and iron due to hypoxia from severe anaemia,
deposition in all tissues. endocrine hypofunction secondary to iron
• Folic acid supplement also seems to be of deposition, or the toxic action of iron
some benefit. enzyme systems leading to tissue injury.
• The iron overload is treated with conti- • The dentin and enamel are indicators of
nuous injections of a chelator, deferiprone, iron deposition, and deciduous and perma-
which mobilizes and excretes the excess nent teeth of patients with thalassemia
iron. contain up to five times the iron concentra-
tion measured in normal patients. High iron Dental Considerations

concentration explains the discoloration of • The severity of anemia and its correction
teeth in patients with β-thalassemia major. should be evaluated before major dental
Dental Management interventions because the decline in
hemoglobin can reach 3 to 4 g/dl during
• Poor healing after surgical dental procedures.
hemolytic episodes.
• Exacerbation of the symptoms of cerebral
• Blood transfusions may be used prior to
or cardiac hypoxia if substantial bleeding
dental treatment.
occurs in apatient who is already anemic.
• Drugs that might induce hemolysis, such
• Surgery for facial deformities
as dapsone, sulfasalazine, and phenacetin,
G6PD Deficiency should be avoided. Analgesics and anti-
Glucose-6-phosphate dehydrogenase (G6PD) biotics can be given safely in therapeutic
deficiency is a hereditary enzyme defect that doses.
causes episodic hemolysis because of a reduced • The hemolytic episodes are self-limited, and
capacity of RBCs to deal with oxidative stresses. most patients with drug- or infection-
Patients with an enzymatic defect, such as induced hemolysis recover fully following
the one found in the hexose monophosphate treatment.
shunt, do not maintain the required level of Pernicious Anemia
reduced glutathione in their RBCs. As a result, The development of a vitamin B12 deficiency
hemoglobin sulfhydryl groups and the cell is a slow process and is most frequently due
membranes themselves are oxidized, leading to impaired absorption rather than dietary
to hemoglobin precipitation in the cell and deficiency. Conditions that can lead to
eventual cell lysis. cobalamin deficiency include:
In the G6PD deficient erythrocyte, the • Pernicious anemia
denatured hemoglobin with stromal proteins
• Gastrectomy
forms particles, called Heinz bodies, as a result
of an oxidative process. These cells circulate • Small bowel
with difficulty through the spleen and liver • Bacterial overgrowth
and are removed from the circulation, • Diverticulosis
resulting in hemolytic anemia. • Blind intestinal loops
In India, this condition is more commonly • Scleroderma
observed in Parsi individuals. • Tapeworm
Drugs and chemicals which cause • Tropical sprue
hemolysis in G6PD deficient patients: • Alcoholism
Analgesics: Acetinilid, aspirin • Medications such as neomycin and
Antimalarials: Primaquine, chloroquine colchicine.
Antibiotics: Sulphonamides, ciprofloxacin, • The most common form of vitamin B 12
norfloxacin, chloramphenicol, nalidixic acid, deficiency is pernicious anemia, which is
dapsone due to atrophy of the gastric mucosa result-
Miscellaneous: Vit K, vit C, doxorubicin, ing in a lack of intrinsic factor secretion.
methylene blue, naphthalene. Intrinsic factor acts by binding to the
vitamin B12 molecule, forming a complex
Treatment that crosses the ileal mucosa and protects
No treatment required except avoidance of the vitamin from proteolysis. The disease
known oxidant drugs such as dapsone. can be the result of an autoimmune reaction
to either the gastric parietal cells or intrinsic • A serum assay for vitamin B12 and folate
factor and is often seen in connection with should be performed using a microbiologic
other autoimmune diseases such as Graves’ or radioisotope technique.
disease.
Schilling Test
Clinical Features Mentioned in the Chapter on tongue disorders.
• Anemia
• Gastrointestinal disorders Treatment
• Neurologic complications Parenteral cyanocobalamin: This treatment
corrects the hematologic changes but will only
Oral Manifestations arrest, not correct, the neurologic changes.
• Glossitis and glossodynia Because the hematologic changes of
• The tongue is “beefy red” and inflamed, pernicious anemia may be reversed by oral
with small erythematous areas on the tip folic acid therapy without arrest of the
and margins. neurologic changes, patients who are anemic
• Loss of filiform papillae, and in advanced should never be given folic acid therapy
disease, the papillary atrophy involves the without the possibility of pernicious anemia
entire tongue surface together with a loss first being ruled out—folic acid removes a
of the normal muscle tone. valuable diagnostic sign (low hemoglobin)
• Erythematous macular lesions also can and allows the neurologic changes, which are
involve the buccal and labial mucosa. mostly irreversible even with B12 therapy to
progress. It is best when prescribing therapeutic
• Dysphagia and taste aberrations
vitamins to choose one without folic acid or
• Discomfort described by denture wearers to ensure that the hemoglobin is normal before
due to the weakened mucosal tissues. instituting vitamin therapy.
• Although the “burning mouth” sensation
diagnosed in pernicious anemia can be due Folic Acid Deficiency
to a neuropathy, other causes of oral Folic acid deficiency causes severe anemia but
burning, including candidiasis, should be does not cause the neurologic abnormalities
considered. seen in pernicious anemia. Folate deficiency
is prevalent in:
Diagnosis
• Diet is devoid of leafy vegetables
• Macrocytic normochromic red cells on the
blood smear. • Alcoholics and drug abusers
• The mean corpuscular volume is increased, • In patients with an increased requirement
the mean corpuscular hemoglobin increased, for folate, such as pregnant women and
and the mean corpuscular hemoglobin young children. Drugs used for cancer
concentration normal. chemotherapy treatment, such as metho-
trexate, azathioprine, 6-mercaptopurine,
• Shape of the RBC varies considerably, the
5-fluorouracil and cytosine arabinoside, are
platelets are abnormally large, and the
known to cause folate deficiency by
neutrophils often are hypersegmented.
interfering with DNA synthesis.
• A bone marrow examination will confirm
these morphologic changes by revealing the Oral Manifestations
presence of megaloblastic marrow changes. May include angular cheilitis and in severe
• Antibodies against the intrinsic factor and cases—ulcerative stomatitis and pharyngitis,
parietal cells of stomach can be detected. recurrent aphthous ulcerations.
Diagnosis Treatment
It is made by detection of hematologic changes • Supportive therapy with blood transfusion
(the same as those in pernicious anemia) with to correct anaemia, thrombocytopenia.
a normal Schilling test and serum vitamin B12 • Immunosuppression with antithymocyte
assays, but low serum assays of folic acid. globulins, cyclosporin is effective at
restoring blood cell production.
Treatment • Patients with histocompatible sibling
Oral doses of 1 mg/d are adequate for most donors can be cured with allogenic HSCT
patients, and a 5 mg tablet suffices to treat even replacing the hematopoietic tissue.
a patient with intestinal malabsorption. • Patients with infections and fever to be
treated aggressively with parenteral broad
Aplastic Anemia (AA)
spectrum antibiotics.
Aplastic anemia is a rare blood dyscrasia in • Antifungals should be added in persistently
which there is complete absence of cellular febrile patients because aspergillosis is
elements of blood (pancytopenia) resulting difficult to diagnose.
from reduced or absent blood cell production
Dental Considerations
by the bone marrow. The cause is considered
to be inherited, idiopathic, acquired. • There are two major problems in the dental
• Environmental exposure to drugs, viruses management of patients with aplastic
and toxins which trigger off an aberrant anaemia: Infection and bleeding.
immune response • Local infections and bacteremias originat-
• Approximately half of the cases are sus- ing in the oral region can have a fatal course
pected to be caused by chemical substances • Gingival bleeding can be reduced by the use
of systemic antifibrinolytic agents, such as
(e.g. paint solvents, benzol, chloram-
aminocaproic acid or tranexamic acid,
phenicol)
as well as local hemostatic measures.
• Most of the acquired and idiopathic AA are Tranexamic acid is given in a dosage of
immune-mediated with activated type 1 20 mg/kg body weight four times a day
cytotoxic T cells implicated starting 24 hours before oral procedures
• Exposure to high levels of X-ray radiation and continuing for 3 to 4 days afterward.
The term “anemia” is, in a sense, a mis- • Oral rinses with chlorhexidine 0.2% in an
nomer since all three cellular elements of the aqueous solution will reduce the amount of
marrow are often involved (pancytopenia). plaque and the number of microorganisms
Clinical Manifestations
in the oral cavity. Scrupulous oral hygiene.
• However, intramuscular injections and
They are related to the pancytopenia: nerve block anesthesias are to be avoided
• Anemia causing pallor, chest pain or because of the risk of thrombocytopenia and
dyspnea, fatigue the bleeding tendency. Intraligamentary
• Thrombocytopenia: Increased bruising, anesthesia can be used safely in these cases.
purpura, petechiae, gingival bleeding,
Suggested Reading
epistaxis, etc.
• Leukopenia/neutropenia: Infections and fever. 1. Burket’s Oral Medicine 9th, 10th and 11th
editions.
Oral Manifestations 2. Oral and Maxillofacial Pathology by
• Most common manifestation is hemorrhage Neville, 3rd edition.
• Bacterial infection 3. Shafer’s Textbook of Oral Pathology, 6th
• Candidiasis edition.
• Viral infections 4. Textbook of Pathology, Harsh Mohan.
10
Temporomandibular Joint Disorders
The temporomandibular joint also known as Also habits such as chewing gum, nail
craniomandibular joint, is described as biting, pencil chewing, etc. can cause para-
bilateral gingylimo-arthroidal diarthrosis, function.
ginglymo because these joints show ‘hinge’ Parafunction often results in MPDS.
type of movement, bilateral because it is
present on both sides and diarthrosis because Intracapsular Disorders
each joint is divided into two components and • Congenital
is a freely movable joint. • Agenesis—unilateral, bilateral
Parafunction: It is defined as a non-functional • Double condyle
oral habit, that is bringing together of the jaws • Hyperplasia of condyle
for reasons other than mastication, deglution • Condylar hypoplasia
and speech. • Infections
Local Factors – Osteomyelitis
• Pericoronitis – Septic arthritis
• Defect in tooth form and occlusion • Rheumatoid—flattened condyle
• Osteoarthritis—osteophytes
Systemic
• Traumatic—trauma to meniscus, fractured
• Epilepsy
condylar head
• Paralysis
• Functional—subluxation, dislocation and
• Dyskinesia
internal disk derangements of the disk
Psychological • Neoplastic—osteoma, osteochondroma
Insoluble personal problems (bruxism): Bruxism • Ankylosis
and clenching may be stress relieving habits,
and are associated with severe attrition, Extracapsular Disorders
occlusal wear facets, prominent linea alba on • MPDS
the cheeks, indentations on the tongue, hyper- • Iatrogenic disorders—prolonged dental
trophy of masseter muscle, pain observed on procedures, trauma during mandibular
waking up in the morning. block
Occupational: Weight lifter, people performing • Infections—osteomyelitis, periostitis
precision work, drivers, tend to clench their • Neoplasia—tumors of the condyle and the
jaws more often than others. ramus.
163
ARTHRITIS Treatment
Methotrexate is often the initial therapy as it
Rheumatoid arthritis is an inflammatory
reduces disease activity, joint erosions and can
disease affecting periarticular tissue and
provide long-term reduction in mortality.
secondarily bone. It starts as a vasculitis of
synovial membrane. It is associated with Prednisolone, and azathioprine are also
round cell infiltration and subsequent forma- given.
tion of granulation tissue—pannus. Aspirin was also used in the past, can lead
to defective platelet aggregation.
The cellular infiltrate causes erosion of
underlying bone and flattening of convex • Rest to joint
condylar surface which is called as ‘sharpened • Soft diet
pencil’ or ‘mouthpiece of flute’ type of • Reestablish occlusion—flat plane occlusal
appearance as seen on OPG or transpharyn- appliance may be helpful if parafunctional
geal view. habits are present.
• Ibuprofen 400 mg TDS for 5–10 days
Signs and Symptoms (contraindicated in asthma due to
• Unilateral or bilateral pain bronchospasm). Other NSAIDs are taken by
• Decreased mandibular movements RA patients can result in gastric ulcerations
• Difficulty in chewing and affect kidney function.
• Deviation of mandible towards affected side • Aspiration of fluid
• Muscle pain • Injection of triamcinolone acetonide 12–15 mg
• Occasional swelling and redness over joint (intra-articular injection of steroids).
area • Exercise to increase the mandibular move-
• Morning stiffness observed—symptoms ments.
relieved by activity • Surgical option for patients with severe
functional impairment or intractable pain.
• Changes in interproximal phalanges of
Swan neck deformity
SYNOVIAL CHONDROMATOSIS
Diagnosis
Chondrometaplasia
Morning stiffness >1 hr
Arthritis >3 joints Synovial chondromatosis (SC) is an uncommon
Arthritis of interphalangeal joints benign disorder characterized by the presence
of multiple cartilaginous nodules of the
Symmetric arthritis
synovial membrane that break off resulting in
Radiographic Changes clusters of free-floating loose calcified bodies
• Narrowing of joint space in the joint (Fig. 10.1). Some cases appear to
be triggered by trauma whereas others are of
• Flattening and erosions of the condylar
unknown etiology.
head
Extension of SC from the TM joint to
• Erosions of the condylar head and glenoid
surrounding tissues (including the parotid
fossa are better appreciated on HRCT
gland, middle ear, or middle cranial fossa)
Serum: Several autoantibodies may be may occur.
detected, but not specific for rheumatoid
arthritis. Clinical Features
RA factor: Anti-cycilc citrullinated proteins • Slow progressive swelling in the pretragus
(anti-CCP) factor present in 80% of adult RA region
patients. • Pain
Temporomandibular Joint Disorders 165
A B
Fig. 10.1: (A) Coronal and (B) Sagittal CBCT showing multiple calcified bodies involving the synovium in a
case of synovial chondromatosis
• Limitation of mandibular movement leading to sclerosis of underlying bone,

• TMJ clicking, locking, crepitus subcondylar cysts and osteophyte formations.
It is essentially a response of the joint to
• Intracranial extension may lead to neuro-
chronic microtrauma or pressure. Chronic
logic deficits such as facial nerve paralysis.
microtrauma may be due to continuous
Radiographs abrasion of the articular surfaces due to age
• Conventional radiography may not lead to related natural wear or due to chronic
the diagnosis, due to superimposition of parafunctional habits (bruxism).
cranial bones that may obscure the calcified Clinical Features
loose bodies.
The incidence of DJD increases with age and
• A CT scan should be obtained if SC is is also related to the rate and extent of dental
suspected after clinical evaluation. attrition.
• The lesion may appear as a single mass or • Unilateral pain directly over the condyle
as many small loose bodies.
• Limitation of mandibular opening
Treatment • Crepitus
Treatment should be conservative and consist • Feeling of stiffness after period of inactivity
of removal of the mass of loose bodies. This • Tenderness and crepitus of the joint on
may be done arthroscopically when only a palpation through the external auditory
small lesion is present, but arthrotomy is meatus.
required for larger lesions. The synovium and • Deviation of mandible to the affected side
articular disc should be removed when they on opening
are involved. Lesions that extend beyond the • Presence of Ely’s cyst
joint space may require extensive resection.
Radiographs
DEGENERATIVE JOINT DISEASE • Narrowing of joint space
• Flattening of articulating surface (Fig. 10.2)
Primarily a disorder of articular cartilage and
the subchondral bone with secondary • Condyle becomes irregular in outline with
inflammation of synovial membrane. It is sharp and pointed osteophytes seen on
localized joint disease without systemic superior surface in transorbital view.
manifestations. It begins as loaded articular • Osteophyte formation seen on tomograms or
cartilage which thins and clefts (fibrillation) CT scans (Fig. 10.3)
and then breaks down during joint activity • Anterior lipping of condyle
Fig. 10.2: TMJ OPG showing bilateral condylar flattening
A B
Fig. 10.3: Coronal and sagittal CT images showing osteophytes and anterior lipping
• Ely’s cyst—a well-demarcated depression Treatment

or cup-like defect seen on condyle called as • Conservative treatment: NSAIDs, heat, soft
Ely’s cyst (Fig. 10.4), which is a misnomer diet, rest, occlusal splints
as it is just a bony defect and not a cyst. • Intra-articular steroids injections
• Joint effusion detected on T2-weighted MRI • Anti-inflammatory effects of doxycycline
as a hyperintense signal (Fig. 10.5). therapy reduces symptoms
Fig. 10.5: T2-weighted MRI showing hyperintense

Fig. 10.4: Coronal CBCT image showing Ely’s cyst signals suggestive of joint effusion (arrows)
• In severe cases with significant loss of In anterior disk displacement with reduc-
function—arthroplasty (removal of osteo- tion, the disk recaptures its original position
phytes and erosive areas) is performed. when patient opens the mouth (Fig. 10.6) and
According to Juniper, the terms ‘disk’ and therefore this condition is accompanied by
‘meniscus’ are both misnomers and fail to opening and reciprocal click. Midway during
describe the exact shape of the intra-articular opening the jaw deviates towards the affected
disk. According to him, the disk resembles the site and at the terminal phase of opening, jaw
cap of a jockey, which snugly fits over the head aligns itself in the midline.
of the condyle and is attached to the medial In the anterior disk displacement without
and lateral poles of the condyle by strong reduction, the disk is occupying a position
ligaments. The disc is a concavoconvex and which is anteromedial to the condyle and
anteriorly is attached to the superior head of hence prevents complete opening so that the
the lateral pterygoid muscle. The inferior head opening reduces from 45 to 30–35 mm. The
of the lateral pterygoid is attached to the jaw deviates towards the affected side, and
pterygoid fovea of the condyle. The disk has because of the pressure of the condyle on the
the following parts: retrodiscal lamina, there is severe pain on
• Anterior band which is thin chewing. As in this condition, the condyle
• Intermediate zone which is very thin does not glide against the posterior band, no
• Posterior band which is thick opening or reciprocal clicks are heard.
Distally the posterior band is attached to However, these patients give history of
the bilaminar zone, the superior lamina is clicking which has disappeared. As the patient
inserted into the squamotympanic fissure, cannot open the mouth fully because of the
and the inferior lamina is inserted on to the physical presence of a malformed disk, antero-
neck of the condyle. Posterior to the disk the medial to the condyle, this condition is also
retrodiscal tissue has a rich neurovascular termed as ‘the closed lock’. The malformed
supply. disk has been described as ‘gum ball appea-
rance’ on MRI (Fig. 10.7).
Pathogenesis of Click
and Internal Disk Derangement
ARTICULAR DISK DISPLACEMENT (ADD)
In a patient having bruxism and clenching
habits, the closing muscles. It is an abnormal relationship between the
Medial pterygoid and masseter are disk, the mandibular condyle, and the arti-
hyperactive. The lateral pterygoid which is an cular eminence, resulting from the stretching
opening muscle also shows contraction to or tearing of the attachment of the disk to the
counterbalance the closing muscles. Greater condyle and glenoid fossa.
the activity of the closing muscles, greater is ADD may result in:
the contraction of the lateral pterygoid, this
• Abnormal joint sounds
results in anterior subluxation of the disc. The
disc now occupies a position such that the • Limitation in mandibular range of motion
posterior band is placed anterior to the head • Pain during mandibular movement
of the condyle in closed position. When patient Loosened disks become displaced anterior
opens his mouth, the condyle slips over the to the mandibular condyle.
posterior band, producing the opening click.
When the patient closes the mouth, the disk Posterior Disc Displacement
again relocates itself anterior to the condyle and When a portion of the disk is found posterior
while so doing produces the reciprocal click. to the top of the condyle.
A B
Fig. 10.6: MRI image showing anteriorly displaced disk in closed mouth position. Disk repositioned to normal
location in open mouth (s/o ADD with reduction)
A B
Fig. 10.7: MRI image showing anteriorly displaced disk which in open position is deformed giving gum ball
appearance (s/o ADD without reduction)
Etiology Classification
• Direct trauma to the joint from a blow to 1. Anterior disk displacement with reduction
the mandible (clicking joint)
• Chronic low-grade microtrauma resulting 2. Anterior disk displacement with intermittent
from long-term bruxism or clenching of the locking
teeth
• Generalized laxity of joints 3. Anterior disk displacement without reduc-
• Combination of mechanisms related to the tion (closed lock).
anatomy of the joint and the facial skeleton,
Anterior Disk Displacement with Reduction
connective tissue chemistry and chronic
loading of the joint increases the suscepti- This condition is caused by an articular disk
bility of certain individuals to a disturbance that has been loosened because of elongation
of the restraining ligaments and displace- or tearing of restraining ligaments and has
ment of the disk. moved from its normal position on the top of
the condyle.
Clinical Features
Pain or dysfunction when accompanied by Clinical Features
capsulitis, synovitis, and joint effusions. • Clicking is accompanied by pain
• Dysfunction due to intermittent locking relationship to the condyle when the mouth
• Pain is most noticeable at the time of the is closed. The disk is folded in the dorsal part
click of the joint space, preventing full mouth
closure.
Palpation and auscultation of the TMJ will
reveal: Clinical Features
Reciprocal click: A clicking or popping sound • Sudden inability to bring the upper and
during both opening and closing mandibular lower teeth together in maximal occlusion.
movements. The clicking or popping sound • Pain in the affected joint when trying to
due to anterior disk displacement with reduc- bring the teeth firmly together.
tion is characterized by a click that occurs at a • Forward displacement of the mandible on
different point during opening and closing. the affected side.
• Restricted lateral movement to the affected
Anterior Disk Displacement without side.
Reduction (Closed Lock) • No restriction of mouth opening.
Closed lock may be the first sign of TMD
Management
occurring after trauma or severe long-term
nocturnal bruxism. It is detected more • ADD resolve over time either with no treat-
frequently in patients with clicking joints that ment or with minimal conservative therapy.
progress to intermittent brief locking and then • Painful clicking or locking should initially
permanent locking. be treated with conservative therapy.
• Recommended treatments for symptomatic
A patient with an acute closed lock will
ADD include splint therapy, manual
often have a history of a long-standing TMJ manipulation and other forms of physical
click that suddenly disappears with a sudden therapy, anti-inflammatory drugs, arthro-
restriction in mandibular opening.This limited centesis, arthroscopic lysis and lavage,
mandibular opening occurs when the disk arthroplasty, and vertical ramus osteotomy.
interferes with the normal translation of the Many of these nonsurgical and surgical
condyle along the glenoid fossa. techniques are effective in decreasing pain
Clinical Features
and in increasing the range of mandibular
motion although the abnormal position of
• Pain directly over the joint during mandi- the disc is not corrected.
bular opening (especially at maximum
• Anterior disk displacement with reduction: Flat-
opening)
plane stabilization splints that do not change
• limited lateral movement to the side away
mandibular position and anterior re-
from the ADD
positioning splints have both been used to
• During maximum mandibular opening, the
treat painful clicking (potential side effects
mandible will deviate towards the side of
of these appliances, which include tooth
the displacement. Palpation of the joints
movement and open bite).
will reveal decreased translation of the
condyle on the side of the disk displace- • Anterior disk displacement without reduction:
ment. Treatment options should depend on the
degree of pain associated with the ADD.
Posterior Disk Displacement Management of a locked TMJ may be non-
Posterior disk displacement has been described surgical or surgical. The goals of successful
as the condyle slipping over the anterior rim therapy are to eliminate pain and to restore
of the disk during opening, with the disk being function by increasing the range of
caught and brought backward in an abnormal mandibular motion. Replacing the disk in
a normal position is not necessary to • Parafunctional habits, e.g. nocturnal

achieve these goals. Flat-plane occlusal bruxing, tooth clenching, lipor cheek biting.
stabilization appliance to decrease the • Emotional distress.
adverse effects of bruxism is advocated.
• Acute trauma from blows or impacts.
Patients with severe pain on mandibular
movement may benefit from either • Trauma from hyperextension, e.g. dental
arthrocentesis or arthroscopy. Flushing the procedures, oral
joint with intra-articular corticosteroids to • Intubation for general anesthesia, yawning,
decrease inflammation or with sodium hyperextension associated with cervical
hyaluronate to increase joint lubrication trauma.
and decrease adhesions has also been repor- • Instability of maxillomandibular relation-
ted to help in decreasing the pain associated ships.
with nonreducing disk displacement.
• Laxity of the joint.
MYOFASCIAL PAIN DYSFUNCTION SYNDROME • Comorbidity of other rheumatic or musculo-
(MPDS) skeletal disorders.
• Poor general health and an unhealthy life-
MPDS or Costen’s syndrome is a disease entity
that results from spasm of the muscles style.
supporting the jaws due to multiple causes
Pathophysiology of MPDS (Laskin’s Theory)
most important being overclosure or over-
extension of the muscles. The pathophysiology of MPDS emphasizes
mainly on the muscular tension caused by oral
Etiology habits and dental irritants. Figure 10.8 gives a
The various factors that have been associated lucid explanation to the mechanism involved
in the cause of MPDS are as follows: in MPDS.
Fig. 10.8: Pathogenesis of MPDS, proposed by Laskin

Clinical Features i. Muscle must be evaluated in its entire

• Patients complain of unilateral, dull pain length including its origin and insertion.
in the ear or preauricular region. ii. The muscles must be evaluated in rest and
• Pain is worse on awakening in the morning. contracted position.
• Tenderness of muscle of mastication is iii. The muscles must be examined bilaterally
present. to compare the difference.
• Mouth opening is limited and painful. The iv. The muscles must be palpated horizon-
jaw deviates to affected side on opening the tally and vertically to the attachments.
mouth. While palpating the muscles, begin palpat-
Laskin’s four cardinal signs of MPDS ing with light pressures before proceeding
1. Unilateral pain: There must be a dull ache to 3–4 pounds. Muscle palpation may be
in the preauricular region. Pain is worse on performed by two methods, i.e.
waking up. 1. Flat palpation: When muscle can be palpated
2. Muscle tenderness must be present on over the bone, e.g. masseter.
palpation. 2. Pincer palpation: When the belly of the
3. Clicking/popping noise must be heard in muscle can be held between the fingers, e.g.
the TMJ. sternocleidomastoid.
4. Mouth opening must be restricted.
Treatment Consideration
Negative Features Multiple therapeutic approach is preferred in
a. Absence of radiographic findings. the management of MPDS beginning with
b. Lack of tenderness in the TMJ on palpation patient education and counseling.
from the external auditory meatus.
Pharmacotherapy
Trigger Points 1. NSAIDs are the drug of choice for imme-
These are localized deep tender areas of taut diate pain relief. Ibuprofen 400 mg t.d.s or
band of skeletal muscle, tendon or ligament nimesulide 100 mg b.d. are good choices of
that has the tendency to cause referred pain analgesics.
in a definite anatomic distribution when 2. Diclofenac gel in pluronic lecithin organo-
stimulated. Presence of such trigger points are gel can be rubbed over the skin followed
characteristic feature of MPDS. The area by hot fomentation which gives relief from
perceived by the irritable trigger point is called pain and improves mouth opening.
the zone of reference. In MPDS, pain is elicited
by applying digital pressure on the trigger 3. Muscle relaxants such as chlorzoxazone
point whereas in trigeminal neuralgia, even 250 mg t.i.d., carisoprodol 350 mg t.i.d. (tab
light touch or breeze is sufficient to stimulate soma) are valuable in reducing muscle
the trigger zone and precipitate an attack of spasm. Diazepam 2–5 mg can be given for
pain. 10 days. Cyclobenzaprine 10 mg before
sleep has been tried recently and found
Jump Sign effective.
It is the withdrawal of head, wrinkling of head 4. Amitriptyline which is a tricyclic anti-
or verbal response given by the patient on depressant can be given in the doses of
palpating the trigger points. 10 or 25 mg at bed time to reduce patient
Tanaka’s recommendations for palpation of anxiety and provide a good refreshing
muscles. sleep.
Intraoral Appliance Therapy ANKYLOSIS

Hard and soft splints can be fabricated that
Ankylosis in Greek terminology means ‘stiff
help to unload TMJ and establish a harmonious
joint’. Hypomobility to immobility of the joint
relation between TMJ and muscles. can lead to inability to open mouth partially
Trigger Point Therapy or completely.
The spray and stretch technique provides Classification of Ankylosis
stimulation of cutaneous afferent nerves and • False ankylosis or true ankylosis
produces trigger point inhibition causing pain • Extra-articular or intra-articular
relief. • Fibrous or bony
Fluoromethane spray is an effective choice • Unilateral or bilateral
for the same. • Partial or complete
Alternatively injection of local anesthesia
Psuedocauses
0.5% procaine, bupivacaine into the trigger
points reduces pain. However, chances of 1. Scar tissue formed in muscle of mastication
myotoxicity and other reactions should be 2. Myositis ossificans
considered before initiating the therapy. 3. Injury to zygomatic arch and union to
coronoid process (forceps delivery)
Relaxation Therapy 4. Ca nasopharynx and antrum
This mode of therapy decreases sympathetic True—may be fibrous or bony:
activity and arousal. Brief methods such as • Fibrous—joint space seen
deep breathing and deep methods such
• Bony—mass of bone seen between condyle
as meditation, progressive muscle relaxa-
and glenoid fossa (condyle cannot be
tion can be performed under the supervision
visualized). This type is due to trauma or
of a trained master to provide muscle relaxa-
infection to condyle, so that the growth of
tion.
mandible on that side comes to a standstill.
Physiotherapy Etiology
Various types of treatments like moist heat, Two main factors predisposing to ankylosis
ultrasound and shortwave diathermy help is trauma and infections:
immensely in reducing pain and dysfunction. • Trauma: Congenital, at birth (forceps
They act by increasing the vascularity of the delivery), hemarthrosis, and condylar
muscle, resolution of inflammation and fractures
fibrosis and increasing the flexibility of
• Infections: Otitis media, parotitis, tonsillitis,
connective tissue. Isokinetic exercises of the
furuncle, abscess around joint, osteo-
jaws also provide a similar effect to the myelitis, actinomycosis
muscles. Other methods such as massage,
accupressure, homeopathic and herbal • Inflammation: Rheumatoid arthritis, osteo-
medicines, botulinum toxin are also used arthritis, septic arthritis.
widely in the treatment of MPDS. Exercises • Systemic diseases: Smallpox, scarlet fever,
like reciprocal relaxation, active and passive typhoid, gonococcal infections, scleroderma,
stretch are found to be effective. In reciprocal Marie-Strumpell disease, ankylosing
relaxation, patient is asked to open against spondylitis
pressure and this method relaxes the closing • Others: Bifid condyle, prolonged trismus,
muscles which are tender in MPDS. prolonged immobilization, burns.
Clinical Features irregular bony projections and depressions.

Unilateral Ankylosis
These irregularities interdigitate between
themselves hence giving a “jigsaw puzzle”
• Obvious facial asymmetry appearance (Fig. 10.9).
• Deviation of mandible and chin on affected
• Bony ankylosis: Complete obliteration of
side
joint space noticed, normal TMJ anatomy
• Receded chin and hypoplastic mandible on
is distorted (Fig. 10.10).
affected side, with teeth appearing in the
ramus • Elongation of coronoid process (compensa-
• Flattening and elongation of unaffected side tory coronoid hyperplasia) on the side of
of face hypomobility and prominent antegonial
• Roundness and fullness of face on affected notch (Fig. 10.11).
side Treatment
• Prominent antegonial notch on affected side
Treatment is always surgical
• Some degree of mouth opening is possible
• Condylectomy
• Unilateral posterior crossbite on ipsilateral
side • Gap arthroplasty
• Interpositional arthroplasty
Bilateral Ankylosis
• Inability to open mouth—oral opening
severely reduced
• Mandible symmetrical, but micrognathic,
“bird face” deformity due to receding chin
• Antegonial notch is well defined bilaterally
• Class II malocclusion seen
• Multiple carious teeth with poor oral hygiene
• Crowding of teeth
• Multiple impacted teeth (teeth appearing in
the ramus)
Radiographic findings: TMJ OPG, transcranial
view, CT/CBCT, MRI are indicated.
• Fibrous ankylosis: Normal anatomy of the
head and glenoid fossa can be appreciated,
In advanced cases there is deformity of the Fig. 10.9: Coronal CT—fibrous ankylosis showing jig-
condylar head and the glenoid fossa with saw puzzle appearance
A B
Fig. 10.10: CBCT image showing bony ankylosis

Fig. 10.11: Sagittal CBCT and 3-D image showing compensatory coronoid hyperplasia and prominent
antegonial notch
HYPERMOBILITY, SUBLUXATION manipulate the mandible back to its original

AND DISLOCATION position.
During normal or unstrained opening of the Clinical Features
mouth, the condylar heads translate forward • Mouth remains open due to associated
to a position under the apices of the articular spasm of the lateral pterygoid and other
eminence. muscles of mastication.
Dislocation • Difficulty in mastication and speaking.
Excursion of the condylar head beyond these • Deviation of chin towards contralateral side
limits and the condyle is fixed anterior and is seen.
superior to the articular eminence (infratemporal
• Affected condyle cannot be palpated.
fossa). In these cases after the condyle reaches
anterior the articular eminence, the closing • In unilateral dislocation, there is a lateral
muscles (medial pterygoid, masseter) go into crossbite and open bite on the contralateral
spasm, thereby placing the condyle in the side, whereas in bilateral dislocation, there
anterior and superior position with respect to is bilateral open bite.
the articular eminence (Fig. 10.12). At this • Definite depression will be seen and felt
stage, lateral pterygoid muscle also goes into in front of the tragus (pre-tragal notch)
spasm. Consequently patient is unable (Fig. 10.13).
A B
Fig. 10.12: Axial and sagittal CBCT showing dislocation of the condyle, anterior and superior to the articular
eminence
Subluxation
Repeated episodes of dislocation where there
is an abnormal anterior excursion of condyle
beyond the articular eminence but the patient
is able to manipulate it back to normal position.
This recurrent, incomplete, self-reducing
habitual dislocation is termed as hyper-
mobility or chronic subluxation of TMJ.
It occurs due to triad of:
• Ligamentous and capsular flaccidity
• Eminental erosion
• Flattening and trauma of TMJ
Fig. 10.13: Deep pre-tragal notch seen in patient with Causes
TMJ dislocation In predisposed individuals yawning, laugh-
ing, severe epilepsy, Ehlers-Danlos syndrome
Causes can precipitate an episode of subluxation.
• Blow to the chin while mouth is open Treatment
• Excessive mouth opening, prolonged dental • Intermaxillary fixation or limiting oral
treatment opening by giving elastics.
• Injudicious use of mouth gag • Use of sclerosing agents such as sodium
Treatment psylliate, sodium morrhuate, sodium
tetradecyl sulfate into the joint space.
To overcome the resistance of the severe
• Surgical procedures like capsule tightening
muscle spasm, and to reduce tension and
procedures (capsulorrhaphy), creating
anxiety, the following steps are taken: mechanical obstacle for condylar head,
• Reassure the patient creation of new muscle balance and removal
• Tranquillizer or sedative to relax the of mechanical obstacle by menisectomy,
muscles high condylectomy, and eminectomy.
• Pressure and massage to the area Differences between subluxation and dis-
• Manipulation location
Manipulation can be done without any
anesthesia, or with LA or under GA and Subluxation Dislocation
sedation, depending upon the severity and Patient can correct it Doctor has to correct it
chronicity of the case. himself
For the procedure of manipulation, the Condyle anterior to arti- Condyle anterior and
cular eminence superior to articular emi-
thumbs of the operator are covered with gauze nence
(to prevent accidental injury in case of sudden Posterior slope of articular Posterior slope of articular
closure) and continuous downward pressure eminence is flat eminence is steep
is given on the posterior teeth, by placing
the thumbs on the occlusal surface, and Suggested Reading
supporting the chin with the other fingers. 1. Burket’s Oral Medicine, 11th Edition.
Downward pressure overcomes the spasm of 2. Common diseases of TMJ, Ogus and Toller.
the muscles plus it brings the locked condylar 3. TMJ Disorders and Occlusion, Jeffery P
head below the level of the articular eminence. Okeson, 7th Edition.
Then backward pressure is given to guide the 4. TMJ Disorder and Orofacial pain, DCNA
entire mandible posteriorly. Jan 2007.
11
Diseases of Maxillary Sinus
The maxillary sinuses are a pair of air-filled IV. Neoplastic diseases

cavities located within the body of the maxilla. a. Benign tumors
They communicate with the nasal cavity • Papilloma
through an ostium which drains into the • Osteoma
middle meatus. The sinuses are lined by
• Ameloblastoma
pseudostratified ciliated columnar epithelium.
• Adenomatoid odontogenic tumor
Though the function of these sinuses is not
clear, it is proposed that they serve to • Complex odontoma
humidify and warm the inhaled air and add • Ossifying fibroma
resonance to the voice in addition to lightening b. Malignant tumors
the skull. • Squamous cell carcinoma
• Adenocarcinomas
Classification of Diseases of Maxillary Sinus
I. Inflammatory disease (sinusitis) V. Fibrous dysplasia
a. Acute Examination of the Patient with Maxillary
b. Chronic Sinus Disease
In addition to the routine history taking and
II. Traumatic lesions
examination, the following specific factors
a. Concussion or laceration of the sinus must be considered while examining a patient
mucosa. with maxillary sinus disease.
b. Blow out fractures of the orbit involving the 1. The patient must be examined for any
sinus. asymmetry, ecchymosis, deformity and
c. Isolated fractures of the sinus. erythema of the skin over the sinus. These
d. Complex fractures associated with middle may be signs of traumatic injury involving
third injuries. the sinus.
e. Oroantral fistula. 2. Presence of epistaxis and epiphora are signs
of malignant tumor or space occupying
III. Cystic lesions lesion within the sinus.
a. Intrinsic cyst: Mucous retention cyst, benign 3. Paresthesia of the infraorbital nerve may be
mucosal cyst, surgical ciliated cyst. present which should alert the clinician of
b. Extrinsic cysts: Dentigerous cyst, radicular a fracture involving the sinus wall or a
cyst, OKC, etc. malignant tumor.
176
Diseases of Maxillary Sinus 177
4. Tenderness of teeth in the absence of any 2. CT Scans

dental pathology may be a feature of CT scans are excellent choice to study various
sinusitis. Such teeth are referred to as Stomp pathologies involving the sinus including
positive, i.e. they are painful when the sinusitis, cysts, tumors, fractures, etc. Coronal
patient jumps or walks fast. and axial sections must be obtained to study
5. Trismus may be caused due to tumors of the entire extent of the lesions. CT scans are
the maxillary sinus destroying the posterior mandatory in cases of fractures and malignant
wall of the sinus and invading the pterygoid tumors involving the sinus.
muscles or locking of the coronoid process.
3. MRI Scans
6. Eye movements must be noted carefully. MRI scans produce an excellent soft tissue
Visual disturbance is associated with blow contrast and valuable in studying cysts and
out fractures and also malignant tumors tumors involving the sinus. Mucosal
involving the orbit. thickening of the sinus wall and accumulation
7. Cervical lymph nodes must be examined in of fluid within the sinus can be studied with
all the cases as they are enlarged in infec- MRI scans.
tions and malignant tumors of the sinus.
4. Radionuclide Scanning
Radiological Evaluation of a Patient Scans obtained after injection of a radioisotope
with Maxillary Sinus Disease such as 99mTc demonstrate the physiological
The following investigations may be performed changes taking place within the sinus.
for a case of suspected maxillary sinus disease. Scintigraphic studies are useful in the
diagnosis of malignant tumors of the sinus to
1. Radiographs
study the complete extent of the tumor.
Radiographic survey is the preliminary choice
of investigation for sinus disease. IOPA views MAXILLARY SINUSITIS
can be made to study the floor of sinus,
diagnose and locate oroantral fistula and i. Sinusitis can be due to bacterial or allergic
displaced root pieces. For large lesions, lateral- cause. Haemophilus influenzae, Streptococcus
occlusal views can be made to visualize the pneumoniae are the common causative
sinus and its floor. Amongst the extraoral organisms of maxillary sinusitis. A rare
views, OPG and Water’s view are the most cause can be due to fungal infection such
important views to study the sinuses. As a rule, as aspergillosis which is usually seen in
cystic lesions are better visualized on OPG immune-compromised patients.
while haziness of the sinus due to sinusitis can ii. Conditions such as deviated nasal septum
be studied more clearly on the Water’s view. (DNS) predispose to sinusitis. Spread of
The posterior wall of the sinus cannot be seen infection from the oral cavity from an
on the Water’s view and an SMV view is infected root apex or displaced root-piece
required to demonstrate this. The normal sinus can also lead to sinusitis.
contains air and hence appears radiolucent. iii. Nasal congestion or obstructions accom-
Any pathology or change within the sinus panied with headache and secretion from
encroaches the air space and hence appears the nose are considered as the triad of
relatively radiopaque. The radiographic sinusitis.
appearances of sinus disease are thus not
specific owing to the fact that transudates, Acute Maxillary Sinusitis
exudates, blood will all produce a similar It may be suppurative or non-suppurative
shadow on the radiograph. inflammation of the antral mucosa.
Clinical Features between the opacity and the sinus is straight

• Tenderness, paresthesia, feeling of heavi- and horizontal. Fluid level indicates pus or
ness on the affected side blood in the sinus. The radiograph must be
• Mild swelling of cheek in severe cases made in a standing position to confirm this
feature (Fig. 11.2).
• Tenderness on percussion of maxillary teeth
• Patient gives a recent history of attack of cold Treatment
and rhinitis (3–4 days) 1. In early stages, antibiotic therapy with
• Heaviness of the head steam inhalation is a good method of
treating sinusitis. Amoxycillin and cephalo-
• Constant throbbing pain exacerbated by
sporin provide good coverage against the
lowering or bending down
organisms involved in acute maxillary
• Pain which is more severe in morning and sinusitis. Use of nasal decongestants like
evening ephedrine sulfate 0.5–1%, xylometazolin
• Unilateral foul nasal discharge that becomes hydrochloride 0.1% helps shrink the
more profuse on lowering of head swollen and inflamed mucosa, and helps
• Fever, chills, sweating, nausea, difficulty in minimize mucosal discharge. Steam
breathing inhalation with mucolytic agents like tinc.
Benzoin, camphor and menthol improves
Radiographic Features the drainage by the ciliary pathways of the
a. The thickening of the mucosa and accumula- antral lining through the ostium.
tion of secretion during sinusitis reduces 2. In severe cases, surgical drainage may have
the air content of the sinus and causes the to be established to relieve the patient.
sinus to appear increasingly radiopaque 3. Chronic maxillary sinusitis cases may
(Fig. 11.1). The thickened mucosa appears require a Caldwell-Luc operation to curette
nearly parallel to the walls of the sinus. It the sinus contents or correction of DNS to
may be of uniform thickness or polypoid. avoid recurrence.
b. In chronic sinusitis, opacification of sinus
takes place which may be accompanied by Chronic Maxillary Sinusitis
sclerosis of the bony walls. It may be due to persistent dental focus,
c. The presence of fluid within the sinus can chronic rhinitis, chronic infection in frontal or
be ascertained if the line of demarcation ethmoidal sinuses, allergic conditions, etc.
Fig. 11.1: Opacification of the right maxillary sinus Fig. 11.2: Maxillary sinusitis case showing fluid level
suggestive of sinusitis in Water’s view (Source: Internet)
Clinical Features
• Sometimes asymptomatic condition
• Pain and tenderness in the area of antrum
in acute exacerbation
• Unilateral foul discharge through posterior
nares
• Cacosmia (fetid odour with bad taste in the
mouth)
Fig. 11.3: Bilateral dome-shaped radiopacities in
Empyema
maxillary antral suggestive of benign mucosal cyst
Sometimes the ostium of the sinus gets blocked
by thickened mucosa or other pathologic differentiated where mucosal thickening of the
conditions. Suppurative infection results in entire antral lining is present.
such cases and the pus accumulates inside the
Contusions of the Sinus
sinus. Such an accumulation of pus within a
cavity is known as empyema. A blow on the face may transmit the force
Radiographically, the sinus appears to be through the bone of the anterior wall of the
completely opacified. Such opacity must be sinus causing a tear in the mucosal lining. The
differentiated from simple mucosal thicken- anterolateral wall may suffer a green stick
ing. Accumulation of pus inside the sinus may fracture but sometimes since this bone is
lead to osteomyelitis. relatively elastic; it gives rise to laceration of
the sinus mucosa and bleeding within the
Mucous Retention Cyst of the Antrum sinus.
This is a common sequelae of an inflamed or
Radiographic Features
hyperplastic lining of the maxillary sinus.
Retention cysts are formed when the duct of a Contusions of the maxillary sinus appear as
seromucinous gland is blocked or damaged haziness of the sinus due to bleeding. Fluid
due to inflammatory reaction. The lesion is level can be demonstrated on a radiograph
usually unilateral, asymptomatic and acciden- made in a standing position.
tally discovered during a routine radiographic Blow out Fractures
survey.
When the globe of the eye sustains a blunt
Radiographic Features injury due to an object larger than its size, the
The cyst appears as a dome-shaped radiopacity kinetic energy is converted into hydraulic
attached to the floor or lateral wall of the sinus. energy and the orbital contents break the floor
An OPG is a clear view to identify such cyst and the medial wall. Thus, it causes herniation
(Fig. 11.3). If the cyst is large, it may fill up the of the orbital contents into the sinus.
entire maxillary sinus and appear as uniform Clinical features of blow out fractures
cloudiness. Sometimes a large cyst may pro- include periorbital edema, subconjunctival
trude through the ostium into the nasal cavity. ecchymosis, hooding of eye/enophthalmos
The differential diagnosis for such cystic and diplopia.
lesions inside the sinus includes odontogenic
Radiographic Signs
cysts. The presence of a hyperostotic border
around the cyst that appears as a white line i. Soft tissue swelling over the orbital rim.
serves to identify odontogenic cysts which are ii. Trap door sign or bright light sign on the
extrinsic in origin. Antral polyps must also be CT (Fig. 11.4).
A B
Fig. 11.4: (A) Subconjunctival ecchymosis of right eye; (B) Trap door sign suggestive of blow out fracture
iii. Polypoid density in the roof of the sinus. iv. A mouth mirror held near the orifice turns
iv. Teardrop herniation of the orbital contents moist when the patient blows with his
into the sinus. nostrils closed. Similarly a wisp of cotton
v. If the distance between infraorbital margin will flutter when it is held near the
and floor of orbit appears more than 2 mm perforation when the patient blows his
on PA Water’s view, it is suggestive of nose.
fracture of the floor of orbit. v. In late stage, symptoms of established
oroantral fistula consist of 4 Ps:
Oroantral Fistula/Communication
Oroantral fistula (OAF) is an unnatural • Pain—previously a dominant feature,
communication between the oral cavity and is now negligible as the fistula allows
the maxillary sinus. The term fistula is used free escape of fluids
to denote communication between the oral • Persistent, purulent or mucopurulent
cavity and the antrum which is chronic and foul unilateral nasal discharge when
lined by the epithelium. The most important head is lowered
cause for the formation of an OAF is iatrogenic • Post-nasal drip
perforation of the floor of sinus during
extraction of an upper molar with the root • Popping out of an antral polyp
piece displaced into the sinus. Other causes
Radiographic Features
include, traumatic injuries to the maxilla such
as gun shot injuries, infections such as syphilis a. Discontinuity of the floor of sinus can be
causing perforation of the palate. seen on an IOPA view or lateral occlusal
view.
Clinical Features
b. The displaced root piece may be present
i. Sudden disappearance of a root piece inside the sinus and appears as a radio-
during extraction into the socket is a sign paque mass with a radiolucent root canal
of an oroantral communication.
inside it.
ii. Presence of bubble formation in the blood
present within the socket when the patient c. In chronic cases, there may be generalized
blows his nose also suggests a newly haziness of the sinus due to chronic
formed fistula. inflammation (Fig. 11.5).
iii. Regurgitation of fluids, nasal twang in the Differential diagnosis: Must include a foreign
voice and features of chronic sinusitis may body in the sinus, antrolith, normal bony
be seen in long-standing cases. projections within the sinus, etc.
A B
Fig. 11.5: Cropped image of OPG and coronal section CT showing oroantral fistula and sinusitis of left
antrum on CT image
Treatment of OAF to the apex of a non-vital tooth. They have a

An OAF must be closed as soon as it is identi- corticated border that separates them from the
fied. The root piece can be retrieved through sinus.
the socket or by a Caldwell-Luc surgery. The Dentigerous cysts are associated with the
fistula can be closed by various surgical crown of an unerupted tooth. They appear as
procedures like buccal advancement flap, peri coronal radiolucency attached to the neck
palatal advancement flap or a combination of the tooth. The associated impacted tooth
flap can be performed to close the fistula. may be pushed deep into the sinus at times
reaching the floor of the orbit or the posterior
Antrolith wall of the sinus (Fig. 11.6). A corticated wall
An antrolith is a calcified mass within the separates the cyst from the sinus. CT scans
sinus. Antroliths form around endogenous must be obtained to confirm the location of
foci such as inspissated pus, mucous plug, the tooth inside the sinus.
blood clot, etc. or around exogenous foci such Globulomaxillary cyst (so-called) was
as a foreign body, a piece of paper. Antroliths considered to be a fissural cyst that arises from
are often asymptomatic but occasional large the epithelial remnants at the site of fusion of
stones may perforate the medial wall of the the maxilla and pre-maxilla but now believed
sinus and protrude into the nasal cavity. to be an odontogenic cyst. It appears on the
Radiographically, they appear as round-, oval- radiograph as inverted pear-shaped radio-
or irregular-shaped calcified masses within lucency between the canine and lateral incisor.
the sinus. It may also show alternate radio- A large expanding cyst may cause displace-
lucent and radiopaque lamellae. ment of the walls of nasal cavity. The inverted
‘Y’ line of Ennis may be obliterated when such
Extrinsic Cysts
large cysts encroach the sinus.
Extrinsic cysts are those that arise outside the
sinus and invade the sinus. The common Benign Tumors
extrinsic cysts include radicular cysts, denti- Benign tumors, such as papilloma and osteoma,
gerous cysts, fissural cysts such as globulo- arise within the sinus. Epithelial papilloma is
maxillary cysts. They may be odontogenic or a soft tissue mass arising from the lining of
non-odontogenic in origin. Radicular cysts the walls of the sinus. Radiographically, it
appear as periapical radiolucency in relation appears haziness within the sinus. Osteomas
A B
Fig. 11.6: Axial and coronal CT showing dentigerous cyst involving the left maxillary sinus
are the most common mesenchymal tumors i. When the medial wall is affected, it causes
of the PNS. It is a slowly growing expansile nasal symptoms such as nasal obstruction,
lesion causing nasal obstruction. The frontal discharge, epistaxis and pain.
sinus is the most common sinus to be affected. ii. When the floor is affected, it causes
On the radiographs, osteomas appear as numbness of the palate, unusual mobility
lobulated sharply defined, rounded homo- of the teeth and swelling of the palate.
geneous mass of much greater opacity. iii. When the lateral wall is affected, it causes
Extrinsic tumors involving the sinus include swelling on the face and vestibule along
ameloblastoma, AOT. with pain and hyperesthesia of the
The most common extrinsic tumor affecting maxillary teeth.
the sinus is ameloblastoma. It is an aggressive iv. When the roof of the sinus is affected, eye
tumor when it occurs in the maxilla and grows symptoms such as diplopia, proptosis,
rapidly causing loosening of the teeth and pain in the cheeks and upper teeth are the
nasal obstruction. It also causes painless presenting features and sometimes
deformity of the middle-third of the face. sudden loss of vision may take place.
Radiographically, it appears as unilocular or v. When the tumor spreads posteriorly, the
multilocular radiolucency involving the sinus. pterygoid muscles are affected and this
The complete extension of ameloblastoma can along with locking of the coronoid process
be studied on a CT scan. causes trismus and obstruction to the
AOT is a benign odontogenic tumor chiefly eustachian tube. Radiographically, the
affecting the anterior part of the maxilla. It tumor appears as haziness of the sinus.
may extend posteriorly to involve the sinus. The affected walls of the sinus are
The lesion present as an expansile radiolucent destroyed and appear discontinuous
mass having an impacted tooth or areas of (Fig. 11.7A to C).
calcification with a Milky Way appearance of Treatment involves surgical removal of the
the lumen. maxilla followed by radiotherapy and re-
habilitation with a suitable prosthesis.
Squamous Cell Carcinoma of the Sinus
It accounts to about 3% of malignant tumors Fibrous Dysplasia of Bone
affecting the sinus. The clinical features It is a benign fibro-osseous lesion that
depend upon the walls of the sinus that are frequently affects the maxillary sinus. It is
affected. believed to be a hamartoma that has limited
Fig. 11.7B: OPG showing osteolytic lesion of the left

maxilla with discontinuity of the floor of the antrum
Fig. 11.7A: Growth involving left maxilla and floating 27
Fig. 11.7C: Coronal CT showing extensive osteolytic lesion destroying the walls of the left maxilla suggestive
of CA maxillary antrum
growth potential. Fibrous dysplasias commonly stippled or a granular appearance (Fig. 11.8A
affect young individuals and presents as and B). It is treated by surgical recontouring
expansile dense radiopaque mass filling the of the excess bone which is best performed after
sinus. It may have a characteristic groundglass, the growth has stopped to avoid recurrence.
Fig. 11.8A: Patient presenting with expansile lesion in the left maxilla
Fig. 11.8B: Axial and coronal CT showing groundglass appearance of fibrous dysplasia
Even if normally FD stops growing after 2. Oral and Maxillofacial Pathology by

adolescence, pregnancy and hormonal factors Neville, 3rd edition.
are reported to trigger sudden spurt in the
growth of FD. 3. Shafer’s Textbook of Oral Pathology, 6th
edition.
Suggested Reading
1. Burket’s Oral Medicine, 9th, 10th and 11th 4. The maxillary sinus and its Dental Implica-
editions. tions, David McGowen.
12
Salivary Gland Disorders
DISEASES OF SALIVARY GLAND C. Necrotizing sialometaplasia (minor

salivary gland pathology)
Classification 4. Obstruction of flow
1. Developmental a. Calcareous deposits (sialolithiasis),
• Aplasia organic masses or inspissated mucus
• Hypoplasia
b. Collapse of ducts because of pressure of
• Absence of one or more pair of glands
adjacent structures.
• Abberancy—addition
5. Mucocele
• Accessory ducts
• Diverticuli—small pouches in which a. True cyst
saliva can stagnate b. Mucus retention
2. Functional c. Mucus extravasation
• It includes increase or decrease in d. Ranula
salivation 6. Sialoadenosis
• Increased—sialorrhea
Non-neoplastic, noninflammatory, asymp-
• Decreased—asialorrhea or xerostomia tomatic enlargement of salivary gland
3. Inflammatory usually bilateral, caused by:
A. Viral a. Barbiturates addiction
1. Mumps or acute non-suppurative-
b. Malnutrition
parotitis
2. Paramyxovirus, cytomegalo virus c. Alcoholism
B. Bacterial 7. Specific infectious diseases
1. Acute bacterial sialoadenitis or acute a. Viral—mumps/epidemic parotitis
suppurative parotitis b. Bacterial—tuberculosis, actinomycosis,
I. Postoperative complication after spirochetes (syphilis)
major surgery 8. Autoimmune diseases
II. Debilitating diseases
a. Sjögren’s syndrome
2. Secondary to blockage of salivary
gland or trauma b. Uveoparotid fever
I. Chronic suppurative c. Mickulicz’s disease
II. Allergic sialoadenitis d. Recurrent non-specific parotitis
185
9. Tumors To study functional disorders and auto-

a. Benign immune diseases.
Parenchymal Warthin’s tumor and oncocytoma are
Interstitial visualized as hot spots.
b. Malignant
5. Ultrasound
Parenchymal
Interstitial It is useful in studying space occupying lesions
within the salivary gland, e.g. cyst benign
History and Investigations tumors and also shows calcific and non-calcific
1. History Taking obstructions.
In the diagnosis of salivary gland pathology 6. CT Scan and CT Sialography
history plays an important role. For example, It is useful in studying the salivary gland and
patients with sialolithiasis give history of ductal pathology.
unilateral pain and swelling related to food
intake. 7. MRI
Mumps patients give history of fever with Considered the best imaging modality to
tender enlargement of parotid gland. study various parenchymal pathologies, e.g.
Sjögren’s syndrome patients will give history tumors, infections.
of severe dryness of oral cavity and eyes.
8. Sialoendoscopy
2. Clinical Examination It can be performed to study obstruction in
Clinical examination is carried out to locate the ducts and its removal.
and study clinical characteristics the salivary
gland pathology, e.g. unilateral or bilateral Sialography
tender swelling of parotid gland with elevated (Neglected step child of radiology).
ear lobules and inflamed ductal orifices in
mumps, milking of the gland to study the Indications
diminished secretion in sialolithiasis, bi- 1. Diagnostic
manual palpation for locating the calculus.
a. Detection of a calculus or calculi or foreign
3. X-rays bodies whether they are radiopaque or
True occlusal of mandible to study calculus radiolucent (mucus plugs).
in the Wharton’s duct, Donovan’s technique b. Determination of extent of destruction of
to study calculus in deeper portion of the duct. gland secondary to obstructing calculi or
Cheek blow out AP view and intrabuccal foreign body so as to decide whether total
view (IOPA) to study parotid calculi. excision of gland is required or simple
Sialography: Radiographic procedure to lithotomy will suffice.
study ductal pattern of salivary gland. This c. Detection of fistula, diverticula or strictures.
involves introduction of dye in the ductal d. Detection and diagnosis of recurrent
system of salivary gland. Parenchymal swellings and inflammatory process.
abnormality, however, cannot be appreciated
e. Demonstration of tumour and determina-
by this method.
tion of its location, size and origin whether
4. Scintigraphy radiograph suggests benign or malignant
Radioactive isotopes like technetium tumour.
pertechnate-99m f. Selection of a site for biopsy
Salivary Gland Disorders 187
g. Detection of residual stones, residual Contrast Medium

tumor, fistula, stenosis or retention cyst a. Water-soluble media (iodinated):
following surgical procedures. • Conray 420
h. Outline plane of facial nerve as guide in • Conray 280
biopsy or surgery. • Hypaque
• Renografin
2. Therapeutic
• Sinografin
Introduction of dye causes dilatation of ductal b. Oil-based media:
system during study may aid in drainage of a
• Iodised oil
ductal contents, e.g. flushing out of small
• Ethiodol
mucus plugs.
• Lipidol
Limitations
Properties
Useful primarily for the study of diseases
i. Should have physiologic properties like
involving ductal system.
saliva
Contraindications ii. Miscible with saliva
a. Patients with known sensitivity to iodine iii. No toxicity
compounds iv. It should be radiopaque
v. Low surface tension and low viscosity to
b. History of asthma
allow the filling of the smaller ductules.
c. Anaphylaxis following use of iodine vi. It should be easily eliminated.
compounds
vii. It should be detoxified by liver and
d. History of urticaria and hypotension excreted through kidney.
e. Sialography performed during a period
Procedure
acute inflammation of gland, may lead to
leakage of dye into the parenchyma and a. X-rays: Pre-procedure radiographic
connective tissue, causing severe foreign evaluation to localize calculus if any and to
body reaction, as in acute inflammation study any bony defects.
ductal epithelium becomes thin and gets b. Procedure: In case of diminished secretion
disrupted. it becomes difficult to localize the ductal
orifice in such cases a piece of lemon can be
f. Administration and retention of iodine
used to increase secretion. Cotton rolls are
contrast medium may interfere with
used to dry the area, the gland is massaged,
subsequent thyroid function test. Such
appearance of a drop of saliva helps to
studies should be performed prior to
localise ductal orifice.
sialography.
Lacrimal dilator is used to cannulate and
Complications dilate the ductal orifice. Thereafter a cannula
i. Chronic inflammatory process may be attached to a plastic catheter is gently
introduced into the ductal orifice and then
aggravated by this procedure.
radiopaque dye is injected gradually with the
ii. Overdistention of gland may cause help of a syringe attached to the catheter.
temporary swelling and discomfort for a Around 2–3 ml of radiopaque dye is injected,
few hours or a few days. radiographs are obtained when the patient
iii. Extravasation of contrast medium may starts getting a sensation of fullness in the
lead to foreign body reaction. salivary gland under study.
• For Wharton’s duct occlusal and lateral 6. Antiviral activity—HIV infection

oblique view are taken. 7. Digestive properties, e.g. amylase helps in
• For Stenson’s duct transpharyngeal and AP digestion of carbohydrates.
view are taken.
Aberrant/Ectopic Salivary Gland
• Same views are again taken at evacuation
phase. Salivary glands may be developed at an
unusual site such glands are referred to as
• Normal salivary gland appear as leafless
aberrant.
tree pattern in sialography.
Common sites are parabuccal and retro-
• Sialoadenitis appears as apple tree in
molar regions and such glands do not have
blossom.
ducts or secretory orifices. Aberrant glands
• Sjögren’s syndrome presents with elongated have also been found at the base of the neck,
delicate ducts and punctate, globular and at level of TMJ articulation, in the middle ear
cavitory sialectasis—branchless tree with and at the surface or within the mandible.
fruit-laden appearance.
• Benign tumor presents as ball in hand Aplasia or Hypoplasia
appearance. Absence of major salivary gland is rare and is
associated with cleft palate, mandibular facial
Scintigraphy
dysostosis.
Scintigraphy is carried out with Tc pertectanate
Hypoplasia of parotid gland is frequently
99m which is injected intravenously and after
observed in Melkersson-Rosenthal syndrome:
specified period with the help of gamma
Fissured tongue, facial palsy, salivary gland
camera images are made.
hypoplasia, cheilitis glandularis’.
Indications
Clinical Significance
1. Study of parenchyma for morphology of
salivary gland and to diagnose space Complete absence of salivary gland can lead
occupying lesions. to xerostomia.
2. Salivary function evaluation—diminished Accessory duct may open into major
in Sjögren’s syndrome salivary gland and this anomaly can be
diagnosed with the help of sialography.
3. To demonstrate accessory salivary glands.
Functions of Saliva Diverticuli
1. Lubrication of mucosa Pouches or out pockets of ductal system. It
may lead to stagnation of saliva and repeated
2. Mechanical
episodes of parotitis
3. Buffering
Diagnosis—sialography
4. Prevent tooth disintegration
a. Provides minerals for post-eruptive Sialorrhea
maturation, e.g. calcium and phosphate. Increased salivation
b. Forms a pellicle to protect enamel
Causes
c. Prevent tooth dissolution
d. Forms a glycoprotein and prevents a. Infancy
attrition and abrasion b. Before eruption of deciduous teeth (because
5. Antibacterial properties especially IgA and of lack of swallowing capacity)
lysosomes break up bacterial wall. c. Insertion of a new complete denture.
Pathologic Xerostomia (Dry Mouth, Asialorrhea)

Local mouth diseases 1. Diseases of salivary gland like aplasia,
a. ANUG hypoplasia, ductal obstruction, severe
b. Erythema multiforme sialoadenitis.
2. Administration of drugs
Systemic Diseases/Factors a. Chlorpromazine
a. Mental retardation b. Antihypertensives
b. Epilepsy c. Belladonna
c. Cerebral palsy and facial paralysis d. Tranquillizers
d. Alcoholic neuritis e. Tricyclic antidepressants
e. Obstructive esophagitis and GERD f. Anti-Parkinson’s drugs
f. Parkinson’s disease g. Antihistamines, atropine, ephedrine
g. Metallic poisoning, e.g. mercury, lead, iron 3. Systemic diseases
h. Medications such as pilocarpine, cevimeline, a. Fever
clonazepam, mercuric salts, etc. b. Dehydration due to loss of fluid in,
vomiting, polyuria, sweating, hemorr-
Clinical Features hage
1. Drooling saliva can cause social embarrass- 4. Psychologic factors: Fear, anxiety
ment and rejection 5. Physiologic: Menopausal
2. Angular cheilitis and skin infection (because 6. Irradiation of salivary gland
of perioral irritation). 7. Uncontrolled diabetes, hyperthyroidism
3. In severe cases, partial or total blockage of 8. Vitamin A and B complex deficiency
air space can occur and can give rise to 9. Sjögren’s syndrome
aspiration pneumonia. 10. Mikulicz’s disease
Treatment Clinical Features

Depends upon etiology of sialorrhea: Patient complains of severe dryness, burning
sensation, inability to chew and swallow food
1. Physical method: Speech and swallowing (dysphagia).
therapy to increase neuromuscular control
• On clinical examination
2. Medications: Such as scopolamine, propan- • Pale, dry and inflamed mucosa with erythe-
thelene, diphenhydramine matous lesions
• Amisulpride 400 mg/day produce signi- • Cracks, fissures at the commissures
ficant improvement • Glistening
• The underlying causes like GERD, GI tract • Irritation caused by dentures and also
disturbances should be treated diminished retention of dentures.
• Intraglandular botulinum toxin injection • Rampant caries
can be used to improve sialorrhea in
Diagnosis
Parkinson’s disease and cerebral palsy.
On the basis of clinical features and history.
3. Surgical: Redirection of submandibular and
parotid ducts. Treatment
Duct ligation has been tried for major 1. Symptomatic treatment:
salivary glands but can cause complications • Sugarless oral rinses, mouth washes and
like ranula formation, pain, swelling, etc. gels increased fluid intake
Topical application of paraffin, almond oil,

Aloe vera and vitamin E products and cold
cream or silicone fluid or petroleum jelly
as moisturisers.
2. Artificial saliva (wet mouth, ora lube)
3. Removal of cause.
4. Drugs
a. Nicotinamide 300–400 mg t.d.s. for 10
days.
b. Pilocarpine 5–10 mg 3–4 times specially
before meals
c. Cevimeline HCl 30 mg t.d.s.
(Pilocarpine and cevimeline are contra-
indicated in pulmonary and cardio- Fig. 12.1: Sialogram showing sharp bend in the
Wharton’s duct (coma area)
vascular diseases and glaucoma)
d. Neostigmine bromide 7.5 mg t.d.s. • Submandibular gland saliva contains more
(Side effect increased peristalsis) of calcium and phosphorus.
• Saliva is more viscous, mucinous and
SIALOLITHIASIS alkaline compared to parotid secretions.
It is the formation of calcified organic matter, • The Wharton’s duct is longer and has
developed in the secretory system of major tortuous course.
and minor salivary glands. • Ductal orifice is small and lumen is larger
Composition possibly leading to stasis of saliva.
• Ductal orifice is at higher level and gland
Organic matter or nidus covered with shells
is at lower level possibly leading to salivary
of calcified material. The structure of sialoliths
pooling due to gravity.
is crystalline primarily composed of hydroxy-
apatite. Chemical composition is calcium • The Wharton’s duct takes right-angled bend
phosphate, traces of carbon, magnesium, KCl, posterior to mylohyoid muscle, this area
NH3. is termed as coma area (Fig. 12.1) and
sialoliths occur more commonly seen in this
Exact cause not known
region.
Factors leading to sialolithiasis:
Parotid Gland
a. Trauma
b. Infection Stenson’s duct opening is at higher level
compared to the gland and also it pierces the
c. Intake of drugs leading to salivary buccinator and takes a right-angled turn to
stagnation open into parotid papilla. Despite these points
Commonly seen in submandibular gland similiar to Wharton’s duct, sialoliths are not
80–90% so common in the Stenson’s duct because
Parotid gland 5–15% mainly salivary secretions are serous.
Sublingual 2–5% Clinical Features
Single or multiple calculi may be formed. a. The patients may have no symptoms and
Sialoliths are more common in submandi- sialolith may be detected during routine
bular duct and gland because: radiographic examinations.
b. Xerostomia is absent in patients with small

calculi.
c. If sialolith causes partial or total blockage
of the affected duct, pooling of salivary
secretions takes place just before meals
leading to transient pain and swelling of the
affected gland which reduces itself after
meals.
d. Clinical examination shows diminished
secretion on the affected side and at times
frank pus is expressed on applying digital
Fig. 12.2: Occlusal view showing multiple sialoliths
pressure on the gland.
in Wharton’s duct
e. Complete blockage often gives rise to
recurrent/chronic swelling which is tender.
Chronic stagnation of the salivary secretion
can give rise to progressive pressure
atrophy leading to destruction of the gland.
f. In certain cases a fistula, sinus tract or ulcer
may occur over the calculus.
g. The presence of calculus can be ascertained
with digital palpation.
h. Other complications from sialolith includes
acute sialoadenitis and strictures.
Diagnosis
a. History
b. Bimanual/bidigital palpation
c. Radiographs
• Lateral oblique
• Occlusal view with reduced exposure Fig. 12.3: Deeply located sialolith visualized on
(Fig. 12.2) occlusal view taken by Donovan’s technique
• Donovan’s technique (Fig. 12.3)
d. Sialography may show filling defect
(Fig. 12.4)
Treatments
Removal of calculus
• If small, removal by probing and by milking
duct.
• If large surgically removed.
• Complete removal of gland may be
advocated in cases where there is complete Fig. 12.4: Sialogram showing filling defect caused
destruction. by sialolith
• Lithotripsy and sialoendoscopy may be • Adults may be affected

helpful and non-invasive treatment for • After the incubation of 2–3 weeks salivary
sialolithiasis. gland inflammation and enlargement
occurs with preauricular pain.
Chronic Necrotizing Sialometaplasia • Associated with malaise, fever and
Benign, self-limiting, reactive inflammatory anorexia.
disorder of salivary tissue of unknown • Enlargement of salivary gland which are
etiology. Could be related to local ischemia tender and present difficulty in eating, if
or infectious process. partial ductal obstruction occurs.
• The ductal orifices are inflamed but there
Clinical Features
is no purulent discharge.
1. Males are mainly affected mostly in 5–6th • One gland may become symptomatic
decade. 24–48 hours before the other gland.
2. Primarily affects palate, lip and retromolar • It may spread and cause bilateral involve-
area. ment. Parotid swellings invariably give rise
3. It has a rapid onset and starts as a tender to raised ear lobules.
erythematous nodule which breaks down • All glandular structures may be affected.
to form a deep ulcer with yellow base. • It is seen in epidemics.
4. Compared to the large size pain is moderate Complications
or dull.
• Myocarditis
5. These lesions occur shortly after surgical • Meningitis and encephalitis
procedures and also have been reported to
• Orchitis, sterility
be connected to vomiting episodes in bulimia.
• Deafness
Diagnosis requires biopsy and histo- • Oophoritis
pathology of the lesion. The lesion does not
• Thyroiditis
shows any evidence of malignancy.
• Pancreatitis
Differential Diagnosis Differential Diagnosis
Major aphthae (associated with history of a. Acute parotitis of infectious origin shows
recurrence and severe pain). the presence of pus discharge.
Malignancy (mucoepidermoid carcinoma, b. Acute alveolar abscess associated with
adenoid cystic carcinoma or squamous cell carious tooth or pericoronitis with no dis-
carcinoma). placement of ear lobule.
c. Recurrent parotid swelling of non-
Treatment inflammation due to sialoadenosis is non-
This is a self-limiting condition and healing tender, soft and of long duration.
takes place within 6–8 weeks.
Treatment
Debridement of the lesion and saline rinses
Prevention with live attenuated vaccine (MMR).
helps in the healing process.
Systemic corticosteroid for painful testicular
Recurrence is rare. involvement.
Mumps/Non-suppurative Parotitis Acute Bacterial Sialoadenitis
• Caused by paramyxovirus Bacterial infections of the salivary glands are
• Most common in children 4–6 years commonly seen in patients with decreased
salivary flow in debilitated and dehydrated • Patients are instructed to milk the gland
patients. several times throughout the day
In the past, retrograde bacterial infection • Stimulation of salivary secretion by sucking
were seen in the patients who have undergone on candy
general anesthesia as a result of xerostomia • Surgical drainage in acute condition
and dehydration secondary to administration • Improvement of oral hygiene
of anticholinergic drugs (as preanesthetic • IV fluid and electrolytes
medication). • Intraductal instillation of penicillin or
In recent times, majority of bacterial infec- saline.
tions occurs in patients with reduced salivary
Allergic Sialoadenitis
flow as there is diminished mechanical
flushing of bacteria which tend to colonise the History of allergy, asthmatic attack
oral cavity and then colonise the duct. • Asymptomatic enlargement or with itching
Although, sialoliths occcur more often in over the gland
submandibular gland, bacterial sialoadenitis • History of change in or new intake of drug
occurs more frequently in parotid gland. It is • Most common drugs associated are etham-
believed that submandibular salivary gland butol, phenobarbital, iodine compounds
secretion has high level of mucin which has and heavy metals.
potent anti-microbial activity, tongue move-
Diagnosis
ments tend to clear the floor of mouth and
protect the Wharton’s duct. Parotid papilla is Diagnosis should be made with caution, if
located adjacent to molars where heavy there is no rash and edema.
bacterial colonization occurs. Treatment
Clinical Features Self-limiting disease
Fever with sudden onset of unilateral or • Avoiding the allergens
bilateral salivary gland enlargement. • Monitoring the patient and prevention of
• Intense pain in salivary gland region. secondary infection.
• Tender, warm, enlarged gland with red skin Sarcoidosis
• Purulent discharge from orifice of Stenson’s
• Bilateral firm painless enlargement
duct
involving the parotid gland
• Leukocytosis
– Decreased or absent salivation
Diagnosis – Sarcoid infiltration is associated with
Purulent discharge expressed can be cultured Heerfordt’s syndrome which is chara-
for various organisms mainly Staphylococcus cterized by:
aureus, H. influenzae, S. viridans, Prevotella and Infection and swelling of parotid gland
Fusobacterium. with fever

Ultrasound, CT scan, and MRI are useful Inflammation of uveal tract of eye
in the diagnosis. Facial palsy.
Treatment Diagnosis
• High antibiotic dose—penicillinase-resistant Biopsy of the minor salivary gland can confirm
antistaphylococcal antibiotics. the diagnosis of sarcoidosis with non-
• Culture antibiotic sensitivity test caseating granuloma.
Treatment Diagnosis
Mainly palliative corticosteroids and other Ophthalmic tests
immunosuppressive and immunomodulator 1. Schirmer’s test: In normal patients 15 mm of
drugs are used. the filter paper is wetted when placed in
lower conjunctival sac for 5 minutes, but in
Sjögren’s syndrome SS only 5 mm.
Autoimmune disorder of exocrine glands first 2. Rose Bengal dye test: Denuded and damaged
described by Henrick Sjögren in 1933. areas of the cornea can be visualized clearly
• Primary Sjögren’s syndrome (SS) is with this dye.
associated with salivary and lacrimal 3. Break up time test: A slit-lamp is used and
glands dysfunction without any auto- interval between complete blink and
immune condition. appearance of dry spot on the cornea is
• Secondary Sjögren syndrome is chara- noted.
cterized by: Salivary gland function is assessed by:
– Lacrimal gland involvement causing 1. Salivary flow rate is diminished in SS.
ocular dryness 2. Minor salivary gland biopsy taken from
lower labial mucosa.
– Salivary gland involvement causing
3. Scintigraphy: Technetium pertechnate 99m,
decreased salivation (xerostomia)
in SS diminished uptake and excretion of
– Along with autoimmune disorders such isotope in the saliva.
as: Rheumatoid arthritis, SLE. 4. Sialography shows thinning of the ducts
Clinical Features
and decrease in the number of ductules. The
typical sialography appearance is described
Post-menopausal women are most commonly as punctate, globular and cavitory pseudo-
affected (40–60 years). sialectasis. It is termed as pseudosialectasis
a. Lacrimal gland involvement gives rise to because the appearance is due to the
dryness of the eyes and continuous feeling pooling of the dye in periductal area and
of dirt or foreign body in the eye. not because of the dilation of the ductules.
Conjunctivitis and corneal ulceration also Overall description is given by the term
a common feature. branchless tree with fruit-laden appearance
b. Dryness of pharynx, larynx and nasal cavity (Rankow) (Fig. 12.5A).
may lead to pneumonia. 5. MRI shows salt and pepper appearances of
the enlarged salivary glands (Fig. 12.5B).
c. Xerostomia—severe dryness of the oral
cavity causing difficulty in speech, mastica- Immunological tests
tion and deglutition. Presence of autoantibodies against anti-SS A
d. Minimum salivation in the oral cavity, if and anti-SS B.
present saliva is thick and ropy. Mirror Treatment
head, tongue blade gets stuck to the mucosa
1. Medical consultation for prevention of
during examination.
pneumonia.
e. Dry and cracked lips with angular cheilitis. 2. Regular examination by ophthalmologist.
f. Oral mucosa is dry and glistening, tongue 3. To manage xerostomia
appear depapillated and at times lobulated. a. Salivary substitutes with topical methyl
g. Candidiasis and increased dental caries are cellulose (Oralube ®, Xero-Lube ® wet
also observed. mouth), continuous with the water.
A B
Fig. 12.5: (A) Sialogram showing branchless fruit-laden tree appearance in Sjögren’s syndrome, (B) MRI
showing salt and pepper appearances of parotid glands
b. Pilocarpine 5 mg 1 tab t.d.s.

c. Cevimeline 30 mg 1 tab t.d.s.
d. Bromhexine
4. Dental considerations
a. Daily use of topical fluoride rinse
b. Topical application of nystatin and
clotrimazole to control candidiasis
c. Patients of SS may be on steroids or
immunosupressants for the treatment of
SLE or rheumatoid arthritis, therefore
one must take precaution against infec-
tion preceding oral surgical procedures.
5. Additional drugs
Fig. 12.6: CT scan multicentric cyst in parotid gland
a. Methotrexate
b. Oral interferon α: 150 IU daily a. Hyperplastic lymph nodes
c. Antimalarial drugs: Hydroxychloroquine b. Lymphocytic infiltrate
d. Rituximab (rituxan), an anti-CD20 mono- c. Cystic cavities
clonal antibody.
Treatment
HIV Associated Salivary Gland Disease Treatment is symptomatic with salivary
Patients with HIV infection may experience substitutes.
salivary gland disease either from AIDS related Salivary gland condition improves with
tumours, i.e. lymphoma, or because of HAART.
Sjögren’s syndrome like condition of unknown
etiology. Sialoadenosis
Such patients on labial biopsy shows It is a non-neoplastic, non-inflammatory
similar changes like Sjögren’s but with pre- enlargement of the salivary gland.
ponderance of CD8 lymphocytes. Parotid glands are more often involved than
On CT and MRI, large multicentric cysts are the submandibular glands. Swelling of pre-
detected within the enlarged parotid glands. auricular portion is more common than the
This enlargement is due to: retroauricular.
Sialochemistry shows increased salivary

potassium and decreased salivary sodium
levels.
Sialoadenosis may occur in a variety of
conditions:
1. Hormonal sialoadenosis associated with
menarche, pregnancy, menopause, etc.
2. Diabetic sialosis
3. Associated with alcoholism
4. Associated with malnutrition specially with Fig. 12.7: Dome-shaped bluish swelling on the lower
lip—mucocele
protein deprivation.
5. May be because of drug administration like to salty discharge following which the
iodine containing drugs, phenylbutazone. lesion deflates, but recurrence is common.
On sialographic examination, the ducts and c. Size varies from 4 mm to 1 cm.
ductules appear to be splayed.
Treatment
Treatment 1. Surgical excision helps to prevent re-
Treatment is symptomatic and is related to the currence, however, adjacent minor salivary
management of causative factors. gland ducts can get traumatized and lead
Mucocele to new mucoceles.
2. Intralesional steroid injections have been
This is a term used to describe swelling caused
by pooling of saliva at the site of injured minor tried.
salivary gland duct. Ranula
It is of two types: Ranula is large mucocele located in the floor
1. Mucus extravasation: It is the common of mouth. It may be because of mucus extra-
mucocele caused by trauma to the minor vasation or mucus retention.
salivary duct giving rise to extravasation of
saliva/mucus in the adjacent connective Clinical Features
tissue. This is surrounded by an area of a. The term ranula is used because of its
inflammation and formation of granulation resemblance to the swollen belly of a frog.
tissue but does not have any epithelial cyst b. It presents as a painless, slow growing, soft
wall, even if it is termed as a cyst. and movable mass located in the floor of
2. Mucus retention cyst: It is less common and the mouth (Fig. 12.8).
caused by the obstruction of minor salivary
duct. The continuous pressure of accumu-
lated salivary secretion forms a cyst-like
lesion which can be lined by epithelium of
dilated duct.
Clinical Features
a. More common in lower lip because it is
more prone to trauma, other sites are buccal
mucosa, floor of the mouth, etc.
b. Typical mucocele appears as a thin-walled
bluish, rounded swelling on the lower lip
(Fig. 12.7) that ruptures easily giving rise Fig. 12.8: Bluish swelling in the floor of the mouth
c. Superficial may appear blue in color and

deeper ranulas may have normal appea-
rance.
d. Deep ranula which herniates through the
mylohyoid muscle and extends along the
fascial planes to the neck region is called
plunging ranula.
Diagnosis
a. Radiography helps to rule out sialolith.
b. Injecting radiopaque dye to delineate
borders and full extent of the lesion.
c. MRI will show cystic lesion giving hyper-
intense signal on T2-weighted image. Fig. 12.9: Nodular swelling on the right parotid
elevating the ear lobule (s/o pleomorphic adenoma)
Treatment
a. Surgical intervention: Marsupialization and the superficial lobe. The size of the tumor
excision varies from several centimetres to very large,
b. Intralesional injection of corticosteroids if left untreated.
Intraorally, occurs more often on palate,
Salivary Gland Tumors followed by upper lip and buccal mucosa as
They may be classified as: a well-defined firm and non-fluctuant mass
1. Benign with normal mucosal coverage.
2. Malignant Diagnosis
Majority of the salivary gland tumors (80%)
As this tumor has good vascular supply, it
occur in the parotid gland. 10–20% occur in
shows enhancement with contrast on CT scan.
submandibular gland and the remaining in
On MRI, it presents as well-demarcated
sublingual and minor salivary glands. lobulated hyperintense swelling within the
80% of parotid and 50% of submandibular substance of the gland (Fig. 12.10).
and minor salivary gland tumors are benign
in contrast 60% of the tumors in sublingual Treatment
gland are malignant. • Superficial parotidectomy.
Pleomorphic Adenoma – Lesions in submandibular gland are
treated by complete removal of the entire
Most common tumor of salivary glands and gland.
majority of these are found in parotid glands.
• It is called mixed tumor because it consists Mucoepidermoid Carcinoma
of epithelial and mesenchymal elements. • Most common malignant salivary gland
• It accounts for 60% of tumors. tumor.
• 4–6th decade. – 60–90% occur in parotid gland and palate
is the second most common site.
Clinical Features
– 3–5th decade.
Slow growing, painless and firm mass which
elevates the ear lobule, if present in parotid Clinical Features
gland (Fig. 12.9). • Low grade tumor shows a long period of
In parotid gland, these neoplasms are most slow and painless growth may resemble
commonly seen in posterior-inferior aspect of pleomorphic adenoma.
A B
Fig. 12.10: MRI image showing nodular tumor mass in the right parotid
– High grade tumor grows rapidly, produce – Intraorally, adenoid cystic carcinoma
pain and ulceration of overlying tissue and presents as mucosal ulceration which
shows early metastasis. help it to distinguish from benign mixed
– Facial nerve palsy may be seen. tumor. Metastasis into lungs is more
common.
Treatment
• Treated by superficial parotidectomy or Treatment
total parotidectomy depending upon the Radical surgical excision. Because of ability of
extent of the lesion. the lesion to spread along the nerve sheaths,
– Postoperative radiation therapy is useful remaining cells can give rise to long-term
adjunct. recurrence even after aggressive surgical
excision.
Adenoid Cystic Carcinoma (Cylindroma)
• 6–10% of salivary gland tumors. Suggested Reading
– Most common tumor of submandibular 1. Burket’s Oral Medicine, 9th, 10th and 11th
and minor salivary glands. editions.
Clinical Features 2. Diseases of the Salivary Gland, Maxillo-
facial Surgical Clinics of North America.
• It is usually presents as firm, slow growing
and unilobular mass in the gland. 3. Diseases of the Salivary Gland, Rankow.
– Occasionally the tumor is painful. 4. Oral and Maxillofacial Pathology by
– If parotid gland is involved facial nerve Neville, 3rd edition.
palsy can occur. 5. Shafer’s Textbook of Oral Pathology, 6th
– It spreads by perineural invasion. edition.
13
Orofacial Pain
Pain is by far the most common symptom with B. Non-neuropathic

which the patient presents to the dental Pain originating from structures other than the
clinician. nerve
It is stated, “There was never yet a Philosopher • CNS
who could endure toothache patiently!” • Extraneural
Pain may be defined as an unpleasant – Dental pain
sensation produced by a noxious stimulus – Adjacent alveolar mucosa
carried as an impulse along a nerve track to – Musculoskeletal
the CNS where it is interpreted as such. – Vascular—migraine, cluster headache,
etc. Migrane—now believed to be neuro-
As per International Association for Study
vascular.
of Pain (IASP), pain is—“An unpleasant
– Referred
sensory and emotional experience associated
with actual or potential tissue damage or C. Unknown Nature
described in terms of such damage.” • Atypical neuralgia
• Psychogenic pain
Classification of Orofacial Pain
Dental Pain
A. Neuropathic
a. Pulpal pain
Pain arising from actual pathology affecting
the nerve 1. Hyperactive pulp
• Hyperemia
• Paroxysmal
• Hypersensitivity
– Trigeminal neuralgia 2. Acute pulpitis
– Glossopharyngeal neuralgia 3. Chronic pulpitis
– Geniculate neuralgia • Open
• Nonparoxysmal • Hyperplastic
4. Necrotic pulp
– Postherpetic
5. Cracked tooth or trauma
– Post-traumatic
b. Periodontal pain
• Neoplasia 1. Periodontitis
– Along nerve 2. Periodontal abscess
199
c. Periapical pain A good mouth mirror, sharp explorer and

1. Acute apical periodontitis a good quality light is mandatory for detection
2. Acute apical abscess of caries. Occlusal caries is easily detectable,
3. Chronic apical periodontitis marginal ridges have to be carefully observed
4. Suppurative apical periodontitis for the presence of opacity (lack of trans-
5. Apical cyst lucency) which is associated with proximal
d. Pericoronitis, dry socket caries.
e. Dentin and cementum exposure • Upper and lower third molars. buccal
f. Occlusal trauma surface and distal surfaces of 17, 27 are more
g. Eruption and exfoliation prone to caries, and are most likely to be
h. Impacted unerupted supernumerary (IUS) missed during clinical examination, and
teeth hence these areas should be examined
i. Cracked tooth syndrome carefully.
j. Aerodontalgia • Periapical abscess, granuloma and cyst may
present with pain which may vary from
Adjacent Alveolar Mucosa severe to mild. Such teeth are tender to
1. Recurrent aphthae percussion. This can be diagnosed with the
2. Erosive lichen planus help of clinical examination of teeth and
3. Herpes simplex/zoster radiographs.
4. ANUG If the teeth are healthy then gingiva should
Musculoskeletal
be examined carefully for the cause of pain.
• Gingiva: Pocket, ulceration, ANUG,
1. Fracture, osteomyelitis periodontitis.
2. Excessive vertical dimension
It is also advisable to ask the patient to
3. Diseases of TMJ and MPDS occlude his teeth, do side to side move-
Practical Approach Towards ments and look for the evidence of occlusal
Diagnosis of Orofacial Pain trauma, e.g. premature contact, plunger
Whenever a patient presents with pain to a cusp, abnormally tilted teeth, etc. as these
dental surgeon, as a first step, tooth related factors can lead to persistent pain in the
causes should be ruled out, as follows: teeth which otherwise look normal. Teeth
Tooth: Enamel should be examined for with periodontal abscess are tender on
attrition, abrasion, erosion, abfraction, lateral percussion, and the painful tooth is
hypoplasia, cracked tooth and carious lesions. easily localized by the patient unlike
Dentin exposure: In case of total wear of enamel, pulpitis affected tooth.
or deep caries, dentin is exposed or involved Many times the teeth and the periodontium
leading to hypersensitivity. are quite normal. At such times, other
Cementum: In cases where the abrasion and mucosal surfaces should be examined for
other wasting diseases involve the tooth at any pathology.
CEJ, cementum is lost, there by exposing root • Mucosa: Ulceration (aphthous, lichen
dentin. Loss of cementum also gives rise to planus, traumatic ulcerations)
bone loss. Cemental caries is also commonly The dental surgeon may encounter pain
seen in older individuals. which is related to the deeper structures,
Pulpitis: Either caries or the wasting diseases like the alveolar bone, e.g. dry socket, osteo-
of the teeth, or trauma, or cracked tooth, may myelitis.
lead to pulpitis which presents as excruciating If the examination of teeth, the perio-
pain. dontium, mucosa, and the alveolar bone
Orofacial Pain 201
reveals no cause for pain, one should suspect surgeon is unable to reach the diagnosis.
MPDS or pain of muscle origin, presenting Psychogenic: Patients presenting with pain
with tender trigger points commonly in of chronic nature, which cannot be attributed
masseter and temporalis muscles. Trismus to any of the above conditions, may be
which is due to spasm of masticatory muscles cautiously considered to be of psychogenic
can present with severe pain. origin. Such pains are constant, unanatomic,
At times, patients clearly complain of pain and can cross the midline and seen in patients
in the TM joint with clicking in which case TM who are rigid and unyielding. However, every
joint disorders should be suspected and effort must be made to rule out physical cause
investigated. These would include anterior for pain before labelling this type of pain as
disc displacement with or without reduction, psychogenic.
arthritis, etc.
Pulpalgia
Patients with neuralgia have distinct acute,
paroxysmal, lancinating, electric shock-like Pulpitis is the most common painful condition
pain precipitated by stimulation of the ‘trigger which brings the patient to the dentist. Caries,
zone’. Despite these characteristic features, cracked tooth, trauma can precipitate pulpitis.
mistaken diagnosis of pulpitis and subsequent Acute pulpitis pain is the most severe pain,
needless endodontic treatment or extractions and it is caused by the severe pressure exerted
have been carried out. on the apical nerve endings because of
Patients who present with unilateral inflammatory changes within the pulp. The
throbbing pain with rapid pounding pulsa- pain is unbearable and increases on lying
tions should be suspected to have pain of down. Pulpitis pain is poorly localized and is
vascular origin, e.g. migraine with or without relieved after excavation of caries with/
aura, cluster headache (pain localized behind without extirpation of pulp.
the eye), temporal arteritis (with visible Reversible pulpitis: Exaggerated quick, sharp
throbbing of the artery). response to cold stimulus, followed by dull
Salivary gland pathologies, like sialolithiasis, ache that disappears; there is no pain on
sialoadenitis, mumps, present with pain and percussion and no radiographic evidence of
swelling of the affected gland with diminished periapical abnormality. Usually after
secretion. excavation of caries or removal of the cause
Maxillary sinusitis at times may be mistaken and restoration of lost tooth structure,
for toothache, but a history of rhinitis, blocked symptoms abate and root canal treatment is
ostium, and unilateral heaviness, increased not required.
pain on bending down and foul discharge can Irreversible pulpitis: Spontaneous lingering
help to pinpoint the diagnosis. dull ache or constant severe unrelenting pain,
Many times the pain from distant organs aggravated by noxious stimuli, and positive
such as myocardium, ENT can be referred to response to cold and heat stimuli, radio-
the teeth. In such cases, absence of positive graphically periapical widening of PDL space.
findings on history, clinical examination and Treatment is either RCT or extraction.
radiography can help to rule out dental cause Chronic pulpitis pain is relatively milder.
for pain. However, diagnose cardiac or ENT In chronic open pulpitis, patient normally
cause of pain is a challenging task. Patients complains of pain after food impaction and
with cardiac complaint have the pain localized in chronic hyperplastic pulpitis, there is pulp
to the left angle of mandible and neck and is polyp with very mild pain. However, in both
relieved by nitroglycerine. It is prudent to seek these cases, patients stop chewing from that
expert advice in cases where the dental particular side, leading to excessive deposition
of calculus on the teeth of the affected segment Occlusal Trauma

sometimes even on occlusal surfaces! Sometimes patients having occlusal abnor-
Closed suppurative pulpitis: In this condition, malities such as premature contacts, high
inflammation leads to necrosed pulp which points in the restorations, plunger cusps may
further gets infected with pyogenic organisms. present with tenderness in the affected teeth.
As the pus is accumulated, and confined to a Such symptoms get aggravated, if patients
very limited area within the tooth, the pressure also have clenching habit or bruxism.
exerted on the apical nerve endings is
tremendous so that patient is literally crying. Bruxism: Pain in masticatory muscles on
LA injection followed by pulp extirpation awakening, persistent grating sound
brings immediate relief to the patient. produced by the patient with nocturnal
bruxism is more disturbing to the spouse!
Periapical Pain
Such patients present with:
This is moderate to severe spontaneous pain • Facets on teeth, unusually severe attrition
that is sharp, throbbing or aching in nature. in younger individuals
The tooth in question is nonvital, tender to
• Indentations on tongue
percussion, more so, if the abscess is confined
to the bone. The abscess may present in the • Prominent linea alba
soft tissues presents as fluctuant pus filled • Masticatory muscle fatigue and pain
swelling extremely tender to palpation, or if especially worse on awakening
there is a fistula formation, the severity of the Such cases respond to occlusal adjustment
pain is less. after the detection of premature contacts and
Acute apical periodontitis: There is a mouth guard to minimize the clenching/
complaint of spontaneous pain which is bruxing habit.
moderate or severe, the tooth involved is
nonvital and tender to percussion. Patient Cracked Tooth Syndrome
complains of severe pain on biting on that Associated with incomplete fracture of tooth
tooth, and radiographic findings include break which may or may not extend to the pulp.
in lamina dura and widening of PDL space. When pulp is involved, patient starts
Such type of pain is also observed at the complaining of severe pain, which is sharp
second seating after inadvertent over- and momentary and is stimulated by biting
instrumentation during endodontic treatment and releasing. Pain in this condition is more
of affected teeth. commonly noted with the release of biting,
Acute apical abscess: It is characterized by owing to the fluids within the dentinal
rapid onset of spontaneous pain and swelling tubules moving to the pulp.
of gingival and alveolar mucosa. Sometimes Patients give history of either habitually
it is confined only to the bone. Radiographi- eating hard substances or inadvertently biting
cally periapical changes may or may not be on hard substance:
present. • Areca nut chewing
Chronic apical abscess: This is due to long-
• Bottle opening/electricians stripping wires
standing focus of infection, with a little or no
with teeth
discomfort to the patient. There is a presence
of a fistula or a sinus tract. • Hard substance eaten
Patients having periapical lesions have to • More common in upper premolars with
be treated with endodontic treatment with or prominent cusps
without periapical curettage and in certain • Teeth having large proximal restorations
cases by extraction. more susceptible to cracks
Orofacial Pain 203
• Continuous and severe pain caused by 4. Damage caused to the interdental papilla
pulpitis. by matrix band and wedge
– Tooth may or may not have filling. 5. No lining given or calcium hydroxide
– Tooth extremely sensitive to percussion dressing not given in pulp exposure cases.
6. Certain composite restorations are highly
Diagnosis technique sensitive and may induce pain in
One should suspect cracked tooth in patients the teeth after a period of time if all steps
who complain of severe pulpitis type of pain are not scrupulously followed.
and the tooth involved is not carious or 7. Leakage; fractured fillings, amalgam restora-
discoloured and the pain is aggravated on tion sunk in the cavity—ditched amalgam
mastication. Teeth having large restorations 8. High points
with a little healthy enamel, dentin intact Galvanism: Two dissimilar metallic fillings
should also raise the suspicion. act as electrodes with saliva as electrolyte.
1. Dry and isolate the tooth. Apply disclosing Patient complains of pain for a brief period
solution for crack to become visible. on closing mouth. This type of pain is also seen
2. Lead shot or no. 1 round bur is also used when filling is touched with probe, spoon,
after covering it with cellophane and asking fork, pin, etc.
patient to bite on it.
3. Ask patient to bite on blunt end of instru- Treatment
ment. Alkaline mouth washes are given, because
4. High intensity light (transillumination) acidic pH of saliva (acting as an electrolyte) is
directed towards the tooth makes the crack necessary for transmission of current.
visible. Adequate replacement of the fillings to over-
5. Use of a plastic probe which shows come the problem of galvanism.
evidence of pocket only in the region of Dry Socket, Alveolar Osteitis
crack helps in the diagnosis.
Not an uncommon post-extraction complica-
Treatment tion wherein pain appears 2–3 days after
If crack involves pulp then pulpectomy extraction.
followed by full crown. Use of orthodontic Pain is severe localized to the socket,
bracket for stabilization and more perma- aggravated by temperature changes.
nently a crown or overlay is indicated. At On examination—absence of clot, fetid
times the crack is deeper and leads to odor, exposed bone in the wall of the socket
irreparable fracture of cusps and extraction of extremely tender due to bare nerve endings.
the involved tooth is the best treatment option. Probable etiological factors for occurrence
of dry socket:
Pain in Filled Teeth
• Due to excessive vasoconstriction, clot not
It occurs because of: allowed to form
1. Residual caries (incomplete excavation of • Due to severe infection, clot may not be
caries) retained
2. Secondary caries (caries beneath the • Organisms like Treponema denticola causing
restoration) lysis of the clot.
3. When intermittent cutting and cooling of
the tooth is not done during cavity Treatment
preparation, pulp will get inflamed leading • Irrigation of socket
to pain. • Control of infection
• Induction of bleeding or freshening of • The patient characteristically has photo-

wound (curetting, surgical debridement phobia, lies down in a dark room and tries
and give sutures). to fall asleep.
• Acryflavin, iodoform, ZOE dressing given
blocks the stimuli and controls the pain as Treatment
the socket heals from the base, but this • Assessment of food triggers
process takes time. • Minimize stress by relaxation techniques
• Commercial preparation like dry socket • Ergotamine tartarate 1–2 mg sublingually,
pastes (alvogyl packed loosely in the sumatriptan given orally, nasally, rectally,
cleaned socket, metronidazole ointment or parenterally are useful in aborting attack.
(metrogyl DG gel) applied locally also helps.
• Drugs used for prevention are propranolol,
• Antibiotics and analgesics to control
verapamil, tricyclic antidepressants like
infection and pain.
amitriptyline.
Maxillary Sinusitis • Methysergide or monoamine oxidase
1. History of attack of common cold, allergic inhibitors such as phenelzine can be used
rhinitis, nasal block to manage difficult cases that do not
2. Heaviness in face, pain increases on respond to safer drugs.
bending or moving head
3. Upper posterior teeth tender to percussion Cluster Headache
4. Nasal twang, fetid odor—halitosis It is associated with throbbing pain with
5. Postnasal discharge followed by tonsillitis rhinorrhea, lacrimation with flushing and
swelling of face.
Treatment
It is a distinct pain syndrome caused by
Antibiotics, decongestants, otrivin nasal episodes of severe unilateral pain occurring
drops, steam inhalation. chiefly around the eye and accompanied by a
number of autonomic signs.
Vascular Pain (Migraine)
• Throbbing pain where 1st vasoconstriction Patients describe the pain as sudden and
of intracranial vessels occurs (which causes stabbing ‘hot as metal rod in and around the
neurological symptoms) followed vasodila- eye’
tion (which results in pounding headache). • Multiple headaches per day for 4–6 weeks
Now considered to be neurovascular. (hence called as cluster headache) followed
• Usually unilateral by pain-free period for months to years.
• Triggered by foods such as nuts, chocolates, • Sudden, unilateral and stabbing pain
stress, sleep deprivation or hunger. causing patients to pace, cry out, strike
• 4 types of migraine are present—classic, objects (as opposed to the behavior of
common, basilar and facial. migraine patients, who lie down in dark
• History of aura—seeing certain flashing of room and try to sleep).
light or shiny objects in front of eyes, which
• No history of aura
lasts for 20–30 mins.
• Aura is followed by increasing severe • Painful episodes at night
unilateral throbbing headache that is • Autonomic signs such as nasal congestion,
frequently accompanied by nausea and lacrimation, sweating of face, ptosis,
vomiting. Headache lasts for a few hours increased salivation and edema of eyelid are
to 2–3 days. accompanying signs.
Orofacial Pain 205
Treatment • Unilateral pain along course of nerve

• Abortion of acute attack with 100% oxygen • Half inch sign—when patient is asked to
• Sumatriptan 50 to 100 mg/day and/or shows the location of pain, he keeps the
ergotamine (1 mg tab sublingually) 2 to finger ½ an inch away to avoid precipitating
4 mg/day are useful therapy the pain attack.
• Lithium is effective for those who can • Cheshire cat smile
tolerate the side effects • No pain between 2 episodes (refractory
• Prevention by ergotamine, prophylactic period)
prednisone and calcium channel blockers • No loss of sensation
• Antihypertensive drugs like nifedipine, • Most common affected branch is the
CO2 inhalation. maxillary division of trigeminal nerve and
Barosinusitis the trigger zone is ala of the nose and upper
lip.
As a result of inflammation or allergy, ostium
gets blocked because of unequal pressure, i.e. Etiology
atmospheric and sinus pressure leading to i. Believed to be due to cross-connection
pain. Seen in pilots and divers and patients between thermo-, noci-, and mechano-
travelling at high altitudes (aerodontalgia). receptors probably because of pressure
Ice-cream Headache and demyelination.
Cold foodstuffs such as ice-cream when ii. Pressure from anterior-inferior cerebellar
swallowed transmits the cold impulses artery and superior cerebellar artery on the
through the walls of the pharynx to the carotid trigeminal nerve root.
arteries giving rise to constriction of the vessel, iii. 10% cases associated with tumors of cere-
which further causes constriction of its bellar pontine region, plaques associated
tributaries and branches resulting in pain. with multiple sclerosis and aneurysms.
iv. Most accepted theory is atherosclerotic
Trigeminal Neuralgia or Tic Douloureux
plaques associated with superior cerebellar
Acute short-acting paroxysmal lancinating artery pressing on the root of trigeminal
pain which lasts for a few seconds and some- nerve.
times a few minutes.
Unfortunately this condition gets mis- Treatment
diagnosed as pulpitis or pain of dental origin i. Rule out dental cause and avoid extraction
and unwarranted and ineffective treatment or endodontic treatment if the exact cause
(extractions) is often meted out to the patient. of pain cannot be diagnosed with certainty
It is a sad yet true when it was stated that as of dental origin.
“nowhere in the history of dentistry so much
ii. Give tegretol (carbamazepine) 200 mg t.d.s.
has been done for so many with so little
depending on severity. Side effects of
benefit” and the common presentation of
carbamazepine—nausea, dizziness,
patient with trigeminal neuralgia is uni-
laterally edentulous jaw! drowsiness, hematologic abnormalities,
rarely erythema multiforme like reactions.
• Trigger zone, i.e. an area on the skin or the
mucosa, stimulation of which triggers iii. Carbamazepine in combination with
paroxysm of pain. Even light touch or baclofen. Baclofen dose—10 mg/day
breeze is enough to cause paroxysm (unlike maximum 80 mg/day.
trigger point in MPDS where digital iv. Phenytoin, lamotrigine, topiramate, and
pressure is required). pimozide are also effective.
v. Gabapentin is effective in certain cases. – Pain is due to inflammation and fibrosis

Dose—300 to 600 mg/day. of the nerve fibers, so that even general
vi. In case drug therapy is ineffective or sensation is perceived as pain.
patient is unable to tolerate side effects, Treatment
surgery is indicated.
• Topical therapy includes use of topical
vii. Surgeries at peripheral portion of nerve
anesthetic agents like lidocaine, analgesics
includes cryosurgery on trigeminal nerve.
like capsaicin or combinations of topical
viii. At the level of gasserian ganglion, proce- anesthetics like EMLA (eutectic mixture of
dure performed is percutaneous radio- local anesthetic—lidocaine and prilocaine)
frequency thermocoagulation (RFTC). capsaicin is believed to suppress substance
ix. Glycerol block and balloon micro- P at the nerve endings.
compression are also advocated.
• Gabapentin has fewer side effects and is
x. Gamma knife stereotactic radiosurgery better tolerated in elderly patients.
uses multiple beams of radiation to a
• Tricyclic antidepressants like amitriptyline,
focused point, which spares normal tissue
nortriptyline, doxepin and desipramine are
(especially useful in elderly patients with
also used.
high surgical risk).
xi. Injection of neurolytic material like boiling • Best therapy is prevention—the use of
water or absolute alcohol. antiviral drugs (famciclovir 500 mg/day or
valacyclovir 1000 mg/day) during acute
xii. Avulsion of concerned nerve, i.e.
phase of disease decreases the incidence
neurectomy.
and severity of post-herpetic neuralgia.
xiii. Rhizotomy—root of nerve is removed.
• Surgery at the level of peripheral nerve or
xiv.Vascular decompression with teflon
dorsal root in cases of intractable pain.
interposed between the superior cerebellar
artery and root of the nerve. • Use of steroids is controversial.
Post-herpetic Neuralgia Glossopharyngeal Neuralgia

In majority of the cases, pain associated with Pain similar to trigeminal neuralgia, but less
herpes zoster infection resolves in a month intense. The trigger zone is along distribution
following the healing of the lesions. Pain that of glossopharyngeal nerve—pharynx, poste-
persists longer than a month is known as post- rior tongue, ear. Pain is triggered by chewing,
herpetic neuralgia. talking, and swallowing.
Etiology Treatment
• Demyelination, wallerian degeneration and • It responds to carbamazepine and baclofen:
sclerosis of nerve due to varicella zoster – Percutaneous radio-frequency thermo-
virus coagulation of nerve at the jugular foramen.
• Increased age is a risk factor, higher in
women: Geniculate Neuralgia
– Pain is burning or itching type Paroxysmal pain associated of cranial nerve
– Pain is continuous VII. Pain is associated along the sensory
– Not paroxysmal distribution of cranial nerve VII, i.e. in ear,
– No trigger zone unlike classical anterior tongue, soft palate.
trigeminal neuralgia • Pain is not as sharp and as intense as
– History of herpes zoster trigeminal neuralgia.
Orofacial Pain 207
• History of herpes zoster of geniculate confirms the evidence that the source of pain
ganglion (Ramsay Hunt syndrome) is elsewhere.
Treatment • Patient should be specifically asked after
LA whether the tooth still hurts.
• Acyclovir reduces duration of pain
• Clinical features of cardiac toothache are
• Carbamazepine and antidepressants
pain is cyclic, increased with physical
Referred Pain exertion or exercise, toothache associated
Toothache as a symptom can present a with chest, left arm or neck pain.
diagnostic problem for the clinician, because • Toothache is relieved by nitroglycerin
pain felt in one tooth may be referred from tablet.
another tooth or from other orofacial struc- • Local provocation of the tooth does not alter
tures. To treat the toothache effectively, the the pain.
clinician must pinpoint the cause of the pain,
and if not odontogenic, has to face the challenge Toothache of Neuropathic Origin
of determining the true origin of pain. • Neuropathic pain is unilateral, severe,
Referred pain is the type of pain where the lancinating, shock-like.
site of pain and the origin of pain are at • Innocuous peripheral stimulation of trigger
different locations. Familiar example is that zone precipitates the pain.
of cardiac pain. Patient with myocardial • LA to the tooth by blockage may eliminate
ischemia perceives pain in the left arm the pain if tooth is proximal to the trigger
shoulder or the mandible. zone.
The clinical basis of non-odontogenic tooth- • Absence of dental pathology to explain the
ache is that the dental therapy directed pain.
towards the tooth fails to resolve the pain and
• Pain responds to anticonvulsants like
also local anesthetic placed at the site of pain
carbamazepine.
fails to reduce the pain. These two observa-
tions are important to differentiate dental pain Toothache Associated with Continuous (Non-
from referred pain. When toothache is not paroxysmal) Neuropathic Pain
accentuated by local provocation, i.e. cold, hot, • May be associated with maxillary sinusitis
percussion referred pain should be suspected. and associated neuritis, post-herpetic
Pain associated with MPDS—tenderness in neuralgia.
the muscles of mastication, trigger point
• Patients may have other neurological
present, pressure on trigger pain typically
complaints like hyperesthesia, hypo-
increases the pain, and LA does not relieve
esthesia, paresthesia, etc.
the toothache. LA or spray and stretch of the
involved muscle relieves the toothache. • Neuropathic pain may occasionally arise
Neurovascular pain associated with from an injury such as external trauma,
migraine has a throbbing characteristic which extraction, pulp extirpation or major oral
simulates pulpal pain. But this appears at surgery.
similar times during the day and has no dental
Toothache of Maxillary Sinus
cause of pain. The pain responds to ergotamine.
or Nasal Mucosa Origin
Cardiac Pain Associated Toothache With acute or chronic sinusitis, feeling of
Absence of dental cause for pain should constant dull-aching pressure can be felt in the
always be an alerting sign. Failure of LA to teeth. Teeth may be sensitive to percussion,
arrest the pain promptly and completely chewing. Common feature of pain is perceived
in multiple teeth rather than a single tooth. AO appears in the IASP classification under
Water’s radiograph may show evidence of air “lesions of the ear, nose, and oral cavity”and
fluid level or thickened mucosa. is defined as a severe throbbing pain in the
teeth in the absence of a major pathology.
Clinical Features
• Atypical odontalgia is a bizarre pain condi-
• Dull constant pain in upper posterior teeth
tion with no local signs of dental pathology
• Pain below the eyes and sometimes even the tooth is absent.
• Toothache increases on lowering the head Criteria for identifying atypical odontalgia
• History of sinusitis and upper respiratory are:
tract infections
– Pain is felt in tooth or tooth site (upper
• Positive findings on Water’s view, confirmed canine, premolar) in middle-aged women.
on CT/CBCT in doubtful cases.
– Pain is continuous and burning type of
• Referral to ENT and treatment of sinusitis
pain lasting for more than 4 months.
generally controls the pain.
• Edematous nasal mucosa with swelling of – No sign of local cause or referred pain.
the turbinates, occluding the outflow from – LA blocking of the painful tooth provides
maxillary sinus ostium can produce painful equivocal results.
condition of maxillary anterior teeth. – Tricyclic antidepressants with anti-
Atypical Facial Pain convulsants like carbamazepine, baclofen
may be useful in controlling pain.
The term has been applied to various facial
pain problems and has been considered to – Capsaicin ointment may also be tried.
represent a psychological disorder although
Neuralgia-inducing Cavitational
no specific diagnostic criteria have ever been
Osteonecrosis
established.
Atypical facial pain (AFP) is defined more The term given to describe this disorder is
by what it is not than by what it is. Feinmann “neuralgia-inducing cavitational osteo-
characterized AFP as a nonmuscular or joint necrosis” (NICO). It is believed to be due to
pain that has no detectable neurologic cause. ischemic necrosis of the bone and gives rise
True love and colleagues described AFP as a to progressive pain over time. It may be
condition characterized by the absence of intermittent and may vary in extent, location,
other diagnoses and causing continuous, and character. It is more frequent in the fourth
variable-intensity, migrating, nagging, deep, and fifth decades of life. It is thought to occur
and diffuse pain. most frequently in the mandibular molar area.
Most NICO sites are thought to involve
In the TMD classification of the AAOP, AFP
edentulous areas or areas associated with
is listed in the glossary of terms and is defined
radiographically successful endodontic
as “a continuous unilateral deep aching pain
procedures. No specific imaging criteria are
sometimes with a burning component.”
diagnostic, however, it is important to radio-
Atypical Odontalgia graph patients presenting with atypical pain
Atypical odontalgia (AO), described as a localized to an area to rule out the possibility
chronic pain disorder, characterized by pain of osteonecrosis.
localized to teeth or gingiva. In the AAOP Surgical treatment of entering and curetting
classification, AO is listed within the category these cavities are considered to be contro-
“facial pain not fulfilling other criteria” and versial and might lead to nerve injury and
is considered to be a de-afferentiation pain. aggravation of symptoms.
Orofacial Pain 209
Phantom Pain – Pain in multiple teeth with frequent

“Phantom tooth pain” defined as persistent change in character and location
pain in endodontically treated teeth or – General departure from normal or physio-
edentate areas for which there is no explana- logical pattern of pain
tion to be found by physical or radiographic
– Pain is of chronic nature
examination. Traditionally the term ’phantom
pain’ is used to describe the pain felt by the – There is lack of response, or unusual and
patient in amputated limb. unexpected response to reasonable dental
treatment.
Causalgia
– No identifiable pathology that can explain
Typical constant burning type of pain the toothache.
experienced by the patient who has undergone
nerve injury. Treatment
Münchausen Syndrome Such conditions are best treated by qualified
(Hospital Hopper or Thick Chart Syndrome) psychologist or psychiatrist.
Münchausen syndrome is a psychiatric Not to tell patient that the pain is imaginary
factitious disorder wherein those affected
Psychogenic aspects of chronic pain: Hackel
feign disease, illness, or psychological trauma
and Carsen have provided a useful guide that
to draw attention, sympathy, or reassurance
to themselves. This condition derives its name uses the acronym “MADISON”
after Baron Münchausen a German nobleman “MADISON” criteria to differentiate
working for the Russian army who used to psychogenic pain from organic pain:
give dramatic and imaginary description of M—Multiplicity of complaints (at multiple
his exploits all of which were essentially sites all having significant degrees of pain)
untrue!
A—Authenticity (patient tries hard to prove
Psychogenic Pain that his pain is authentic)
It is displacement of pain from psyche,
D—Denial tendency. Patient denies having
peripherally into somatic structure where it
is more tolerable to ego; more common in any stress and refuses to deal with it
females in the postmenopausal stage. I—Interpersonal variability whereby the
• Pain is constant, unanatomic (crosses degree of pain described by the patient
midline) and is deep. It is poorly localized varies depending on who comprises the
and vaguely described. Patient is rigid, patient’s audience
unyielding and obsessive.
• Patient is also obsessive about pain. S—Singularity, patient’s tendency to
• It is very important to rule out all possible catastrophize the pain, expressing the sense
causes of pain before labelling it as psycho- that only he or she experiences such intense
genic pain. pain
• Somatoform pain disorder is a type of a O—“Only you can be of assistance to the
mental disorder in which the patient may patient in such a plight” is the usual state-
complain of physical condition with ment made by the patient to the doctor
absolutely no physical signs. Such a pain
when confined to the tooth is referred to as N—“nothing helps”—agonized cry-
psychogenic toothache. It is characterized verbalization subsequent to protracted and
by following findings: fruitless search to find cure.
Burning Mouth Syndrome • Careful clinical examination for oral lesions

Burning mouth syndrome is defined by the such as candidiasis, lichen planus, other
IASP as a burning pain in the tongue or other erosive lesions should be performed
mucous membranes associated with normal • Possibility of salivary gland disorders and
signs and laboratory findings. The cause and diabetes mellitus, anemia, vit B12 deficiency
pathogenesis is unknown and the diagnosis should be ruled out.
is essentially clinical.
Treatment
Clinical Manifestations • Consists of counseling and reassurance to
• Seven times more common in women than the patient
men • Drug therapy should include tricyclic
• More common in postmenopausal women antidepressants, clonazepam, and recently
• Tongue is most common site of involve- 2-month course of 600 mg of alpha lipoic
ment acid has been shown to reduce BMS pain.
• Burning can be intermittent or constant, but
drinking, eating, placing candy or chewing Suggested Reading
gum relieves the symptoms 1. Burket’s Oral Medicine, 9th, 10th and 11th
• The patients with BMS are often appre- editions.
hensive and generally anxious, and have 2. Dental Clinics of North America, April
symptoms that suggest depression such as 1997; 4(2):367–383.
decreased appetite, insomnia. 3. Orofacial pain by Bell, 7th edition.
14
Oral Cancer and Precancerous Lesions
Oral cancer is generally preceded by some submucous fibrosis. Oral lichen planus is
benign lesions or conditions for a varying regarded as possible precancerous condition.
length of time. Interestingly they share the The above mentioned precancerous lesions
same etiologic factors with oral cancer, parti- and conditions are described in details in
cularly the use of tobacco, and exhibit the same Chapter 3 Red and White Lesions.
site and habit relationships. Many of them
Neoplasm
show a high potential to become cancers and
therefore termed “precancerous”. Even though Willis’ definition: It is an abnormal mass of
only a small proportion of precancers actually tissue, growth of which exceeds and is
progress to oral cancer, this development forms uncoordinated with that of normal tissue and
a source for over 70% of oral cancer in India. which persists in the same excessive manner
Individuals with precancer run a risk that is even after cessation of the stimuli which
69 times higher for them to develop oral cancer evoked the change.
compared to tobacco users who do not have Neoplasm is also defined as growth of new
precancer. The recognition and management cells which proliferate without control and
of oral precancerous lesions therefore consti- which serves no useful function.
tute a vital oral cancer control measure. Oral Main factors for carcinogenesis:
precancer is distinguished into “precancerous 1. Chemicals: A few examples of chemicals
lesions” and “precancerous conditions”. which acts as carcinogens are:
• Carcinoma of scrotum in chimney
PRECANCEROUS LESIONS sweepers
• Aniline dyes—carcinoma of bladder
A precancerous lesion is a morphologically
• Polycyclic aromatic hydrocarbon (tar
altered tissue in which cancer is more likely
and tar products)
to occur than its apparently normal counter-
2. Viral: Virus which are carcinogenic are:
part. The examples are—erythroplakia,
leukoplakia and palatal changes associated • Epstein-Barr virus—Burkitt’s lymphoma
with reverse smoking. in African children
• Bittner’s milk factor—transfer of carci-
Precancerous Conditions noma breast via mothers milk as seen in
A precancerous condition is defined as mice.
“generalised state associated with a significantly 3. Ionizing radiation: Examples are:
increased risk for cancer”. Examples are— • Carcinoma lung common in cobalt mine
syphilis, sideropenic dysphagia and oral workers
211
• Malignancy is common in people tion. Most patients will invariably give

painting fluorescent watch dials history of tobacco and clinical examination
• Leukemia is common in survivors of can show evidence of either frank or subtle
atomic explosion and radiologists (Dr lesions suggestive of malignancy. For
Edmund Kells—Ca skin) example:
4. Hormonal factors • Chronic ulcer with elevated margins
• CA breast (Fig. 14.1)
• CA cervix • Fixed ulcer (Fig. 14.2)
• CA prostate • Exophytic growth (cauliflower appea-
rance, Fig. 14.3)
Modes of Spread • Erythroplakia or speckled leukoplakia
1. Infiltration: Malignant cells infiltrate into lesion with reddish granular area and
surrounding tissues and this spread proliferative verrucous leukoplakia (PVL)
resembles crab (karkinos). Malignant • Fixed lymph node
tumors are not encapsulated unlike benign
tumors.
2. Lymphatics: Lymphatic permeation, i.e.
along the channel and lymphatic embolism,
i.e. tumor cells forming embolus. For
example, carcinomas.
3. Blood spread: Malignant cells may enter and
spread via vascular channels, e.g. sarcomas
4. Spread through natural spaces, e.g. renal
pelvis to bladder
5. Through serous cavity, e.g. from ovary to Fig. 14.1: Carcinoma presenting as perforating ulcer
intestine and fungating nodule
6. Inoculation: Surgeons might implant
malignant cells at site from which skin graft
is taken.
7. Perineural, e.g. adenoid cystic carcinoma.
8. Perivascular
Diagnostic AIDS
1. Clinical examination: By far the most
important step in the diagnosis of oral
cancer is history taking and clinical examina- Fig. 14.2: Carcinoma presenting as a fixed ulcer
A B
Fig. 14.3: Examples of carcinoma presenting as exophytic growth

Oral Cancer and Precancerous Lesions 213
2. X-rays, tomography: Helpful in detecting 4. CT with contrast can also show bony and
bone involvement. However, early lesions soft tissue involvement and metastatic
may be missed. lymph nodes (Fig. 14.4).
5. MRI is ideal when malignancy is localized
3. Ultrasound: It helps in studying soft tissue to the soft tissues. For example, deep seated
involvement including lymph node meta- tongue lesions, floor of the mouth, lymph
stasis. node involvement, etc. (Fig. 14.5).
A B
Fig. 14.4: CT scan showing metastatic lymph node with necrotic center in a patient with CA of retromolar region
A B
C D
Fig. 14.5: (A) Carcinoma tongue with lymph node metastasis; (B) MRI showing decortication of lingual plate
and air-space encroachment; (C) MRI coronal section showing CA tongue; (D) MRI showing lymph node
metastasis with areas of necrosis (arrows)
6. Radionuclide scanning (99Tc) is helpful in 9. FNAC (fine needle aspiration cytology):

detecting malignant lesions or areas with Indicated in lymph node enlargements
increased metabolic activity which are missed suspected to be of malignant origin. The
on conventional radiograph (Fig. 14.6) and aspirate obtained by this method can show
FDG-PET is ideal for localizing distant malignant cells and provide a clue about
metastasis. the primary lesion.
7. Biopsy is the gold standard in diagnosis of 10. FNAB (fine needle aspiration biopsy): As the
oral cancer and also helps to ascertain the name suggests, instead of aspiration, the
degree of dysplasia. needle is rotated within the lesion to
8. Cytologic smear: Cells obtained by scraping obtain tissue biopsy.
the superficial part of the lesion are stained 11. Use of toluidine blue: Intravital staining
with Papanicolaou stain and it gives the helps in the selection of site of biopsy as
indication of the nature of the lesion, being a basic dye stains the dysplastic cells
however, it cannot be a substitute for having greater DNA content (Fig. 14.7)
biopsy. (refer to red and white lesions Chapter 3).
A B
C D
Fig. 14.6: (A) CA floor of the mouth; (B) OPG showing no appreciable bony changes; (C and D) Radionuclide
scans AP and lateral view showing hot spots
A B
Fig. 14.7: CA alveolus showing positive toluidine blue test

Differences between benign and malignant N—Nodal Involvement

lesion • Nx: Lymph nodes cannot be evaluated
Benign tumor Malignant tumor • N0: Tumor cells absent from regional
lymph nodes
Macroscopic features
1. Single, localised Multiple or diffused • N1: Regional lymph node metastasis
2. Round elliptical ped- Irregular shape present (at some sites: Tumor spread to
unculated or sessile closest or small number of regional lymph
(regular shape) nodes)
3. Surface of the lesion Surface irregular thrown
is smooth with normal into ulcers or exophytic • N2: Tumor spread to an extent between N1
mucosa or skin growth and N3 (N2 is not used at all sites)
4. Encapsulated Non-encapsulated • N3: Tumor spread to more distant or nume-
5. Slow growth Rapid growth
rous regional lymph nodes (N3 is not used
6. Necrosis uncommon Necrosis common
7. Removal is easy Removal is difficult
at all sites)
8. Root resorption and It is rare
displacement of teeth M—Metastasis
9. Metastasis absent Metastasis present • M0: No distant metastasis
10. Recurrence uncommon Recurrence common
11. Not fatal
• M1: Metastasis to distant organs (beyond
Fatal
12. Fetid odor absent Fetid odour regional lymph nodes)
Microscopic features
Squamous Cell Carcinoma
13. Tumor cells similar to Tumors are anaplastic
parent cells Etiology
14. Tumor confined by Unconfined
adjacent tissue • Tobacco is the main risk factor known to be
15. Tumor cells do not Tumor cells penetrate associated with carcinoma.
penetrate connective connective tissue • Malignancy without tobacco habit has been
tissue capsule associated with viral etiology HPV.
16. Does not grow beyond Can grow beyond its
its blood supply • Associated premalignant condition such
blood supply
17. Nuclear changes Nuclear changes present as—Plummer-Vinson syndrome, tertiary
absent syphilis, etc.
Radiographic features • Immunosuppression: Carcinoma has been
18. It shows expansion It causes destruction reported in patients who are HIV positive
19. Septa present— Irregular with bays and
with or without tobacco habit.
multilocular promontories
20. Displacement of ana- Destruction of ana- • Other factors are genetic predisposition, old
tomical landmarks tomical landmarks age, chronic trauma.
Clinical Features
TNM Classification
• Ulcerative lesions of long-standing duration
T—Tumor Size with everted margins fixed to underlying
• T0: No signs of tumor tissues.
• Tx: Tumor size cannot be evaluated • Exophytic growth with rough irregular
surface (Fig. 14.8).
• Tis: Carcinoma in situ
• It may present itself as speckled leukoplakia
• T1: Tumor size less than 2 mm or erythroplakia.
• T2: Tumor size between 2 and 4 mm • Submandibular and cervical lymph nodes
• T3: Tumor size more than 4 mm are palpable and fixed.
margin of the malignant tumor is irre-

gular and ragged. Such an appearance is
described as bays and promontories type
of appearance.
• Radiographic lesion of carcinoma may be
large or small, shallow or deep but it does
not have corticated border (unlike benign
tumour). Extensive destruction of bone
weakens jaw and this might give rise to
pathological fracture (Fig. 14.9).
• As carcinoma grows close to the anatomical
landmarks like maxillary antrum or inferior
Fig. 14.8: Squamous cell carcinoma presenting as alveolar canal, it gives rise to a distinct
an exophytic growth break in the continuity of the landmark, e.g.
floor of the maxillary antrum (Fig. 14.10).
• The part affected is immobilised, e.g. in
Malignant tumor may give rise to very little
ability to protrude tongue.
resorption of teeth which is irregular and
• Pain is absent in early stages. superficial termed as spiked resorption
• Mobility of the teeth in the involved region unlike benign tumors which give rise to
and at times secondary osteomyelitis. clear-cut and extensive root resorption
Radiographic Features termed as blunt resorption (Fig. 14.11).
• Malignant tumors involving bone giving
• Squamous cell carcinoma starts in alveolar
rise to rapid destruction of alveolar bone
or cheek mucosa and invades tongue. It is
around the roots and a floating or hanging
not a bone tumor but a tumor in bone. At
tooth appearance.
early stages even if the lesion is present in
the mouth, X-ray picture may be negative, Differential Diagnosis
as the lesion progresses, it gives rise to • Juvenile periodontitis: Seen in younger
destruction or erosion of underlying bone. patients with no active proliferative soft
• Unlike benign tumors, malignant tumor tissue growth. Bilaterally symmetrical
spreads very fast and hence do not have a lesions involving molars and incisors giving
fibrous capsule, i.e. radiographically the Mirror image appearance on OPG.
A B
Fig. 14.9: Lateral oblique view showing irregular radiolucency with pathological fracture in patient with
squamous cell carcinoma of left mandibular alveolus
Fig. 14.10: CA maxilla showing tooth hanging in space Fig. 14.11: CA alveolus showing floating tooth
appearance with break in the floor of the maxillary sinus appearance with spiked root resorption
• Endo-perio lesion: This shows distinct radiographs is through use of scans taken with
margins around the lesion which is sclerotic 99
Tc MD and PET scan which can show bone
and follows outline of original lamina dura. involvement which has less than 30% of
Whereas a floating tooth of carcinoma will demineralization of bone.
have irregular ragged margin along the Metastatic diseases are best treated by—
region. surgery, radiation therapy—chemotherapy in
As there is an ulcerative lesion, secondary varying combinations.
infection may set in giving rise to osteo-
myelitis. In which case it becomes difficult Radiographic Features
to differentiate between carcinoma and • Two types
osteomyelitis. Osteoblastic: Multiple radiopaque foci in
• Eosinophilic granuloma: Younger individual bone. Primary is in prostate or breast,
with bilateral scooped out osteolytic lesions especially when hormonal therapy is given.
and no history of tobacco intake. Osteolytic: Primary in lungs, liver, rectum,
Metastatic Carcinoma stomach. This gives rise to multiple punched
out radiolucent lesions in the skin or
Metastatic carcinoma is reported to be the
geographic skull.
most common malignant tumor in the bone,
however, in the jaws it is found to be rare. The Diffuse radiolucency with poorly defined
common bones to be affected in metastasis are ragged borders. Metastatic lesions may show:
vault of the skull and vertebrae. The most • Unilateral widened PDL space in absence
common malignancy to metastasize to the of periodontal disease or local factors.
jaws are from primary sites in the breast, • Well-defined radiolucency similar to benign
lungs, kidney, thyroid, prostate, colon, tumor without corticated margins.
stomach. They may be asymptomatic or • Diffuse radiolucencies with ill-defined
painful. According to HM Worth, unsolicitated margins (Fig. 14.12)
complaint of numbness or paresthesia of lips
• Cortical erosion and perforation without
and chin is a striking symptom with which
expansion
the patient presents.
• Generalized radiopacity
They may present as unexplained perio-
dontal disease and paraesthesia. • Pathological fracture
Approximately 85% of metastatic carci- To differentiate metastatic malignancy from
noma occurs in mandible. One method to squamous cell carcinoma arising in the oral
detect bony metastasis before it appears on cavity, the following findings are useful:
A B
C D
Fig. 14.12: Patient with history of CA thyroid presenting with: (A) Reddish exophytic growth in 38 region;
(B) OPG showing osteolytic lesion of the left body of the mandible; (C and D) CT scan showing destruction of
mandibular alveolus caused by metastatic malignancy
1. Clinically either growth or an ulcerative According to Worth, it may occur intra-

lesion is invariably seen in squamous cell orally in 38 and 48 regions resembling a
carcinoma, whereas the metastatic malig- socket (but no history of extraction and
nancy might occur without any clinical radiographically no lamina dura).
evidence at least in the early stages.
Etiology
2. The alveolar bone loss is more apparent
with floating teeth appearance I squamous Ultraviolet radiation, thus chronic sun expo-
cell carcinoma whereas centrally occurring sure is important in the development of BCC.
osteolytic lesion with intact alveolar bone A long latency period of 20–50 years is typical
is more commonly seen in metastatic between the time of UV damage and clinical
malignancy onset of BCC. X-ray exposure as well as
chemical like arsenic has been associated with
Basal Cell Carcinoma basal cell carcinoma development. A modest
• Also known as rodent ulcer role has been ascribed to immunosuppression
• Commonly seen in upper half of the face, as well.
most commonly on the exposed surface of Syndromes like xeroderma pigmentosum
the skin, face and scalp. (due to an inability to repair UV induced DNA
• It is slow growing and it rarely metastasizes damage) and nevoid BCC syndrome are
but it can cause significant local destruction characterized by multiple basal cell carci-
and disfigurement, if neglected. nomas occurring at early age.
Clinical Features not well-defined and often extends well

• Commonly seen in fourth decade of life. beyond clinical margins. Ulceration
• Male : Female—3 : 2 bleeding and crusting are uncommon. It
• Seen in white individuals (fair skin) on may be mistaken for scar tissue.
middle third of the face. But may occur Differential Diagnosis
anywhere on the sun-exposed part of the
skin. • Actinic keratosis
• Bowen’s disease
Subtypes of BCC
• Keratoacanthoma
1. Nodular BCC: Begins as a small slightly • Melanocytic nevi
elevated papule with a central depression
• Sebaceous hyperplasia
which ulcerates heals over and then
breakdown again (Fig. 14.13). • Seborrheic keratosis
2. Pigmented BCC: It contains increased brown • Squamous cell carcinoma
or black pigment and are seen more
Treatment and Prognosis
commonly in individuals with dark skin.
3. Cystic BCC: These lesions are translucent • BCC shows equally good results from
blue-gray cystic nodule that may mimic surgical excision of the tumor or from X-ray
benign cystic lesion. radiation.
4. Superficial BCC: This variety presents as • Prognosis of BCC is good since the
scaly patches or papules that are pink to red neoplasm grows slowly and does not tend
brown in color often with central clearing. to metastasize and responds well to
A thread-like border is common. It is more treatment.
common on trunk.
Osteogenic Sarcoma
5. Micronodular BCC: It is an aggressive
variety, prone to ulcerations. May appear • Malignant tumor of bone.
yellow white when stretched and is firm to • Affects long bones and rarely affects jaw
touch. It may have a seemingly well- bones (7% of all sarcomas). But most
defined border. common type of primary sarcoma affecting
6. Morpheaform and infiltrating BCC: These are jaws.
aggressive BCC subtypes with sclerotic • Arises from osteoblasts.
plaques or papules. The borders are usually • Incidence is increased Paget’s disease and
irradiated bone and bones likely to be
traumatized like tibia.
Clinical Features
• Common in younger age group, mean
age—33 years
• Starts as a swelling with pain with a short
history (Fig. 14.14 A and B)
• Swelling shows rapid growth (doubles its
size in 32 days)
Fig. 14.13: Basal cell carcinoma presenting as papular
• Loosening of teeth
lesion with central depression on middle third of the • Distant metastasis: Rapid through blood
face stream to lungs
A B C
Fig. 14.14: (A and B) Patient presenting with exophytic growth in left maxilla obliterating the nasolabial fold;
(C) Water’s view showing complete obliteration of left maxillary sinus; (D) CT scan showing invasive growth
involving the left antrum with sunburst appearance in osteogenic sarcoma
Radiographic Features manner giving rise to ‘sunray or sunburst

Early sign: Widening of PDL space. appearance’ (Fig. 14.14 C and D). Periosteal
reaction is also seen.
It has three types of appearances: Osteolytic,
osteoblastic and osteosclerotic. Chondrosarcoma
Osteolytic: It resembles carcinoma but the bone It can arise centrally or peripherally in the
loss of more concentric nature as lesion starts periosteum. Mostly develops from cartilage
in the centre of the bone, unlike carcinoma located in the bone either centrally or
which starts peripherally. Therefore, patho- peripherally from the cartilage cap of an
logic fractures are more common in sarcoma osteocondroma. Common in pelvis, ribs,
than carcinoma. spine, and long bones.
Osteoblastic and osteosclerotic: They give rise to
bone formation as seen on X-ray. Typical Clinical Features
picture shows dense radiopaque mass attached • In jaws, chondrosarcoma is most often
to mandible at periphery of which perpendi- found in anterior alveolar process of
cularly bone striae are arranged in a radial maxilla.
• Average age: 40 years (younger than chondro- Malignancies of Hematopoietic Origin

sarcoma elsewhere) • Leukemia
• Males > Females in the ratio of 2 : 1 • Lymphoma
• Painless swelling at an early stage with – Hodgkin’s lymphoma
partial asymmetry is the first complaint but – Non-Hodgkin’s lymphoma
as it slowly enlarges it becomes painful and – Burkitt’s lymphoma
hard. • Multiple myeloma
These lesions are described in details in
• Teeth adjacent to the lesion may be gingival enlargement and hematopoietic
resorbed, loosened or exfoliated. diseases respectively.
• Chondrosarcoma can be seen in irregular
normal bone or benign lesions. Suggested Reading
1. Burket’s Oral Medicine, 9th, 10th and 11th
Radiographic Features editions.
Radiolucency with hazy interior, large lobule 2. Oral and Maxillofacial Pathology by
of cartilage may give rise to a soap bubble Neville, 3rd edition.
appearance. Multiple radiolucencies with 3. Shafer’s Textbook of Oral Pathology, 6th
sclerotic foci as seen in osteosarcoma. edition.
15
Immunological Diseases
The term ‘immunity’ refers to the resistance of live or killed microorganisms or their
exhibited by the host towards injury caused products used for immunization.
by microorganisms and their products.
Immunity against infectious diseases can be Natural passive immunity is the resistance
of two types: passively transferred from mother to baby.
The fetus acquires some ability to synthesize
1. Innate Immunity antibodies (IgM) from about twentieth week
of life but immunological capacity of the infant
The resistance to infections which an indivi- is still inadequate at birth. The maternal
dual possesses by virtue of his genetic and antibodies (IgG) protect the fetus till around
constitutional make up. Some examples of
6 months of age from various infections.
innate immunity are:
a. Cough reflex: The cilia on the respiratory Artificial passive immunity is the resistance
epithelial cells propel particles upwards. passively transferred to a recipient by the
b. Tears contain the antibacterial substance administration of antibodies. The agents used
lysozyme, first described by Fleming (1922). for this purpose are hyperimmune sera of
animal or human origin, convalescent sera and
c. A method of defence against viral infections
pooled human gammaglobulin, e.g. ATS (anti-
is the production of interferon by cells
tetanus serum).
stimulated by live or killed viruses and
certain other inducers. The specific reactivity induced in a host by
an antigenic stimulus is known as the immune
2. Acquired Immunity
response. The immune response can be of two
The resistance that an individual acquires types (Fig. 15.1):
during life is known as acquired immunity. It
is of following types: • Humoral immunity (antibody-mediated):
Primary defence against most extracellular
Natural active immunity results from either a bacterial pathogens, helps in defence against
clinical or an unapparent infection by a viruses that infect through the respiratory
microbe. A person who has recovered from or intestinal tracts, prevents recurrence of
an attack of measles develops natural active virus infections and participates in the
immunity. pathogenesis of Type 1, Type 2, Type 3
Artificial active immunity is the resistance hypersensitivity and certain autoimmune
induced by vaccines. Vaccines are preparations diseases.
222
Immunological Diseases 223
Fig. 15.1: Types of immune response (Source: Internet)
• Cellular immunity (cell-mediated): Primary T helper cells which in turn can stimulate
defence against fungi, viruses and either B cells (humoral immunity) or cytotoxic
facultative intracellular bacterial pathogens, T cells (cell-mediated immunity) depending
participates in the rejection of homografts on the antigenic stimulus.
and graft-versus-host reaction, provides Cell-mediated immunity: Cytotoxic T
immunity against cancer and mediates lymphocytes are sensitized by contact and
delayed type of hypersensitivity (Type 4) activated by lymphokines secreted by
and certain autoimmune diseases. activated helper T lymphocytes. T lympho-
When the immune system is first exposed cytes attack and destroy foreign material
to an antigenic stimulus, it is engulfed by directly or through release of soluble media-
antigen presenting cells which stimulates tors, i.e. cytokines.
Humoral immunity: Antigen presenting cells A. Disorders of Specific Immunity

like macrophages phagocytize a pathogen and i. Humoral immunodeficiencies (B cell
present an antigen to a matching helper T cell. defects)
At the same time, some pathogens contact a. X-linked agammaglobulinemia
B cells matching the pathogen’s antigens. b. Selective immunoglobulin deficiencies
Helper T cells multiply, secrete lymphokines (IgA, IgM or IgG subclasses)
which stimulate the B cells to multiply and ii. Cellular immunodeficiencies (T cell
specialize into plasma cells. The plasma cells defects)
secretes antibodies which cause removal of a. Thymic hypoplasia (DiGeorge syndrome)
antigenic stimulus by undergoing following iii. Combined immunodeficiencies (B and T
reactions: cell defects)
Neutralization: The effect of the antigen, a. Cellular immunodeficiency with
toxin or virus is neutralized on mixing with abnormal immunoglobulin synthesis
its antibody. Examples, include the toxin- (Nezelof syndrome)
antitoxin reaction in the diagnosis of diphtheria. b. Ataxia-telangiectasia
c. Wiskott-Aldrich syndrome
Agglutination: Specific antibodies (agglutinins)
that have been formed in response to the B. Disorders of Complement System
occurrence of particulate antigen in host a. Complement component deficiencies: Systemic
tissues combine with a homologous antiserum lupus erythematosus is associated with low
to form a three-dimensional mosaic complex C3 and C4
that can be visualized microscopically, and b. Complement inhibitor deficiencies: Disorders
sometimes macroscopically. Agglutination of the proteins that act to inhibit the comple-
reactions are used for the diagnosis of ment system (such as C1-inhibitor) leading
infections due to salmonellae (Widal test) and to an overactive response, causing condi-
rickettsiae (Weil-Felix test). tions such as hereditary angioedema and
Precipitation: The antigen is in a soluble form hemolytic-uremic syndrome.
and, on combination with the antibody, either
C. Disorders of Phagocytosis
sediments or remains suspended in the form
of floccules. Examples of diagnostic precipita- a. Chronic granulomatous disease
tion tests include the Kahn and VDRL tests. b. Chediak-Higashi syndrome
c. Job’s syndrome
Opsonization: Antibody opsonization is the
process by which a pathogen is marked for Secondary Immunodeficiencies
ingestion and destruction by a phagocyte. Immune responsiveness can be depressed
Opsonization involves the binding of an non-specifically by many factors. Cell-
opsonin, e.g. antibody, to an epitope on an mediated immunity in particular may be
antigen. impaired in states of malnutrition. Many
therapeutic agents such as X-rays, cytotoxic
Primary Immunodeficiency Disorder (PID)
drugs and corticosteroids may have severe
Refers to a heterogeneous group of disorders adverse effects on the immune system. The
characterized by poor or absent function in most important of these secondary immuno-
one or more components of the immune deficiencies is acquired immunodeficiency
system. Most PIDs result from inherited syndrome (AIDS) caused by the human
defects in immune system development and/ immunodeficiency virus (HIV) (explained in
or function; however, acquired forms have detail in chapter on sexually transmitted
also been described. disease.
Autoimmune Disorders conjunctiva. Lesions have a predilection for

The function of the immune system is to the mucous membranes and they are
recognize and differentiate self from non-self. histologically indistinguishable from bullous
Autoimmune disorder strikes when the pemphigoid. The most common oral manifes-
immune system mistakes self for non-self. tation is desquamative gingivitis. MMP is
characterized by the presence of IgG auto-
Autoimmunity is a condition in which
antibodies specific for bullous pemphigoid
structural or functional damage is produced
antigen 2 (BP180 or type XVII collagen) which
by the action of immunologically competent
forms a part of the anchoring filament
cells or antibodies against the normal
complex together with laminin 5 which also
components of the body.
appears to function as an adhesion molecule.
Autoimmune bullous diseases are rare dis-
orders affecting skin and mucous membranes Systemic Lupus Erythematosus (SLE)
that are mediated by pathogenic autoantibodies SLE is a multisystem autoimmune inflamma-
against desmosomal or hemidesmosomal tory disorder. The main feature is the formation
antigens of squamous epithelium. These of antibodies to DNA which can initiate
conditions are elaborated in chapter on immune complex reactions. In addition to
ulcerative and vesicobullous lesions.
Criterion Definition/examples
Pemphigus
1. Malar rash Fixed erythema over the malar
The pemphigus syndrome includes diseases eminences, tending to spare
that are characterized by loss of epidermal the nasolabial folds
cell—cell cohesion (acantholysis) and auto- 2. Discoid rash Erythematosus raised patches,
antibodies against desmosomal cadherins. may scar
This group comprises the two classical forms 3. Photosensitivity Skin rash as a result of un-
of pemphigus: Pemphigus vulgaris (PV) and usual reaction to sunlight
pemphigus foliaceus (PF). PV is characterized 4. Oral ulcers Usually painless
by suprabasilar acantholysis and anti-Dsg3
5. Arthritis Non-erosive: Jaccoud’s arthro-
IgG autoantibodies, whereas PF is chara-
pathy
cterized by subcorneal acantholysis and anti-
6. Serositis a. Pleuritis—pleuritic pain,
Dsg1 IgG autoantibodies.
pleural rub, pleural effusion
Bullous Pemphigoid b. Pericarditis—ECG changes,
rub, pericardial effusion
Bullous pemphigoid (BP) is a chronic, auto-
immune, subepidermal, blistering skin disease 7. Renal disorder a. Proteinuria (>3+ or 0.5 g/day)
b. Cellular casts in urine
that rarely involves mucous membranes. BP
is characterized by the presence of immuno- 8. Neurological a. Seizures
disorder b. Psychosis
globulin G (IgG) autoantibodies specific for
the hemidesmosomal BP antigens BP230 9. Hematological a. Hemolytic anemia
(BPAg1) and BP180 (BPAg2) (type XVII disorder b. Leukopenia
c. Lymphopenia
collagen).
d. Thrombocytopenia
Mucous Membrane Pemphigoid 10. Immunological a. Anti-DNA antibodies
The pathological hallmark of mucous disorder b. Anti-Sm antibodies
c. Anti-phospholipid antibodies
membrane pemphigoid is a subepithelial loss
of adhesion, which can result in permanent 11. Anti-nuclear Exclude drug causes
scarring of the affected area, particularly the antibody
systemic lupus and chronic discoid lupus, a • The TMJ becomes involved in approxi-
distinct syndrome of drug-induced lupus is mately half of the affected patients. The
recognized. The criteria for diagnosing systemic characteristic radiographic findings are a
lupus erythematosus are published by the result of villous synovitis, which leads to
American College of Rheumatology (ACR). formation of synovial granulomatous tissue
Also refer to Chapter 3 on red and white (pannus) that grows into fibrocartilage and
lesions. bone, releasing enzymes that may destroy
the articular eminence and the anterior
Rheumatic fever is a systemic disease that can
aspect of the condylar head, permitting
involve the heart, joints, skin, and brain, the
anterosuperior positioning of the condyle
illness typically develops two to three weeks
when the teeth are in maximum inter-
after an untreated group A beta hemolytic
cuspation and resulting in an anterior open
streptococcal pharyngeal infection. It is
bite.
believed to be caused by antibody cross-
• Erosion of the anterior and posterior
reactivity. This cross-reactivity is a type II
condylar surfaces at the attachment of the
hypersensitivity reaction and is termed as
synovial lining may result in ‘sharpened
molecular mimicry.
pencil’ appearance of the condyle (Fig. 15.3).
Rheumatoid Arthritis • Erosive changes may be so severe that entire
condylar head is destroyed, with only the
• Rheumatoid arthritis (RA) is a systemic
neck remaining as the articulating surface.
inflammatory disorder characterized by
Similarly, the articular eminence may be
symmetrical synovitis of peripheral joints
destroyed to the extent that a concavity
and tendon sheaths. replaces the normally convex eminence.
• The metacarpophalangeal joints, wrists, • Joint destruction eventually leads to
and metatarsophalangeal joints are most secondary degenerative joint disease.
commonly involved at the onset, but any • Subchondral sclerosis and flattening of
synovial joint may be affected. As disease articulating surfaces may occur, as well as
advances, progressive damage to bone and subchondral ‘cysts’ and osteophyte forma-
soft-tissues occurs, with consequent joint tion.
subluxation or deformity. The fingers classi- • Fibrous ankylosis or osseous ankylosis may
cally exhibit “swan neck” or “boutonniére” occur; reduced mobility is related to the
deformities (Fig. 15.2). duration and severity of the disease.
Fig. 15.2: Swan-like deformity Fig 15.3: Sharpened pencil appearance of right condyle
The 1987 American Rheumatology Association heart and kidneys. It is characterized by

criteria: At least four criteria must be fulfilled alterations of the microvasculature, distur-
for classification as rheumatoid arthritis (RA). bances of the immune system and by massive
deposition of collagen. It is of two types:
1. Morning stiffness of joints—lasting at least 1 hour
before maximal improvement for at least 6 weeks 1. Localized scleroderma: Two types
2. Arthritis in 3 or more joint areas—soft tissue • Linear scleroderma: Band of sclerotic indura-
swelling or effusion in 3 or more joint areas tion and hyperpigmentation occurring
simultaneously for at least 6 weeks
on one limb or side of the face. The lesion
3. Arthritis of hand joints—swelling of wrist, meta-
carpophalangeal, or proximal interphalangeal
of localized linear scleroderma of the
joints for at least 6 weeks head and face is called en coup de sabre.
4. Symmetric arthritis—simultaneous involvement • Circumscribed scleroderma (morphea):
of the same joint areas bilaterally for at least 6 Small violaceous skin patches or larger
weeks skin patches (guttate morphea) that
5. Rheumatoid nodules—subcutaneous nodules
indurate and lose hair and sweat gland
over bony prominences, extensor surfaces, or
in juxta-articular regions
function.
6. Rheumatoid factor—detected by a method that 2. Systemic sclerosis (SSc)
is positive in <5% of normal controls
7. Radiographic changes—typical RA changes on
• Limited cutaneous SSc: Patient shows
hand and wrist radiographs, e.g. erosions, peri- Raynaud‘s phenomenon for years at
articular osteopenia presentation. Skin sclerosis is limited to
hands, feet, face, and forearms, or is
• First-line, symptomatic therapy is usually absent. Significant late incidence of
with NSAIDs, which relieve symptoms pulmonary hypertension, trigeminal
of inflammation but do not alter the neuralgia, calcinosis, and telangiectasia
progression of disease or its prognosis. is present.
Some newer NSAIDs are more selective for • Diffuse cutaneous SSc: Patient shows onset
the COX-2 isoenzyme with lower incidence of Raynaud’s phenomenon within 1 year
of gastrointestinal complications, but these of onset of skin changes. Truncal and
COX-2 drugs may also increase the risk of acral skin involvement is observed. Early
thrombotic complications relative to and significant incidence of interstitial
standard NSAIDs. lung disease, oliguric renal failure, diff-
• The course of RA is characterized by use gastrointestinal disease, and myo-
episodic flare ups and remissions, super- cardial involvement is present. There is
imposed on progressive damage to bones presence of anti-DNA topoisomerase I
and joints. Most patients require long-term (anti-Scl-70) antibodies and absence of
therapy with immunomodulatory disease- anticentromere antibodies.
modifying antirheumatic drugs (DMARDs),
Clinical Features
such as methotrexate, sulphasalazine,
hydroxychloroquine and gold. • Typical features of the face involvement are
shrunken nose (mouse facies), microcheilia,
Systemic Sclerosis reduced mouth aperture and microglossia
Systemic sclerosis (SSc) is a clinically hetero- (Fig. 15.4).
geneous generalized disorder which affects • In addition, radial furrowing around the
the connective tissue of the skin and internal lips (purse string appearance), telangiectasia
organs such as gastrointestinal tract, lungs, (hard palate and lips) and changes in
• Esophageal involvement is diagnosed by

conventional radiography (barium swallow)
which shows a stiff glass tube appearance by
manometric measurements.
• In lungs, with increased fibrosis, a cystic
transformation takes place, representing the
so-called end-stage-lung or honeycomb lung.
• Affection of the kidney has the worst prog-
nosis and highest mortality of all internal
organs involved. The primary event seems
to be the damage of endothelial cells with
thickening and proliferation of the intima
with deposits of glycoproteins and muco-
Fig. 15.4: Mouse facies and purse string appearance
polysaccharides in the interlobular and
small arcuate arteries. These changes lead
the pigmentation (mottled or diffuse to narrowing or even obliteration of vessel
hyperpigmentation resembling Addison’s lumina and ultimately to infarction of
disease or focal hypopigmentation as post- glomeruli and tubuli.
inflammatory pigment incontinence) are Radiographic Features
typical.
• Due to fibrosis of muscles of mastication;
• Sclerosis limits expression, leading to a mandibular resorption is seen in angle,
mask-like stiffness of the face. coronoid process, etc. (Fig. 15.6).
• The tongue becomes hard and rigid making • Uniform thickening of periodontal ligament
speaking and swallowing difficult. space is seen in less than 10% of patients.
• A subgroup of patients characterized by The posterior teeth are involved more
extensive calcinosis, Raynaud’s pheno- frequently than the anterior teeth.
menon, esophageal dysmotility, sclero- • Calcinosis of soft tissues around the jaws
dactyly and widespread telangiectasia is can be misinterpreted as a radiographic
described as CREST syndrome. intrabony lesion.
• Acro-osteolysis may cause articular
Circulating antinuclear antibodies are
deformities and dissolution of terminal
present in >90% of scleroderma patients.
phalanges (Fig. 15.5).
Several are highly specific for the disease like
anticentromere, antitopoisomerase I, etc.
Fig. 15.6: Resorption at the site of muscle attach-

Fig. 15.5: Acro-osteolysis of fingers ments: At the angle of ramus bilaterally
The therapy is directed at three pathogenic • Diminished secretion of tears (aqueous layer)
compartments: leads to chronic irritation and destruction
• Vascular system of the corneal and bulbar conjunctival
• Immune system (inflammation, immuno- epithelium [keratoconjunctivitis sicca
modulation, autoimmunity) (KCS)].
• Fibrosis • Sialography demonstrates formation of
punctate, cavitary defects which are filled
Vasoactive Substances with radiopaque contrast media producing
• Calcium channel blockers: Nifedipine a cherry blossom or branchless fruit-laden
• ACE-inhibitors captopril, enalapril tree appearance radiographically.
Anti-inflammatory and Treatment

Immunosuppressive Substances Antimalarial medications and corticosteroids
• Glucocorticoids: Methylprednisolone are being reevaluated in the treatment of
• Azathioprine, cyclophosphamide Sjögren’s syndrome. Hydroxychloroquine
(plaquenil) may be useful for treating the
Antifibrotic Substances arthralgias and fatigue associated with
• D-penicillamine Sjögren’s syndrome. Rituximab (rituxan), an
anti-CD20 monoclonal antibody that depletes
Sjögren’s Syndrome (SS) B lymphocytes, holds promise as a therapy
• SS is an autoimmune disorder characterized for severe inflammatory manifestations of
by exocrine gland dysfunction and destruc- Sjögren’s syndrome.
tion, mainly the salivary and lacrimal Also refer to chapter on salivary gland
glands, leading to dryness of mouth and disorders.
eyes. Sjögren’s syndrome appears unique
for two reasons. First, it has a broad clinical Idiopathic Thrombocytopenic Purpura
presentation, extending from local exocrino- • Idiopathic thrombocytopenic purpura (ITP)
pathy to involvement of multiple organs; it is the condition of having a low platelet
may be found alone (primary SS) or in count (thrombocytopenia) of no known
association with other autoimmune diseases cause (idiopathic). Although most cases are
(secondary SS) like rheumatoid arthritis. asymptomatic, very low platelet counts can
lead to a bleeding diathesis and purpura.
• Dryness of mouth (xerostomia) and eyes are
• ITP may be either acute or chronic. The
the major glandular manifestations of SS.
acute form is most common in children
Patients complain of difficulty in chewing
between the ages of two and six years; the
and swallowing, sore mouth, and a sandy
chronic form is most common in adult
feeling or itchiness in the eyes.
females between 20 and 40 years.
• The oral mucosa is dry, sticky, and erythe- • In many cases, the cause is not actually
matous, often with secondary candidiasis. idiopathic but autoimmune, with IgG
The tongue appears fissured and there is antibodies against platelets being detected
atrophy of the filiform papillae. in approximately 60% of patients. The
• Teeth show increased plaque formation, coating of platelets with IgG renders them
hypocalcification, and caries at the gingival susceptible to opsonization and phago-
margins. cytosis by splenic macrophages.
• Recent evidence suggests that the stimulus refers to that caused by atrophic gastritis,
for autoantibody production in ITP is parietal cell loss, and lack of intrinsic factor
due to abnormal T helper cells reacting only.
with platelet antigens on the surface of • Antibodies to intrinsic factor and parietal
antigen presenting cells. This important cells cause the destruction of the oxyntic
finding suggests that therapies directed gastric mucosa, in which the parietal cells
towards T cells may be effective in treating are located, leading to the subsequent
ITP. loss of intrinsic factor synthesis. Without
intrinsic factor, the ileum can no longer
Also refer to chapter on bleeding and clotting
absorb the B12.
disorders.
Also refer to chapter on tongue.
Pernicious Anemia
• It is caused by loss of gastric parietal cells, Suggested Reading
which are responsible for the secretion of 1. Textbook of Microbiology by Ananth-
intrinsic factor, a protein essential for narayanan.
subsequent absorption of vitamin B12 in the
ileum. While the term ‘pernicious anemia’ 2. Textbook of Oral Medicine by Burket, 9th,
is sometimes also incorrectly used to 10th and 11th editions.
indicate megaloblastic anemia due to any 3. Textbook of Oral Radiology by White and
cause of B12 deficiency, its proper usage Pharaoh, 6th edition.
16
Endocrine Disease and Dysfunction
Endocrine disease or dysfunction is best and anatomically distinct—anterior lobe

regarded as hyperfunction or hypofunction of (adenohypophysis) and posterior lobe
endocrine tissue or failure of target organs to (neurohypophysis).
appropriately respond to hormones. These
Hypopituitarism
functional abnormalities are most commonly
caused by acute or chronic pathosis such as • When single or multiple pituitary hormones
tumors, infection or degenerative changes are not produced in normal amount.
affecting the endocrine glands. The present • Panhypopituitarism (Simmond’s disease)—
chapter describes the clinical and radiographic total absence of pituitary secretions.
oral manifestations of the various endocrine The nature and clinical manifestation of
diseases and discusses special dental manage- pituitary hypofunction depends on which
ment considerations in patients with suspected target organs or tissues are affected. Hypo-
or proven endocrine dysfunction. pituitarism can result from:
• Space occupying lesion of sella turcica, e.g.
DISEASES OF PITUITARY GLAND craniopharyngioma, adenomas of pituitary
Anatomy and Physiology gland, metastatic carcinomas, sarcoidosis
and histiocytosis.
The pituitary gland is situated in the sella
• Sheehan’s syndrome is a form of hypo-
turcica and is composed of functionally
pituitarism caused by infarction of the
Adenohypohysis— Neurohypophysis— pituitary associated with post-partum
secretes secretes hemorrhage.
Adrenocorticotropin Antidiuretic hormone (ADH)
Signs and Symptoms
(ACTH) regulates the flow of water
through kidneys Growth hormone does not act on a single
Growth hormone (GH) Oxytocin—contraction of target organ but has a more general metabolic
uterus and milk ejection effect. Deficiency in children produces
Follicle-stimulating Luteinizing hormone (LH) dwarfism which is caused by craniopharyn-
hormone (FSH) and interstitial-stimulating
hormone (ICSH) gioma or is idiopathic.
Thyroid-stimulating Clinical Features
hormone (TSH)
Lactogenic hormone i. Growth retardation noticed till 2nd to 3rd
(prolactin, LTH) year.
Melanocyte-stimulating ii. Hypoglycemia: Due to lack of GH and
hormone (MSH) cortisol
231
iii. Lack of gonadotropin: Delayed onset of puberty eruption, over retained deciduous teeth and
iv. Deficiency of vasopressin or ADH: Diabetes incomplete apexification of permanent teeth
insipidus are also common findings in such cases.
v. Despite retarded growth normal body Treatment
proportion in contrast with primary hypo-
Use of growth hormone prepared from human
thyroidism who have infantile proportions
(head larger in proportion to body). pituitary gland. Hypopituitarism caused by
tumors may require surgery or radiotherapy.
Oral Changes Deficiency of end organ hormones are
No dental anomaly is pathognomonic for a corrected by hormone replacement therapy
particular endocrine disorder. In hypo- when appropriate.
pituitarism, both facial and dental develop-
Hyperpituitarism
ments are slowed. Facial height is affected
because the mandible is underdeveloped Excess secretion of growth hormone caused
owing to lack of condylar growth and a short by a pituitary adenoma produces gigantism
ramus, and this can lead to severe mal- in children and acromegaly in adults
occlusion and crowding of the teeth. Delayed (Fig. 16.1A to C).
Fig. 16.1A: A 45-year-old female patient presenting with prominent nose, lower jaw and increased diastema
Fig. 16.1B: OPG and lateral cephalogram of the same patient showing mandibular prognathism and spacing
between the teeth
Endocrine Disease and Dysfunction 233
Fig. 16.1C: MRI showing pituitary adenoma in the same patient
Signs and Symptoms 4. Lips and nose greatly enlarged in

1. Increased secretion of growth hormones acromegaly. Mandible is enlarged more in
before closure of epiphysis leads to an proportion to maxilla and hence leading to
increase in bone length and within a class III malocclusion. Palatal vault is
proportional manner, giving rise to flattened.
pituitary gigantism. 5. Tongue increases in size and may show
2. After closure of epiphysis, excessive crenations on lateral borders.
secretion of growth hormone leads to
6. Tremendous flattening of the dental arches
periosteal overgrowth and thickening of
and fanning out and spacing of the teeth is
soft tissues cause a characteristic coarsening
common.
of facial features termed as acromegaly.
3. Fingers and hands enlarge so that no 7. In edentulous patient, enlargement of the
jewellery fits. alveolus may prevent comfortable fit of the
4. Increased in size of calvarium, therefore, complete denture.
changed hat size.
Diagnosis
5. Erosion of articular surfaces and symptoms
such as arthralgia, headache, visual • Clinical findings
problems and carpal tunnel syndrome. • Radiographically—skull reveals cortical
Oral Changes thickening, frontal sinus enlargement and
erosion of sella turcica.
1. Overgrowth of mandible leading to
prognathism (lantern jaw). • Growth hormone concentrations can be
2. Excessive dental development including measured by radioimmunoassay techniques.
eruption of the teeth is apparent clinically
as well as radiographically. Treatment
3. Radiographically: Marked thickening of Depends on the nature and location of the
cranium and the cortical plates of mandible lesion. Both surgery and radiotherapy are
and often shows sinus enlargement. used effectively to irradicate functional
Periosteal calcifications may be seen at tumors. A possible complication of treatment
muscle and tendon insertions. is development of panhypopituitarism.
Thyroid Diseases Hyperthyroidism (Thyrotoxicosis)

Anatomy and physiology: Located in midline, Types
butterfly-shaped organ, consists of two lobes • Graves’ disease
on either side of trachea at the level of cricoid • Toxic nodular goiter (toxic adenoma)
cartilage connected by an isthmus. • Hyperthyroid phase of subacute thyroiditis
• Hyperthyroidism associated with acro-
Developmental Disorder
megaly
1. Develops as a downgrowth of 4th pharyn- • Due to excessive pituitary TSH
geal pouch and ultimobranchial body. The
anlage of the median lobe arise at the base Graves’ Disease
of the tongue (foramen cecum) and as Most common form of hyperthyroidism,
downgrowth occurs the thyroglossal duct usually affecting middle aged females charac-
maintains continuity between the lingual terized by:
and pharyngeal areas. By the sixth week in • Nodular thyroid enlargement
utero, this structure usually is obliterated, • Exophthalmus
however, epithelial remnants may persist • Pretibial myxedema
anywhere along the path of descent of the Significant percentage of patients with
thyroid anlage leading to thyroglossal Graves’ disease have a circulating thyroid
duct cysts. The vast majority of these cysts stimulator in their serum known as long-
occur in the midline and move superiorly acting thyroid stimulator (LATS) which has
with swallowing or protrusion of the characteristics of an antibody.
tongue. Signs and Symptoms
2. Inadequate descent of the gland known as
lingual thyroid gland. The lesion persists Signs Symptoms
as a raised purplish mass, usually located Thyroid enlargement Nervousness
at the base of the tongue. Radioisotope Tachycardia Increased sweating
studies and biopsy are used to establish the Widened pulse pressure Hypersensitivity to heat
diagnosis. Warm moist skin Palpitations, increased
Synthesis and secretion of the thyroid appetite
hormones is controlled by thyroid-stimulating Tremors Fatigue
hormone (TSH) produced in anterior pitui- Eye signs Insomnia
tary. TSH in turn is regulated by thyrotropin- Atrial fibrillation Muscle weakness
releasing hormone (TRH) which is elaborated
by the hypothalamus and transported to Eye signs: Exophthalmus is produced by
pituitary. When thyroid hormone levels are excessive retro-orbital tissue and lymphocytic
depleted in the tissues TSH synthesis is infiltration of the ocular muscle (Fig. 16.2).
stimulated in the pituitary thus increasing the Pretibial myxedema is characterized by the
secretion of thyroid hormones following a nonpitting mucinous infiltration of the tissues.
negative feedback loop. Thyroid hormones are Thyroid storm: Untreated thyrotoxicosis can
essential for normal growth and maturation lead to a rare and life-threatening condition
and are known to affect oxygen consumption known as thyroid storm. This condition is
and protein synthesis throughout the body. precipitated by infection, trauma or dental
Enlargement of the thyroid gland is seen in surgery under local anesthesia with epine-
iodine deficiency and neoplastic disease. phrine.
2. Propranolol: A beta adrenergic blocker,

remission occurs within one year and if
thyroid laboratory results returns to
normal, patients are weaned from drug
therapy.
3. Surgery: In patients who do not experience
a prolonged remission from antithyroid
therapy.
4. Radioisotope therapy.
Most common side effect of this treatment
is hypothyroidism therefore sometimes
Fig. 16.2: Graves’ disease/thyrotoxicosis patient with hormonal replacement is required to stabilise
exophthalmus and thyroid swelling (Source: Internet)
the patient.
Characterized by
• Rapid onset of muscle weakness
• Profuse sweating Evaluation of current thyroid status: Euthyroid
patients (laboratory findings in normal range)
• Marked tachycardia
can be managed uneventfully, while patients
• Fatigue and fever
with active disease have increased likelihood
• Nausea, vomiting and abdominal pain of cardiovascular complications that could
• Congestive heart failure and cardiac precipitate a life threatening episode in dental
arrhythmias chair. Specifically the use of epinephrine in
• Patient may become psychotic and comatose local anaesthetic or in gingival retraction cord
• Profound hypotension can lead to death is strictly contraindicated until thyroid
Treatment hormones levels are brought under control.
Emergency treatment of thyroid storm consists Hypothyroidism and Myxedema
of large doses of propyluracil, propranolol, It is a condition caused by a deficiency of
potassium iodide, hydrocortisone and intra- thyroid hormone. Characterized by an
venous fluids. insidious and progressive slow-down of body
Oral Changes metabolic functions.
No pathognomonic oral signs and symptoms The etiology of hypothyroidism is multi-
are associated with hyperthyroidism. factorial:
• Thyroid gland malfunction
Diagnosis
• As side effect of radioisotope therapy in
• History and clinical examination patients of Graves’ disease
• Increased level of T3 and T4 • Subtotal thyroidectomy
• Other more useful tests like—serum thyro-
xine, serum T3 and thyroidal radioactive Symptoms
iodine uptake. • Fatigue, muscle weakness
• Coarse, dry skin
Treatment
• Edema of extremities
1. Antithyroid drugs such as: Propylthiouracil
or methimazole. It interferes with the • Cold intolerance
synthesis of thyroxine. • Hoarseness
• Slight weight gain with loss of appetite Early recognition of hypothyroidism in

• Paresthesia, arthralgias infants is essential to prevent permanent brain
• Muscle cramps damage.
• Constipation Signs and Symptoms
In advanced form of the disease, i.e. Cretinism results from aplastic thyroid gland
myxedema, the skin is infiltrated by a muco- or a gland replaced by fibrous scar tissue and
protien and mucopolysaccharides resulting in lymphocytes.
a puffy, edematous appearance. Deposition in
cardiac tissues may cause problems like Clinical Features
cardiomyopathy, pleural and pericardial
• Generalized retarded growth
effusions.
• Delayed ossification of bones, epiphyseal
Diagnosis dysgenesis, cerebral hypoplasia
It is based on: • Jaw and tooth anomalies
• Signs and symptoms • Skin becomes thick, dry and wrinkled
• Serum T4 levels • Macroglossia, thickening of the lips, open
• Radioimmunoassay for serum TSH. With bite and persistent drooling
this test, a greater than two-fold increase in • Broad face, short and flattened nose
serum TSH is regarded as initial indication • Mental retardation and dwarfism
of primary hypothyroidism. (Fig. 16.3A,B)
Treatment Oral Changes

Sodium levothyroxine to replace deficient Athyreotic cretinism, there is dysgenesis of
thyroid hormone. thyroid gland in utero that interferes with
normal development of cranium facial bones,
Dental Considerations jaws and primordia of teeth. The newborn
Alteration in metabolism with impaired athyreotic infant typically has massive
healing following oral surgical or periodontal macroglossia coarse face and broad nose, lips
procedures, untoward reaction to anesthesia are puffy, thickened and protruded, retarded
or analgesic compounds. Therefore, elective jaw development, micrognathia with open
dental treatment is postponed till hypothyroid bite, retarded eruption of primary teeth and
patients are properly treated from medical delayed exfoliation of these teeth, absence of
standpoint and potential underlying cardiac, dentin and enlarged pulp chambers are the
neurologic and metabolic abnormalities are features of cretinism.
investigated and controlled.
Diagnosis
Cretinism Cretinism is often suspected at birth, however,
Affects infants and young adults due to lack the typical physical appearance and beha-
of thyroxine during fetal and perinatal period. vioural changes may not become apparent
It is the most common cause of mental until 3rd to 6th month of life. In infants with
retardation. T4 values less than 7 μg/dl, repeat T4 and
serum TSH test to confirm the diagnosis.
Causes
• Incomplete development of thyroid gland Treatment
• Iodine deficiency Cretinism is treated with thyroid hormone
• Defect in thyroxine synthesis replacement therapy.
Fig. 16.3A: An 8-year-old boy presenting with stunted growth, depressed nasal bridge and enlarged tongue—
cretinism
Fig. 16.3B: OPG showing anterior open bite
DISEASES OF ADRENAL GLAND Epinephrine supports blood pressure by

increasing heart rate, increases oxygen
Anatomy and Physiology consumption by tissues and glucose release
The adrenals are triangular-shaped structures by the liver.
that are situated on the superior poles of the Norepinephrine increases peripheral
kidneys. They produce or secrete number of resistance by its vasoconstriction effects.
compounds that are essential for maintenance
of life and adaptation to stress. Each gland is Both increase lipolysis, increase blood sugar
divided anatomically and functionally into level by stimulating glycogenolysis, elevate
medulla and a cortex. body temperature, and increase basal metabolic
rate. Most importantly during emergency
Adrenal Medulla situations these compounds help the body in
Arises from ectodermal tissues. Functions as adapting to stress. Thus release of endogenous
a part of sympathetic nervous systems. It epinephrine during stressful dental procedure
manufactures and secrete two catechol- can produce significant changes in blood
amines—epinephrine and norepinephrine. pressure and pulse rate.
Adrenal Medullary Disease • Maintains fluid and electrolyte balance by

Pheochromocytoma: This catecholamine controlling sodium and potassium levels
producing tumor arises from the chromaffin and by monitoring renal tubular function.
cells of the adrenal medulla or from the extra-
adrenal tissues of the sympathetic nervous DISEASES OF ADRENAL CORTEX
system (paraganglioma). Major clinical symp-
Addison’s Disease
tom associated with this tumor is paroxysmal
hypertension. Primary adrenocortical insufficiency.
Sipple syndrome: Characterized by endocrine Causes
neoplasm (pheochromocytoma, and medullary • Idiopathic destruction of the adrenal cortex
carcinoma of thyroid) and multiple mucosal (autoimmune basis)
neuromas involving lips, tongue, larynx and • Granulomatous infiltration of the cortex by
eyelids. It is inherited as autosomal dominant tuberculosis, amyloidosis, inflammatory
trait. necrosis or neoplastic disease of the gland
Adrenal Cortex Affects all age group and both sexes
It secretes three major class of hormones: equally.
• Glucocorticoids—which affects inflamma- Signs and Symptoms
tory process, carbohydrate and protein
All are related to deprivation of aldosterone
metabolism
and cortisol. In Addison’s disease, sodium
• Mineralocorticoids (aldosterone) which
excretion is increased and potassium excretion
affects water and electrolyte balance
is decreased resulting in high blood levels of
• Sex hormones (testosterone, estrogen and potassium and low concentration of sodium
progesterone) and chloride. This electrolyte imbalance
Synthesis and secretion of the glucocorti- produces increased diuresis with dehydration,
coids is regulated by pituitary adrenal axis. decreased fluid volume, hypotension and
In stress, noxious stimuli, surgical trauma— potential circulatory collapse.
hypothalamus produces corticotropin
releasing factors (CRF) which stimulates Cortical Depression
secretion of ACTH by anterior pituitary, • Increases hypotension
ACTH in turn, promotes the synthesis and • Disturbances in carbohydrates, protein and
secretion of cortisol in the adrenal cortex. metabolism leading to hypoglycemia and
Functions of Glucocorticoids diminished glycogen storage in the liver
• It increases glucose level by increasing • Neuromuscular functions are inhibited—
gluconeogenesis in the liver muscle weakness
• Promotes mineral, protein and nucleic acid • Reduced resistance to infections, trauma
catabolism and stress
• Influences lipolysis and distribution of • Cardiac output decreased—circulatory
adipose tissue in the body failure
• It is used therapeutically to suppress or modify • Low cortisol—stimulates pituitary ACTH
the immune and inflammatory response output and increase release of melanocyte
stimulating hormone (MSH) which
Functions of Mineralocorticoid Steroids accounts for hyperpigmentation of skin and
Synthesis and secretion is regulated by renin- mucous membranes with Addison’s
angiotensin system (RAS) in the kidney. disease.
Addison’s disease often occurs in associa- Cushing’s Syndrome

tion with other diseases including diabetes Hypersecretion of one or more hormone
mellitus, thyroid and parathyroid dys- produced by adrenal cortex (adrenocortical
function. Common clinical manifestations are hyperfunctions) causes distinct clinical
generalized weakness, fatigue, hypotension syndromes.
and abnormal pigmentation. Increased • When androgens increase—adrenal virilism
pigmentation may take the form of diffused
• Increased aldosterone—aldosteronism
tanning, black freckles on the skin of face and
extremities, areas of vitiligo and bluish black • Increased glucocorticoid—Cushing’s syn-
discoloration of the areolas and mucous drome
membranes of lip, mouth, rectum and vagina. Biologic effects of hydrocortisone over-
Weight loss, dehydration, anorexia, vomiting production:
and nausea are also common complaints. • Protein metabolism: Thinning of skin, reddish
striae, loss of bone matrix and demineraliza-
Oral Changes
tion, poor wound healing, muscle wasting
Pigmentation of face and mucosa. The and weakness, capillary fragility and
pigmented areas are bluish black in colour and bruising, impaired growth in children.
involve the mucosa of cheek, gingiva, palate,
• Carbohydrate metabolism: Abnormal glucose
tongue and lips. It is important to differentiate
tolerance curve, overt diabetes mellitus.
the lesions from hyperpigmentation of Peutz-
Jeghers syndrome and neurofibromatosis. In • Lipid metabolism: Centripetal fat distribu-
these later disorders, steroid replacement tion, moonfacies.
therapy of course does not result in reversal • Electrolyte balance: Sodium retention,
of the changes. potassium loss, hypertension, hypervolemia.
• Hematopoietic effects: Eosinopenia, lympho-
Diagnosis penia, polymorphonuclear leukocytosis,
Laboratory studies reveals: erythrocytosis.
• Low serum sodium level • General effects: Hypercalciurea and renal
• High serum potassium level calculi, gastric ulceration, psychosis,
• Elevated blood urea nitrogen (BUN) impaired immunologic tolerance.
• Diagnosis is confirmed by failure of These syndromes may be caused by
administered synthetic ACTH to produce congenital or acquired hyperplasia of the
an appropriate rise in blood cortisol levels. gland. Adenoma and adenocarcinomas also
Treatment cause adrenocortical hyperfunction.
• Replacement of glucocorticoid in a dose Signs and Symptoms
approximating normal daily requirement. • Rounded moon facies with plethoric (fluid
The dose is divided such that larger amounts filled, edematous) appearance
are given in the early morning hours and
• Truncal obesity with prominent supra-
less in the late afternoon. Supplemental
clavicular and dorsal cervical fat pads
mineralocorticoids may also be required.
giving rise to characteristic “buffalo hump”
• In stressful situations, additional steroids
appearance.
may be given.
• If secondary adrenal insufficiency results • Thin distal extremities
due to failure of pituitary gland to secrete • Muscle weakness and wasting
ACTH then give corticoid replacement • Skin is atrophic and there is poor wound
therapy. healing, easy bruising and osteoporosis
• Purple straie (stretch marks) commonly Normal level of calcium maintenance

appearing on abdomen depends on dietary intake of calcium, gastro-
• Increased production of androgens— intestinal absorption of calcium and renal
hypertrichosis and abnormal facial hair in calcium excretion. If serum calcium decreases,
women PTH increases and vice versa.
Oral Changes Absorption of calcium in small intestine is
dependent on vitamin D. PTH from para-
No pathognomonic changes involving the oral
thyroid gland promotes renal formation of
structures. In children, growth and develop-
active metabolite of vitamin D (1, 25-dihydroxy-
ment including skeletal and dental age may
cholecalciferol) which increases calcium
be retarded.
absorption from GIT.
Treatment Parathormone and vitamin D are principle
Based on correction of underlying physiologic mediators of calcium and phosphate homeo-
abnormality. If a lesion is in the pituitary stasis.
gland, therapy usually consists of combination
Actions of PTH
of surgery and irradiation. Tumors involving
the adrenal cortex are removed surgically and PTH maintains blood calcium level by its
often require postoperative administration of action on three target levels:
corticosteroids to maintain normal gluco- • Bone: Increases resorption
corticoid level. • GIT: Increases absorption
• Kidney: Increases tubular reabsorption of Ca
DISEASES OF PARATHYROID GLAND and decreases reabsorption of phosphate
Anatomy and Physiology PTH stimulates osteoclastic osteolysis and
activates adenyl cyclase in bone and kidney
Parathyroid glands are four in number,
leading to formation of cyclic adenosine mono-
located on posterior aspect of thyroid gland.
phosphate. The hormone calcitonin which is
They secrete parathyroid hormone (para-
probably produced in thyroid gland has an
thormone, PTH), a polypeptide that plays an
antagonistic action to PTH. It reduces serum
important role in calcium and phosphorous
calcium by direct inhibition of bone resorption.
metabolism. Calcium is an important consti-
tuent of biologic membranes and it exerts an Hypoparathyroidism
influence on membrane permeability and It is caused by decrease in PTH level leading
excitability. Calcium also plays an essential to hypocalcemia and increased neuromuscular
role in contraction of all type of muscles. excitability. The four types of hypopara-
Normal serum calcium level is 8.8 mg/ thyroidism are:
100 ml to 10.4 mg/100 ml. • DiGeorge’s syndrome
Approximately 40% of total blood calcium
• Postoperative hypoparathyroidism
is bound to serum proteins chiefly albumin.
The remaining nonprotein bound calcium is • Idiopathic hypoparathyroidism
ultrafilterable and consists of ionized calcium • Pseudo-hypoparathyroidism
and calcium complexed with phosphate and 1. DiGeorge’s syndrome: It is the congenital
citrate. absence of parathyroid gland and thyroid,
The ionized calcium is the fraction that aortic arch anomalies and congenital heart
affects biologic processes and must be kept defects. Thymic aplasia results in severe
normal by the parathyroid and other homeo- immune deficiencies that may not be consis-
static mechanisms. tent with life.
2. Postoperative hypoparathyroidism: Most Diagnosis

common type, resulting due to inadvertent • Serum calcium level below 7 mg/dl
removal or injury to parathyroid gland • Serum phosphate level is elevated
during thyroid surgery. • Serum alkaline phosphate level is normal
3. Idiopathic hypoparathyroidism: Rare form of • Urinary calcium is low or absent
hypoparathyroidism and has unknown Treatment
etiology.
Hypoparathyroidism is treated by supple-
4. Pseudo-hypoparathyroidism: PTH levels are mental calcium and vitamin D depending on
normal but the defect exists in target organs the severity of hypoparathyroidism and the
(bone and kidney) which are unresponsive nature of the associated sign and symptoms.
to action of PTH. These patients are Hyperparathyroidism
typically small, have short metacarpals and
Hypersecretion of PTH, characterized by
metatarsal bones, mental retardation.
hypercalcemia, hypophosphatemia and
Plasma levels are often increased and the
abnormal bone metabolism. The disease is
bone may show evidence of osteitis fibrosa more frequently seen in 20–50-year-old
cystica. patients and mostly females.
Signs and Symptoms Signs and Symptoms
Due to hypocalcemia Primarily referred to bones, kidney and GIT.
• Tetany Bone: Increased osteoclastic osteolysis,
• Paresthesia of lip, tongue, fingers and feet oeteoporosis, fibrous degeneration and cyst
• Myalgia and spasm of facial muscles formation—osteitis fibrosa cystica. Bone pain
and pathological fractures are also noted.
• Twitches of facial muscles by tapping on
Kidney: Around half of the patients have renal
facial nerve—Chvostek’s sign.
calculi. Other symptoms are hematuria, back
• Trousseau’s sign (carpopedal spasm) which pain, urinary tract infection and hypertension
occurs when blood supply to the hand is are common.
reduced by application of the blood pressure
GIT: Anorexia, nausea, vomiting and crampy
cuff above the systolic blood pressure.
pain. 20% of patients demonstrates peptic ulcer.
• Weakness, cramps, palpitations, bizzare Patient presents with muscle weakness,
behavior pattern. fatigue, weight loss, cardiac irregularities,
• Skin is coarse, scaly and dry and nail beds insomnia, headache and polyuria.
are deformed, hair is thin and alopecia may Some authors have described the clinical
be present. features of hyperparathyroidism as:
• Painful bones
Oral Changes • Renal stones
• Dental age is delayed • Abdominal groans
• Enamel hypoplasia and abnormal dentin • Psychic moans
formation • Muscular overtones
• Bands of enamel hypoplasia and pits and Oral Changes
grooves observed • Radiographically skull shows groundglass
• Incomplete root formation and premature appearance, moth eaten appearance or salt
narrowing of the apices. and pepper appearance.
• The trabecular pattern of alveolus and Differential Diagnosis

mandible is indistinct 1. Paget’s disease: Calcium metabolism is
• Generalized loss of lamina dura is regarded normal but the rate of bone formation
as pathognomonic of hyperparathyroidism. exceeds rate of bone resorption, resulting in
elevated blood alkaline phosphatase level.
• Central and peripheral lesions known as
2. Osteomalacia: Blood calcium and phos-
browns tumor occur which has same
phorous levels are decreased.
histologic features as giant cell reparative
3. Fibrous dysplasia: Localised osseous changes,
granuloma. Termed as brown because of
there is no loss of lamina dura.
the color due to hemorrhage. 4. Multiple myeloma: Skull is often involved,
• A history of recurrent osseous or soft tissue Bence-Jones proteins can be demonstrated
lesions is highly suspicious of this endo- in the urine and there is characteristic serum
crinopathy (Fig. 16.4A and B). protein abnormalities on electrophoresis.
Fig. 16.4A: A 30-year-old patient presenting with swellings in the left maxillary and mandibular posterior
region
Fig. 16.4B: OPG showing generalized disappearance of lamina dura thinning of the lower border of mandible
and osteolytic lesions involving maxilla and mandible on left side
Diagnosis patients suffer from multitude of symptoms

• Increased serum calcium levels such as polyuria, polyphagia, polydypsia
• Decreased blood phosphorus levels and those associated with vascular changes
(macro- and microangiopathies).
• Alkaline phosphatase level increased
• This topic is elaborated in Chapter 1—
• Urinary excretion of calcium increased Definition, Case history and Examination.
• Increased PTH by radioisotope study
Diabetes Mellitus Suggested Reading
• Caused by the deficiency of insulin secreted 1. Burket’s Oral Medicine, 8th, 9th and 11th
by beta cells of islet of Langerhans and Edition.
results into hyperglycemia, glycosuria. The 2. Textbook of Oral Pathology, Shafer.
17
Management of Medically Compromised
Patients and Drug Interactions
MANAGING PATIENTS WITH INCREASED • Appointments should be scheduled in

MEDICAL RISKS afternoons.
• If an attack occurs, stop dental treatment,
1. Respiratory Disorders—Asthma clear oral cavity of materials and potential
Asthma is a diffuse obstructive disease of the obstructions.
airways characterized by high degree of • Administer medications usually used by
reversibility with appropriate therapy. patients, if medications prove ineffective,
obtain medical assistance.
Clinical Features • Administer oxygen via nasal cannula if
Paroxysmal dyspnea with coughing, whee- patient remains in respiratory distress after
zing and rales caused due to obstruction of bronchodilators.
airways due to respiratory smooth muscle • Administration of 1:1000 epinephrine
spasm, increased mucous secretion and edema subcutaneously.
of the mucous membrane precipitated by
2. Tuberculosis
allergens.
Refer to chapter on granulomatous diseases.
Status asthmaticus: Life-threatening
3. Syncope
complication of asthma when a patient conti-
nues to have a significant respiratory distress It is defined as a transient loss of conscious-
despite administration of sympathomimetic ness. Syncope may result from cardiovascular,
drugs and theophylline. neurologic, metabolic or psychologic disorders.
In dental practice, syncope most commonly
Dental Management results from
• History taking to assess triggers of attacks, • Vasodepressor: Severe anxiety, sudden fright,
frequency, usual severity and duration of apprehension, grief and acute pain (LA
attacks. injection) can precipitate syncope.
• Orthostatic hypotension: Venous pooling,
• Drug history of nebulizers and inhalers
prolonged supine position, abnormal
• Patients should be instructed to get medica- autonomic reflex.
tions at every visit. • Dysrhythmia
• Sedation is recommended to prevent A significant interruption of cerebral
psychogenic triggers (nitrous oxide and perfusion for more than 10–15 seconds results
chloral hydrate). in loss of consciousness and cerebral hypoxia.
244
Management of Medically Compromised Patients and Drug Interactions 245
Significant warning signs of impending dilated blood vessels produce spider petechiae
syncope: Complaints of feeling ill, nausea, on the nose, baggy eyes and puffy facial
diaphoresis (excessive perspiration), decreased features.
pulse, reduced blood pressure. Systemic effects of interest to the dentist:
Signs of syncope: Sudden appearance of • Malnutrition: Chronic alcoholics suffer from
palor involving vermilion border of the lips vitamin B complex deficiency and protein
and ala of the nose (immediately after painful deficiency. Features of hypoglycemia are
procedure like injection, extraction, etc.). more evident in alcoholics.
Rapid fall in blood pressure, bradycardia, • Neurologic disorders: Damage to central and
weak pulse, strained, shallow or abolished peripheral nervous system coupled with
respiratory efforts, seizures resulting from deficiency of thiamine has a depressant
cerebral ischemia. effect. Impaired coordination, disturbances
in gait and speech and reduced manual
Management
dexterity occurs as intoxication progresses.
1. Prevention: In cases of psychogenic causes • Gastritis, ulceration of gastric mucosa,
for syncope, prior counseling of patients is esophageal tears, varices, hemorrhoids are
needed. Efforts for stress reduction through a consequence of chronic alcohol consump-
pharmacological and nonpharmacological tion. Hence, asprin and salicylates should
methods should be undertaken. Patient be avoided by such patients.
should be encouraged to have a light meal • Chronic alcohol abuse adversely affects the
prior to dental procedures. liver resulting in fatty infiltration of liver
2. Stabilization: Patient should be positioned and cirrhosis which in turn affect the carbo-
supine with lower extremities above the level hydrate metabolism, protein metabolism
of the head. Objects in the oral cavity should and depletion of levels of potassium,
be removed. Emergency protocol must be magnesium and phosphate levels. Effects
activated. on liver affect the microsomal enzyme
3. Respiratory and cardiovascular stability induction further altering the pharmaco-
should be evaluated and confirmed using kinetics of drugs administered. Bleeding
vital signs such as heart rate, rhythm, blood and clotting factors produced by liver are
pressure. affected.
4. Communicating and questioning conscious • Chronic alcohol consumption has a dele-
terious effect on heart and cardiovascular
patient to correlate physical signs.
system due to increased levels of toxic
5. Use of aromatic ampules near patients nose, lipoproteins, decreased cardiac efficiency
cold or wet towels and depression of ventricular contractility.
6. Supplement 100% oxygen by nasal cannula Drugs interact with alcohol consumption:
7. If profound bradycardia and hypotension Disulfiram and metronidazole.
persists, start IV isotonic crystalloid solu-
tion and anticholinergic agents like 0.4 mg 5. Bleeding Diathesis
of atropine sulfate. Hemophilia (refer to Chapter on hematologic
disorders).
4. Treatment of Alcoholic Patients
Alcohol is the most widely used mood altering 6. Hypertension
beverage. Any acute increase in blood pressure from
Recognition of alcoholic patient: Tell-tale breath baseline may require immediate management.
of alcoholism, tremor of hand, persistent If the diastolic blood pressure is greater than
redness of the forehead, cheek and nose, 90 mm Hg, hypertension exists.
Clinical Features In case of an acute hypertensive attack in

Morning headache, blurred vision, tingling of dental office:
the extremities, tinnitus. • Place the patient in upright position
• Terminate the dental procedure
• Take vital signs, consult patient’s physician
• Complete history of medications used, as and arrange for medical follow-up
certain drugs such as nifedipine are • Administer nifedipine 10 mg orally or
associated with gingival enlargement. sublingually
• Patient should be seated and should have
been resting longer than five minutes before 7. Hypotension
measuring the blood pressure. Hypotension exists when systolic blood
• Measurement of blood pressure in a quiet pressure is less than 90 mm Hg and diastolic
place prior to treatment. blood pressure is less than 60 mm Hg. Patient
presents with dizziness while standing.
• Consultation with medical physician of
patient for consent regarding treatment. Possible Diagnosis for Hypotension
• Efforts should be directed to reduce stress • Syncope: Patient has slow pulse, cold
in the dental operatory. clammy hands, nausea, cerebral depression,
• Reduced appointment length. unconsciousness.
• Hypovolemia: Patient has rapid pulse and
• Important side effect of antihypertensive
low blood pressure.
medication is a tendency towards postural
hypotension; the dentist must be aware of • Cardiogenic shock: Patient may have tachy-
this reaction when raising the patients from cardia or bradycardia, peripheral perfusion
a reclining position. is poor with cold limbs and signs of peri-
pheral hypoxia.
• Use of CNS depressants such as barbitu-
• Allergic conditions: Patient has severe
rates should be avoided in patients taking
tachycardia accompanied by hypotension,
monoamine oxidase inhibitors.
bronchospasm, and dyspnea.
• Use of local anesthetics containing epine-
phrine in patients is acceptable provided Hypotension in Dental Office
that the maximum concentration of 1:10000 • Place the patient in a supine or Trendelen-
is used. Not more than five capsules (10 ml) burg position
of local anesthetics should be used. • Assure airway, administer 100% oxygen
• Substitute vasopressors such as phenyl- • Terminate dental procedures
ephrine or levonordefrin should be used in • Administer water by mouth in case of
patients who are taking monoamine oxidase hypovolemia
inhibitors.
• Administer 0.5 mg of epinephrine subcuta-
• If patient with hypertension is on β blocker neously if allergy is cause of hypotension.
and adrenaline is administered, there is (Epinephrine causes increased sympathetic
unopposed action of β receptors, which tone, increased heart rate and contractility.)
leads to exaggerated vasoconstriction, and • Administer 0.5 mg of atropine subcuta-
angina attack is precipitated. neously if syncope is likely. (Atropine is
• Use of gingival retraction cords, hemostatic a vagolytic that directly counteracts the
agents containing epinephrine is contra- increased vagal output that generates
indicated. syncope.)
Management of Medically Compromised Patients and Drug Interactions 247
8. Diabetes • Practicing caution in the treatment of an

Refer to Chapter 1 (medical history) for details allergic patient undergoing corticosteroid
therapy as these patients may be unlikely
9. Myocardial Infarction to tolerate stress and thus is far more likely
Refer to Chapter 1 (medical history) for details to manifest an episode of hypersensitivity.
• Penicillin group of drugs are most
10. Angina commonly prescribed in dental practice and
Refer to Chapter 1 (medical history) for details are most likely drugs to cause allergic and
anaphylactic reactions. Antibiotics should
11. Jaundice be prescribed responsibly, when absolutely
Refer to Chapter 1 (medical history) for details required. Skin testing should be conducted
prior to the use of this group, and in case of
12. Anemia allergy to penicillin, erythromycin can be
Refer to Chapter 1 (medical history) for details considered as an alternative to it.
• Lichenoid reactions: Refer to Chapter 3 on
13. Allergic Reactions and Anaphylaxis
white lesions.
Anaphylaxis is defined as an unusual or
exaggerated allergic reaction of an organism 14. Pregnancy
to foreign protein or other substances. All Pregnancy is not a disease and should not be
agents used in dentistry ranging from anti- treated as one. However, there are certain
biotics, analgesics, anesthetic agents, dressings, specific considerations to be noted during
disinfectants, restorations can act as potential dental treatment of such patients.
allergens.
Important Aspects
Clinical Features • Concerns regarding teratogenicity: The first
Preoperative management trimester being most sensitive to effect of
• Obtaining correct history of patients medications, infections, radiation.
regarding allergies to medication, food or • Pregnancy may unmask a prediabetic state
other agents and avoidance of those drugs. • Hypoglycemia may frequently be associated
• Allergies to local anesthetics: True allergic with pregnancy.
reactions to local anesthetics are rare. In case • Susceptibility to infections is raised due to
patient is allergic to amide group of local altered immune status.
anaesthetics (e.g. lidocaine, bupivacaine,
prilocaine, etc.). They can be substituted for
the ester-linked anesthetic agents (procaine, • Dental treatment are best provided in the
propoxycaine, tetracaine) due to absence of second trimester. Elective surgical proce-
cross-reactivity. In patients allergic to both dures are best performed after parturition.
groups, agents such as diphenhydramine • Absolute minimal use of medications,
hydrochloride can be used. avoidance of drugs with teratogenic poten-
• Most allergic reactions to anesthetics occur tial. (Thalidomide, steroids, tetracyclines,
due to preservatives used for local anes- nitrous oxide sedation, vitamin A, etc.)
thetic (methyl paraben) or preservatives for • Avoidance of use of vasoconstrictors in
vasoconstrictors (sodium metabisulphite) anesthetics.
as these agents are used extensively in food • Use of benzodiazepines for control of
products, cosmetics, etc. which can result anesthesia should be with obstetrician
in cross reactivity. consent.
• Radiation exposure only if absolutely • As these patients are susceptible to

necessary, with lead shielding, using high infections which may produce fetal defects,
speed films, long cone high voltage units they should be scheduled at different times
with optimum collimation may be preferably in absence of children patients.
performed, but are best avoided in the first Suggested Reading
trimester.
• In later stages of pregnancy as pregnancy editions.
proceeds, pressure of fetus may put 2. Medical problems in Dentistry, Cawson
pressure on abdominal vessels leading to and Skully.
postural hypotension and syncope. This can 3. Oral and Maxillofacial Pathology by
be avoided by having the patient lie on her Neville, 3rd edition.
left side for a few minutes before she is 4. Shafer’s Textbook of Oral Pathology, 6th
raised. edition.
18
Differential Diagnosis of
Miscellaneous Diseases
Differential diagnosis of various lesions in the i. Inability to open mouth

oral cavity are already discussed in various ii. Difficulty with speech
chapters, however, in this chapter differential iii. Inability to eat and chew food properly
diagnosis of various important clinical presen- iv. Difficulty in cleaning teeth
tations such as trismus, halitosis, etc. are v. Difficulty in dental treatment
described.
Causes of Trismus
TRISMUS 1. Congenital
• The word trismus is derived from the Greek • Congenital disorders are a rare cause of
word “trismos” meaning gnashing and is trismus. These include trismus pseudo-
defined as a prolonged, tetanic spasm of the camptodactyly syndrome, craniocarpotarsal
jaw muscles by which normal opening of dysplasia, hemifacial microsomia, birth
the mouth is restricted (locked jaw). injury, etc.
• In general, it includes all the conditions in
2. Traumatic
which there is inability to open mouth to
the normal distance. • Surgical removal of impacted third molars
• Normal adult oral opening ranges from is by far the most common cause of post-
35 to 50 mm measured between the incisor surgical trismus.
teeth and usually includes a measurement • Fracture involving mandible usually gives
of overbite. rise to trismus.
• The muscles of closure are approximately • Fracture with dislocation of a condylar head
10 times more powerful than the opening can result in a mechanical obstruction and
muscles. The relative weakness of the limit jaw function.
opening musculature explains why patients • Fracture of zygomaticomaxillary complex
have an inability to open the mouth when can limit jaw function by direct impinge-
pathosis limits mandibular motion, e.g. in ment of the complex on the coronoid
tetanus there is spasm of both closing and process of the mandible.
opening muscles but patient presents with • Hemarthrosis of TM joint and hematomas
trismus. of the muscles of the mastication are relati-
• Patients suffering from trismus may present vely common causes of trismus.
to the dentist with a variety of complaints, • It can be caused by needle tract infection,
these are: trauma and inflammation of medial
249
pterygoid muscle. The most common Tetanospasmin is responsible for all the
injections resulting in this phenomenon are clinical features of trismus, it acts by inter-
the inferior alveolar nerve block and poste- fering with the release of acetylcholine.
rior maxillary infiltrations. Both involve the As more muscles are involved rigidity
penetration of muscle and deposition of becomes generalized. Contraction of facial
anesthetic solution into a highly vascular muscle produces a typical expression
space. A small amount of intramuscular called as ‘risus sardonicus’.
hemorrhage may result in discomfort when • Abscesses involving the spaces surroun-
anesthesia wears off. Multiple injections ding the muscles of mastication are a
increase the chance of bleeding from muscles common cause of trismus. There is often
or blood vessels causing a hematoma history of toothache, recent restoration,
leading to trismus. root canal treatment, recurrent peri-
• Anterior dislocation of the TMJ meniscus coronitis, or recent extraction.
is a relatively common cause of trismus. • Facial cellulitis, acute parotitis, acute TMJ
arthritis, otitis externa and peritonsillar
3. Neoplasia abscess can cause trismus.
a. Benign: A wide variety of benign neoplasms • Ludwig’s angina which is cellulitis
have been reported as a cause of limited oral involving the submandibular, sublingual
opening, e.g. osteochondromas, osteomas, and adjacent spaces commonly caused
involving the condyle and coronoid process, by lower third molar infection often
myxoma and hemangiomas in the region of presents with trismus, dysphagia and if
condyle. left untreated can lead to asphyxia and
life-threatening emergency.
Decreased opening secondary to tumors
• Dysphagia is often associated factor and
usually results from mechanical obstruction
clinical examination may reveal swelling,
to mandibular movement.
rednesss, pain and trismus.
b. Malignant: All malignant tumors involving • Pharyngeal spread of infection has more
the jaws, muscles of mastication and serious consequences but paradoxically
associated structures can cause limitation reveal less external signs.
of mandibular movement. Most commonly • Peritonsillar abscess presents with pain
nasopharyngeal and oropharyngeal carci- radiating to the ear, drooling of saliva
nomas which give rise to coronoid locking. and pain on swallowing, dehydration,
Trotter‘s triology of symptoms occurring cervical lymphadenopathy and trismus,
with nasopharyngeal tumor which includes tilting of head towards the affected site
lower jaw pain, palatal asymmetry and and intraorally gross unilateral swelling
deafness or fullness in the ear. Trismus is a of the palate and anterior tonsillar pillar,
common feature. downward displacement of tonsil and
displacement of uvula to the opposite side.
4. Reactive
b. Chronic
a. Acute • It involves:
• Tetanus is a rare and very important – Temporomandibular joint ankylosis
cause of trismus because it is accom- – Degenerative joint diseases
panied by a high mortality rate. – Rheumatoid arthritis
It is caused by Clostridium tetani, which – Post-radiation fibrosis of the muscles
produces two exotoxins—tetanospasmin of mastication
and tetanolysin. – Myofascial pain dysfunction syndrome.
Differential Diagnosis of Miscellaneous Diseases 251
5. Psychogenic HALITOSIS
Hysteria is a common cause of trismus. These ‘Halitus’ means breath and ‘osis’ means
patients should undergo psychiatric assess- condition, so halitosis is a condition in which
ment, most of the patients with hysterical there is an abnormal or obnoxious breath.
trismus open their mouth under IV sedation Cacosmia: Patient has perception of evil odor
or general anaesthesia. in the nose. Either it is a subjective symptom
EMG of these patients reveal no activity of or an aura of epilepsy.
inframandibular muscles when patient tries Odors arising from the mouth:
to open the mouth but there is increase activity • Morning breath: It is because of:
of closing muscles. In cases of physical trismus
– Lack of salivation
there is increase activity of inframandibular
muscles when patient tries to open the mouth. – Failure of movement and swallowing to
remove desquamated epithelial cells , food
(However, long-standing trismus with any debris, microorganisms, etc.
cause can lead to fibrosis of masticatory
– Excessive snoring
muscles.)
• Hunger breath: Hunger can cause halitosis
6. Drug Induced due to hypoglycemia and is cured by a meal.
Acute dystonic reactions may occur as a result • Diet: Fried food, tea, coffee, onion, garlic, etc.
of neuroleptic or antiemetic medication. • Smoker’s breath: In the smokers, the odor is
Strychnine poisoning is possible cause of exuded from lungs, bronchi, mouth, nose
trismus. It can also cause heightened aware- and PNS.
ness, intensified visual impressions, and Pathological Conditions of the Mouth
convulsions of the spinal tract which mimics
• Poor oral hygiene
tetanus with appearance of risus sardonicus.
• Gingivitis and periodontitis (at times frank
7. Miscellaneous Causes pus is present)
• Submucous fibrosis • Degenerating blood from the mouth:
• Post-burn scars – Bleeding gums
• Post-surgical scarring – Post-extractions
• Scleroderma – Post-tonsillectomy
• Vincent’s infection: ANUG and Vincent’s
• Tubercular meningitis
angina
• Epilepsy
• Gross caries
• Myositis ossificans • Unclean dentures and ortho plates
• Tetany (calcium deficiency leading to • Ulcers and tumors
muscle spasm) • Pericoronitis
– Chvostek’s sign: Tapping the facial nerve • Furred tongue (increased coating) and
at the angle of mandible causes twitching fissured tongue.
of facial muscles.
– Trousseau’s sign: Carpopedal spasm which Pathological Conditions of Nasopharynx
occurs when blood supply to the hand • Sinusitis with postnasal discharge
is reduced by the application of blood • Rhinitis (ozena—an atrophic rhinitis with
pressure cuff above the systolic blood mucopurulent discharge associated with
pressure. Klebsiella pneumoniae)
• Rabies (hydrophobia). • Septic adenoids and tonsils
• Pharyngitis SWELLINGS IN FLOOR OF THE MOUTH

• Respiratory tract infection and influenza
The various causes are:
Conditions of Lung and Bronchi • Ranula: A ranula is a mucocele that occurs
• Abscess in the floor of mouth, a retention cyst in
• Bronchiectasis sublingual salivary gland. A plunging
• Cavitation in the lung (area of stagnation) ranula is one that penetrates the mylohyoid
• Lung abscess muscle with possible enlargement in upper
midline of neck.
• Empyema
• Mucocele: It is one of the most frequent
Conditions of Alimentary Tract bluish lesions occur on lower lip, but it can
These conditions do not produce halitosis as occur anywhere on oral mucosa. It occurs
is usually believed. It has been claimed that when a duct of minor salivary gland is
there is a peculiar odor from the breath of the severed by trauma and the secretions
patient who is bleeding from the GI tract, spilled and pooled in superficial tissues
however, generally there is an aroma of (extravasation cyst). The other type is
melena surrounding the bed of the patient but retention cyst, which occurs because of
this is more often from flatus coupled with accumulation of saliva in the ductal
lack of oral hygiene. elements/parenchyma.
• Sialolithiasis: These are calcareous deposits
Dehydration in the duct of major/minor salivary glands
All conditions which cause dehydration will or within the gland themselves. These give
result in halitosis, e.g. hospitalized patients rise to diminished salivation on the affected
with no oral intake, even sleep, mouth side with or without pain and swelling in
breathing, heavy exercise, prolonged public relation to intake of food.
speaking. • Sialoadenitis: A painful enlargement of
Fetor Hepaticus salivary gland may be produced by
inflammation or infection of the gland
Halitosis which occurs in acute liver failure caused by ductal occlusion.
and described as animal like, musty or mousey
• Dermoid cyst and epidermoid cyst: These are
and interestingly compared to the aroma of
developmental anomalies basically cystic
fresh corpse.
teratomas resulting primarily from trapped
Renal Failure germinal epithelium. The floor of the mouth
In chronic renal failure, patient presents with is most common area in head and neck
dry and discolored tongue, foul odor because region. The cyst may be in the midline or
of urea secreted by the saliva and described placed laterally, they are nontender and soft
as ammonical breath or urine-like smell. to rubbery in consistency.
These cyst are originating in the loose
Substances Excreted via Lungs subcutaneous or submucosal tissue and are
• Ketones: Diabetic ketosis—fruity or sweet encapsulated, hence are freely movable in
aromatic odor called as acetone breath. all directions, and also the skin can be easily
• Paraldehyde anticonvulsant drug moved over them.
• Disulfiram: Anti-abuse drug given as a The lumen of the simple cyst is filled with
deterrant to alcoholics (converts alcohol fluid or keratin and no other specialized
into aldehyde) who get symtoms of structure, such a cyst is called as epider-
halitosis and cacogeusia. moid cyst.
The lumen may contain other elements such • Odontogenic infection: Abscess
as sebaceous material as well as keratin, Cellulitis (Ludwig’s angina): It may present
then the lesion is called as dermoid cyst. as tender generalized swelling in the floor
If the lumen contains elements such as blood, of the mouth which elevates the tongue and
muscles, teeth, it is called as a teratoma. floor of the mouth and makes the sub-
lingual folds very prominent. It may be
• Sebaceous cyst: Superficial dome shaped
associated with submandibular submental
mass usually occur in hair-bearing area.
and other space infections giving rise to
These are painless and slow growing in medical emergency.
nature. This cyst is attached to the skin or
• Minor salivary gland pathologies such
is a part of the skin but it is not attached to
as cystic lesions and benign tumors
the underlying structures. Therefore, it can
(pleomorphic adenoma). It may present as
be moved freely over the underlying struc-
swelling in the floor of the mouth.
tures but it cannot be moved independently
Clinical examination, sonography, CT scan,
of the skin.
scintigraphy and MRI can help in diagnosis
• Hemangioma: These are benign tumors of almost all the swellings in the floor of the
composed of blood vessels, can be capillary mouth as these are of soft tissue origin and
or cavernous. They are bluish in color and conventional radiography will not help in the
blanch on pressure (diascopy) and the soft diagnosis.
tissue swelling produced by hemangioma
is emptiable. PERFORATION OF PALATE
• Lymphangioma: These are similar to
The various causes of perforation of palate are:
cavernous hemangiomas, but consists of
• Developmental: Cleft palate
lymphatic vessels usually congenital, most
• Traumatic: Iatrogenic trauma caused by
commonly seen on dorsal surface, or lateral
inadvertent injury during extraction
borders of tongue. Dialated lymphatic
(slipping of elevator).
channels impart a pebbly appearance to the
surface of the lesion and unlike heman- Necrosis caused by chemical/thermal burn
(phossy jaw, metal poisoning).
gioma, it cannot be evacuated by digital
pressure. Aspiration yields lymph fluid • Infectious: Syphilitic gumma of palate
which is high in lipid content. Avascular necrosis associated with
uncontrolled diabetes mellitus or with deep
• Lingual thyroid: It presents as a swelling on fungal infections, such as mucormycosis,
the tongue in the midline and is suggestive blastomycosis, etc.
of ectopic location of the thyroid tissue, this • Osteomyelitis: Osteomyelitis with various
can be diagnosed with the help of etiologic factors such as odontogenic
scintigraphy with 131I. It can be confirmed infections, systemic infections, radiation
with biopsy which will show typical therapy, etc. involving the palate can result
thyroid tissue. into perforation.
• Choristoma: It is a tumor-like growth of • Necrotizing sialometaplasia: It is a self-limiting
normal tissue in an abnormal location. minor salivary gland disorder which rarely
Osseous and cartilaginous choristomas are can result into perforation of the palate.
most commonly seen on the tongue dorsum • Herpes zoster: Alveolar necrosis and
(near foramen cecum). The swelling is firm exfoliation of teeth has been observed as a
and have a smooth surface. It can be complication of herpes zoster involving the
pedunculated or sessile. jaws.
• Neoplastic: Squamous cell carcinoma: SWELLINGS AT ANGLE OF MANDIBLE

– Adenoid cystic carcinoma (cylindroma) The various causes are:
– Mucoepidermoid carcinoma • Developmental: Branchial cleft cyst
– Osteolysis known to be associated with • Traumatic
above malignancies can often result in – Fracture mandible
palatal perforation. – Haematoma
• Midline lethal granuloma: This term is no • Inflammatory
longer used. It is presently attributed to – Periapical infection
neoplastic lesion that is lymphoma which – Periodontal infection
causes perforation of the palate, and – Pericoronal infection related to 3rd molar
involvement of nasal cavity. It is to be – Submandibular space infection
differentiated from Wegener’s granulo- – Osteomyelitis
matosis where in the palatal and nasal – Tuberculous lymphadenitis
lesions are independent. – Syphilis
• Miscellaneous: Perforation caused by suction – Actinomycosis
disc which in the past was used in – Salivary gland pathology:
fabricating maxillary dentures for the Sialoadenosis
purpose of increasing retention. Sialolithiasis
Sialoadenitis
DISCHARGING SINUS Mumps

The term ‘sinus’ means a tract lined by • Neoplastic
epithelium which connects a pathological – Benign tumors
cavity with the exterior/intraoral surface, e.g. Osteoma
discharging sinus associated with pericoronal Ameloblastoma
abscess in third molar. Odontogenic myxoma
The term ‘fistula’ means an abnormal Pleomorphic adenoma
pathway between two anatomical cavities, Warthin’s tumor, etc.
e.g. oroantral fistula. – Malignant tumors

Squamous cell carcinoma
The causes are:
Osteosarcoma
• Periapical infection
Mucoepidermoid carcinoma, etc.
• Periodontal infection
• Reactive lymphadenopathy: Secondary to
• Pericoronal infection infections and malignancy.
• Fracture of mandible with infection • Miscellaneous: Masseteric hypertrophy.
• Osteomyelitis
• Sialoadenitis (parotid and submandibular BALD (DEPAPILLATED) TONGUE
gland infection) Differential diagnosis includes:
• Tuberculosis (cold abscess and scrofula) • Iron deficiency anemia (Plummer-Vinson
• Actinomycosis (sulphur granules) syndrome)
• Osteomyelitis secondary to intrabony • Pernicious anemia
tumors • Sjögren’s syndrome
• Carcinoma with secondary infection • Oral submucous fibrosis, scleroderma
• Post-radiation therapy Lesions which Heal with Scarring

• Chronic candidiasis 1. Major aphthous
• Syphilitic glossitis 2. Cicatricial pemphigoid
• Epidermolysis bullosa 3. Epidermolysis bullosa
• Geographic tongue 4. Post-radiation fibrosis
• Median rhomboid glossitis 5. Burn injury
6. Interstitial glossitis of syphilis
Numbness of the Chin
7. SMF can be considered
The various causes could be:
1. Periapical abscess, osteomyelitis Lesions which involve Oral Cavity and Eyes
(Sight-Threatening)
2. Post-traumatic, post-injection, post-surgical
1. Behçet syndrome
3. Cyst/benign tumor/malignancy causing
pressure on the nerve 2. Stevens-Johnson syndrome
4. Metastatic malignancy 3. Sjögren’s syndrome
4. Cicatricial pemphigoid
5. Diabetic neuropathy
5. Herpes zoster
6. Pre-herpetic symptoms
6. Congenital syphilis
7. Vit B12 deficiency
7. Reiter’s syndrome
8. Hansens disease
9. Paget’s disease and osteopetrosis Suggested Reading
Necrotic Ulcerations editions.
1. ANUG 2. Differential Diagnosis of Oral and Maxillo-
2. Agranulocytosis facial Lesions, Wood and Goaz, 5th edition.
3. Aplastic anemia, leukemia 3. Oral and Maxillofacial Pathology by
4. Cancer chemotherapy Neville, 3rd edition.
5. Cyclic neutropenia 4. Shafer’s Textbook of Oral Pathology, 6th
6. Necrotizing sialometaplasia edition.
19
Forensic Odontology
Forensic Science survive most of the insults and consequences

The word forensic is derived from the Latin encountered at death and during decom-
word forensis meaning public. The word position.
science can be defined as systematized Comparative Dental Identification
knowledge through study using the scientific
It is the conventional method of postmortem
method.
dental identification, and includes four steps:
Forensic Odontology • Oral autopsy
Forensic odontology has been defined by the • Obtaining dental records
Federation Dentaire International (FDI) as • Comparing post- and antemortem dental
‘that branch of dentistry which, in the interest data
of justice, deals with the proper handling and • Writing a report and drawing a conclusion
examination of dental evidence, and with the
proper evaluation and presentation of dental Oral Autopsy
findings.’ • Also known as necropsy or postmortem,
involves examination of the deceased,
Role of Dentist in Identification of usually with dissection to expose the
Unknown Body from Dental Records organs, to determine the cause of death.
The positive identification of living or • It has a systematic protocol starting with
deceased persons using the unique traits and examination of external features of the
characteristics of the teeth and jaws is a body.
cornerstone of forensic science. Forensic • The forensic dentist should have know-
dentists can compare characteristics recorded ledge of postmortem findings like rigor
in a patients dental chart, usually obtained mortis, livor mortis, decomposition and
from the private dentist, with the dental postmortem artifacts.
characteristic found in a unknown person or • Rigor mortis render the jaws rigid and the
a found body. If the characteristics are the use of mouth-gags, or intraoral myotomy
same, the unknown person/body can be is essential for jaw separation.
identified. • Teeth may become brittle in burn cases,
The teeth are the hardest substance in the they need to be reinforced with cyano-
human body and may be the only method to acrylate cement, polyvinyl acetate, or clear
identify the deceased. Teeth potentially can acrylic spray paint prior to examination.
256
Forensic Odontology 257
• Access for radiographs is made by • Insufficient information—insufficient ante-

removing the contents in the floor of the and postmortem information.
mouth in a tunneling fashion from beneath • Excludes identification—comprehensive
the chin. differences indicate mismatch.
• A thorough examination of the soft tissue
injuries, fractures, or foreign bodies is done. Identification from Dental DNA
• All information is entered in standard Teeth can resist extreme conditions and
‘interpol postmortem form’ which is color- according to pretty and sweet, are an excellent
coded in pink. source of DNA. Polymerase chain reaction
allows amplification of even highly degraded
Obtaining Dental Records
DNA. This facilitates comparison of ante-
• Dayal and colleagues state that dental mortem sample like hair from hairbrush,
records may be obtained from the treating epithelial cells from toothbrush or a biopsy
dentist, specialist or hospital records. specimen. If the decedent’s antemortem
• The original records in the form of dental sample is unavailable, the DNA pattern is
charts, radiographs, casts and/or photo- compared with parent or sibling.
graphs are collected and transcribed onto
the standard ‘interpol antemortem form’ Extraction of Dental DNA
which is color coded as yellow. Owing to its neurovascular nature, pulpal
tissue is considered to be the best source of
Comparing Post- and Antemortem Dental Data
DNA.
The postmortem evidence and dental records • Method: Cryogenic grinding
are compared for tooth morphology and – Cooling whole tooth with liquid nitrogen
associated bony structures, pathology and to extremely low temperatures and then
dental restorations. mechanically grinding it to fine powder.
Writing a Report and Drawing Conclusions This requires crushing of the entire tooth.
A detailed report and factual conclusion is • Extraction of DNA can also be done from
clearly stated based on the comparison. There dentin and cementum.
might be differences in the dental findings like • Less destructive method is to open the root
a tooth which is filled in postmortem data may canal and obtain the scraping from the pulp
be intact in the dental records. Having with a notched medical needle. And use the
compared and weighed the two sets of data, material obtained for DNA isolation.
one should ask a set of questions: Are • Multiple teeth may be utilized for optimum
similarities significant? Can the differences be results.
explained? Palatal Rugae in Identification
Based on these following range of con- • The rugae pattern on the deceased’s maxilla
clusions can be drawn: or maxillary denture can be compared to
• Confirms identification beyond reasonable the old dentures recovered from the victims
doubt, includes radiographic support. house or plaster model available with the
• Probable identification, data is comparable treating dentist.
but lack of ante- and postmortem informa- • A useful method for identification in
tion prevents confirmation of the identity. edentulous patients.
Usually no radiographic support. • Palatal rugae are ridges on the anterior part
• Possible identification explainable differences of the palatal mucosa on each side of mid-
exist. palatine raphae, behind the incisive papilla.
Classification of Palatal Rugae Sex Differentiation

Suggested by Lysell: Sex can be determined based on data from
• Primary rugae (>5 mm) morphology of skull and mandible, metric
• Secondary rugae (3–5 mm) features, as well as DNA analysis of teeth.
• Fragmentary rugae (2–3 mm) Sex determination from craniofacial morphology
Thomas and Kotze have further detailed the and dimensions
patterns of primary rugae into branched, • It is based on the measurements of the skull
unified, crosslinked, annular, and papillary. using lateral cephalometric tracings.
• Sex differentiation is made from variables
Analysis of Rugae Pattern such as length of the cranial base, mastoid
• Thomas and Van Wyk have manually height and width, and total face height.
traced rugae patterns on clear acetate and • They have also discovered that the maxi-
then superimposed on photographs. mum length of the skull also gives an
• ‘RUG FP-ID MATCH’ is a computer accurate estimate of the height of an
software program developed by Limson individual.
and Julian. • In general, the male skull is larger than
• On digitized images of the palate points are females with endocranial volume about
plotted on medial and lateral extremities of 200 cc.
the rugae. • Rigorous training in osteology and
• The plotted points are processed by the measuring techniques is essential for sex
software and information is stored. identification from the above parameters.
Sex difference in tooth size
Dental Profiling
Teeth are used for gender differentiation by
It includes extracting a triad of information— measuring their mesiodistal and buccolingual
the decedent’s ethnic origin, gender and age. dimensions. The canines show the maximum
Identifying Ethnic Origin from Teeth genderwise difference. Premolars, first and
second molars as well as maxillary incisors also
Human diversity permeates to dental morpho-
have significant difference.
logy as well, and dental anthropologist have
Dental index: Aitchison presented the
catalogued this diversity. As a result, it is
‘incisor index’ which is calculated by the
possible today to identify an individuals
formula
ethnic origin based purely on one’s dentition.
Ii = [MDI2/MDI1 ] × 100
Genetic and Environmental Influences where, MDI2 = maximum mesiodistal dia-
on Teeth meter of maxillary lateral
• Dental features have a complex mode of incisor
inheritance and are combination of heredi- MDI1 = maximum mesiodistal dia-
tary and environmental factors to which a meter of central incisor.
person is exposed. This index is higher in males compared to
• Dental features used to describe population females. This means that in females lateral
differences are broadly categorized as incisors are much smaller than central incisors,
metric (tooth size) and non-metric (tooth whereas in males the difference between the
shape). Metric features are based on mesiodistal dimension of central incisors and
measurements, and non-metric in terms of lateral incisors is less than that in females.
presence or absence of a particular feature, ‘Mandibular canine index’ by Rao also
e.g. whether Carabelli’s cusp is present or not. helps in sex determination.
Sex Determination by DNA Analysis Demirijian’s Method

Sivagami and coworkers state, amelogenin • This method made use of a scoring system.
(AMEL) is one of the major matrix proteins • The development of seven mandibular
secreted by the ameloblasts of the enamel. The teeth on left side was divided into eight
AMEL gene, coding for a highly conserved stages each (Fig. 19.1).
protein, is located on the X and Y chromo- • These are named from ‘A’ to ‘H’. Third
somes in humans. The two alleles are similar molar was not used in original method.
for the exonic sequences but differ in the • Each tooth is assigned a ‘maturity score’
intronic sequences. Thus, the females have two that corresponds to its developmental stage.
identical AMEL genes but the males have two • Maturity score for each tooth is added. The
nonidentical genes. total maturity score is then plotted on the
Dental Age Estimation chronological age conversion table.
A, beginning of calcification in the form of
Methods
an inverted cone or cones; B, mineralized
Age estimation using the dentition may be cusps are united to show coronal morphology;
grouped into three phases: C, crown half formed, pulp chamber is
• Estimation of age in prenatal, neonatal, and evident; D, crown formation is completed up
early postnatal: to cementoenamel junction, with beginning of
– It makes use of histological techniques, root formation; E, initial formation of the root
which enable observation of tooth
mineralization up to 12 weeks before it
is actually apparent on radiographs.
– The neonatal line is considered as an
indicator of birth. The neonatal line may
take about three weeks after birth to form.
– Estimating age in this group may have
legal implications in cases that involve
foeticide and infanticide.
– For age estimation of skeletal remains
histological sections and radiography is
not practical. An alternative is to measure
the dry weight of the mineralized tooth
cusps developed by stack. The developing
teeth in a child at six months IU weigh
about 60 mg, 0.5 g in a newborn and
1.8 g at the six months postnatal.
• Age estimation in children and adolescents:
– Two events that may be used are:
Tooth eruption
Tooth calcification
Schour and Masler’s Method
The chart produced by them is based on
histological sections which permit direct
comparisons with radiographs. This chart was Fig. 19.1: Eight stages (A to H) of mineralization of
modified by Ubelaker. tooth (Demirijian system)
bifurcation; F, the apex ends in a funnel shape; Limitations

G, the walls of root canal are now parallel, its • None of the variables could be used alone,
apical end partially open; H, the apical end of except dentin translucency.
the root canal is completely closed; the • Training in histological sections were
periodontal membrane of uniform width necessary.
around the root and the apex • Equipment like stereomicroscope was
• Role of third molars in successful age required.
estimation is known to be notoriously • When only one tooth is used the age range
untrustworthy mainly because of a great increased significantly.
variation in genesis:
– Valuable indicator in age range of 16–23 Dentin Translucency
years. • Root dentin starts to become translucent
– When all four third molars have comple- during third decade of life beginning at the
tely calcified, the chances of the individual apex and advancing coronally.
being 18-year-old is 96.3% and 95.1% for • The alteration is believed to be due to the
males and females, respectively. decreased diameter of dentinal tubules
– When all four-thirds molars are unavailable caused by increased intratubular calcifica-
then lower-third molars are best predictors tion. Hence, difference in between intra-
of age. tubular organic and extratubular inorganic
material is equalized which results in
– This has great implication because 18-
increased translucency of affected dentin.
year-old is the age of majority in many
Age = B0 + B 1X + B 2X2, for zones of
jurisdictions around the world.
translucency ≥9 mm
• Age estimation in adults.
And, Age = B0 + B1X, for zones of translucency
Gustafson’s Method >9 mm
In 1950, Gosta Gustafson developed a method B0 = regression constant
based on morphological and histological B1, B2 = regression coefficient
changes of the teeth. This assessed regressive X = translucency length
changes such as:
Age Estimation by Incremental
• Amount of occlusal attrition (A) Lines of Cementum
• Coronal secondary dentine deposition (S) • Kagerer and Grupe suggested the possi-
• Loss of periodontal attachment (P) bility of age estimation from acellular
• Cementum apposition at the root apex (C) cementum incremental lines.
• Root resorption at the apex (R) • Mineralised unstained cross-sections of
• Dentine translucency (T) teeth preferably mandibular central and
For each of these variables a score 0–3 is third molars are used.
assigned. Increase in total score corresponds • In addition, hypomineralized bands in
to an increase in age. However, improvements these incremental lines give an indication
made by Johanson are widely accepted. He of pregnancy, trauma and renal disorders.
proposed seven grades (0, 0.5, 1, 1.5, 2, 2.5, Radiographic Method of
and 3) Kvaal and Associates
Formula • This method used pulp size measurement
Age = 11.02+ (5.14A) + (2.3S) + (4.14P) + 3.71C) of six teeth (maxillary central and lateral
+ (5.57R) + (8.98T) incisor, second premolar, mandibular
incisors, canine and first premolars) on Bite Mark Appearance

periapical radiographs. Type of Injury
• It measures—pulp-tooth length (R), pulp-
• Compression of skin surface due to tooth
root length (P), tooth-root length (T), pulp-
pressure during a bite causes indentations
root width at CEJ (A), mid-root level (C).
initially. They seldom stay for a few
Mean value of all ratios excluding T is M,
minutes, due to elastic nature of skin, unless
mean value of B and C is W.
the victim is dead.
• It uses the formula:
• This is followed by brief period of edema
Age = 129.8 – 316.4 (M) – 66.8 (W-L)
over the bite area.
Bite Marks • Once edema subsides subcutaneous
It is defined by McDonald as “a mark caused bleeding occurs which appears as reddish
by the teeth either alone or in combination or purplish discolorations.
with other mouth parts”. Identifying the Injury as Bite Mark
• It may be caused by humans or animals on
• Gross features: Circular or elliptical mark
tissue, food items, or other items.
found on the skin with a central area of
• There are significant differences in human ecchymosis.
and animal bite.
• Class features: The pattern may vary in size
• Human bite mark is broad, U-shaped and and shape which helps to differentiate
circular or oval whereas of animals is between different types of teeth, e.g.
narrow in anterior aspect and is V-shaped incisors—rectangular marks, canines—
and elongated and also the morphology of triangular or rectangular, premolars and
teeth is different. molars—spherical or point-shaped.
Classification of Bite Marks • Individual features: Class features may have
characteristics like fracture or rotations
McDonald’s Classification
which are known as individual features.
• Tooth pressure marks: Produced on tissue as • Site of bite marks: Can be found on any part
a result of direct pressure by teeth. It is of body. Like females are bitten most often
produced by incisal or occlusal surfaces of on breast and legs, male children on their
teeth. genitals, etc.
• Tongue pressure marks: When sufficient
amount of tissue is taken into mouth, the Bite Mark Investigation
tongue presses it against rigid areas like • Ideally bite evidence should be collected
lingual surfaces of teeth and palatal rugae. when it is first presented and observed. It
The marks thus left are referred to as should not be forgotten that the primary
‘suckling’. concern is patient care and collection of the
• Tooth scrape marks: Caused due to scraping bite mark evidence should not interfere
of teeth across the bitten material. with timely patient treatment.
Webster’s Classification • When associated with laceration and
• Type I: The food item fractures readily with abrasion chances of infection are high, i.e.
limited depth of tooth penetration HIV, hepatitis B, syphilis, etc.
• Type II: Fracture of fragment of food item The protocol for bite mark investigation
with considerable penetration of teeth. involves following steps:
• Type III: Complete or near complete pene- • Visual examination
tration of the food item with slide marks. – Type of injury
– Contour, texture and elasticity of the site • Evidence collection from the suspect should
– Physical appearance: Color and size, be obtained using a signed and witnessed
orientation and location of bite mark informed consent or a court order.
– Differences between upper and lower After a detailed extraoral and intraoral
arches and between individual teeth, examination, the following evidence should
be obtained.
• Photography
1. Photographs of the suspects teeth in
– Photograph provides permanent record occlusion and open bite.
of appearance of the bite marks
2. Maxillary and mandibular impression
– Photograph should be taken immedia- with rubber base material poured in
tely as the injury rapidly changes its dental stone.
appearance due to healing 3. Bite registration and centric occlusion
– Color and black and white photographs using a thin sheet of wax.
from different angles should be taken 4. Saliva swab from the buccal vestibule.
Two views Labeling and storing the above evidence in
1. Orientation photograph to show suitable containers is mandatory.
the bite mark location on the body Bite Mark Analysis and Comparison
2. Close up photograph taken with the
This is a challenging task because one has to
rigid reference scale placed with the
consider the jaw movements of the suspect
same plane as the injury
also the movement on the part of the victim,
• Saliva swab: Saliva deposited on the skin flexibility of the bitten tissue and distortion
may have WBCs and sloughed epithelial introduced during photography.
cells. These are potential source of DNA It is important to consider certain chara-
thus enabling a direct link to the suspect. cteristics of the bite mark. Such as presence or
The bite mark area should not be washed absence of a particular tooth, mesiodistal
before collecting the saliva swab. A cotton dimension, rotation, fracture, diastema and
swab moistened with distilled water should other unusual features of the teeth which may
be used for swabbing. This rehydrates the help in implicating the suspect. Measurements
dry cells in the bite area. The swab is then obtained from the bite mark should be
labeled and stored in the refrigerator. The compared with the suspects dental model.
refrigeration prevents degradation of Direct method of comparison: Where the
salivary DNA and also growth of bacteria. suspects model is placed directly over the bite
In the absence of visible bite marks, high mark itself or the photograph of the bite mark.
intensity light source such as UV light can Indirect method: Incisal and occlusal edges
be used to locate the stains from body fluid of the suspects teeth are traced on the clear
and enable saliva traces to be recovered. acetate and superimposed on life-sized
• Impressions: Impressions should be made photograph.
when tooth indentations exist. The material Computer software program can be used
of choice is vinyl polysiloxane. The (3-D/CAD supported photogrammetry
impression material should be reinforced approach) and holds promise for the future.
with dental stone, self-cure acrylic. If the
bite mark is on an area accessible to the Conclusions of Bite Mark Analysis
victim’s dentition impression of the victims 1. Positive identification: Indicates that there is
teeth also should be made for suspected definite and characteristic match between
self-inflicted bites. the suspects teeth and the bite mark.
2. Possible identification: Implies that suspects prints, if it has to withstand the rigors of court
teeth could have made the bite mark but interrogation.
there is no characteristic match to be
Dentist as an Expert Witness
absolutely certain.
For a practicing dentist not accustomed to the
3. Excludes identification: When the suspects
court procedure the experience as an expert
teeth and bite mark show no characteristic
witness can be intimidating. The witness is
and comparable features indicating that the
first questioned by the side for which he is
suspects teeth could not have definitely
appearing. After this the lawyers of the
caused the bite mark.
opposite side will do cross-examination,
Lip Prints which is the most challenging aspect of court
appearance. The opposition lawyer may try
Presence of wrinkles and the grooves on the to weaken the expert witness and the evidence
lips have been described as ‘sulci labiorum that is presented. It is important for the expert
rubrorum’. Examination of the imprint witness not to become biased or angry during
produced by the lips is termed as “cheiloscopy”. cross examination as this tends to make them
Lip prints are usually left at the crime scene careless and vulnerable and get easily trapped
and can provide a direct link to the suspect. It by the shrewd laywers. It is important to
is interesting to note that use of lipstick is not remain calm and dispassionate and speak up
essential to leave lip print. The vermilion clearly for everyone concerned to hear.
border of the lips has minor salivary gland and Always present the evidence and con-
the edges of the lip has sebaceous glands with clusions based on facts as truth is paramount
sweats glands in between. Secretions of oil and and repeatable. If the expert does not know a
moisture from these enable development of answer to the question he should say so and
latent lip prints similar to latent finger prints. not guess the answers or answer the questions
Although invisible these prints can be lifted that are beyond ones expertise. Opinion
using materials like aluminum powder and should be presented in such a way that is
magnetic powder. accurate and simple enough for a lay person
Major disadvantage of lip print investiga- to understand.
tion is that the lip prints may not remain
unchanged throughout one's life, the zone Suggested Reading
close to vermilion border is extremely mobile 1. Chapter on Forensic Odontology by Ashith
and therefore the prints produced may differ Acharya and B. Sivapathsundharam;
in appearance depending upon the pressure Shafer’s Textbook of Oral Pathology, 5th
applied and its direction. Rigid protocol has edition.
to be established by the forensic odontology 2. DCNA: Forensic Odontology. Volume 45,
speciality to obtain and to analyze the lip Number 2, April 2001.
20
Evidence-Based Dentistry
INTRODUCTION Definition
EBM is defined as ‘the integration of the best
In the last century, majority of the decisions
research evidence with clinical expertise and
regarding treatment plan were based on patient values’ and described as ‘the conscien-
personal experience and wisdom of well- tious, explicit, and judicious use of current best
established physicians and surgeons. evidence in making decision about care of
As these decisions were based on individual individual patient’ (Fig. 20.1).
experiences, preferences and bias, they may Applying EBM principles to dentistry, the
be open to criticism or scientific and logical American Dental Association developed the
questioning. following definition for the term ‘Evidence-Based
Dentistry’ or ‘EBD’: “An approach to oral health care
Presently the decision making is preferably that requires the judicious integration of systematic
based on scientific evidence gathered and pub- assessments of clinically relevant scientific evidence,
lished by various experts in the field. Evidence relating to the patient’s oral and medical condition and
based dentistry provides a sound, reliable and history, with the dentist’s clinical expertise and the
unbiased decision making platform. patient's treatment needs and preferences.”
Fig. 20.1: Different dimensions of evidence-based decision making process
264
Evidence-Based Dentistry 265
TRADITIONAL VS EVIDENCE-BASED DECISION MAKING
Concept Traditional method Evidence-based approach

Use of explicit rules Use of inductive reasoning Reproducible and dynamic system
Acknowledging bias Observations not controlled or
blinded
Perpetuates ineffective Inadvertently Minimizes
or harmful treatments
Quantitative estimates of risk Usually qualitative risk/benefit Explicit quantitative calculations,
determinations i.e. relative risk, absolute risk
Relevant appraisal of treatment Universally applied treatment Individual preferences are given
outcomes goals weightage
Clinical experience Trial and error Continous enhancement
Literature Read for concepts Reading is an absolute require-
ment
Critical evaluation mandatory
Economics Cost/benefit, cost/effectiveness Decision makers must use and
arbitrary make available explicit rules
Manufacturers have great flexibility
Statistics Secondary consideration Statistical and clinical significance
must both be present
Quality assessment Arbitrary Permits flexibility of wide range of
treatment alternatives
EVIDENCE HIERARCHY represent the highest levels of evidence,

whereas case reports and expert opinion are
Evidence-based practice involves tracking the lowest. This ladder of evidence was
down the available evidence, assessing its developed to a larger extent for questions
validity and then using the best evidence to related to interventions or therapy. For
inform decisions regarding care. Rules of questions related to diagnosis, prognosis or
evidence have been established to grade causation, other study designs such as cohort
evidence according to its strength. Some studies or case control studies will often be
research designs are more powerful than more appropriate.
others in their ability to answer research Figure 20.2 illustrates evidence hierarchy.
questions on the effectiveness of interventions. The pyramid shape is used to illustrate the
This notion has given rise to the concept of increasing risk of bias inherent in study
“hierarchy of evidence”. This hierarchy of designs as one goes down the pyramid. In
evidence is based on the concept of causation progressing up the pyramid, the number of
and need to control bias. studies and correspondingly the amount of
The hierarchy provides a framework for available literature decrease, while at the same
ranking evidence that evaluates health care time their relevance to answering clinical
interventions and indicates which studies questions increases. Systematic reviews (SR)
should be given most weight in an evaluation and meta analysis are considered the gold
where the same question has been examined standard for evidence because of their strict
using different types of study. Systematic protocols to reduce bias. SRs and meta-
reviews and randomized control trials analysis are followed respectively by
these cohorts prospectively for the outcome

of interest. Cohort studies are not as reliable
as RCT studies, since in cohort studies the two
groups may present with different variables
in addition to variable under study which can
affect or modify the response of the groups.
Randomized Controlled Trial
Type of study in which participants with
similar clinical parameters are randomly
divided into two groups. One group receives
the desired intervention (e.g. drug under trial)
and another group receives no active
treatment (placebo). Both these groups are
followed up for a period of time. In certain
Fig. 20.2: Hierarchy of evidence for questions about
trials more than one group may receive the
the effectiveness of an intervention or treatment active intervention (two different drugs).
Systematic Review
individual RCT studies, cohort studies, case- Evidence is gathered from various scientific
control studies and expert opinion. In the studies carried out to solve a problem or to
absence of scientific evidence the consensus answer a question. This data is subjected to
opinion of experts in appropriate fields of review process, i.e. comprehensive and
research and clinical practice is used. unbiased. As systematic review is an evalua-
Case Report tion of various scientific studies reported in
the literature, it provides a reliable overview.
Ii is a report on a single patient. Because they
are reports of cases and use no control groups Meta-analysis
with which to compare outcomes, they have In meta-analysis, two or more similar studies
no statistical validity. are subjected to statistical analysis to generate
Case Series a weighted average. The quantitative data
so available will be reliable and useful for
Report on series of patients with an outcome
treatment planning, for accuracy of diagnostic
of interest. No control group is involved.
testing and for determining association
Case Control Studies between risk factor and disease. Meta-analysis
These are studies in which patients who which is at top of pyramid has advantage of
already have a specific condition (cases) are utilizing statistical analysis of various studies
compared with people who do not (control). to reach an accurate and unbiased decision.
Less reliable than RCTs and cohort studies
because showing a statistical relationship does STEPS IN EVIDENCE-BASED DENTISTRY
not mean that one factor necessarily caused
the other. Steps in Using Evidence-based Dentistry
Cohort Studies 1. Create an answerable question
Involves identifying two groups (cohorts) 2. Track down the best evidence to answer the
of subjects, one that receive the exposure of question
interest and another that did not and following 3. Critically appraise the information
Evidence-Based Dentistry 267
4. Apply the results to one’s patient EBD. The BMA provides Medline free of
5. Evaluate one’s performance charges to members with modems and
Medline is also available for a small fee on
Advantages and Disadvantages of the internet.
Evidence-based Dentistry
• Evidence-based dentistry exposes gaps in the
Advantages
evidence.
For individuals
This can be frustrating, particularly for
• Enables clinicians to upgrade their know-
inexperienced doctors. Senior staff can help
ledge base routinely
to overcome this problem by setting
• Improves clinicians understanding of
questions for which there is likely to be
research methods and makes them more
good evidence. The identification of such
critical in using data
gaps can be helpful in generating local and
• It relies on evidence rather than personal national research projects.
experience and authority for clinical
decision making • Medline and the other electronic databases used
• Improves computer literacy and data for finding relevant evidence are not comprehen-
searching techniques sive and are not always well indexed.
• Improves reading habits At times even a lengthy literature search
For clinical teams is fruitless. For some older dentists the
• Gives team a framework for group problem computer skills needed for using databases
solving and for teaching regularly may also seem daunting. Although
the evidence-based approach requires a
• Enables juniors to contribute usefully to
minimum of computer literacy and
team
keyboard skills, while these are now almost
For patients universal among dental students and junior
• More effective use of resources doctors, many older dentists are still
• Better communication with patients about unfamiliar with computers and databases.
the rationale behind management decisions On the other hand, creative and systematic
Disadvantages searching techniques are increasingly
available and high quality review articles
• It takes time both to learn and to practice.
are becoming abundant.
For example, it takes about two hours to
properly set the question, find the evidence, • Amount of evidence: Currently our 2 million
appraise the evidence and act on the biomedical articles are published annually
evidence and for teams to benefit all in some 20,000 journals. There are about 500
members should be present for the first and journals related to dentistry. Clearly not all
last steps. of these articles are relevant to all areas of
• Establishing the infrastructure for practicing dental practice, nor can one hope to read
evidence-based dentistry costs money. any more than a small minority.
Hospitals and general practitioners may A number of publications that are widely
need to buy and maintain the necessary read in dentistry are not subjected to peer
computer hardware and software. CD- review and even when they are subjected,
ROM subscriptions can vary from ` 250 to there is tendency for “publication bias”. This
` 2000 a year, depending on the database bias occurs when there is the tendency both
and specifications. But the shortage of by researchers and by editors to publish
resources need not stifle the adoption of positive reviews.
Negative trials can be equally valuable and guidelines, positions and statements.
concerns have been raised that increasing www.ada.org. [Online] 2002. [Cited: december
sponsorship of medical trials by commercial 30, 2010.] http://www.ada.org/1754.aspx.
concerns could result in non-publication of 2. Jane L Forrest, Syrene A. Miller, Michael G.
negative or unhelpful findings. Newman. Introduction to Evidence-based
Decision Making. Henry H. Takei, Perry R.
Conclusion Klokkevold, Fermin A Carranza Michael G.
The principles of evidence-based health care Newman (book author). Carranza’s Clnical
provide structure and guidance to facilitate the Periodontology. 10 e.s. l.: Elsevier, 2006,
highest levels of patient care. pp. 12–21.
3. Newman Michael G. Improved clinical
Evidence can enhance clinical judgment but
decision making using the evidence-based
does not replace it. Evidence derived from
approach. Annals of Periodontology. 1996;
critical appraisal needs to be integrated with
1:1–9.
clinical experience and patient values so that
4. Paul Benzamin. Promoting Evidence-based
the patient is benefited.
Dentistry Through “The Dental Practice
All practitioners need to refine their Based Research Network”. J of Evid Based
evidence-based skills and desire to meet the Dent Pract. 2009; 9:194–196.
challenges of practicing dentistry in a new and 5. Sutherland, Susan E. Evidence-based
exciting way. Dentistry: Part I. Getting Started. Journal of
Canadian Dental Association. 2001; 67:204–206.
Suggested Reading 6. Sutherland, Susan E. Evidence-based
1. American Dental Asssocitaion (ADA). Dentistry: Part IV. Research Design and
ADA policy on evidence-based dentistry. Levels of Evidence. Journal of Canadian
Professional issue and research, ADA Dental Association. 2001; 67:375–378.
21
Orofacial Syndromes
The term syndrome is derived from the Greek 3. Pierre Robin Anomalad
word syndrom which means to run together • Cleft palate
or concurrence and it refers to a set of • Mandibular micrognathia
symptoms which occur together. In genetics • Glossoptosis (airway obstruction caused by
a pattern of multiple malformations thought lower, posterior displacement of the tongue)
to be pathogenetically related. A few common
syndromes involving head and neck region 4. van der Woude Syndrome
are enlisted below. • Cleft lip, cleft palate
• Hypodontia
1. Mandibulofacial Dysostosis/Treacher-
• Narrow arched palate
Collins Syndrome/Franceschetti-Zwahlen- Klein
Syndrome • Congenital heart disease, heart murmur
and cerebral abnormalities
• Hypoplastic zygoma
• Syndactyly of the hands
• Narrow face with depressed cheeks
• Ankyloglossia, and
• Downward slanting palpebral fissures • Adhesions between the upper and lower
• Coloboma (notch on outer portion of lower gum pads.
eyelid)
5. Ascher Syndrome
• Ear anomalies (deformed pinnae, absence
of external auditory canal) • Double lip
• Blepharochalasis (recurrent episodes of
• Under developed mandible with retruded
swelling cause stretching and atrophy of the
chin, hypoplasia of condyle and coronoid
upper eyelid skin. This results in the
process, prominent antegonial notch.
relaxation of the tarsal fold allowing tissue
• Lateral facial clefting, macrostomia, cleft to slack over the palpebral fissure.)
palate. • Non-toxic thyroid enlargement.
• Hypoplastic parotid gland.
6. Beckwith-Wiedeman Syndrome
2. Oculoauriculovertebral Syndrome/ • Macroglossia
Goldenhar Syndrome • Omphalocele (protrusion of part of the
• Incomplete development of the ear, nose, intestine through a defect in the abdominal
soft palate, lip, and mandible (condylar wall at the umbilicus)
hypoplasia) on usually one side of the body. • Visceromegaly
269
• Gigantism 13. Mazabraud Syndrome

• Neonatal hypoglycemia • Fibrous dysplasia
• Increased risk of childhood visceral tumors • Intramuscular myxomas
(Wilms’ tumor, adrenal carcinoma)
14. Maffucci Syndrome
• Nevus flammeus of forhead and eyelids.
• Skeletal chondromatosis
• Maxillary hypoplasia
• Soft tissue angiomas
7. Down’s Syndrome
15. Segmental Odontomaxillary Dysplasia
• Learning disability
• Unilateral enlargement of the maxillary bone
• Short stature and brachycephaly
• Fibrous hyperplasia of overlying gingival
• Midface retrusion
soft tissue
• Mongoloid slant
• Primary teeth in affected area show enamel
• Macroglossia defects
• Hyperdontia • Radiographs reveal thickened trabeculae
8. Melkersson-Rosenthal Syndrome that are vertically oriented
• Non-tender, persistent swelling of one or • Smaller maxillary sinus on affected side
both lips 16. Crouzon Syndrome
• Facial paralysis • Premature closing of cranial sutures
• Fissured tongue • Brachycephaly (short head), scaphocephaly
9. Eagle Syndrome (boat-shaped head), trigonocephaly
(triangle-shaped head)
• Elongated styloid process, history of
• Severely affected patients show cloverleaf
tonsillectomy
skull
• Vague facial pain while swallowing,
• Ocular proptosis
turning head, or opening mouth
• Visual and hearing impairment
10. Gardner’s Syndrome • Radiographs of skull show beaten-metal
• Colonic polyps pattern
• Osteomas • Hypoplastic maxilla
• Increased prevalence of odontomas, super- 17. Apert Syndrome
numerary teeth, impacted teeth
• Craniosynostosis
• Epidermoid cyst of skin
• Acrobrachycephaly
• Desmoid tumors
• Flattened occiput, tall forehead
11. Multiple Endocrine Neoplasia (MEN) • Ocular proptosis, downward slanting lateral
• Marfanoid body built palpebral fissures
• Narrow face and thick lips • Middle third of face is hypoplastic
• Neuromas on lips, anterior tongue • Open mouth appearance
• Medullary carcinoma of thyroid • Syndactyly of second, third and fourth
digits of hands and feet
12. McCune-Albright Syndrome • Mental retardation
• Polyostotic fibrous dysplasia • Trapezoid like appearance of lips
• café au lait pigmentation • Cleft palate bifid uvula
• Multiple endocrinopathies (sexual precocity, • V-shaped maxillary arch
pituitary adenoma, hyperthyroidism) • Shovel-shaped incisors
Orofacial Syndromes 271
18. Ehlers-Danlos Syndrome • Narrow, high-arched palate

• Hperelasticity of the skin • Prolonged retention of deciduous teeth,
• Cutaneous fragility delayed or complete failure eruption of
• Papyraceous scarring permanent teeth
• Vascular type—bruising • Short lower face height
• Type VIII—marked periodontal disease in • Acute gonial angle, anterior inclination of
ealy life the mandible
• Gorlin sign 22. LEOPARD Syndrome
• Recurrent subluxation of TMJ
• Multiple lentigines
19. Gorlin Syndrome/Nevoid Basal Cell • Electrocardiographic—conduction abnor-
Carcinoma Syndrome malities
• Multiple basal cell carcinoma • Ocular hypertelorism
• Odontogenic keratocyst • Pulmonary stenosis
• Epidermal cysts of skin • Abnormal genitalia
• Calcified falx cerebri • Retardation of growth
• Rib anomalies
• Sensorineural deafness
• Spina bifida occulta of cervical or thoracic
• Freckle-like macules on facial skin
vertebrae
23. Noonan’s Syndrome
20. Sturge-Weber Syndrome
• Lesion in humerus
• Port-wine stain or nevus flammeus
• Leptomeningeal angiomas on ipsilateral • Gingival fibromatosis
cerebral cortex • Psychomotor retardation
• Convulsive disorder • Orbital involvement
• Mental retardation • Obstructive sleep apnea
• Contralateral hemiplegia • Deciduous teeth shed prematurely
• Tramline calcifications • Permanent dentition is defective with
• Occular invlovement—glaucoma, vascular absence of numerous teeth
malformations
24. Rubinstein-Taybi Syndrome
• Gingival hyperplasia
• Talons cusps
21. Cleidocranial Dysplasia • Growth and mental retardation
• Hypoplastic clavicle • Broad thumbs and great toes
• Patient can approximate shoulders in front • Thin upper lip
of the chest • Retrognathia, micrognathia
• Neck appears long and shoulders are • Narrow high-arched palate
narrow • Submucosal cleft palate
• Short stature
• Large head with frontal and parietal 25. SAPHO Syndrome
bossing • Synovitis
• Ocular hypertelorism, broad and depressed • Acne
nose • Pustulosis
• Delayed closure of sutures and fontanels • Hyperostosis
• Wormian bone formation • Osteomyelitis
26. Zimmermann-Laband Syndrome 32. PFAPA Syndrome

• Gingival fibromatosis • Periodic fever
• Hypoplasia of the distal phalanges • Aphthous stomatitis
• Nail dysplasia • Pharyngitis
• Joint hypermobility • Cervical adenitis
• Hepatosplenomegaly 33. Sweet’s Syndrome
• Nose and pinnae are usually large and
• Hematologic disease (including leukemia)
poorly developed
• Immunologic disease (rheumatoid arthritis,
• Mental retardation
inflammatory bowel disease)
27. Paillon Lefevre Syndrome • Behçet’s syndrome
• Palmoplantar keratosis 34. Peutz-Jeghers Syndrome
• Diffuse follicular hyperkeratosis • Freckle-like lesions of hands, perioral skin
• Nail dystrophy and oral mucosa
• Hyperhidrosis • Intestinal polyposis
• Keratosis on elbows and knees
35. CREST Syndrome
• Periodontitis in both deciduous and perma-
nent teeth • Calcinosis cutis
• Loss of attachment • Raynaud’s phenomenon
• Esophageal dysfunction
28. Haim-Munk Syndrome • Sclerodactyly
• Palmoplantar keratosis • Telangiectasia
• Periodontitis is milder 36. Osler-Weber-Rendu Syndrome
• Skin manifestations are more severe
• Also known as hereditary hemorrhagic
29. Ramsay Hunt Syndrome telangiectesia
• Herpes zoster—cutaneous lesions of • Papules in nasal and oropharyngeal
external auditory canal mucosae (telangiectasias)
• Recurrent spontaneous epistaxis
• Involvement of ipsilateral facial and
• Arteriovenous malformation involving
auditory nerves
lungs, liver or CNS
• Facial paralysis
• Hearing deficits 37. Laugier-Hunziker Syndrome
• Vertigo • Longitudinal melanonychia
• Genital melanosis.
30. Behçet’s Syndrome
38. Plummer-Vinson/Paterson-Kelly Syndrome
• Aphthous like ulceration involving soft
palate and oropharynx • Iron deficiency anemia
• Genital ulcerations • Glossitis
• Atrophy of lingual papillae
• Positive pathergy
• Dysphagia
• Skin lesions—erythema nodosum, pseudo-
• Esophageal webs
folliculitis, acneiform nodules
• Koilonychia
• Eye lesions—anterior or posterior uveitis
39. LADD Syndrome/Lacrimo-auriculo-dento-
31. Magic Syndrome digital Syndrome
• Mouth and genital ulcers • Aplasia or hypoplasia of lacrimal and
• Inflamed cartilage salivary glands
Orofacial Syndromes 273
• Cup-shaped ears • Balanitis circinata

• Dental—hypodontia, microdontia, mild • Erythematous papules or ulcers involving
enamel hypoplasia buccal mucosa, tongue, palate
• Digital anomalies • Geographic tongue
40. Mikulicz’s Syndrome 45. Grinspan Syndrome
Parotid and lacrimal enlargement secondary • Hypertension
to another disease, such as tuberculosis, • Diabetes mellitus
sarcoidosis, lymphoma, and Sjögren's • Erosive lichen planus
syndrome.
46. Cushing’s Syndrome
41. Sjögren’s Syndrome
• Central obesity
• Xerostomia
• Buffalo hump
• Xerophthalmia
• Moon facies
• Keratoconjunctivitis sicca
• Red-purple abdominal striae
• Rheumatoid arthritis
• Hirsutism
• Frothy saliva
• Poor healing
• Fissured tongue
• Secondary candidiasis • Osteoporosis
• Diffuse enlargement of salivary gland • Hypertension
• Sialography shows fruit-laden branchless • Mood changes
tree appearance • Hyperglycemia
• Muscle wasting
42. Cowden’s Syndrome
• Multiple, small papules on facial skin 47. Frey Syndrome
(mouth, nose, ears) • Facial flushing and sweating along the
• Acral keratosis on dorsal surface of hand distribution of auriculotemporal nerve
• Palmoplantar keratosis during chewing
• Cutaneous hemangiomas, neuromas, • Pain and increase in temperature of
xanthomas and lipomas localised skin
• Multiple papules affecting gingiva, dorsal 48. Chediak-Higashi Syndrome
tongue, buccal mucosa
• Recurrent pyogenic infection
43. Stevens-Johnson Syndrome • Partial albinism, nystagmus
• Ocular, genital and mucosal ulcerations • Peripheral neuropathy
• Severe ocular involvement may cause • The infections involve mucous membranes,
scarring skin, and the respiratory tract
• Conjunctivitis
49. Costen’s Syndrome
• Fever
• Vertex and occipital pain
• Sore throat
• Otalgia, glossodynia
• Fatigue
• Pain about the nose and eyes associated
44. Reiter’s Syndrome with disturbed temporomandibular joint
• Nongonococcal urethritis function.
• Arthritis • “Stuffy deaf” sensation
• Conjunctivitis • Neuralgic pain
50. Goltz-Gorlin Syndrome • Trigeminal neuralgia due to perineural

• Microphthalmia, colobomas of the iris and spread
choroid. • Soft palate immobility
• Distinctive peripheral corneal lesions • Difficulty opening mouth
consisting of discrete vascularized sub- 52. Wiskott-Aldrich Syndrome
epithelial opacities
• Eczema
• Oral, esophageal, and laryngeal fibro-
• Thrombocytopenia (low platelet count)
vascular papillomas
• Immune deficiency
• The teeth erupt late and are usually hypo-
• Bloody diarrhea (secondary to the thrombo-
plastic.
cytopenia).
• The nails are often dysplastic
• Hands and feet may be ‘split’ with Suggested Reading
syndactyly of the third and fourth fingers—
1. Syndromes of Head and Neck—Robert J
‘lobster claw’ appearance.
Gorlin, Jens J Pindborg.
51. Trotter’s Syndrome 2. Textbook of Oral and Maxillofacial
• Nasopharyngeal carcinoma Pathology—Neville.
• Unilateral conductive deafness due to 3. Textbook of Oral Medicine—Burket, 9th,
middle ear effusion 10th and 11th editions.
22
Routine Blood Investigations
Hemoglobin (Hb) Eosinophils: 1–4%

It is oxygen carrying material in RBCs Basophils: 0–1%
Females: 12–16 g/100 ml of blood Shift to left—increase in number of
Males: 14–18 g/100 ml of blood immature neutrophils.
Increased in polycythemia Shift to right—increase in number of
Decreased in iron deficiency anemia mature neutrophils.
Hematocrit (HCT) Neutrophil count increased in acute
bacterial infections like acute appendicitis.
It is measurement of packed red cell volume
in a volume of blood. Lymphocyte count is increased in chronic
bacterial infection, e.g. tuberculosis, leprosy.
Females: 37–47%
Males: 40–52% Eosinophils increase in allergic conditions
and parasitic infestations.
Increased in polycythemia, dehydration
Decreased in aplastic anemia Platelet Count
Red Blood Cell (RBC) Count 150000–400000 cells/cu mm
Males: 4.5–6.2 million cells/cu mm Increased in polycythemia
Females: 4.5–5.5 million cells/cu mm Decreased in leukemia, dengue fever, drug-
Increased in polycythemia induced thrombocytopenia.
Decreased in aplastic anemia, leukemia. Red Cell Indices
White Blood Cell (WBC) Count Red cell indices are useful tools for measuring
Normal value 5000–11000 cells/cu mm the size, shape and hemoglobin content of
Leukocytosis value above 11000 seen in RBC. They utilize hematocrit, hemoglobin
acute infectious conditions. and RBC count.
Leukopenia is value below 5000 seen in
Mean Corpuscular Volume (MCV)
patients with typhoid fever.
This gives volume of average RBC
Differential White Cell Count Normal value: 82–98 cu microns
Neutrophils: 50–70% Decreased in iron deficiency anemia,
Lymphocytes: 25–40% thalassemia
Monocytes: 3–8% Increased in megaloblastic anemia
275
Mean corpuscular hemoglobin (MCH) International Normalized Ratio (INR)

This gives the hemoglobin content of • As prothrombin time estimated in different
individual RBC. laboratories is not comparable due to
Normal range is 27–32 micrograms. difference in the source of thromboplastin
Values below this suggest microcytic anemia used and difference in type of instrumen-
and above suggest macrocytic anemia. tation.
• Hence, an attempt to introduce standardiza-
Mean Corpuscular Hemoglobin
tion lead to development of INR
Concentration (MCHC)
• It relates all thromboplastins to the
MCHC estimates the average amount of standard of human brain thromboplastin
hemoglobin in 100 ml of packed RBC with the use of internal sensitivity index (ISI)
32–38 g/100 ml • INR of normal patient is 1
Increased in hereditary spherocytosis. (ISI)
Decreased in microcytic anemia. ⎧ Prothrombin time of patient ⎫
• INR = ⎨ ⎬
⎩ Prothrombin time of control ⎭
Reticulocyte Count
• When INR is below 3.5 normal extraction
0.5 to 1.5% of red blood cells counted of tooth can be done without any change in
Reticulocytes are immature form of RBC anticoagulant therapy.
and represent a stage between nucleated
RBC and mature RBC. Reticulocytes count is Partial Thromboplastin Time (PTT)
increased when RBC formation is increased Normal value is 25–40 secs.
and is associated with various anemias and The PTT is prolonged in factor VIII, IX, XI
blood loss. and XII deficiencies and in the deficiencies of
Erythrocyte Sedimentation Rate those factors necessary for common pathway,
i.e. I, II. V and X. PTT is also prolonged in
Males: 0–10 mm/hr patients undergoing heparin therapy.
Females: 0–20 mm/hr
It is a non-specific test, and values above Activated Partial Thromboplastin Time (APTT)
normal indicates infections, trauma, infarc- • It is a screening test for intrinsic limb and
tions, etc. common pathway of coagulation system.
ESR tends to rise in following situations— • Blood samples are collected in tubes with
acute inflammation, bacterial infections like oxalate or citrate to arrest coagulation by
tuberculosis, bacterial endocarditis, rheuma- binding calcium. The specimen is then
toid arthritis, SLE, neoplastic conditions and delivered to the laboratory. In order to
pregnancy. activate the intrinsic pathway, phospho-
ESR is lowered in heart failure, poly- lipids, an activator (such as silica, celite,
cythemia, and sickle cell anemia. kaolin), and calcium (to reverse the
anticoagulant effect of the oxalate) are
Coagulation Tests
mixed into the plasma sample. The time is
Prothrombin Time (PT) measured until a clot forms.
Normal value is 11–15 secs. • The test is termed “partial” due to the
Prothrombin time is prolonged in factor I, absence of tissue factor from the reaction
II, V, VII and X deficiencies and occurs with mixture.
anticoagulant therapy, cirrhosis, hepatitis • Normal range below 45 sec. (Note: PTT is
obstructive jaundice, colitis and salicylate insensitive to large changes in intrinsic
therapy. coagulation pathway. A 70% decrease in
Routine Blood Investigations 277
factor levels may still provide normal PTT Phosphorus (Inorganic)

hence even a small change in PTT is of a Normal value is 2.5–4.5 mg/100 ml.
great significance). Increases in—hypoparathyroidism and
• It is increased in hemophilia. secondary hyperparathyroidism.
Bleeding Time (Duke) Decreases in—primary hyperparathyroidism,
vitamin D deficiencies and malabsorption
Normal value is 3–5 mins.
diseases and chronic antacid usages.
This gives some information concerning
vascular and platelet interaction. Normal Magnesium (Mg)
bleeding time should not exceed five minutes, Normal value is 1.5–2 mEq/L.
it is usually prlonged in thrombocytopenia, Increased levels are seen in renal failure and
von Willebrand’s disease and platelet large doses of antacids that contain magnesium.
dysfunction. Decreased levels are associated with
Clotting Time alcoholism, diabetic acidosis, malabsorption,
Normal value is 4–8 mins. hypocalcemia and hypokalemia.
In theory, the blood sample is drawn Iron
cleanly and there is no tissue thromboplastin Normal value is 50–175 μg/100 ml.
contamination, the clotting time should Increased levels are associated with
measure the intrinsic and common pathways. hemolytic anemias, hemochromatosis, and
In practice, only severe factor deficiencies in pernicious anemia.
these pathways cause a prolonged clotting
Decreased levels are found in iron
time. The chief use for clotting time is in the
deficiency anemias and anemias secondary to
management of heparin therapy.
chronic infections.
Blood Chemistry
Total Iron Binding Capacity (TIBC)
Total Protein Normal value is 250–410 μg/100 ml.
Normal value is 6–8 g/100 ml. Increased levels are seen in iron deficiency
Increases in dehydration, dysgamma- anemia and anemias secondary to blood loss.
globulinemia. Decreased levels are seen in chronic
Decreases in hepatocellular disease, mal- infections and liver disease.
absorption disease and starvation.
Albumin SERUM ELECTROLYTES
Normal value is 3.5–5 g/100 ml.
Sodium (Na)
Increases in dehydration
Decreases in chronic glomerulonephritis, Normal value is 135–145 mEq/L.
ulcerative colitis, hepatocellular damage Hyponatremia is seen in cirrhosis, conges-
secondary to hepatitis, leukemia tive heart failure, adrenal insufficiency,
nephrosis, excessive use of diuretics, inappro-
Calcium priate ADH secretion and water intoxication.
Normal value is 8.5–10.5 mg/100 ml. Hypernatremia is caused by excessive
Increases in hyperparathyroidism, malig- water loss in vomiting, diarrhea, severe
nancy with bone metastasis. sweating and diabetes mellitus.
Decreased levels seen in hypopara-
thyroidism, tetany, acute pancreatitis, renal Potassium (K)
failure, starvation. Normal value is 3.2–5.5 mEq/L.
Hypokalemia is associated with inadequate and low HDL increases the ratio and is
intake or loss from GI tract or urinary tract, undesirable as it increases the chances of CAD.
e.g. vomiting, diarrhea or use of diuretic Conversely high HDL and low total
medicines. cholesterol lowers the ratio and is desirable.
Hyperkalemia is associated with release of Normal value is 2–6.
cellular potassium secondary to surgery, crush Optimal desirable level is less than 2.
injury, hemolysis of RBCs, renal failure and High-risk level is more than 6.
acidosis.
LDL
Chloride (Cl)
LDL is referred to as “bad cholesterol” because
Normal level is 95–105 mEq/L. it carries cholesterol, triglycerides and
Serum chloride levels usually follow serum phospholipids from liver to the tissues and
Na level; however, chloride will be reduced organs where it gets deposited increasing the
in vomiting. chances of CAD.
Normal value is 60–100 mg/dl.
LIPID PROFILE Optimal desirable level is less than 60 mg/dl.
The lipid profile is a group of blood tests High-risk level is more than 100 mg/dl.
which are carried out to determine the risk of VLDL
coronary artery disease (CAD). It carries the highest amount of triglycerides
The tests included in lipid profile are total and helps cholesterol build up on walls of
cholesterol, triglyceride, HDL, LDL, VLDL arteries. Hence, increased levels are harmful.
and total cholesterol to HDL ratio. Normal value is 5–40 mg/dl.
Cholesterol Optimal desirable level is less than 5 mg/dl.
Normal level is 150–300 mg/100 ml. High-risk level is more than 40 mg/dl.
Increased levels seen in idiopathic hyper- Serum Triglycerides
cholesterolemia, secondary hypercholestero- Normal value ranges between 35 and 150 mg/
lemia caused by nephrosis, chronic obstructive 100 ml.
biliary disease, diabetes.
Increased levels are seen in congenital
Decreased levels in hyperthyroidism, hyperlipidemia, nephrotic syndrome, diabetes
malnutrition and secondary liver cirrhosis. mellitus, and myocardial infarction.
HDL Glucose
HDL is referred to as “good cholesterol” Normal value is 65–110 mg/100 ml.
because it carries cholesterol and phospho- Increased in diabetes mellitus, acromegaly,
lipids from tissues and organs to the liver for Cushing’s syndrome
degradation and elimination Decreased levels are seen in islets cell tumor
Normal value is 40–60 mg/dl. of pancreas, advanced cirrhosis
Optimal desirable level is more than Glycosylated hemoglobin (HbA1C)
60 mg/dl. Has been confirmed as a sensitive monitor
High-risk level is less than 40 mg/dl. of glucose control in both type 1 and type 2
Total cholesterol to HDL ratio: The total choles- diabetes.
terol to HDL ratio is helpful in predicting As the life of RBC is 120 days, HbA1C
atherosclerosis and CAD. High total cholesterol reflects the blood glucose level averaged over
Routine Blood Investigations 279
time rather than at the time of venipuncture Serum Glutamic Pyruvic Transaminase (SGPT)
only. It is, therefore, considered better Normal value is 6–36 mU/ml.
indicator of diabetic control than individual Values are elevated in liver damage and
blood glucose levels. myocardial damage.
Average range is 5.5 to 9% of total
hemoglobin. Blood Urea Nitrogen (BUN)
Values as high as 16.6% ± 7.6% are seen in Normal value is 10–20 mg/100 ml.
untreated diabetes. Increased in conditions with decreased
Uric Acid GFR, prerenal and postrenal azotemia.
Decreased in advanced liver diseases and
Normal value is 2.5–8 mg/100 ml.
low protein diets.
Increased in gout, leukemia, multiple
myeloma, renal failure, use of aspirin and Bilirubin
diuretics.
Two forms direct (conjugated) and total
When raised uric acid level is associated (conjugated and unconjugated)
with high cholesterol level, incidence of Normal values
myocardial infarction secondary to coronary
Total bilirubin is 0.8 mg/100 ml
artery disease is increased.
Conjugated bilirubin is 0.5 mg/100 ml
Decreased in uricosuric drugs intake,
Unconjugated bilirubin is 0.3 mg/100 ml
Wilson’s disease and use of ACTH.
Depending of type of bilirubin responsible
0.7–1.4 mg/100 ml
for total bilirubin elevation we can distinguish
Increased in kidney disease, muscle disease. between hepatocellular and obstructive forms
Alkaline Phosphatase of liver diseases.
Normal value is 1.5–4.5 Bodansky units, Acid Phosphatase
30–110 IU
Normal value is 0.5–11 mU/ml.
Increased in Paget’s disease, hyperpara-
Prostate is rich in acid phosphatase.
thyroidism, liver disease.
Increased acid phosphatase usually indicates
Decreased in hypophosphatasia, hypo-
that carcinoma of the prostate has metasta-
thyroidism.
sized to bone.
Lactic Dehydrogenase (LDH)
Amylase
Normal value is 90–200 mU/ml.
Normal value is 60–150 Somogyi units/100 ml.
Increased in malignancies, inflammations,
necrotic processes, and infections. For example, Increases in acute pancreatitis, recurrent bouts
myocardial infarction, pulmonary embolism, of chronic pancreatitis, pancreatic duct
pulmornary infarction, hepatitis, leukemia, obstruction secondary to carcinoma, spasm,
lymphoma and congestive heart failure. etc., salivary gland disease, bowel obstruction,
and upper gastrointestinal surgery.
Serum Glutamic Oxaloacetic Transaminase
(SGOT) Creatine Phosphokinase (CPK)
Normal value is 10–50 mU/ml. Normal value is 5–50 I mU/ml.
Increased in myocardial infarction, Increases in myocardial infarction, cerebral
hepatitis, liver cirrhosis and liver neoplasms, infarction and Duchenne type muscular dys
muscle injury and after surgery. trophy.
Tumor Markers
Tumor markers are those biological substances synthesized and released by cancer cells or
produced by the host tissues in response to the presence of cancerous tissue.
Broad classification of tumor markers
1. Proliferation markers Ki-67, PCNA, p27 kip/gene, DNA polymerase alpha, p105, p120,
statin
2. Oncogenes c-erbB-2 gene, ras gene, myc gene, bcl-2 gene
3. Growth factors and receptors Epidermal growth factor receptor (EGFR)
Transforming growth factor β-HCC
Fibroblast growth factor receptor
Insulin and insulin-like growth factor receptor.
4. Tumour suppressor genes p53, retinoblastoma susceptibility suppressor gene.
5. Serological tumor markers a. Markers associated with cell proliferation
b. Markers related to cell differentiation (carcinoembryonic
proteins like carcinoembryonic Ag, α-fetoprotein
c. Markers related to metastasis
d. Related to other tumor-associated events
e. Related to malignant transformation
f. Inherited mutations
g. Monoclonal Ab-defined tumor markers
Tissue markers of potential and established malignancy

Cell surface markers Carbohydrates—particularly blood group antigens
Squamous carcinoma antigens Ca-1, TA-4, SQM and 3H-1
Histocompatibility antigens
Growth factors and receptors
Intracellular markers Cytokeratins
Filaggrin
Involucrin
Desmosomal protiens
Carcinoma antigen 17.13
Quantitative DNA
Silver binding nucleolar organiser regions
Oncogenes
Arachidonic acid products
Gamma-glutamyl transpeptidase
Lactate dehydrogenase
Guanidine benzonatate
Basemement membrane markers Laminin
Collagen IV
Matrix markers Tenascin
Index
Abfraction 12, 200 Aurothioglucose 71
Acantholysis 36, 38, 71, 225 Auspitz sign 61
Acanthosis nigricans 97 Autoimmunity 225
Accupressure 172 Azidothymidine 130, 132
ACE-inhibitors 229 Azoles 55
Achlorhydria 96, 155 Azotemia 279
Acrobrachycephaly 270
Bacitracin 147
Acrodermatitis enteropathica 50
Baclofen 205, 206, 208
Acrodynia 111
Balanitis 26, 273
Acromegaly 232–234, 278
Ballooning degeneration 19, 21, 23, 35
Acroosteolysis 228
Actinomycoses 120 Barosinusitis 205
Bayonet technique 134
Acute lymphonodular pharyngitis 20, 21
Beaten-Metal pattern 270
Addison’s disease 238, 239
Beckwith-Wiedeman syndrome 90, 269
Aerodontalgia 200, 205
Behçet’s syndrome 33, 272
Allopurinol 71
Bell’s palsy 18, 22
Amisulpride 189
Bence-Jones proteins 151, 242
Ammoniacal odor 53
Benign migratory glossitis 86, 93
Amyloidosis 97
Bernard-Soulier syndrome 145
Angioneurotic edema 28, 29, 99
Betnesol 27, 70
Anti-cyclic citrullinated proteins 164
Bidigital palpation 191
Antioxidants 66, 74
Birbeck granules 123
Antipsychotics 98
Bismuth 110, 111
Antipyretics 119
Bismuthism 110
Antiretroviral 97 Bismuth Grippe 110
Antirheumatic 227 Bisphosphonate-induced osteonecrosis 151
Antroliths 181 Bittner’s milk factor 211
Arecholine 73 Blanching 74, 104
Argyll-Robertson pupil 23, 116 Bleomycin 30, 149
Argyria 112 Blepharochalasis 269
Arsenic 112 Bodansky 279
Arthrocentesis 169,170 Bon-bon sign 98
Arthropathy 225 Boutonniere deformities 226
Arthroscopy 170 Bowen’s disease 219
Asboe-Hansen sign 38 Bronze appearance 108
Ascher syndrome 269 Bronzing 105
Aspergillosis 162, 177 Browns tumor 243
Astemizole 56 Bruxism 163, 165
Asthma 4, 164, 244 Buffalo hump 239, 273
Athetosis 85 Bulimia 192
281
Bullae 13 Cretinism 90, 91, 236, 237

Bullous pemphigoid 39 Crohn’s disease 25
Bulls eye 25 Crouzon syndrome 270
Burtonianline 110 Cushing’s syndrome 239, 273
Butterfly rash 72 Cyanosis 83, 112, 153
Cacosmia 179, 251 Cylindroma 198
Cysticercosis 98
Calcitonin 240
Cytomegalovirus 24
Caldwell Luc surgery 178, 181
Cannon’s disease 61 D-penicillamine 229
Capsaicin 23, 208 Dacarbazine 149
Capillary hemangioma 104, 128 Daunorubicin 82
Castleman’s disease 38 DDAVP 142
Cat-scratch disease 126 Demirijian’s method 259
Causalgia 209 Dentigerous cyst 181
Cauterising agent 52 Desmoglein 36
Cavernous hemangioma 103, 104 Desmopressin 142
Chancre 35, 114 Dexamethasone 38, 151
Chediak-Higashi syndrome 148, 224, 273 Dialysis 53
Cheilitis glandularis 188 Diascopy 103, 253
Cheiloscopy 263 DiGeorge’s syndrome 240
Cherry blossom appearance 229 Diphenhydramine 147, 189
Chloasma 109 Diplopia 179, 182
Choristoma 253 Diphtheria 47
Chvostek’s sign 241, 251 Disulfiram reaction 252
Cicatricial pemphigoid 40, 41 DMARDS 227
Cleidocranial dysostosis 271 Donovan’s technique 186
Clicking 169–171 Duchenne dystrophy 279
Clindamycin 6 Dysarthria 98
Clobetasol 33, 38, 70, 72, 131 Dystonia 98
Clofazimine 122
Clonazepam 210
Eagle’s syndrome 270
Cloverleaf skull 270 Ebbing tide appearance 62
Clozapine 98 Eczema 274
Clubbing 10, 11 Ehlers-Danlos syndrome 87, 141, 271
Coastline of California 106, 107 Electrogustometry 88
Coastline of Maine 106, 107 Electromyography 88
Cobblestone appearance 39, 121 Ely’s cyst 165, 166
Colchicine 160 Eminectomy 175
Coloboma 269, 274 EMLA 206
Condyloma acuminatum 124, 131 Emphysema 82
Condyloma lata 115 Empyema 179, 252
Cooley’s anemia 158 Enalapril 229
Coombs’ test 156 Encephalitis 18, 20
Costen’s syndrome 170,273 Enophthalmus 179
Cowden’s syndrome 85, 273 Ephelides 104
Coxsackie virus 20, 21 Ephelis 104
Craniosynostosis 270 Epidermolysis bullosa 38, 41, 87
CREST syndrome 272 Epiphora 176
Index 283
Epistaxis 103, 162, 176 Gorlin sign 87, 271

Epitope 224 Graft-versus-host disease 71, 223
Epstein-Barr virus 127, 211 Granulocytopenia 147
Erythroplakia 67 Graves’ disease 234
Ethambutol 120, 193 Grinspan syndrome 69, 70, 273
Ethiodol 187 Griseofulvin 70
Ethionamide 122 Groundglass appearance 241
Ethosuximide 83 Gumma 114, 115,116, 253
Eugenol 57, 136 Gustafson’s method 260
Exophthalmus 234, 235
HAART 195
Famciclovir 23, 206 Haim-munk syndrome 272
FDG-PET 214 Hairy tongue 92, 93, 110
Fibroma 16 Hairy leukoplakia 127
Filliform papillae 110 Hallopeau 17, 39
Fimbriae 97 Hand-Schüller-Christian disease 123, 124
Fluconazole 55, 56, 127 Hansen’s disease 121
Fluocinolone 27, 33, 38 Happy puppet syndrome 91
Fluoroquinolones 147 Heerfordt’s syndrome 122, 193
Fluorouracil 161 Heinz bodies 158, 160
Flute appearance 164 Hemangioma 253
Foliate papillae 87 Hemarthrosis 78
Fontana stain 118 Hemochromatosis 108
Fordyce’s granules 11, 50 Hemoglobinopathies 155
Formaldehyde 137 Hemolytic-uremic syndrome 224
Formocresol 52 Hemophilia 141,142, 145, 245
Foscarnet 44, 129 Herpangina 20, 21
Franceschetti-Zwahlen-Klein syndrome 269 Herpetic whitlow 35, 133
Frenectomy 90 Herpetiform ulcers 31, 32
Frey’s syndrome 278 Herpes simplex 17, 21
Frog-like position 78 Herpes zoster 22, 27, 207, 253, 272
Fusospirochetal infections 45 Histoplasmosis 17, 25
Gabapentin 23, 206 HIV-salivary gland disease 129
Gadolinum 88 Hodgkin’s lymphoma 149
Galvanism 203 Hunters glossitis 94
Ganciclovir 24, 25, 131 Hutchinson’s freckle 105, 114
Hutchinson’s incisors 114, 116, 117
Gardner’s syndrome 270
Hutchinson’s triad 114, 116
Garlic odor 112
Hyperparathyroidism 241, 242, 277
Genodermatoses 61
Hypoparathyroidism 240, 241
Gentian violet 33
Hypophosphatasia 279
Geometric glossitis 18, 19
Hypophosphatemia 241
Giemsa stain 19, 21, 114,118
Hypopituitarism 232
Globulomaxillary cyst 181
Hypothyroidism 232
Glossodynia 100
Hypovitaminosis 62
Glossoptosis 269
Glossopyrosis 100 Ice-cream headache 205
Goldenhar syndrome 269 Imatinib mesylate 82
Goltz-Gorlin syndrome 274 Immunofluorescence 38
Immunological diseases 223 Lobster claw appearance 274

Immunophenotyping 82 Ludwig’s angina 98, 253
Inverted Y line of Ennis 181 Lugol’s iodine 64
Isoniazid 94, 120 Lupus erythematosus 119
Itraconazole 55 Lyell disease 25
Lymphangioma 91, 253
Jaccoud’s arthropathy 225
Lymphomas 149
Jarisch-Herxheimer reaction 118
Jaundice 9, 156, 157 Macroglossia 90, 91, 236, 269, 270
Jigsaw appearance 173 Macrostomia 269
Job’s syndrome 224 Macule 14
Junctional nevus 105 MADISON criteria 209
Juvenile periodontitis 216 Maffucci syndrome 270
Jump sign 171 MAGIC syndrome 272
Mandibulofacial dysostosis 269
Kahn test 224 Marfanoid 270
Kaposi’s sarcoma 125, 127
Marie-Strumpell disease 172
Kenacort 70, 74
Mask-like 228
Keratoacanthoma 219 Masseteric hypertrophy 254
Keratoconjunctivitis sicca 229
Mazabraud syndrome 270
Ketoacidosis 82, 152
McCune-Albright syndrome 106, 270
Ketoconazole 55, 56, 127 Measles 54
Kissing disease 24
Median rhomboid glossitis 56, 58, 92
Kissing lesion 58
Megaloblastic anemia 230
Koch’s disease 118, 134 Melanoma 106
Koebner’s phenomenon 70
Melasma 109
Koilonychia 95, 272
Melena 252
Koplik’s spot 50, 54 Melkersson-Rosenthal syndrome 92, 188, 270
LADD syndrome 272 Mercaptopurine 30, 82, 161
Lancinating pain 201, 205 Mercury poisoning 111
Langerhan’s cell histiocytosis 123 Metaplasia 59
Laskin’s theory 170, 171 Metastasis 217
Laugier-Hunziker syndrome 272 Methemoglobinemia 41
Leopard syndrome 271 Mickulicz’s disease 185, 273
Lepromin skin test 121 Micro-abscesses 61
Leprosy 121 Micro-aneurysms 103
Lesch-Nyhan syndrome 43 Microcheilia 227
Letterer-Siwe disease 123, 124 Microcytic anemia 158
Leukemia 80 Microdontia 273
Leukoplakia 61–68 Microglossia 227
Levamisole 33 Micrognathia 236, 269, 271
Levodopa 98 Microphthalmia 274
Lichen planus 67–71 Microstomia 43
Lichenoid reaction 28, 71, 72 Migraine 204, 207
Linea alba 51, 65 Minocycline 108
Lipshultz bodies 19 Moeller’s glossitis 87
Lithotomy 186 Molluscum contagiosum 132
Lithotripsy 192 Moniliasis 49
Low molecular weight heparin (LMWH) 144 Monilid reaction 59
Index 285
Mono spot test 24 Oroantral fistula 177, 181

Monroe’s abscess 61, 94 Orthostatic hypotension 244
Moon’s molars 117 Osteitis fibrosis cystica 241
Moon facies 239 Osteogenic sarcoma 219
Morphea 227 Osteomas 182, 270
Morsicatio buccarum 52 Osteomyelitis 253–255, 271
Mucocele 196 Osteonecrosis 22
Mucoepidermoid carcinoma 192, 254 Osteopetrosis 255
Mucormycosis 44, 45, 253 Osteoporosis 239, 273
Mulberry molars 114 Osteosarcoma 221
Multiple endocrine neoplasia 270 Otalgia 273
Mumps 192, 201 Oxytocin 231
Munchausen syndrome 209 Ozena 251
Myasthenia gravis 36, 98
Mycoplasma 25, 26 Pagano–Levin agar 55
Myeloproliferative disorder 146, 153 Paget’s disease 242, 279
Myofacial pain dysfunction syndrome 170, 250 Pagophagia 95
Myositis ossificans 172, 251 Palifermin 82
Myxedema 235, 236 Palmoplantar keratosis 272, 273
Pancytopenia 162
Necrotizing ulcerative gingivitis 45, 128 Panhypopituitarism 231, 233
Necrotizing ulcerative periodontitis 128 Pannus 164, 226
Necrotizing sialometaplasia 192, 253 Parkinsonism 87, 98
Neuralgia-inducing cavitational Paterson-Kelly syndrome 95, 272
osteonecrosis (NICO) 208
Pathergy test 33, 272
Neurofibromatosis 101, 106
Paul-Bunnell test 24
Neurolysis 23
Pemphigus 36–39, 71
Neuromuscular disorders 98
Peutz-Jeghers syndrome 106, 272
Neurosyphilis 114, 118
Phossy jaw 112, 253
Nevoid basal cell carcinoma syndrome 218, 271
Pilocarpine 189, 190, 195
Nevus 105
Pleomorphic adenoma 253, 254
Nevus flammeus 270, 271
Plummer-Vinson syndrome 95, 146, 155
Nezelof syndrome 224
Portwine stain 102, 271
Nikolsky’s sign 26, 38, 40, 71
Posaconazole 45
Noguchi’s medium 118
Prednisolone 29, 38, 150
Noma 47, 48
Pregnancy gingivitis 79
Non-Hodgkin’s lymphoma 149
Prevotella intermedia 45
Noonan’s syndrome 271
Probenecid 118
Nystagmus 148, 273
Propylthiouracil 235
Nystatin 55, 127
Pseudo-hypoparathyroidism 240, 241
Omphalocele 269 Psoriasis 61
Oncocytoma 186 Pulse Doppler ultrasound 87
Oncogenes 280 Purse string appearance 228
Oncovin 150 PUVA therapy 70
Oophoritis 192 Pyostomatitis vegetans 39
Opalescent appearance 51, 65, 71 Pyridoxine 94
Opsonization 224 Pyrizinamide 120
Orchitis 192 Pyruvate kinase deficiency 155
Radiation mucositis 52 Sialoadenosis 195, 196

Radiofrequency thermocoagulation (RFTC) 206 Sialochemistry 196
Rampant caries 2, 189 Sialoendoscopy 186, 192
Ramsay Hunt syndrome 22, 272 Sialography 187, 188, 229, 273
Ranula 196, 197, 252 Sialolithiasis 190, 252
Raynaud’s phenomenon 227, 228, 272 Sialometaplasia 192, 253
Reed-Sternberg cell 149 Sialorrhea 189
Reiter’s syndrome 17, 61, 94, 273 Sickle cell anemia 156–158
Rendu-Osler-Weber syndrome 103, 272 Siderophenic dysphagia 62
Renografin 187 Simmond’s disease 232
Reye’s syndrome 2, 20 Sinografin 187
Rhagade 114 Sipple syndrome 238
Rheumatic heart disease 6, 226 Sjögren’s syndrome 194, 195, 229, 273
Rheumatoid arthritis 164, 226, 229 Spasmodic torticollis 98
Rhinorrhea 25, 204 Spherocytosis 156
Rhizotomy 206 Spina bifida occulta 271
Riboflavin 86, 94, 99 Splenectomy 152
Rickets 117 Starry sky appearance 150
Rifampicin 120, 122 Status asthmaticus 244
Riga-Fede disease 43, 97 Stevens-Johnson syndrome 25, 26, 255, 273
Riley-Day syndrome 43 Stomp positive 177
Risus sardonicus 250, 251 Streptokinase 145
Rituximab 150, 195, 229 Sturge-Weber syndrome 103, 271
Robinow’s syndrome 85 Subluxation 174, 175, 271
Rodent ulcer 218 Sumatriptan 204, 205
Roseola infantum 18, 115 Sump of the oral cavity 63
Rubinstein-Taybi syndrome 271 Sunburst appearance 220
Rutherford syndrome 85 Sunray spicules 150, 220
Sutton’s disease 31, 32
Sabouraud agar medium 55
Sabre tibia 116, 227 Swan-neck 164, 226
Sweet’s syndrome 272
Saddle nose 114, 116
Symblepharon 11, 41
Scaphocephaly 270
Schilling’s test 96 Syncytium 19
Syndactyly 269, 270, 274
Schirmer’s test 194
Synovitis 226, 271
Schourand Masler’s method 259
Scintigraphy 188, 194 Syphilis 114, 115
Syphilitic glossitis 116
Sclerodactyly 272
Scleroderma 96, 227, 228 Tabes dorsalis 114, 115
Scopolamine 189 Tacrolimus 70
Scrofula 119, 254 Tanaka’s recommendations 171
Scurvy 78, 145 Tantumoral rinse 53
Sequestrum 112 Tardive dyskinesia 43
Serpenginous border 61 Target lesions 25, 26
Sharpened pencil appearance 164, 226 Tc pertechnetate 88, 186, 194
Sheehan’s syndrome 231 Tegretol 205
Shotty lymph nodes 114 Telangiectasia 228, 272
Shovel shaped incisors 270 Temporomandibular joint disorders 169, 173, 175
Sialoadenitis 193, 252 Tenovate 70
Index 287
Terfenadine 56 Valacyclovir 23, 129, 206

Tertiary syphilis 97, 114, 115 Valganciclovir 25
Tetanolysin 250 van der Woude syndrome 269
Tetanospasmin 250 Varicella zoster 20, 21, 126, 206
Tetanus 249–251 Varicosities 87, 153
Tetany 241, 251 Vermicular movements 98
Thalassemias 158
Verruca vulgaris 50, 131
Thrush 49, 50, 54, 55
Verrucous leukoplakia 63
Thyroglossal duct cyst 92
Vinblastine 30, 149
Thyrotoxicosis 235
Tinnitus 82 Vincent’s angina 45, 47
Toluidine blue 64, 65, 214 Vincristine 30, 150, 151
Tourniquet test 142 von Ebner’s glands 89
Tram line calcifications 103, 271 von Recklinghausen’s disease 107
Tranexamic acid 5, 162 von Willebrand’s disease 141, 145
Transillumination 203
Waldenström macroglobulinemia 38
Trap door sign 179
Waldeyer’s ring 149
Treacher-Collins syndrome 269
Trench mouth 45 Wallerian degeneration 206
Tretinoin 66 Wandering rash 93
Triamcinolone 27, 38, 70 Warfarin 55, 140, 144
Trigeminal neuralgia 205 Warthin’s tumor 186, 254
Trigger point 171, 172 Water’s view 177
Trigger zone 201, 205 Webster’s classification 261
Trigonocephaly 270 Wegener’s granulomatosis 122
Trismus 172, 177, 249–251 Weil-Felix test 224
Trotter syndrome 250, 274 Western blot test 132
Trousseau’s sign 241, 251
Wheal 29
Tubercular ulcer 44
Wickham’s striae 67
Tuberculin test 130
Widal test 224
Tuberculoid leprosy 121
Wiskott-Aldrich syndrome 274
Tuberculosis 118, 121, 129
Tuberculous osteomyelitis 119 Wizened old man appearance 116
Tuberculum impar 58, 92 Wormian bones 271
Tuberous sclerosis 87 Xenografts 26
Turkish towel appearance 63
Xeroderma pigmentosum 218
Tzanck cells 38
Xerophthalmia 273
Ulcer 15 Xerostomia 129, 189, 229
Ultrasound 88, 172, 186
Unfractioned heparin-coumarin method 144
Zidovudine 97, 108, 109, 134
Urokinase 145 Ziehl-Neelsen 122, 129
Urticaria 28, 29 Zimmermann-Laband syndrome 272
Uveoparotid fever 122, 185 Zoledronic acid 151
Uvulopalatopharyngoplasty 99 Zoster sine eruption 23

Oral Medicine H Umarji

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CBS Publishers & Distributors Pvt Ltd

First eBook Edition: 2018

Published by Satish Kumar Jain and produced by Varun Jain for

1. Definition and Introduction 1

2. Ulcerative and Vesiculobullous Lesions 17

3. Red and White Lesions 49

7. Granulomatous Diseases and STDs 113

8. Cross-Infection Control 133

9. Bleeding and Clotting Disorders and Hematological Diseases 138

10. Temporomandibular Joint Disorders 163

11. Diseases of Maxillary Sinus 176

12. Salivary Gland Disorders 185

13. Orofacial Pain 199

14. Oral Cancer and Precancerous Lesions 211

15. Immunological Diseases 222

16. Endocrine Disease and Dysfunction 231

17. Management of Medically Compromised Patients and Drug Interactions 244

18. Differential Diagnosis of Miscellaneous Diseases 249

19. Forensic Odontology 256

20. Evidence-Based Dentistry 264

21. Orofacial Syndromes 269

22. Routine Blood Investigations 275

ORAL MEDICINE The case history includes the following parts:

A—Assessment, which involves arriving at health status. The possibility of drug

questions may be of two types, open-ended fulminating infections such as Ludwig’s

B—Bleeding Disorders vii. It is ideal to carry out surgical procedures

ii. Infections must be treated aggressively everyday. Pigmentation of oral tissues

floor of the mouth should also be inspected 11. Final Diagnosis

• Bullae are circumscribed elevated serous • Pustule is a circumscribed elevated lesion

Fig 1.1: Line diagram and picture of vesicle

Fig. 1.2: Line diagram and picture of bullous lesion

Fig. 1.3: Pustule

Fig. 1.4: Line diagram and picture of papules

Fig. 1.5: Line diagram and picture of plaque

Fig. 1.6: Line diagram and picture of macule

Fig. 1.10: Line diagram and picture of ulcer

surface as a polyp. It may be present in the

Type of virus 5. Each ulcer is surrounded by an inflamma-

Fig. 2.1: Multiple vesicles and ulcerations in primary HSV infection

Fig. 2.2: Primary HSV infection—geometric glossitis and palatal lesions

formation and there is always a danger of serum is diagnostic in primary. HSV

COXSACKIE VIRUS INFECTION

HZ infection may be deep seated and get

Fig. 2.6: Herpes zoster involving mandibular division of trigeminal nerve

Chickenpox Large atypical lymphocytes 20–80% of

• DNA hybrid capture. acyclovir prevented recurrent EM in HSV

9. Gingiva rarely affected. involvement of lungs, liver or kidneys.

Fig. 2.9: Stevens-Johnson syndrome

Histopathology: Shows intraepithelial lesions Treatment

In patients with diabetes or acidity or peptic

edematous attached gingiva occasionally

Fixed Drug Eruption Diagnosis: For contact allergy—patch test

Fig. 2.13: Examples of minor aphthous ulcers

Fig. 2.14: Examples of major aphthous ulcers

Major aphthae (PMNR, Sutton’s disease)

3. Resemble herpetic ulcers as they are small Behcet’s Syndrome

2. Steroids are mainstay and particularly Clinical Features

Fig. 2.16: Examples of recurrent herpes labialis