Essentials of Oral Medicine

Essentials
of
Oral Medicine
https://t.me/RoyalDentistryLibrary
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Essentials
of
Oral Medicine
Gautam Srivastava MDS

Reader in Oral Medicine, Diagnosis and Radiology
Lenora Institute of Dental Sciences
Rajahmundry, Andhra Pradesh (India)
E-mail: srivastava15@yahoo.com
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Essentials of Oral Medicine

© 2008, Gautam Srivastava
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form
or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the
author and the publisher.
This book has been published in good faith that the material provided by author is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In
case of any dispute, all legal matters are to be settled under Delhi jurisdiction only.
First Edition: 2008

ISBN 978-81-8448-212-6
Typeset at JPBMP typesetting unit
Printed at Rajkamal Press
Dedicated to
My parents, who taught me that the only

way to get anywhere in life is to work hard
and
my wife and son, who bring so much joy to my life
Thank you for being there
FOREWORD
It gives me great pleasure to write the foreword for this book Essentials of Oral
Medicine. The book consists of systematic rendering of the subject with a whole
chapter on “Ill Effects of Tobacco, Areca Nut and Alcohol.” It is well-illustrated
with appropriate clinical pictures and provides students with a clear
understanding of this science. The design and presentation of this book bears
testimony to the meticulous and tireless effort put in by the author, who is a
good academician and an excellent teacher. I am sure this book will be well-
appreciated and accepted by the dental profession. I congratulate Dr. Gautam
Srivastava for his excellent academic venture and wish him all success in his
endeavors.
Swarnalatha J Wesley MDS
Principal
Lenora Institute of Dental Sciences
Rajahmundry
Andhra Pradesh
PREFACE
This book is primarily intended for undergraduate students. However, students pursuing
postgraduation will find this book equally useful. The book contains twelve chapters, which reflect
basic as well as applied aspects with emphasis on current developments in oral medicine. The
organization of each chapter follows a logical sequence and is supported by high quality colored
diagrams and photographs to enable the student comprehend the subject fully and logically. A list of
important references covering all chapters is provided for the benefit of those interested in to have
detail information. The entire text has been word processed, which greatly facilitated editing and
updating the various chapters repeatedly as and when recent literature and reviews became available.
I would be most grateful to my readers both teachers and students for their constructive criticism of the
book.
Gautam Srivastava
ACKNOWLEDGEMENTS
The publication of this book would not have been possible without the efforts and cooperation of
many people. Firstly, my special thanks to my father Prof Bir Bahadur, who read the proof and offered
many marvelous suggestions and criticisms. I owe gratitude to my wife Shalini for her excellent job in
designing and drawing the figures, which made the book attractive. I would like to thank my teachers
Dr P Sudha, Dr R Heera, Dr VV Kamath, Dr DN Bailoor, Dr Bharat M Mody and Dr R Gopa Kumar for
their valuable guidance during my graduation and postgraduation. I wish to express my thanks to my
colleagues Dr NDVN Shyam for his valuable suggestions. I acknowledge the cooperation of my students
who judiciously read the proof and offered valuable suggestions. I am grateful to my students who
acted as models for the photographs of various procedures. I wish to thank Shri JP Vij, Chairman and
Managing Director of M/s Jaypee Brothers Medical Publishers (P) Ltd for giving me the opportunity to
author this book. I also acknowledge the support I received from Mr Nikhil Bardhan, Asst Incharge,
Hyderabad branch. The library facilities of College of Dental Surgery, Mangalore and Manipal, AB
Shetty Memorial Institute of Dental Sciences, Mangalore and Govt Dental College and Hospital,
Vijayawada are colossally recognized. Finally, I wish to thank my mother Dr Vijaya Devi Mathur for
her constant help, not only during the writing of this book throughout my dental education.
CONTENTS
1. Dental Recordkeeping .................................................................................................. 1
2. Biopsy ............................................................................................................................ 10
3. Orofacial Pain .............................................................................................................. 18
4. Temporomandibular Joint Dysfunction .................................................................. 31
5. Tobacco, Areca Nut and Alcohol .............................................................................. 56
6. Oral Precancer ............................................................................................................. 65
7. Oral Cancer .................................................................................................................. 80
8. Oral Candidosis ........................................................................................................... 99
9. Vesiculobullous and Ulcerative Lesions ............................................................... 104
10. HIV/AIDS in Dental Care ........................................................................................ 136
11. Pregnancy and Dental Care ..................................................................................... 155
12. Systemic Diseases and Dental Care ...................................................................... 168

I Oral Health and Heart Health
II Asthma and Dental Care
III Diabetes Mellitus and Dental Care
IV Bell’s Palsy
Glossary ........................................................................................................................ 223
Index ............................................................................................................................. 243

Chapter
Dental Recordkeeping
1
INTRODUCTION 7. Adequate recording of patient information,
medical/dental history, clinical and
Patient records must provide an accurate picture
of the condition / or conditions present on initial radiographic findings, diagnosis and
examination as well as the clinical diagnosis, treatment including fees charged, and
treatment options, the proposed and accepted referrals
treatment plan, a record of the treatment 8. Responsibility for record completion remains
performed, details about any referrals, and the with practitioner providing services
prognosis and/or outcome of the treatment where
applicable. Patient Consent
Following is a list of situations where the patients
Recordkeeping Principles signature is desirable to see to it that the records
In keeping and maintaining acceptable patient are closest to accuracy:
records, a careful practitioner should adhere to 1. Medical history including date
the following basic principles: 2. Consent for treatment including associated
1. All entries should be recorded in ink, fees
typewritten or be in an acceptable electronic 3. Presurgical and postsurgical instructions for
format major procedures or those done under
2. All entries should be accurate and clean sedation or general anesthetic
3. All entries should be signed, initialed or 4. Consent for sedation and general anesthesia
otherwise credited to treating clinician 5. Financial arrangements
4. All entries should be dated and entered at 6. Consent to obtain and/or release information
time of patient visit in chronological order (late a. Personal use
entries should be identified as such) b. To transfer records to another dentist
5. Radiographs and other diagnostic aids, such c. To transfer records to physician
as study models, should be properly labeled, d. To transfer records to alternate physician
dated and the interpretation of the findings e. For referrals
documented when considered appropriate by f. Legal use (lawsuit)
the practitioner g. Third party (coroner (forensic odontologist),
6. All items and/or pages properly identified law enforcement agencies, third party
by patient name payment)
2 Essentials of Oral Medicine
7. When patients refuse radiographs, treatment 11. Name, address and phone number of patients
or referral to another practitioner medical specialist (s), if obtainable
12. Emergency contact name and telephone
PATIENT RECORD number
13. Previous dentist
The extent of the detail required for each individual
14. For minors, name of parent or legally
dental record will vary from patient to patient. It
authorized representative
will also depend on the conditions with which
the patient presents, and the complexity of the Financial Information
treatment that is required. Certain baseline data,
however, should be common to all dental patients. 1. Name of the person or agency responsible for
This information includes: payment
1. Demographic data 2. Insurance information, if applicable
2. Financial information
Dental History
3. Dental history
4. Medical history The dental history should contain information of
5. Clinical examination personal dental health and previous dental care.
6. Diagnosis and treatment plan Information obtained regarding a patients dental
7. Referrals and consultations history can supplement the clinical examination,
8. Follow-up notes and assists in the planning dental care that is
9. Emergency treatment record necessary and suited to improve the patients
10. Laboratory record dental health status. The dental history should
11. Drugs record address the following:
12. Financial record 1. Chief complaint (painful tooth/teeth, bleeding
13. Confidentiality gums, crooked teeth, hole in tooth, bad breath,
discoloration of teeth, loose tooth/teeth, teeth
Demographic Data set, sores, growth, white patch, burning
sensation, etc)
The following general information should be 2. History of present illness
obtained from every patient at the initial a. Origin: When did the problem start?
appointment and updated at regular intervals: b. Duration: Since how long has the problem
1. Name been present?
2. Age c. Progress: How is the problem progressing
3. Sex e.g., getting better, getting worse or
4. Date of birth remaining static?
5. Address d. Aggravating and relieving factors: Any
6. Telephone numbers (residence and office) factors that aggravate the problem or any
7. E-mail ID factors that relieve the problem?
8. Occupation e. Radiation: Is the problem radiating e.g.,
9. Name and address of any referring health refered pain?
professional, if applicable 3. Previous dental care (scaling, restoration,
10. Name, address and phone number of patients extraction, denture, root canal therapy,
primary physician, if obtainable radiographs, etc)
Dental Recordkeeping 3
4. Date of last dental visit carcinogenic agent in alcoholic beverages is

5. Emotional concerns (fear, pain, time, money, ethanol per se (in and of itself).” It must be also
embarrassment) borne in mind that polycyclic aromatic
6. Oral hygiene habits hydrocarbons and nitrosamines are also widely
a. Brushing with toothpaste and toothbrush present in tobacco and foodstuffs.
(frequency)
Medical History
b. Brushing with toothpowder and
toothbrush (frequency) A general medical history should be taken at the
c. Flossing (frequency) initial appointment to assist in proper diagnosis
d. Interproximal brush (frequency) and treatment, and to allow safe dental care. This
e. Others (finger, salt, charcoal, brick powder, can be accomplished using a suitable question-
chewing neem sticks etc) naire and accompanying verbal discussion. In
7. Oral habits situations where the patient has trouble reading,
a. Mouth breathing the dentist may take the medical history orally
and make appropriate notes on behalf of the
b. Tongue thrusting
patient. It may also be necessary to obtain medical
c. Thumb/finger sucking
information from family members if the patient is
d. Grinding teeth
unable to provide it (e.g., language barrier,
e. Biting lips/tongue/cheeks/fingernails
Alzheimer’s patient).
8. Dietary habits (sugar intake)
Any drug allergies, current drug regimens,
9. Tobacco habits (frequency × years) or quit
medical alerts or conditions appropriate to the
a. Pack Year: The risk of development of
patient should be prominently noted on the patient
diseases due to tobacco smoking is related
record. This history should be updated at regular
to the intensity of the exposure, frequently
intervals and this fact noted in the patient record.
expressed in terms of “pack year.” Pack It is important that the collection of necessary
year is a way to measure the amount a medical history information be done in a
person has smoked over a long period of systematic manner. In doing so, the following key
time. It is calculated by multiplying the areas must be addressed for all patients and both
number of packs of cigarettes smoked per positive and negative responses recorded:
day by the number of years the person has 1. Family history of disease
smoked. For example, 1 pack year is equal 2. Adverse reactions to any medicines or
to smoking 1 pack per day for 1 year, or materials e.g., penicillin, aspirin, erythro-
2 packs per day for half a year, and so on. mycin, local anesthetics, latex allergy (latex
10. Alcohol habits (frequency × years), (type of gloves and latex rubber dams)
alcoholic beverage) or quit 3. Drug or alcohol dependency
Specific alcoholic beverages have been shown 4. A listing of all medications currently being
to contain specific impurities or contaminants taken
which can be carcinogenic. N-nitrosodiethyl- 5. Details of past hospitalizations
amine is present in some beers and whisky and 6. List of surgical procedures
has been associated with an increased risk of oral 7. Women (pregnancy, birth control pills)
cancer. Polycyclic aromatic hydrocarbons, some 8. Cardiovascular disorders e.g., angina pectoris,
of which are considered to be carcinogenic are myocardial infarction, congestive cardiac
found in many brands of whisky. However, Kabat disease, hypertension, valvular disease,
and Wynder (1989) concluded that the “main rheumatic fever, stroke etc
9. Respiratory disorders e.g., bronchitis, asthma, update it whenever necessary. For those patients
tuberculosis, emphysema, cystic fibrosis etc with little or no history of dental disease and
10. Neurological disorders e.g., epilepsy, Bell’s relatively healthy oral tissues, this can be
palsy, cerebral palsy, Alzheimer’s disease, etc accomplished with a notation such as “nothing
11. Hematological disorders e.g., anemias, abnormal detected” for most of the areas.
leukemias, lymphomas, bleeding disorders Components of a comprehensive clinical
12. Endocrine disorders e.g., hyperthyroidism, examination include:
hypothyroidism, hyperparathyroidism, 1. Examination of patients chief complaint
diabetes mellitus etc 2. Vital signs (temperature, respiratory rate,
13. Gastrointestinal disorders e.g., gastritis, pulse, blood pressure)
peptic ulcer, jaundice, cirrhosis, hepatitis etc 3. Pallor, icterus, cyanosis, and clubbing
14. Renal disorders e.g., acute and chronic renal 4. Extraoral
failure etc a. General appearance (well build,
15. Dermatological disorders e.g., eczema, fungal moderately build, ill build)
infection, psoriasis etc b. Height, weight, and gait
16. Psychiatric disorders e.g., anxiety, c. Facial symmetry (symmetrical, asymme-
depression, schizophrenia, bipolar disorder trical)
etc d. Facial profile (convex, straight, concave)
17. Nutritional disorders e.g., anorexia nervosa, e. Head (normal, brachycephalic (short head),
bulimia etc dolichocephalic (long head))
18. Infectious diseases e.g., AIDS, syphilis,
f. Eyes (normal, exophthalmia, enophthal-
infectious mononucleosis etc mia, hypertelorism (increased intercanthal
19. Cancer/radiation treatment /chemotherapy distance), strabismus or squint (convergent
20. Organ transplants (solid organs or bone
or divergent), blue sclera)
marrow)
g. Nose (normal, saddle nose, parrot’s beak)
21. Medical implants (joint replacement, heart
h. Neck
valve replacement, pacemaker, indwelling
I. Lymph nodes (Figs 1.1A to E)
catheters)
i. Size: Estimate the size in millimeters
22. Ever had or been tested positive for any
ii. Number: Single or multiple
immunocompromising disease
enlarged lymph nodes
iii. Location: Unilateral or bilateral
Clinical Examination
iv. Tenderness: When palpated the
The clinical examination is tailored to the patients lymph node may be painful (tender)
chief complaint. A visual examination should or not painful (nontender)
precede other diagnostic procedures. The clinical v. Mobility: When palpated the lymph
examination consists of recordings on an node may be fixed to the underlying
odontogram (tooth chart) which may include tissue or freely movable under the
written descriptions of the conditions (e.g., fingers
decayed teeth, missing teeth, and restored teeth) vi. Consistency: Describe the lymph
that are present on examination of the patient. node as hard (stone), firm (like a
However, other conditions such as intrinsic tensed muscle), soft (like a water
staining and hypoplasia require separate written balloon)
descriptions. It is important that there is sufficient II. Other neck masses (thyroglossal duct
space to record all relevant information and to cyst, epidermoid cyst, dermoid cyst,
Fig. 1.1A: Palpation of the submandibular lymph nodes Fig. 1.1D: Palpation of the middle jugular lymph nodes
Fig. 1.1B: Palpation of the submental lymph nodes Fig. 1.1E: Palpation of the lower jugular lymph nodes
roma, fibroma, hemangioma, plunging

ranula, salivary gland tumors, sialoa-
denitis, esophageal fibroma, sarcoi-
dosis, metastatic carcinoma, intra-
thoracic goiter)
i. Muscles of mastication (normal, hypertro-
phied, paralyzed)
j. Salivary glands (normal, enlarged)
5. Temporomandibular joint examination
a. Assessment of pain location
Fig. 1.1C: Palpation of the upper jugular lymph nodes b. Opening pattern
c. Vertical range of movement (Fig. 1.2A and B).
submental lymphadenitis, submental d. Joint sounds on vertical opening
abscess, thyroid gland tumors, ectopic e. Jaw excursions (lateral and protrusive)
thyroid, carotid body tumor, branchial f. Joint sounds on lateral and protrusive
cleft cyst, cystic hygroma, neurofib- excursions
Fig. 1.2A: Unassisted mandibular opening without pain Fig. 1.3A: Palpation of the lateral pole
Fig. 1.2B: Maximum assisted mandibular opening Fig. 1.3B: Palpation of the posterior disc attachment
g. Muscle and joint palpation

i. Extraoral muscles
ii. Temporomandibular joint (Figs 1.3A
and B)
iii. Intraoral muscles (Figs 1.4A and B)
6. Intraoral soft tissue examination
a. Lips
b. Labial mucosa
c. Buccal mucosa
d. Buccal vestibule
e. Retromolar area
f. Oropharynx Fig. 1.4A: Palpation of the lataral pterygoid area
g. Palate (hard and soft)

7. Intraoral hard tissue examination
h. Lingual vestibule a. Appliances present
i. Tongue (posterior, dorsal, lateral, ventral) b. Occlusion (Class I, Class II ( Div I, Div II),
j. Floor of mouth
Class III)
k. Salivary gland ducts
c. Overjet
Diagnosis
Diagnosis is an assessment of the clinical
findings, which may help in identifying a specific
disease. There are a number of related terms, which
are as follows:
1. Spot diagnosis
2. Working diagnosis (provisional diagnosis or
tentative diagnosis)
3. Differential diagnosis
4. Definitive (final diagnosis)
Fig. 1.4B: Palpation of the tendon of temporalis
d. Overbite Spot Diagnosis

e. Crossbite Diagnosis made quickly on the spot. It can be a
f. Crowding perfectly good diagnosis e.g., a patient returns
g. Spacing three days after removal of a tooth complaining of
h. Decayed teeth pain, bad taste, exhibiting inflammation and
i. Missing teeth discharge at the extraction site. The spot diagnosis
j. Restored teeth is that the patient probably has a “dry socket.” In
k. Sensitive teeth such case, various diagnostic tests are not required
unless the condition does not respond to the
l. Impacted teeth
routine treatment.
m. Supraerupted teeth
n. Migrated teeth Working Diagnosis (Provisional diagnosis or
o. Fractured teeth tentative diagnosis)
p. Mobile teeth Diagnosis made when the clinical presentation
q. Regressive alterations corresponds to a particular disease so that
r. Developmental disturbances preliminary treatment may proceed. Example,
s. Edentulous (unerupted teeth, bony ulceration on the lateral border of the tongue in
spicules, retained roots, shallow vestibule, relation to a sharp edge of a grossly decayed tooth
hyperplastic tissue) may simply be a traumatic ulcer in response to
8. Periodontal examination chronic irritation. With that as a working
a. Deposits (plaque, stains, calculus) diagnosis, the sharp edge of the tooth may be
b. Gingiva (size, shape, color, consistency, grinded off or the tooth extracted and a
texture) reevaluation of the patient scheduled after a week
c. Gingival bleeding or suppuration or two. If the ulcer resolves, the clinician can safely
d. Gingival recession and finally diagnose it as a “traumatic ulcer.”
e. Frenal attachments (normal, high, low) However, if the ulcer has not resolved, the working
f. Furcation involvement diagnosis is discarded, and further investigations
g. Probing of pocket depths when indicated started.
Differential Diagnosis Treatment Plan

It is a process of identifying a specific disease from The treatment plan would include specific
other diseases that may produce similar signs and information regarding the nature of the
symptoms. Once the diagnostician has listed all procedures, materials to be used, number of
the diseases that produce similar signs and appointments needed to accomplish this care,
symptoms, an algorithm (a precise rule or set of behavior management techniques and fee for
rules specifying how to solve some problem) may proposed procedures. The treatment plan should
be used or prepared, which may help in narrowing be supported by a complete and accurate clinical
down the list of diseases. Further investigations record and take into account the relative urgency
may then be carried out, until a single disease or and severity of the patients condition. The patients
cluster of diseases remain. At that point, all choice of treatment should be recorded along with
additional investigations to confirm the diagnosis the estimated costs.
within the cluster of diseases are performed,
leading to a definitive diagnosis. Referrals and Consultations
Definitive (Final diagnosis) Notes of referrals to specialists or other health care

professionals as well as copies of correspondence
Diagnosis derived after using differential
and reports should be incorporated into the
diagnosis is the definitive or final diagnosis. Once
record. If a patient requests access to their dental
the definitive diagnosis is derived, the suitable
treatment is delivered. However, if the disease fails records or reports from other practitioners, they
to respond to the treatment, it may be necessary to must be disclosed. When a patient refuses to be
turn back to the differential diagnosis and try all referred to another specialist, a note should be
over again. made in the record and if possible, the note should
In cases of soft tissue and bony diseases, be signed by the patient or legally authorized
histological examination of biopsy specimen often representative.
determines the final diagnosis. Hematological
diseases or autoimmune diseases may be proved Follow-up Notes
by hematological examination and serology. An entry must be made in the patients record that
However, not all diseases can be diagnosed easily, accurately and objectively summarizes each visit.
as the range of abnormal is as wide as that of The following information should be included:
normal. 1. Date of visit
2. Reason for visit
Investigations 3. Changes in the medical history, if any
Based upon the clinical examination, the dentist 4. Clinical findings
may employ additional diagnostic tools to 5. Diagnostic procedures
complete the oral health assessment. Such 6. Treatment rendered
diagnostic aids may include: percussion test, 7. Local anesthetic used including type and
vitality tests, radiographs, photographs, vital quantity
staining, biopsy, fremitus test, butterfly test, 8. Medication given to the patient
transillumination test, caries activity tests, 9. Referrals to specialists or other health care
laboratory tests, and study casts. professionals and the results of such referrals
Emergency Treatment Record 6. Directions for use

7. Condition being treated
A dental emergency exists if the person needs
If the prescription is given by phone from
immediate relief of pain, or control of infection or
outside the office, the details should be recorded
bleeding. The emergency treatment record should
on a piece of paper and later transferred to the
include:
patient record.
1. Personal information
2. Thorough medical history and relevant dental
Financial Record
history
3. Findings of the emergency Fees charged and payments received must be
4. Record of services performed recorded including date of the transaction, method
5. Record of prescriptions of payment, and source (e.g., patient, third party
6. Record of referrals payer).
7. Record of follow-ups
Confidentiality
Laboratory Record Dental records are collections of sensitive patient
This is a record containing particulars of information compiled to allow dental
purchases of all dental prosthetic, restorative or practitioners to provide dental treatment, ensure
orthodontic devices and should include the continuity of services, and maintain optimal
following information: standards of care. Every effort must be made to
1. Name of laboratory ensure that the information provided by the
2. Address of laboratory patient is protected against unauthorized use or
3. Nature of device disclosure. Dentists must educate their employees
4. Materials used with regard to maintaining the confidentiality of
5. Date of device prescribed patient information.
6. Device prescribed for whom
BIBLIOGRAPHY
Drugs Record 1. American Academy of Pediatric Dentistry.
Drugs must be prescribed, administered by a Clinical Guideline on Recordkeeping. Clinical
guidelines 2004-2005;134-9.
dentist in accordance with the Drugs and
2. College of Dental surgeons of British Columbia.
Cosmetics Act and Rules. The following Dental Records Management 2003;1-42.
information must be recorded on the patients 3. Delrose DC, Steinberg RW. The clinical
record: significance of the digital patient record JADA
1. Date of prescription 2000;131:57S-60S.
2. Name of drug 4. Giglio JA, Laskin DM. Establishing the differential
3. Strength of drug diagnosis of neck lesions. Quintessence Int
2000;31:637-41.
4. Quantity of drug
5. Royal College of Dental Surgeons of Ontario.
5. Form of drug
Guidelines on Dental Recordkeeping 2002;1-12.
Chapter
Biopsy
2
INTRODUCTION 3. Brush biopsy
French dermatologist Ernest Henry Besnier 4. Laser biopsy
coined the word “biopsy” in 1879. In Greek, it 5. Fine needle aspiration biopsy
means Bios meaning life and opsis meaning
vision. As the diagnosis made clinically is purely Excisional Biopsy
provisional, biopsy is essential for final diagnosis. Excisional biopsy is the total removal of the
There is no harm in supplementing the pathological tissue along with margin of normal
provisional diagnosis with biopsy even when the tissue. It is indicated when the size of the
clinician is sure that the lesion is benign. pathological tissue is less than 2 cm.
However, the provisional clinical diagnosis is
very important in guiding the biopsy technique. Incisional Biopsy or Wedge Biopsy
Definition Incisional biopsy is the partial removal of the

pathological tissue along with margin of normal
According to Richard W.Tiecke, biopsy may be tissue. It is indicated when the size of the
defined as surgical or non-surgical removal of pathological tissue is more than 2 cm.
tissue from a living organism for microscopic
analysis, chemical analysis, or bacterial analysis Intraoral Punch Biopsy
or a combination of all. An alternative technique to the traditional
1. Microscopic analysis: Histopathological incisional biopsy is the punch biopsy. The punch
examination or cytological examination biopsy instrument has a circular blade attached
2. Chemical analysis: Protein estimation of to a plastic handle. The diameter of circular blade
aspirated fluid can be adjusted from 2 to 10 mm. The biopsy
3. Bacterial analysis: Bacterial culture specimen can be removed with a help of curved
scissors or a scalpel. There are chances that the
Types of Biopsy
biopsy specimen being sucked in. If the resultant
1. Excisional biopsy wound is large, it is usually sutured. A study
2. Incisional biopsy carried out by Moule et al (1995) has shown that
a. Intraoral punch biopsy punch biopsies produce fewer artifacts. The site
b. Modified Ellis drill biopsy of the lesion may indicate punch biopsy or
Biopsy 11
incisional biopsy. Lesions on the gingiva and Sullivan-Schein dental subsidiary of Henry
palate do not give enough access for punch Schein, Inc, exclusively distributes the Oral CDx
biopsy. oral brush biopsy. In comparison to exfoliative
cytology Oral CDx, brush biopsy has an upper
Modified Ellis’ Drill Biopsy hand because of two reasons:
Drill biopsy is a type of incisional biopsy, which 1. The dysplastic or cancerous cells are located
is indicated in central lesions. The biopsy is deep to the keratin layer
performed under local anesthesia or general 2. The procedure consists of microscopic
anesthesia, following which the mucoperiosteal screening a cytological smear consisting of
flap is reflected and a window is made in the 1000’s of normal cells to identify abnormal
cortex with the help of bur. However, sometimes cells because the exfoliating normal cells are
the cortex may be thin or perforated and bur is in enormous numbers because of epithelial
not required for window preparation. Once the turnover
cortex is removed the underlying pathology is Brush biopsy is also being effectively used in
exposed, which can be curetted and placed in the medical field as a diagnostic tool for
10% formalin. bronchial, duodenal, pancreatic, biliary, and
rectal cancers. For more information on Oral CDx
Brush Biopsy brush biopsy one can email to
oralcdx@oralscan.com.
Majority of oral cancer cases are diagnosed in The Oral CDx brush biopsy kit is free and
advanced stages as the early stages of oral cancer includes:
are asymptomatic and appear innocuous and the 1. Sterile brush
classical clinical characteristics associated with 2. Precoded glass slide
advanced oral cancer like ulceration, induration, 3. Alcohol or polyethylene glycol fixative
bleeding, and cervical lymphadenopathy are pouch
absent. Thus, detection of oral cancer in the early 4. Test requisition form, which includes
asymptomatic stages dramatically improves patients demographic data
patients survival rate and minimizes extensive 5. Preaddressed container
debilitating treatment procedures. Therefore, the
US Collaborative Oral CDx study group
Advantages
undertook a study to evaluate the sensitivity of The advantages of Oral CDx brush biopsy are
Oral CDx (Oral Scan Laboratories, Inc.). The Oral enlisted below (Table 2.1).
CDx is a diagnostic system that combines a Table 2.1: Advantages of Oral CDx brush biopsy
painless oral brush biopsy (full transepithelial • Local anesthesia is not required
oral biopsy), which is taken in the dental office,
• Reduced chair side time
with advanced computer analysis. The Oral CDx
• Simple procedure which is easy to master
oral brush biopsy test was developed precisely
to evaluate benign-appearing oral lesions and • Quick results
was evaluated in a prospective multicenter
Indications
clinical trial that involved 35 United States
academic dental sites and the findings were The indications of Oral CDx brush biopsy are
published in the JADA, Vol.30, October 1999. enlisted below (Table 2.2).
Table 2.2: Indications of Oral CDx brush biopsy in computer-assisted analysis of oral brush
• Precancerous lesions • Herpes simplex virus infection biopsy specimen. The pathologist classifies the
• Oral squamous cell • Human papilloma virus specimens displayed on the high-resolution
carcinoma infection colour video monitor into four categories, which
are enlisted below (Table 2.3). After submitting
• Candidiasis • Pernicious anemia
the Oral CDx brush, biopsy specimen to the
• Pemphigus vulgaris • Radiation effects
speciality laboratory the dentist receives a faxed
report consisting of coloured images of the
Procedure “atypical” or “positive cells.” The coloured
No local anesthetic is required. Slightly moisten images enable the dentist to demonstrate to the
the biopsy brush with the patients saliva if the patient the abnormal test results.
lesion is dry. Press the biopsy brush firmly
Oral CDx Computer
against the lesion. Rotate 5-10 times (depending
on the thickness of the lesion) while maintaining The Oral CDx is a nonalgorithimic neural
firm pressure until pink tissue or pinpoint network computer whose technology was
bleeding is observed. The cellular material developed in the late 1980s for SDI missile
collected on the brush is transferred to the defense system. The Oral CDx computer is
precoded bar glass slide by rotating and dragging specifically designed to detect as few as two
the brush lengthwise. The fixative packet is abnormal oral epithelial cells scattered among
quickly squeezed onto the precoded bar glass more thousands of normal cells distributed on
slide to avoid air-drying. Set the slide aside to each oral brush biopsy specimen. In addition, the
dry for 15 minutes, and then place it in the slide Oral CDx computer also complements the
holder. Complete the test requisition form, and existing oral cancer screening modalities that use
send the specimen to Oral Scan Laboratories in vital dyes like toluidine blue. Toluidine blue is a
Suffern, N.Y. in the preaddressed container. At metachromatic vital dye that increases visual
the Oral Scan laboratory, the precoded bar glass detection of oral precancer and cancer after
slide is stained with modified Papanicolau stain negative clinical examination. The nonalgorithi-
which is scanned by the Oral CDx computer for mic neural network computer is a type of
abnormal cells. The abnormal cells identified by artificial intelligence that attempts to imitate the
the Oral CDx computer are displayed on the way a human brain works by creating
high-resolution colour video monitor for connections between processing elements, the
interpretation by a pathologist specially trained computer equivalent of neurons rather than a
Table 2.3: Classification of Oral CDx specimens

Categories Interpretation Action
• Negative No epithelial abnormality Careful clinical follow-up
• Atypical Abnormal epithelial changes of uncertain Refer for scalpel biopsy and histological
diagnostic significance evaluation
• Positive Definite evidence of dysplasia or carcinoma Refer for scalpel biopsy and histological
evaluation
• Inadequate Incomplete transepithelial biopsy Repeat the brush biopsy procedure
Biopsy 13
digital computer, in which all computations An important principle to remember is that even
manipulate zeros and ones. Neural networks are though the surgeon is employing laser as an
particularly effective for predicting events when alternative to scalpel the principles of the biopsy
the networks have a large database of prior procedure are same for example the biopsy
examples to draw on. Bernard Widrow of specimen should include both normal and
Stanford University pioneered the field of neural pathological tissues. Focused mode is preferred
networks in the 1950s. The nonalgorithimic over defocused mode because in focused mode,
neural network computer is currently used the intensity of the laser beam is high and the
prominently in voice recognition systems, image
laser beam hits a focal spot on the tissue surface.
recognition systems, industrial robotics, medical
For the patient and the surgeon eye protection is
imaging, aerospace applications, and data
very essential, as the laser beams are harmful.
mining.
Different lasers require different types of safety
Laser Biopsy glasses and these should never be interchanged
for example argon lasers require dark green
Lasers can be effectively used for incisional and safety glasses. General anesthetic gases should
excisional biopsies. Lasers have a definite edge be kept away from laser beams as fires and
over the conventional scalpel because of the explosions may be ignited when lasers hit them.
following reasons: In addition, instruments with reflective surfaces
1. Patient acceptance like mouth mirror, polished restorations should
2. There is little or no bleeding be kept away from lasers, as they tend to reflect
3. Dry operating field the laser beam. The laser plume created when
4. Excellent visibility
tissue vaporizes produces “fulguration artifact”
5. Reduced operating time
in the biopsy specimen thus when laser biopsy
6. No trauma to adjacent tissues
is performed the pathologist should be informed.
7. Pain is reduced to 90 % due to sealing of
The surgical applications of dental lasers are
nerve fibers
enlisted below (Table 2.4).
8. Bacterial counts are reduced thereby
providing a relatively sterile operating field
Fine Needle Aspiration Biopsy
9. There is little or no postoperative swelling
due to sealing of blood vessels and Aspiration biopsy is very inexpensive, quick and
lymphatics easily performed technique. The complete
10. Because of minimal bleeding and sealing of transtumor sample is composed of cells, tissue,
blood vessels and lymphatics chances of or fluid and is useful in diagnosis of fluctuant
metastasis is eliminated when performing lesions, deep-seated submucosal lesions and
biopsy on oral squamous cell carcinoma metastasis in enlarged cervical lymph nodes. A
Table 2.4: Surgical applications of dental lasers

• Fibroma • Oral submucous fibrosis • Mucous membrane pemphigoid
• Papilloma • Oral squamous cell carcinoma • Tongue lesions
• Epulis • Aphthous ulcers • Hemophilia
• Leukoplakia • Herpetic lesions • Idiopathic thrombocytopenia purpura
• Lichen planus • Pemphigus vulgaris • Slurge-Weber syndrome
10 ml syringe, 22-gauge needle, frosted glass 4. Vascular lesions such as haemangioma

slides, 10% formalin is all that is needed. The skin 5. Patients who are on anticoagulant therapy
should be prepared with iodine prior to
aspirating the enlarged cervical lymph nodes. Principles of Biopsy Procedure
The needle is inserted into the fluctuant swelling 1. A written consent from the patient prior to
or the enlarged cervical lymph nodes and moved the biopsy procedure is very important, as
up and down. Once the cells, tissue, or fluid is there are risks involved in biopsy procedures
aspirated, the needle is withdrawn from the such as paresthesia, and swelling.
swelling and sent for either protein estimation 2. The type of biopsy will be based on the
or cytological examination. The various colours approximate size of the lesion. In case the
of aspirated fluid are enlisted below (Table 2.5). size of the pathological tissue is less than 2
cm, excisional biopsy is preferred. Incisional
Table 2.5: Various colours of aspirated fluid biopsy is indicated when the size of the
Pathology Aspirate colour pathological tissue is greater than 2 cm.
3. During the biopsy procedure, consideration
• Odontogenic keratocyst Thick yellow cheesy material
should be given to anatomical structures like
• Dentigerous cyst Straw coloured fluid
neurovascular bundles that should be
• Radicular cyst Straw coloured fluid handled with care. For example when
• Residual cyst Amber coloured fluid incisional biopsy of the palate is performed
• Traumatic bone cyst Nonproductive the incisions should run parallel to the nerves
(antero-posteriorly) and not (medio-
• Aneurysmal bone cyst Red coloured fluid
laterally).
• Infected cyst Pus
4. In order to select the biopsy area vital stains
• Ameloblastoma Straw coloured fluid like toluidine blue, lugol’s iodine, or acridine
• Haemangioma Red coloured fluid help in identifying areas of dysplasia,
carcinoma in situ and invasive carcinoma.
Indications for Biopsy Avoid biopsy from centre of large tumors,
as they are necrotic.
1. Lesions that cannot be diagnosed by clinical
5. Infiltration with a local anesthetic well away
and radiological examination
(atleast 2 cm) from the biopsy site is
2. Lesions that which do not respond to
preferable as there are chances of biopsy
treatment
specimen being distorted due to artificial
3. Precancerous lesions and conditions
water logging. Infiltration should be slow
4. Lesions, which exhibit rapid growth, and minimal to prevent separation of
paresthesia, or loss of function epithelium from connective tissue and rapid
5. Cancerophobia swelling.
6. Nerve block is not preferred as the
Contraindications for Biopsy haemostatic effect of adrenaline is lost.
1. Acute inflammatory conditions such as 7. Insert 000 silk suture material into the
cellulitis pathological tissue and tie a loose knot above
2. Normal anatomical variations such as linea the tissue surface. The knot should not be
alba very close to the tissue surface as the knot
3. Patients with bleeding disorders has a tendency to crush the lesion.
Biopsy 15
8. Elevate the 000 silk suture with the knot. may be used alternatively to prevent
9. An elliptical-shaped incision is made around autolysis. “Michel’s solution” is the choice
the pathological tissue with a scalpel, which of fixative in Vesiculo-bullous lesions and not
should include normal adjacent tissue. 10% formalin as formalin fixes the biopsy
10. The size of the biopsy specimen should be specimens by forming intermolecular
atleast 1 × 1 cm in size, as inadequate size bridges between proteins and cross-links
may pose problems such as shrinkage after between protein end groups thus the
fixation and there may be chances of repeat specimen is rendered unusable for
biopsy. immunofluorescence test. Alternatively, the
11. In case of excisional biopsy, the lesion should biopsy specimen can be immediately frozen.
be oriented. This can be achieved by placing 15. Biopsy specimens from different anatomical
a suture at one known margin, for example sites should be placed in different containers
the anterior or superior margin. This would and properly labeled.
enable the pathologist to confidently indicate 16. Suture the surgical area with 000 silk non-
the precise location of any residual tumor. resorbable suture material. Resorbable
12. In order to avoid artifacts the biopsy sutures such as polyglactin are now
specimens should be handled with care as replacing traditional 000 silk sutures.
improper handling may produce “crush 17. A non-eugenol containing periodontal
defects.” The ‘traditional’ technique using dressing can be used for covering gingival
toothed tissue forceps to grasp the specimen biopsy sites and in case of palatal biopsies; a
is acceptable providing care is taken and the preconstructed acrylic plate should be placed
area grasped is away from the main site of beneath the non-eugenol containing
interest. periodontal dressing.
13. The excised biopsy specimen is not placed 18. Securely seal the bottle and label it.
in a bottle having narrow mouth and neck, 19. Fill up the biopsy form with the necessary
as the biopsy specimen tends to get crushed. details.
Rusted containers should be avoided, as iron 20. Send the biopsy specimen to the pathologist
oxide will interfere with staining. for microscopic examination.
14. The excised biopsy specimen is placed in 10
% neutral buffered formalin fixative, which Modifications of Biopsy Procedure (Table 2.6)
has a pungent and distinct odour. The 1. In diagnosis of precancerous lesions such as
volume of the fixative should be atleast 10 leukoplakia or erythroplakia, importance
times the volume of the specimen. It is not should be given to areas, which are non-
advisable to place the biopsy specimen on homogenous, speckled, or erythematous as
gauze and then place it in the glass bottle they have a higher incidence of having
containing formalin because the gauze tends dysplastic features or transforming into
to absorb the formalin if its volume is not malignancy. If there are numerous
great enough. Glutaraldehyde is the fixative erythematous areas, multiple biopsies
of choice if the biopsy specimen is required should be performed.
for electron microscopy. In case 10 % 2. In diagnosis of lichen planus or lichenoid
formalin is not available, the biopsy reactions, area of non-erosive lesional tissue
specimen should be placed in absolute should be chosen without adjacent normal
alcohol. Normal saline or anesthetic solution tissue as erosive areas usually show non-
specific inflammatory changes and 4. Mucoceles should be excised completely

ulceration. with lot of care along with associated minor
3. In diagnosis of oral cancer, a pie-shaped deep salivary glands as they have a tendency to
incisional biopsy specimen involving the recur.
margin of the ulcer along with 1 cm margin 5. In diagnosis of minor salivary gland tumors
of normal mucosa, however, 2 cm margin of of the palate, incisional biopsy should be
normal mucosa is indicated in squamous cell performed and should be as deep as possible
carcinoma of tongue. If the margin of normal because the lesions can be deep to the palatal
mucosa is less than 1 cm, there is an increased mucosa. Due attention should be given to
recurrence rate of oral squamous cell nerve and vessels of that area.
carcinoma. The incisional biopsy should be
6. In diagnosis of vesiculobullous lesions such
deep involving submucosa to rule out
as pemphigus, the site of the biopsy should
extensive spread. A study carried out by
be adjacent to vesicle or bulla where the
Kinsukawa et al (2000) demonstrates that
epithelium is normal.
cytokeratins are present in the peripheral
blood in two out of ten patients 15 minutes Artifacts in Oral Biopsies
after incisional biopsy of an oral squamous
cell carcinoma, thereby demonstrating that In order to investigate the various artifacts in oral
there was dissemination of cancer cells, biopsies, Seoane et al (2004) randomly selected
which may result in metastasis. 354 oral biopsy samples. The various artifacts
Table 2.6: Types of biopsies
Pathology Type of biopsy
• Ameloblastoma Incisional biopsy
• Cyst Aspiration biopsy
• Epulis Excisional biopsy
• Extraoral soft tissue swellings Fine needle aspiration cytology (FNAC)
(Major salivary gland tumor) Fine needle cutting biopsy (FNCB(
• Fibroma Excisional biopsy
• Leukoplakia Excisional biopsy
Incisional biopsy
Multiple incisional biopsies if lesion is extensive
Punch biopsy
• Lichen planus INcisional biopsy of non-erosive lesional tissue
• Minor salivary gland tumor Deep incisional biopsy
Punch biopsy
• Mucocele Excisional biopsy
• Oral submucous fibrosis Incisional biopsy
• Squamous cell carcinoma Incisional biopsy involving the margin of ulcer
• Traumatic ulcer Incisional biopsy involving the margin of ulcer
• Vesiculobullous lesions Incisional biopsies of mucosa close to bufla, erosion, or ulcer
Punch biopsy
Biopsy 17
identified by them were crush 27.1%; 2. Sufficient absorbent material like gauze or
haemorrhage 19.8%; splits 11.3%; and fragmenta- paper napkins should be placed around the
tion 6.2%. bottle in case there is an accidental spillage
of the fixative
Information to Accompany the Biopsy 3. The bottle should be placed in a sealed plastic
Specimen container, which is then placed in a
1. Name of the doctor who has referred the cardboard box and secured properly
biopsy 4. The cardboard box should be labeled
2. Type of biopsy “Pathological Specimen – Handle with Care”
3. Fixative used 5. Name and address of the sender should be
4. Patients demographic data clearly displayed
5. Description of lesion
6. Summary of clinical findings BIBLIOGRAPHY
7. Medical history if relevant
1. Johnsaon Seoane J, Varela-Centelles P, Ramirez
8. Provisional diagnosis J, Cameselle-Teijeiro J, Romero M. Artifacts in oral
9. Radiographs incisional biopsies in general dental practice: A
10. If the biopsy specimen contains calcified pathology audit. Oral Diseases 2004;10:113-7.
structures, the pathologist should be 2. Oliver RJ, Sloan P, Pemberton MN. Oral biopsies:
informed about it so that they are decalcified Methods and applications. Br Dent J 2004;196:
prior to processing and sectioning of the 329-33.
biopsy specimen because they may damage 3. Ord RA, Blanchaert RH (Eds). Oral Cancer-The
the microtome or specimen during Dentist’s Role in Diagnosis, Management,
sectioning. Rehabilitation, and Prevention; Quintessence
Publishing Co, Inc London 1999.
Precautions to be Taken while Sending
the Biopsy Specimen by Postal Service 4. Sciubba JJ. Improving detection of precancerous
and cancerous oral lesions: Computer-assisted
1. The bottle containing the biopsy specimen analysis of the oral brush biopsy. JADA
should be tightly sealed 1999;130:1445-55.
Chapter
Orofacial Pain
3
DEFINITION OF PAIN Components of Trigeminal Nerve
The International Association for the Study of The trigeminal nerve has two components
Pain or IASP defines pain as “an unpleasant including:
sensory and emotional experience associated 1. Sensory component
with actual or potential tissue damage, or 2. Branchial motor component
described in terms of such damage.” Each trigeminal nerve division has
proprioceptive fibres, touch, and pain, and
The Trigeminal Nerve temperature fibres.
1. The large A–α fibers transmit proprioceptive
The gasserian ganglion consists of cell bodies,
information
which have peripheral and central processes. The
2. The A–β fibers transmit touch information
peripheral processes make up the afferents and
3. The A–δ and C fibers transmit touch, itch,
are in the V1, V2, and V3 divisions of trigeminal
warmth, cold, and nociceptive information
nerve (Fig. 3.1). The central processes make up
the sensory root, which enters the pons.
Trigeminal Nucleus
The trigeminal nucleus consists of four parts (Fig.
3.2)
1. Mesencephalic nucleus
2. Principal sensory nucleus
3. Spinal nucleus
a. Subnucleus oralis
b. Subnucleus interpolaris
c. Subnucleus caudalis
d. Motor nucleus
Trigeminal Nerve—Sensory Component

The peripheral processes of A–β fibers transmit
touch information. The central processes of these
Fig. 3.1: Trigeminal nerve distributions fibers arise from the gasserian ganglion and
Orofacial Pain 19
Fig. 3.3: Touch pathway
Fig. 3.2: Trigeminal nucleus
synapse in the principal sensory nucleus,

subnucleus oralis, and subnucleus interpolaris.
The principal sensory nucleus, subnucleus oralis,
subnucleus interpolaris give rise to second order
neurons which cross the midline (Fig. 3.3). The
peripheral processes of A–δ and C fibers transmit
touch, itch, warmth, cold, and nociceptive
information. The central processes of A–δ and C
fibers arise from gasserian ganglion and synapse
in the subnucleus caudalis. The subnucleus
Fig. 3.4: Trigeminal nerve pain pathway
caudalis give rise to the second order neurons,
which cross the midline and ascend to join the
The Postcentral Gyrus
second order neurons from principal sensory
nucleus, subnucleus oralis, and subnucleus The third order neurons arise from the ventro-
interpolaris as ventral trigeminothalamic tract posterior thalamic nuclei and end in areas S1
(Fig. 3.4). (postcentral gyrus) and S2. The postcentral gyrus
represents structures like mouth, teeth and has
Trigeminal Leminiscus unilateral sensation (Fig. 3.6). The S2 area is
present in the lower end of postcentral gyrus and
The principal sensory nucleus gives rise to second has bilateral representation of the sensation.
order neurons, which ascend, ipsilaterally as
dorsal trigeminothalamic tract. Both the dorsal
TRIGEMINAL NEURALGIA
and ventral trigeminothalamic tracts end in the
ventro-posterior medial thalamic nuclei and (Fothergill’s disease, neuralgia epileptiformae,
comprise the trigeminal leminiscus (Fig. 3.5). tic-doloureaux, trifacial neuralgia)
Fig. 3.7: Trigger zones
Fig. 3.5: Trigeminal leminiscus

6. Posttraumatic trigeminal neuralgia
7. Failed trigeminal neuralgia
Etiology
1. Microvascular compression of the trigeminal
nerve root
2. Failure of central inhibitory mechanism
Fig. 3.6: Cerebrum

3. Vascular disease of trigeminovascular
system
It is the most common facial neuralgia. Right 4. Multiple sclerosis
side of face is frequently affected than left side.
Pain is initiated by physical stimulation of
Microvascular Compression of the
specific areas known as trigger points or zones.
Trigeminal Nerve Root
Trigger zones (Fig. 3.7) are found in region
innervated by trigeminal nerve. The physical Microvascular compression of the trigeminal
stimuli may be touch, shaving, or brushing the nerve root is most often caused by superior
teeth. cerebellar artery which leads to the irritation of
nerve root causing demyelination and ectopic
Classification of Trigeminal Neuralgia firing resulting in hyperactivity in the trigeminal
1. Typical trigeminal neuralgia nucleus (Figs 3.8A and 3.8B). Hyperactivity of
2. Atypical trigeminal neuralgia the trigeminal nucleus can lead to sudden painful
3. Pretrigeminal neuralgia attacks that last for seconds to 2 minutes. The
4. Multiple sclerosis related trigeminal painful attacks are accompained by tic-like
neuralgia cramps of the facial muscles and hence the name
5. Secondary or tumor related trigeminal tic doloureux. Sixty percent of the cases involve
neuralgia V2 and V3. Trigeminal neuralgia is characterized
Orofacial Pain 21
Fig. 3.8A: No vascular compression
Fig. 3.9: Progression of trigeminal neuralgia
The various drugs used to treat trigeminal

neuralgia include:
1. Carbamazepine—Antiepileptic drug (first
drug of choice)
2. Phenytoin sodium—Antiepileptic drug
(second drug of choice)
3. Baclofen—Muscle relaxant (second drug of
choice)
4. Neurontin—Antiepileptic drug
Combination therapy is helpful when a single
drug is not effective. Because of side effects and
Fig. 3.8B: Vascular compression
incomplete cure, most patients prefer to undergo
surgical treatment. Figure 3.10 shows the medical
treatment drug regimen given by Green et al
by periods of exacerbation and remission. The
(1991) and Figure 3.11 for adverse effects of
periods of exacerbation are short early in the
medications.
disease course and increases later (Fig. 3.9).
Peripheral Nerve Block, Sectioning, and
Treatment
Avulsion
1. Medical
This procedure involves administration of
2. Peripheral trigeminal nerve blocks
peripheral nerve blocks, injection of alcohol,
3. Surgical (when medications fail)
cutting (sectioning) of peripheral nerve and
4. Radio surgery
avulsion of the nerve. This procedure provides
temporary relief and numbness and is indicated
Medical Treatment
in patients who are unfit for surgery. As the
The drugs used to treat trigeminal neuralgia recurrence rate is very high, surgery is the main
reduce the hyperactivity of trigeminal nucleus. treatment for long-term disease control.
from the trigeminal nerve root. It is preferred

open surgical method to treat trigeminal
neuralgia.
Procedure
1. Hair is shaved and a small incision in made
behind the ear under general anesthesia,
following which a opening is made to gain
access. This procedure is termed as
suboccipital craniotomy (Fig. 3.12)
2. With the help of operating microscope, the
surgeon looks for the area of microvascular
compression caused by superior cerebellar
Fig. 3.10: Drug regimen (Green et al, 1991) artery
3. Shredded Teflon® felt implants are used in
microvascular decompression surgery
because they are inert and do not react with
the local environment
4. Microinstruments are used to mobilize the
offending vessels and to place the inert
shredded Teflon® felt implants (Fig. 3.13)
5. Closing of the bony opening and suturing
the skin, marks the end of the surgery (Fig.
3.14)
Complications
1. Hearing loss
2. Facial anesthesia
Fig. 3.11: Adverse effects of medications
Surgical Treatment
Surgical treatment includes:
1. Microvascular decompression surgery
2. Rhizotomies
a. Microsurgical rhizotomy
b. Percutaneous glycerol rhizotomy
c. Balloon compression rhizotomy
d. Percutaneous radiofrequency rhizotomy
Microvascular Decompression Surgery

The main aim of microvascular decompression
surgery is to alleviate microvascular compression Fig. 3.12: Incision and craniotomy
Orofacial Pain 23
Fig. 3.13: Insertion of Teflon implants
3. Inflammation
4. Postoperative infection
5. Delayed healing
6. CSF leak
7. Cerebellar damage
8. Brain stem infarction
9. Stroke
10. Ataxia (muscular incoordination)
11. Death
Rhizotomies
Rhizotomy is destruction of ganglion and
Fig. 3.14: Closing and suturing sensory root. Indicated when medications fail.
Types of Rhizotomies Balloon Compression Rhizotomy

(Fig. 3.16)
1. Percutaneous glycerol rhizotomy
Performed under general anesthesia. Regarding
2. Balloon compression rhizotomy
pain control, this surgical procedure has greater
3. Percutaneous radiofrequency rhizotomy potential than glycerol rhizotomy. The needle is
4. Microsurgical rhizotomy 10.5 cm long, 14 gauge and is made up of stainless
steel. Once the needle is placed near the gasserian
Complications of Rhizotomies ganglion, a 4.0 french silicone balloon catheter is
1. Permanent facial numbness or anesthesia introduced through the needle. The balloon is
dolorosa inflated causing injury by compression to the
gasserian ganglion and nerve root. Effective
2. Temporary weakness in muscles of
when V 1 is involved
mastication
3. Loss of sensation of cornea, which can lead
to keratitis and blindness
Percutaneous Glycerol Rhizotomy

(Fig. 3.15)
Performed under local anesthesia. Needle is
inserted through the foramen ovale to the
gasserian ganglion. Radiograph is taken to guide
the needle to the gasserian ganglion. The glycerol
produces mild injury to the ganglion, which
results in facial numbness. Usually, there is
recurrence of pain.
Fig. 3.16: Ballon compression rhizotomy.
Components in Mullan Set (Fig. 3.17)

1. Beveled access needle and sharp stylet
2. Blunt obturator
3. Scalpel
4. Syringe
5. Microcompression balloon catheter
Complications
1. Facial numbness
2. Weakness of muscles of mastication
Fig. 3.15: Glycerol rhizotomy 3. Loss of sensation to cornea
Orofacial Pain 25
Fig. 3.17: Mullan compression set Fig. 3.18: Radiofrequency rhizotomy
Percutaneous Radiofrequency Rhizotomy Patients experience minimal pain and in most

(Fig. 3.18) cases, can resume their regular activities within
a day or two after treatment. It is one of the most
Performed under intravenous sedation. An
advanced techniques in the treatment of
electrode is placed at the gasserian ganglion. The
disorders affecting the brain and its adjacent
electrode is heated with radiofrequency current
structures. Gamma Knife treatment is not
causing thermal injury to the ganglion. experimental. The Gamma Knife has been in use
Complications may include facial numbness. for over 30 years, and has been used successfully
to treat more than 100,000 patients worldwide.
Microsurgical Rhizotomy Therefore, it is not surprising that the Gamma
Indicated when V3 is involved. The trigeminal Knife is regarded as the “gold standard” for
nerve root is sectioned. Complications may stereotactic radiosurgery.
include numbness of the lower part of face. It
has now been replaced by microvascular Lesions Treated by Gamma Knife
decompression surgery. Radiosurgery
1. AV malformations
Gamma Knife Radiosurgery
2. Meningioma
In 1951 Lars Leksell, Professor of Neurosurgery 3. Gliomas
in Sweden, introduced the concept of 4. Acoustic neuromas
radiosurgery. The Gamma Knife® is a 5. Pituitary tumors
remarkable tool that allows surgeons to operate 6. Parkinson’s disease
on abnormal areas of the brain and its 7. Metastatic tumors
surrounding tissue without making an incision 8. Trigeminal neuralgia
(Fig. 3.19). Using a technique called stereotactic 9. Epilepsy
radiosurgery, it is designed to precisely target 10. Glaucoma
and destroy abnormalities within the head using 11. Cluster headache
highly focused gamma rays. 12. Uveal melanoma
Fig. 3.19: Gamma knife unit
The Gamma Knife Team wearing stereotactic frame, MRI is taken to

1. Neurosurgeon determine size and shape of lesion. The digital
2. Radiation oncologist image is then transferred to Leksell Gamma
3. Medical radiation physicist Plan® computers installed with Leksell Gamma
4. Anesthesiologists (children) Plan® software, which allows the gamma knife
5. Nursing staff team to:
1. Determine the exact relationship between the
Treatment Procedure target lesion and the stereotactic frame.
2. Calculate how to set the controls of the
The stereotactic frame is attached at four points gamma knife to treat the targets optimally
around the patients head with pins that penetrate with an accuracy of within 0.1 millimeter.
about 2 millimeters. To prevent any discomfort 3. To calculate the dose and exposure time.
when the frame is attached, the patient is given Once treatment planning is complete, the
local anesthesia (injected just under the skin). patient is moved to the treatment room that
Frame fitting usually takes about 20 minutes. The houses the gamma knife unit. The patient then
function of the frame is to prevent the head from lies down on the couch of the gamma knife, and
moving during imaging and treatment so that the head is positioned in the appropriate
the radiation is delivered accurately and to collimator helmet (Fig. 3.20). The gamma knife
establish spatial references. With the patient unit contains 201 cobalt 60 sources of
Orofacial Pain 27
Fig. 3.21: Production of gamma rays
Fig. 3.20: Helmet
approximately 30 curies each, arrayed in a

hemisphere. Cobalt 60decays into Nickel 60 and
one electron plus two gamma rays (Fig. 3.21). 201
focused beams of gamma rays are produced (Fig.
3.22). The gamma rays produced are aimed
through a collimator to a common focal point
with extreme accuracy of better than 0.33 mm.
The trigeminal nerve root is the common focal Fig. 3.22: Principles of gamma knife therapy
point and receives a therapeutic dose of gamma
rays. The surrounding brain tissue absorbs
finished. After the treatment, the stereotactic
minimal gamma rays. Higher doses of gamma
rays result in better pain control. frame is removed. There is no need for
The diameter of collimators can be 4 mm, postanesthesia recovery or intensive care unless
8 mm, 14 mm, and 18 mm depending on size of the treatment was carried out under general
gamma rays needed to accurately target the anesthesia especially children. The patient will
lesion. There are no loud noises during the probably be discharged from the hospital the
treatment. A video and two-way voice following day. As the patients experience
communications system allows the patient to be minimal pain, most people can resume their
in contact with the gamma knife team regular activities within a day or two after
throughout the treatment. The patient may also treatment.
listen to his/her own favorite compact disc. The
Advantages
total time the patient will be exposed to radiation
usually ranges from 15 to 60 minutes but may be 1. State-of-the-art technology
up to several hours, depending on the complexity 2. Supported by extensive study
of the treatment. The couch will automatically 3. Noninvasive
move out of the unit when the treatment is 4. Precise and accurate
5. Safe An alternative theory states that AFP is a disease

6. Good clinical outcome of trigeminovascular system. Other authors state
7. Mortality rate is less that some aspects of AFP can be seen as a form
8. No convalescence (recover health after of reflex sympathetic dystrophy (regional pain
illness) syndrome).
9. Cost-effective Both AFP and regional pain syndrome share
10. The time factor common features such as, the initiating noxious
stimuli are of low intensity and there is pain relief
Complications after sympatholytic intervention.
1. Headache
2. Scalp tenderness Clinical Features
3. Swelling 1. Age: Around 35-40 years
4. Cranial nerve dysfunction 2. Sex: More commonly seen in women
5. Focal brain swelling 3. Anatomical location: Usually one side of the
6. Focal brain necrosis face is affected, but bilateral occurrence is not
uncommon
ATYPICAL FACIAL PAIN
Introduction Clinical Presentation
Unfortunately, there is a lack of a uniform AFP is characterized by an intense, deep, and
definition and overall accepted diagnostic criteria constant pain. The pain is burning or aching, and
of atypical facial pain or AFP. In the past, the it is poorly localized. AFP does not follow
term AFP served as a diagnostic “wastebasket” anatomical pathways of the peripheral nerves.
for facial pains that are not classified. Because of Allodynia, dysesthesia, and paresthesia are
the vagueness of this term, the IASP discontinued common additional complaints. Unlike
to list AFP in their classifications of chronic pain. trigeminal neuralgia, eating, talking, and other
Instead, the broader term AFP has been replaced facial functions are usually not impaired.
by two specific subentities, namely: Majority of the patients with AFP have no
1. Atypical odontalgia (phantom tooth pain) limitations in their ability to work. Sleep is not
2. Glossodynia and sore mouth (oral affected.
dysesthesia)
However, in the clinical environment the term
Treatment
AFP is still widely accepted.
AFP is considered the least manageable form of
ETIOLOGY AND PATHOPHYSIOLOGY chronic pain. However, even small
neurodestructive interventions carried out for
The cause and pathophysiology of AFP remain
enigmas. There are several theories about the therapeutic purposes generally aggravate the
pathophysiology of AFP. In general, the pain. Tricyclic antidepressants, such as
symptoms of AFP are initiated or reinforced by amitriptyline, as well as MAO inhibitors
a local, often surgical trauma (such as, extraction (Selegiline Hcl) have been successful in specific
of teeth and interventions on the maxillary sinus). cases. Another alternative is the use of
One view has AFP as a psychosomatic disease benzodiazepines e.g., clonazepam. Additional
and is associated with anxiety and depression. treatment options include:
Orofacial Pain 29
1. Transcutaneous electric nerve stimulation 1. Mild

(TENS) 2. Moderate
2. Psychotherapy 3. Severe
3. Sympathetic nerve blocks They noted that moderate BMS is the most
frequent, followed by the severe and mild forms.
Furthermore, Basker et al (1978) reported that
BURNING MOUTH SYNDROME
intermittent BMS was more common than
(Stomatodynia, stomatopyrosis, oral dysesthesia) continuous BMS.
“Burning mouth syndrome” or BMS is a Lamey and Lewis (1989) proposed three
condition characterized by burning and painful patterns of BMS as it might vary over the day
sensations in a mouth with normal mucosa.” (Fig. 3.23).
When the symptoms of the burning mouth are Type 1 is characterized by a symptom free
limited to the tongue the term “glossodynia” is period in the morning and burning
preferred. sensation increasing during the day to
be the most severe in the evening.
Clinical Features Type 2 is characterized by continuous burning
1. Age: 40-49 years (females) and 30-59 years sensation over the day.
(males) Type 3 is characterized by symptom free
2. Sex: Most frequent in women beyond middle periods over the day.
age
3. Sites: Tongue, denture bearing mucosa, lips
and buccal mucosa are the most frequently
affected sites
Symptoms
Almost all patients with BMS describe their
symptoms as “a burning feeling.” Patients with
BMS frequently describe other symptoms such
Fig. 3.23: Patterns of BMS
as:
1. Xerostomia Etiological Factors
2. Altered or loss of taste sensation
BMS is considered multifactorial and the
Assessment etiological factors may be divided into three main
groups:
To assess how severe is the burning sensation a
linear analogue scale is used. On the scale the Local Factors
score “0” means no burning and “10” indicates
1. Xerostomia
intolerable burning. In a study by Lamey and 2. Candidiasis
Lamb 1988, they found a median score of “8.” 3. Fusospirochetal infection
4. Local allergic reactions to Hg and denture
Classification based materials
Basker et al (1978) divided BMS into: 5. Temporomandibular joint dysfunction
Systemic Factors BMS Protocol

Systemic etiological factors, which might cause The BMS protocol is a questionnaire, which is
BMS, can be divided into the following main given to the patient to identify, the:
groups: 1. Location of the burning mouth symptoms
1. Deficiencies of different types 2. Description of the symptoms
2. Hormonal disturbances
3. Estimation of the intensity of the symptoms
3. Immunological disturbances
4. When do these symptoms occur?
Deficiencies 5. Time of the day these symptoms occur
1. Fe deficiency 6. Factors aggravating the symptoms
2. B1, B2, B6, B12 deficiency 7. Factors relieving the symptoms
3. Combined deficiency of these vitamins 8. Any altered taste sensation
4. Folic acid deficiency 9. Any other symptom
Hormonal and Immunological
BIBLIOGRAPHY
Lamey and Lamb 1988, singled out diabetes
mellitus as a possible etiological factor for BMS. 1. Bell WE. Orofacial Pains Classification, Diagnosis,
As xerostomia was a frequent accompanying Management; Year Book Medical Publishers, Inc.;
London 1989.
symptom in patients with a number of
immunological disorders, Grushka et al (1987) 2. Bergdahl M, Bergdahl J. Burning mouth
syndrome: Prevalence and associated factors.
emphasized the importance of immunological
Oral Pathol Med 1999;28:350-4.
disorders as one of the etiological factor.
3. Bergdhal J, Anneroth G. Burning mouth
syndrome: Literature review and model for
Psychogenic Factors
research and management. J Oral Pathol Med
1. Anxiety 1993;22:433-8.
2. Depression 4. Juniper RP, Glynn CJ. Association between
3. Neurosis paroxysmal trigeminal neuralgia and atypical
4. Psychasthenia facial pain. Br. J Oral and Maxillofacial Surg
5. Cancerophobia 1999;37:444-7.
6. Dependent personality disorder 5. Kaufman A.M, Patel M. Your Complete Guide to
Trigeminal Neuralgia. Center for Cranial Nerve
Treatment Disorders, Winnipeg, Manitoba, Canada 2001.
6. Law AS, Lilly JP Trigeminal neuralgia mimicking
BMS protocol to evaluate the BMS odontogenic pain. Oral Surg Oral Med Oral
1. Oral and medical investigations Pathol Oral Radiol Endod 1995;80:96-100.
2. Diagnosis of oral and medical diseases 7. Turp JC, Dr Dent M, Gobetti JP. Trigeminal
3. Treatment of diagnosed oral and medical neuralgia versus atypical facial pain: A review of
diseases the literature and case report. Oral Surg Oral Med
4. In patients with resistant BMS, a Oral Pathol Oral Radiol Endod 1996;81:424-32.
psychological examination is performed, 8. Wilson-Pauwels L, Akesson EJ, Stewart PA.
followed by psychotherapy Cranial Nerves; B.C.Decker Inc; Toronto 1998.
Chapter
Temporomandibular
4 Joint Dysfunction
TEMPOROMANDIBULAR JOINT (TMJ) ANATOMY
INTRODUCTION
The temporomandibular joint is a unique joint
as:
1. It functions bilaterally in unison
2. The articular disc is movable during the joint
movements
3. The articular surfaces are covered by
fibrocartilage and not hyaline cartilage
4. The fibrocartilage is considered as the
growth center, which contributes to the
overall growth of mandible (endochondral
ossification)
TMJ SYNONYMS
Fig. 4.1: Classification of joints
1. Ginglymus joint
2. Diarthrodial joint
b. Secondary: In a secondary cartilaginous
3. Mandibular joint
joint, the articulation tissues are in the
4. Synovial joint
5. Craniomandibular articulation sequence, bone-cartilage-fibrous tissue-
cartilage-bone, e.g., pubic symphysis.
Classification of Joints (Fig. 4.1) 3. Synovial joints: The synovial joints consist
of two bones, covered by hyaline cartilage,
1. Fibrous joints: The two bones are connected
united and surrounded by a capsule
by fibrous connective tissue
2. Cartilaginous joints: There are two types of
Type of Joint
cartilaginous joints, primary and secondary
a. Primary: In a primary cartilaginous joint, The TMJ (Fig. 4.2) is a synovial joint between the
the bone and cartilage are in direct condylar head and articular fossa of the
collocation, e.g. costochondral junction. squamous part of temporal bone. It is a synovial
Articular Fossa
It is a depression anterior to the external auditory
meatus, which is limited anteriorly by articular
eminence and posteriorly by posterior glenoid
process or posterior glenoid tubercle. The center
of the articular fossa is thin and it is possible to
drive the condyle into the middle cranial fossa
by a powerful blow to the mandible.
Fibrous connective tissue: A layer of avascular
fibrous connective tissue forming the articular
zone, lines the articular eminence, condylar head
and, articular fossa. The avascular fibrous
Fig. 4.2: Temporomandibular Joint connective tissue consists of collagen fiber
bundles with fibroblasts situated between the
fiber bundles. The number of fibroblasts
joint as the joint cavity is filled with synovial decreases with age. The avascular fibrous
fluid. The TMJ differs from other synovial joints connective tissue is thickest on the articular
as its articular surfaces are covered by eminence especially on the posterior slope. This
fibrocartilage and not hyaline cartilage. It is often
is mainly an adaptation to the stress generated
said that the TMJ is not weight-bearing joint as
when the condyle and articular disc glide across
its articular surfaces are covered by fibrocartilage
the posterior slope of articular eminence. The
and not hyaline cartilage. This statement is not
thickness of avascular fibrous connective tissue
true: the joint is weight bearing.
on the condylar head is thick in comparison to
Structures Involved in the TMJ articular fossa where it is relatively thin.
1. Articular eminence Condyle

2. Articular fossa
The condyle comprises of head and neck. The
3. Condyle
condylar head or the articulating surface is
4. Capsule
covered by a thick avascular fibrous connective
5. Ligaments
tissue containing fibroblasts. Below the avascular
6. Synovial lining
fibrous connective tissue is a layer comprising
7. Articular disc
of prechondrocytes and chondrocytes. The
Articular Eminence chondrocytes lay down cartilage, which is
It is bony eminence present on the inferior aspect transformed into bone by a process known as
of the zygomatic process of the temporal bone. endochondral ossification. The fibrocartilage is
The lateral aspect of the articular eminence is present in condyle and articular eminence.
often referred to as articular tubercle. However, Presence of fibrocartilage helps in adapting
it is important to note that the two terms articular stress. In the aging condyle, there is less amount
eminence and articular tubercle are used of cartilage and overloading may lead to
synonymously by many authors. degenerative joint diseases.
Temporomandibular Joint Dysfunction 33
Capsule
The fibrous capsule (Fig. 4.3) is a loose envelope,
which defines the anatomical and functional
boundaries of the joint. Anteriorly and
posteriorly, the capsule is loose, to allow
mandibular movement. Medially and laterally,
the capsule is firm, to stabilize the mandible
during movement. The medial capsule is not as
strong as the lateral capsule, which is reinforced
by the lateral ligament.
1. Anteriorly: Capsule is attached
approximately 4 mm anterior to the apex of
the articular eminence.
2. Posteriorly: Capsule is attached to the Fig. 4.3: Lateral ligament and capsule
anterior lip of the petrotympanic fissure.
3. Superiorly: Capsule is attached to the
margins of the articular fossa.
4. Inferiorly: Capsule is attached to the neck
of the condyle medially and laterally.
5. Medially: Capsule is short and merges into
the periosteum below the medial pole of the
condyle (Fig. 4.4).
6. Laterally: Capsule merges into the
periosteum below the condylar neck (Fig.
4.4).
Ligaments
The TMJ is supported by lateral ligament (see Fig. 4.4: Coronal section of temporomandibular joint
Fig. 4.3) and two accessory ligaments (Fig. 4.5).
The lateral ligament is present lateral to the
capsule. It runs from the inferior border of
zygomatic process of the temporal bone
obliquely downwards, backwards to be inserted
into the neck of the condyle. The two accessory
ligaments that protect TMJ joint during wide
excursions are stylomandibular ligament and
sphenoman-dibular ligament. The stylomandi-
bular ligament runs from the tip of the styloid
process to the angle and posterior border of the
mandible. In comparison, the sphenomandibular
ligament runs from the greater wing of the
sphenoid bone to the lingula of the mandibular
ramus. Fig. 4.5: Accessory ligaments
Synovial Lining consists of hyaluronic acid – protein complex

The capsule consists of two layers: outer fibrous with very few glycosaminoglycans (GAGs). The
layer and inner synovial lining. The synovial hyaluronic acid is responsible for slippery or
lining (Fig. 4.4) lines all the intra-articular viscous consistency of the fluid. The synovial
structures except the articular eminence, articular fluid consists of a protein known as lubricin,
fossa, articular disc, condyle, and the which helps in lubrication of the joint. The
fibrocartilage. The symovial lining consists of two synovial fluid reduces the friction between the
layers: The first layer is the synovial intima, which articular surfaces by serving as a lubricant,
faces the joint space and consists of type A and provides nutrition to the non-vascularised tissue
type B cells (Table 4.1). The second layer is the of the articular surfaces and the disc, and
subintima, which is a supportive layer and removes debris from the joint space.
consists of loose fibrous connective tissue. The
Articular Disc
synovial subintima consists of extracellular
matrix, which shows morphologic differences Articular disc should not be termed as meniscus
based on electron microscopic features. It is as meniscus is semilunar shaped and disc is
generally differentiated into three types: areolar biconcave and rigid. The articular disc consists
(loose collagen), fibrous (dense collagen), and of dense avascular fibrous tissue. The articular
adipose (lipid globules). The capillaries that lie disc is divided into anterior, intermediate, and
beneath the synovial intima are fenestrated posterior zone. The articular disc fits like a cap
suggestive of rapid exchange of water and over the condyle. Its lower surface is concave and
solutes. In the deeper layers of the synovial upper surface is convex. Medially and laterally,
subintimal tissue, substance P nerve fibres, the disc is attached to the capsule (see Fig. 4.4).
calcitonin gene related peptide nerve fibers, and Anteriorly and posteriorly, the disc divides into
Vater-Pacini corpuscles are found. superior and inferior lamellae. Anteriorly the
disk splits into two lamellae: upper and lower
Table 4.1: Cells of the synovial intima lamellae (Fig. 4.6). The upper lamella is attached
Type A Type B to the anterior edge of the articular eminence.
• Bone marrow derived • Arise from the mesenchyme The lower lamella is attached to the anterior
monocytes of the original skeletal surface of the condylar head. Between these two
blastema lamellae, the muscle fibres of the superior head
• Closely related to • Closely related to fibroblasts of lateral pterygoid are inserted. Posteriorly the
macrophages disk splits into two lamellae: upper and lower
lamellae (the bilaminar region) (Fig. 4.6). The
• Characterized by promi- • Characterized by prominent
upper lamella gives way to loosely textured mass
nent Golgi apparatus rough endoplasmic reticulum
of tissue containing many blood vessels, nerves,
• Phagocytic function • Secretory function
fat, and elastic fibers. The loosely textured mass
Synovial fluid: The synovial lining produces of tissue is attached to the capsule posteriorly and
synovial fluid. In a healthy TMJ there is very little petrotympanic fissure superiorly. This loosely
amount of synovial fluid. Increased amount of textured mass of tissue is known as retrodiscal
synovial fluid indicates joint pathology. The pad. The lower lamella is attached to the neck of
chemical composition of synovial fluid indicates the condyle. The lower lamella limits the anterior
that it is a dialysate of plasma. The synovial fluid movement of the disc, thus when it is damaged
Fig. 4.6: Temporomandibular joint anatomy
the articular disc can translate anterior to downwards along the medial surface of the
condyle, resulting in disc displacement. When lateral pterygoid muscle. It then turns laterally
the mandible is at rest the ideal articular disc crossing the posterior border of the condylar neck
position in the articular fossa is with the posterior where it divides into several branches that
band at approximately 12 o’clock position. The innervate the capsule and disk attachments
articular disc divides the joint space into superior posteriorly, laterally and medially.
and inferior compartments, adapts to the
Masseteric Nerve
articular surface thereby increasing the stability
The masseteric nerve is a motor nerve, which
of the joint, protects the articular surface, acts as
innervates the anterior capsule and anterior disc
a shock absorber, and helps in joint movements.
attachment. After it leaves the mandibular nerve,
it runs laterally along the medial border of the
Innervation of TMJ
lateral pterygoid muscle, to emerge through the
The nerves that innervate the TMJ are anterior part of the mandibular notch, behind the
auriculotemporal nerve, masseteric nerve, and tendon of the temporalis muscle, to innervate the
the posterior deep temporal nerves. They are masseter muscle.
derived from the mandibular nerve after its
passage through the foramen ovale, which is Posterior Deep Temporal Nerve
located medial to the articular eminence. The posterior deep temporal nerve is a motor
nerve, which innervates the anterior capsule and
Auriculotemporal Nerve anterior disc attachment. After it leaves the
The auriculotemporal nerve is a sensory nerve mandibular nerve, it turns upwards and passes
with autonomic nerve function. After it leaves superior to the lateral pterygoid muscle to
the mandibular nerve, immediately below the innervate the deep surface of the temporalis
skull base, it runs posteriorly and slightly muscle.
Receptors
The TMJ contains four types of nerve receptors
(Fig. 4.7) namely, Ruffini receptors, Golgi tendon
organs, encapsulated Vater-Pacini corpuscles,
and free nerve endings.
Fig. 4.7: Temporomandibular joint receptors
TEMPOROMANDIBULAR JOINT PAIN
INTRODUCTION
Pain is the most common chief complaint in
temporomandibular joint disorder. It is very
difficult to evaluate because of individual
differences in experience. Pain can demonstrate
variety of qualities (Table 4.2). Each variety of
pain is characteristically associated with
pathology (Fig. 4.8).
Table 4.2: Varieties of qualities

• Piercing • Aching
• Shooting • Stinging
• Burning • Squeezing
Fig. 4.8: Varities and association
• Grinding • Numbing
• Throbbing • Itching
whether the patient has problems with any other
• Cramping • Tingling joints or any known systemic disease.
DIAGNOSIS HISTORY OF PAIN

When pain is present in the temporomandibular The starting point in diagnosis of
joint region, an accurate diagnosis is of prime temporomandibular joint pain is to obtain an
importance. Any disorder that affects other accurate description of the complaint. It should
synovial joints may also affect temporomandi- be first taken in the patients own words and then
bular joint. Therefore, it is important to ask retold in technical language as indicated.
Description of Pain analgesia. If there are no pain-free intervals, it is

classified as continuous or uninterrupted.
Anatomic Location of Pain
Paroxysmal pain is characterized by sudden
The patients ability to locate the pain with bursts of jabs, which may vary in intensity and
accuracy has diagnostic value. The patients duration. When the jabs occur frequently, the
description of the location of pain identifies only pain may become continuous.
the site of pain. It is the clinician’s responsibility
to determine whether that is the true source. Duration of Individual Pains
Momentary pain is expressed in seconds. Longer-
Intensity of Pain lasting pains are classified in minutes, hours, or
The intensity of pain should be established by days. A pain that is continuous from one day to
differentiating between mild and severe pain. the next is said to be protracted.
1. Mild pain: Patient describes the pain and
does not display any physical reactions. Localization Behavior
2. Severe pain: Patient describes the pain and The localization behavior of the pain should be
displays physical reactions that are included in its description. If the patient is able
objectively evident to the clinician. to define the pain to an exact anatomic location,
it is classified as localized pain. If the patient is
Mode of Onset
not able to define the pain to an exact anatomical
The mode of onset of pain has diagnostic value. location, it is classified as diffuse pain.
The onset may be spontaneous or self-generated.
It may be induced by yawning, chewing, Effect on Functional Activities
drinking hot and cold fluids, or bending over. It The effect on functional activities should be
may be accidentally triggered by minor observed and described. Common functions
superficial stimulation by touching the skin, lips, include movement of face, jaw, or tongue,
face, and tongue. mastication, deglutition, brushing of teeth,
shaving, and washing the face.
Quality of Pain (varieties)
The quality of pain should be classified according Concomitant Symptoms
to how it makes the patient feel. When the pain Any concomitant or accompanying symptoms
has a stimulating or exciting effect on the patient should be described. The accompanying
it is classified as bright. When the pain has a symptoms include:
depressing effect that causes patient to withdraw 1. Hyperesthesia: Increased sensitivity to
it is classified as dull. stimulation
2. Hypoesthesia: Decreased sensitivity to
Temporal Behavior
stimulation
Temporal behavior can be classified as 3. Anesthesia: Absence of all sensations
intermittent, continuous, and paroxysmal. If the 4. Paresthesia: Abnormal sensation
pain comes and goes (pain-free intervals), it is
5. Dysesthesia: Unpleasant sensation
classified as intermittent. Intermittent pain
means that during the pain-free intervals the
Temporomandibular Joint Pain
patient is comfortable. The intermittent pain-free
intervals should not be confused with the effect The origin of temporomandibular joint pain is
of analgesics that induce periods of comfort by not simple to diagnose. The most common source
of temporomandibular joint pain is due to

temporomandibular joint problem. The principal
challenge is to differentiate whether the pain is
arthrogenous, myogenous, or referred pain.
Arthrogenous Pain
Aggravated by jaw functions (biting, chewing,
talking, mouth opening, or lying down on the
side).The temporomandibular joint is tender on
palpation. Patient should be asked to point to the
worst spot with one finger. If the worst spot is
identified over the joint, it may be arthrogenous
in origin
Myogenous Pain
Pain that is not aggravated by jaw functions
indicates some other source of pain other than Fig. 4.9: Myofascial trigger point
the joint. Patients with muscular disorders
usually describe or point to diffuse areas often Choice of Anesthetic
in the area of muscle distribution (temple, orbit,
The long duration bupivacaine should not be
front of the head).
used, as it is neurotoxic and may infiltrate to the
Referred Pain central nervous system. Lignocaine or prilocaine
is the choice of anesthetic.
Referred pain is described as the pain felt at an
area that is innervated by a nerve, which does
Procedure
not mediate the primary pain. For e.g., patient
may complain of pain in the temporomandibular The needle should be directed from slightly
joint area, but the source may be the salivary behind and towards the neck of the condyle. The
glands. Usually myogenous pain may be referred needle should meet the neck of the condyle.
to the joint. This is especially true if the While keeping the needle in contact with the neck
myofascial trigger points (Fig. 4.9) involve the of condyle, the patient is instructed to open and
strenocleidomastoid muscle, masseter, medial close the mouth repeatedly within a small range
pterygoid, and lateral pterygoid muscles. of movement. By opening and closing the mouth
However, referred pain from any source (such repeatedly within a small range of movement,
as the salivary glands) may be felt in the the clinician will know whether the needle is
temporomandibular joint area. against movable condyle or not. The needle is
then withdrawn a few millimeters to avoid
Anesthetic Nerve Block injection into joint spaces. The goal of this
procedure is to block the auriculotemporal nerve
A good aid for establishing differential diagnosis
trunk behind the neck of the condyle.
is an anesthetic nerve block of the
auriculotemporal nerve. If the pain is eliminated
Complications
after the block, it is arthrogenous in origin. If the
pain is not eliminated after the block, it is As the facial nerve, runs adjacent to the joint,
myogenous or referred in origin. anesthesia can infiltrate and cause temporary
hemifacial anesthesia. Therefore, prior to the nerve entrapment. In the temporomandibular

procedure the patient should be informed about joint region, the auriculotemporal nerve,
temporary hemifacial anesthesia. If temporary masseteric nerve, and posterior deep temporal
hemifacial anesthesia occurs, the blink reflex on nerves can be entrapped. Entrapment of these
the ipsilateral side will be impaired and requires nerves gives rise to pain within the peripheral
taping of the upper eyelid to protect the cornea. areas of the particular nerve distribution. For e.g.,
entrapment of the lingual nerve can produce
Nerve Entrapment symptoms related to the tongue such as pain,
The process by which the peripheral nerve is altered taste sensation, burning sensation, and
subjected to mechanical irritation by numbness causing deviation in speech
compression, rubbing, or traction is known as articulation.
TEMPOROMANDIBULAR JOINT SOUNDS
INTRODUCTION in men and is higher during childhood and

Temporomandibular joint sounds (Table 4.3) adolescence, and then decreases with age.
indicate joint abnormality. Higher frequency of
Conditions Associated with Clicking
joint sounds is associated with more advanced
disease. However, the absence of joint sounds Disc Displacement with Reduction
does not exclude joint pathology. The most common cause of TMJ clicking is disc
displacement with reduction. Clicking during
CLICKING mouth opening can occur early, intermediate, or
Temporomandibular joint clicking refers to a late, depending on the advance of tissue damage,
distinct cracking or snapping sound. The particularly of the posterior disc attachment. The
prevalence of clicking is higher in women than more herniated and elongated the attachment,
Table 4.3: Varietis of TMJ sound

TMJ sound Description
• Reciprocal click Noise made on opening and closing from centric occlusion position that is
reproducible on every opening and closing. Can be eliminated with anterior
repositioning of jaw
• Reproducible opening click Noise with every opening, no noise when closing
• Reproducible laterotrusive click Noise with every full laterotrusive movement, no noise on opening
• Reproducible closing click Noise with every closing, no noise when opening
• Nonreproducible click Present on opening or in laterotrusion but not repeatable
• Crepitus (fine) Fine grating noise suggestive of mild bone-on-bone contact
• Crepitus (coarse) Coarse grating noise suggestive of gross bone-on-bone contact
• Popping Distinctly audible sound on opening
the later the opening click will occur. Clicking chondromatosis, osteoarthrosis, and intra-
during mouth closure usually takes places during articular fractures. All these conditions occur
the last third of closing movement and, in most rarely, but can cause clicking in combination with
instances, immediately before tooth contact. crepitations.
Local Soft Tissue Thickenings Muscular Incoordination

When the mandibular disc and condyle with a The superior and inferior head of the lateral
normal interrelationship pass a local thickening pterygoid muscle control the movements of the
on the articulating surface, clicking can occur. condylar head and disc. Disturbance in the
Clicking then occurs after muscular strength has function of this muscle can result in an
been sufficiently great to overcome the obstacle incoordinated movement of the condylar head
(local soft tissue thickenings). These thickenings and disc during jaw movements, which in turn
are somewhere along the posterior slope of the can produce clicking sounds.
articulating eminence.
Clinical Registration of Clicking
Joint Hypermobility
In a normal joint immediately after maximum The presence or absence of clicking should be
proved with a stethoscope. The clinician may
jaw opening the condylar head is located at the
listen to one joint at a time with a conventional
apex of the articular eminence. Clicking can arise
stethoscope or may listen to both the joints at a
when the mandibular condyle and articular disc
time using double stethoscope. However, the use
with a normal interrelationship pass the apex of
of a stethoscope to record joint sounds is
the articular eminence. The apex of the articular
eminence can serve as an obstacle for the unreliable. A false-negative diagnosis can result
when the mandibular condyle slides off and on
mandibular condyle and articular disc in
to the disc without any clicking.
hypermobile joints. When the muscular strength
overcomes the obstacle (articular eminence),
Crepitations
condylar velocity increases and, the condyle-disc
assembly passes the apex of the articular Crepitations can be either fine or coarse. Fine
eminence. Opening click arises at the end of crepitations are fine grating noises suggestive of
mouth opening and the mandible deflects mild bone-on-bone contact and coarse
toward the contralateral side. In most cases, no crepitations are coarse grating noises suggestive
sound occurs during jaw closing, but sometimes of gross bone-on-bone contact. Crepitations are
occurs at the very beginning of mouth closure. more common in complete denture patients, and
patients with loss of molar support. Crepitations
Loose Intra-articular Bodies can also occur in patients with osteoarthrosis,
Loose intra-articular bodies can have different rheumatoid arthritis, and synovial chondro-
origins. They can arise because of synovial matosis.
RESEARCH DIAGNOSTIC CRITERIA—TMD CLINICAL EXAMINATION
Temporomandibular disorder (TMD) is a 2. Measurements need to be conducted with

collective term embracing a number of clinical the patients jaw muscles in a passive state.
problems that involve the muscles of mastication, 3. The joints and muscles should not receive
the temporomandibular joint, or both of these. additional weight at anytime.
Examination of the articulatory system should 4. Millimeter measurements should be clearly
be comprehensive enough to avoid missing any recorded in single or double digits.
signs or symptoms yet simple enough for all 5. The patient should be sitting in the
practitioners to perform routinely on all patients. examination chair at approximately 90
The overall examination should include an degress to the examiner.
assessment of pain, opening pattern, vertical 6. Examiner needs to wear gloves at all times.
range of movement and joint sounds. 7. Replacement prosthesis should not be
The masticatory muscles and joint should be removed from the patients mouth during the
palpated, the common signs of bruxism should examination. However, biteplates and other
be noted, the patients headache experience appliances that do not replace teeth should
should be discussed, and the occlusion carefully be removed.
examined. 8. If the patient has a beard, a neck brace or
1. General directions for examination any other potential physical barrier that may
2. Assessment of pain location interfere with the muscle or TMJ palpation,
3. Opening pattern indicate this.
4. Vertical range of movement 9. The examination is most efficient if
5. Joint sounds on vertical opening performed in the order mentioned above.
6. Jaw excursions (lateral and protrusive)
7. Joint sounds on lateral and protrusive Examination
excursions Assessment of Pain Location
8. Muscle and joint palpation
1. At the beginning of the examination, the
a. Extraoral muscles
patient should be asked if he or she is in pain
b. Temporomandibular joint
and the side and location of the pain noted.
c. Intraoral muscles
2. If the patient indicates pain in the midline, it
should be scored as both right and left sides
GENERAL DIRECTIONS FOR
painful.
EXAMINATION
3. If it is unclear whether the patient is
1. All questionnaire and examination items indicating a joint or muscle, the examiner
need to be completed unless the patient should press on the area as lightly as possible
refuses or is unable to cooperate. In this case, to help identify the correct site.
write “PR” (patient refuses) in large block 4. If the patient identifies joint pain but the
letters adjacent to the examination item and examiner identifies the site as muscle, the
note why the patient refuses or cannot do examiners finding is the one that should be
item. recorded.
Opening Pattern Maximum Unassisted Mandibular Opening

1. Ask the patient to open the mouth as wide Obtaining measurement
as he/she can even it is painful and close. 1. Ask the patient to place the mandible in a
2. This initial opening puts the muscles in a comfortable position.
functional state. 2. Ask the patient to open the mouth as wide
3. Next, the patient is asked to open the mouth as possible (unassisted), even if he/she feels
three times with the opening pattern scored pain.
based on movement deviation. 3. In measuring maximum unassisted
4. Note that the examiner holds the lower lip mandibular opening, the mm ruler should
during opening to reveal the lower teeth. be placed at the incisal edge of the maxillary
5. Be careful not to apply too much pressure or incisors with the specific tooth noted and
guidance. with the ruler held vertically to the
6. There are four categories of opening pattern: labioincisal edge of the opposing mandibular
a. Straight incisor.
b. Deviation (right or left) Pain
c. Corrected deviation
1. Ask the patient if he/she felt any pain on
d. Other (If the deviation is jerky that does
maximum unassisted mandibular opening.
not fit any other category or of the patient
2. The location of pain is scored in two ways:
has more than one opening pattern).
muscle pain and joint pain.
Vertical Range of Movement 3. Record muscle pain as “None” (0), “Right
Side” (1), “Left Side” (2), or “Both” (3).
If the patient is wearing a denture or partial and
4. Also, record joint pain as “Present” (1) or
it is loose, it should be compressed against the
“Absent” (0).
ridge during the opening measurement.
5. If the patient has no pain, circle “NA” (9) for
Unassisted Mandibular Opening location.
without Pain 6. If the patient indicates a feeling of pressure
Obtaining measurement or tightness, score as “None.”
1. Ask the patient to place the mandible in a
Maximum Assisted Mandibular Opening
comfortable position.
2. Ask the patient to open the mouth as far as Obtaining measurement
possible (unassisted), without feeling any 1. Ask the patient to place the mandible in a
pain. comfortable position.
3. In measuring unassisted mandibular 2. Ask the patient to open the mouth as wide
opening without pain, the mm ruler should as possible, even if he/she feels pain.
be placed at the incisal edge of the maxillary 3. After the subject has opened the mouth, in
incisors with the specific tooth noted and order to assess maximum assisted
with the ruler held vertically to the mandibular opening place your thumb on
labioincisal edge of the opposing mandibular maxillary central incisors and cross your
incisor. index finger over to the mandibular centrals.
4. If opening is less than 30 mm, the measure- 4. This position gives you the advantage to
ment should be repeated. force the patients mouth open wider.
5. Use moderate pressure and be careful not to clear beginning and end, which usually sounds
push the mandible beyond the patients like a “click.”
tolerance. 2 = Coarse crepitus: Coarse crepitus is continuous,
6. In measuring maximum assisted mandibular over a longer period of jaw movement. It is not
opening, the mm ruler should be placed at brief like a click or pop; the sound is not muffled;
the incisal edge of the maxillary incisors with it is the noise of bone grinding against bone, or
the specific tooth noted and with the ruler like a stone grinding against another stone.
held vertically to the labioincisal edge of the
3 = Fine crepitus: Fine crepitus is a fine grating
opposing mandibular incisor.
sound that is continuous over a longer period of
Pain
jaw movement on opening or closing. It is not
1. Ask the patient if he/she felt any pain on
brief like a click; the sound may make
maximum assisted mandibular opening.
overlapping continuous sounds. It may be
2. Score pain locations as in maximum
described as a rubbing or crackling sound on a
unassisted mandibular opening.
rough surface.
3. If the patient indicates a feeling of pressure
or tightness, score as “None.” Scoring of Clicking Sounds
Joint Sounds on Vertical Opening Reproducible opening click: Click is considered
reproducible if it occurs during two of three
General Instructions openings from maximum intercuspation.
1. The temporomandibular joint sounds are Reproducible closing click: Click is considered
measured by palpation during vertical reproducible if it occurs during two of three
opening and closing. closings.
2. In this part of the examination, the object is 1. The measurements of reproducible opening
to determine the presence or absence of
and closing clicks are measured using an mm
specific joint sounds.
ruler.
3. This is done by placing your fingers over the
2. With the millimeter ruler, measure the
patients temporomandibular joint, anterior
interincisal distance at which the first
to the tragus of the ear.
opening and closing clicks are reported /
4. Although a stethoscope may also be used to
heard.
assess joint sounds, the stethoscope
3. The mm ruler should be placed at the incisal
assessment is less reliable than the palpation
edge of the maxillary incisors with the
method.
specific tooth noted and with the ruler held
5. The patient is asked to repeat the opening
and closing maneuver three times and report vertically to the labioincisal edge of the
if sounds are present. opposing mandibular incisor.
6. If so, the sounds are categorized as click, Reproducible reciprocal click
coarse crepitus, and fine crepitus and are 1. If a reproducible click is measured on both
scored separately for opening or closing. vertical opening and closing, ask the patient
to protrude the mandible, and to open and
Definition of Sounds close from this protruded position.
0 = None 2. If the click is eliminated, can be eliminated
1 = Clicking: Clicking is defined as a distinct from this protruded jaw position circle “Yes”
sound, of brief and very limited duration, with a (1)
3. If the click is not eliminated, can be Pain

eliminated from this protruded jaw position 1. Ask the patient if he/she felt any pain when
circle “No” (0). moving the mandible towards the left side.
4. If the patient lacks either a reproducible 2. Score pain locations as in right lateral
opening or closing click, circle “NA” (9). excursion.
3. If the patient indicates a feeling of pressure
Jaw Excursions (lateral and protrusive) or tightness, score as “None.”
The next part of the examination assesses both Protrusion
the degree of excursion and pain on lateral and Obtaining measurement
protrusive movement. 1. Ask the patient to open the mouth slightly
and protrude the mandible.
Right Lateral Excursion
2. If the patient has a deep overbite, ask him/
Obtaining measurement her to open wider so he/she can protrude
1. Ask the patient to open the mouth slightly without getting interference from the
and move the mandible as far as possible to maxillary incisors.
the right, even if it is uncomfortable. 3. Record this measurement in the same
2. With the teeth slightly separated, use a manner as right lateral excursion.
millimeter ruler to measure from the Pain
labioincisal embrasure between the between 1. Ask the patient if he/she felt any pain when
the maxillary central incisors to the moving the mandible forwards.
labioincisal embrasure of the mandibular 2. Score pain locations as in right lateral
central incisors. excursion.
Pain 3. If the patient indicates a feeling of pressure
1. Ask the patient if he/she felt any pain when or tightness, score as “None.”
moving the mandible towards the right side.
2. The location of pain is scored in two ways: Joint Sounds on Lateral and Protrusive
muscle pain and joint pain. Excursions
3. Record muscle pain as “None” (0), “Right
1. Sounds on excursions are assessed in the
Side” (1), “Left Side” (2), or “Both” (3). manner similar to that for assessing sounds
4. Also, record joint pain as “Present” (1) or on vertical opening.
“Absent” (0). 2. The fingers are placed over the joint and the
5. If the patient has no pain, circle “NA” (9). patient is asked to perform lateral and
6. If the patient indicates a feeling of pressure protrusive excursions.
or tightness, score as “None.”
Muscle and Joint Palpation
Left Lateral Excursion
Obtaining measurement General Instructions for Muscle and Joint
1. Ask the patient to open the mouth slightly Palpation for Tenderness
and move the mandible as far as possible to 1. Examining the muscles and joint capsules for
the left, even if it is uncomfortable. tenderness requires that you press on a
2. Record this measurement in the same specific site using the fingertips of the index
manner as right lateral excursion. finger only with standardized pressure, as
follows: palpations will be done with 2 lbs 2. Palpate fibers over the infratemporal fossa,
of pressure for extraoral muscles, 1 lb of immediately above the zygomatic process.
pressure on the joints and intraoral muscles.
2. Palpate the muscles while using the opposite Masseter
hand to provide stability to the head.
Origin of Masseter
3. The subject’s mandible should be in a resting
position, without the teeth touching. 1. Ask the subject to clench and then relax to
4. Palpate the muscles while they are in a help identify muscle.
passive state. 2. Palpate the origin of the muscle beginning
5. Ask the patient to lightly clench and relax in the area 1 cm immediately in front of the
the muscles, in order to identify and palpate TMJ and immediately below the zygomatic
correct muscle site. arch, and palpate anteriorly to the border of
6. Because the site of maximum tenderness the muscle.
may vary from patient to patient, it is Body of the Masseter
important to press in multiple areas in the
1. Ask the subject to clench and then relax to
region specified to determine if tenderness
help identify muscle.
exists.
2. Start just below the zygomatic process at the
7. Before beginning the palpations, say: “In the
anterior border of the muscle.
next part of the examination, we would like
3. Palpate from here down and back to the
you to record whether you feel pain or
angle of the mandible across a surface area
pressure when I palpate or press on certain
about two fingers wide.
parts of your head and face.”
8. Ask the subject to determine if the palpation Insertion of the Masseter
hurts (painful) or if he/she just feels
1. Ask the subject to clench and then relax to
pressure. If it hurts, ask the subject to indicate
help identify muscle.
if the pain is mild, moderate, or severe.
2. Palpate the area 1 cm superior and anterior
9. Record pressure as “No Pain.”
to the angle of the mandible.
Extraoral Muscles
Posterior Mandibular Region
Temporalis Posterior mandibular region (stylohyoid and
Temporalis (posterior) posterior belly of digastric)
1. Ask the subject to clench and then relax to 3. Ask the subject to tip the head back a little.
help identify muscle. 4. Locate the area between the insertion of the
2. Palpate posterior fibers behind the ears to sternocleidomastoid muscle and the
directly above the ears. posterior border of the mandible.
Temporalis (middle) 5. Place finger so it is going medially and
1. Ask the subject to clench and then relax to upwards (and not on the mandible).
help identify muscle. 6. Palpate the area immediately medial and
2. Palpate fibers in the depression about 2 cm posterior to the angle of the mandible.
lateral to the lateral border of the eyebrow.
Temporalis (anterior) Submandibular Region
1. Ask the subject to clench and then relax to Submandibular region (medial pterygoid,
help identify muscle. suprahyoid, and anterior belly of digastric)
1. Locate the site under the mandible at a point completely together. (change examination
2 cm anterior to the angle of the mandible. gloves.)
2. Palpate superiorly, pulling toward the
mandible. Intraoral Muscles
3. If a subject has a lot of pain in this area, try Explain to the patient that you will now be
to determine if the subject is reporting muscle palpating the inside of the mouth: (“Now I am
or nodular pain. going to palpate inside your mouth. While I do
4. If it is nodes, indicate on the exam form.
these palpations, I would like you to keep your
jaw in a relaxed position.”).
Temporomandibular Joint
Lateral Pole Lateral Pterygoid Area
1. Place index finger just anterior to the tragus 1. Before palpating, make sure the fingernail
of the ear and over the subject’s of the index finger is trimmed to avoid false
temporomandibular joint. Ask the subject to positives.
open slightly until the examiner feels the 2. Ask the subject to open the mouth and move
lateral pole of the condyle translated the jaw to the side that is being examined.
forward.
(“Move your jaw towards this hand.”).
2. Use 1 lb pressure on the side that is being
3. Place the index finger on lateral side of
palpated, supporting the head with the alveolar ridge above the right maxillary
opposite hand. molars.
4. Move finger distally, upward, and medial to
Posterior Disc Attachment
palpate.
1. This site can be palpated intrameatally. 5. If the index finger is too large, use the little
2. Place tips of the right little finger into the finger (5th digit).
subject’s left external meatus and the tip of
the left little finger into the subject’s right Tendon of Temporalis
external meatus. 1. After completing, the lateral pterygoid,
3. Point the fingertips towards the examiner rotate your index finger laterally near the
and ask subject to slightly open the mouth coronoid process, ask the subject to open
(or wide open if necessary) to make sure the slightly, and move your index finger up the
joint movement is felt with the fingertips. anterior ridge of the coronoid process
4. Place firm pressure on the right side and then 2. Palpate on the most superior aspect of the
the left side while the subject’s teeth are process.
RESEARCH DIAGNOSTIC CRITERIA—TMD EXAMINATION FORM
Do you have pain on the right side of your face, the left side, or both sides?
1. None………0
2. Right ……...1
3. Left ……….2
4. Both……….3
Could you point to the areas where you feel pain?
Right
1. None………0
2. Jaw Joint…..1
3. Muscles……2
4. Both……….3
Left
1. None………0
2. Jaw joint…..1
3. Muscles……2
4. Both……….3
Opening Pattern
1. Straight ...................................................................... 0
2. Right lateral deviation (uncorrected ..................... 1
3. Right corrected (“S”) deviation ............................. 2
4. Left lateral deviation (uncorrected) ...................... 3
5. Left corrected (“S”) deviation ................................ 4
6. Other .......................................................................... 5
7. Type (specify) .............................................................
Vertical Range of Movement (maxillary incisor used)
1. Unassisted mandibular opening without pain ____ mm
2. Maximum unassisted mandibular opening ____ mm
3. Maximum assisted mandibular opening ____ mm
Muscle pain Joint pain
None Right Left Both Present Absent NA

0 1 2 3 1 0 9
0 1 2 3 1 0 9
Joint Sounds
Right Left
Opening
None ........................................... 0 0
Click ............................................ 1 1
Coarse crepitus .......................... 2 2
Fine crepitus .............................. 3 3
Measurement of reproducible opening click ____ mm ____ mm
Right Left
Closing
None ........................................... 0 0
Click ............................................ 1 1
Coarse crepitus .......................... 2 2
Fine crepitus .............................. 3 3
Measurement of reproducible closing click ____ mm ____ mm.
Reproducible reciprocal click eliminated on protrusive opening
Right Left
No ................................................ 0 0
Yes ............................................... 1 1
NA ............................................... 9 9
Excursions
1. Right lateral excursion ____ mm
2. Left lateral excursion ____ mm
3. Protrusion ____ mm
Muscle pain Joint pain

None Right Left Both Present Absent NA
0 1 2 3 1 0 9
0 1 2 3 1 0 9
Joint Sounds on Excursions

Right sounds
None Click Coarse crepitus Fine crepitus
Excursion right 0 1 2 3
Excursion left 0 1 2 3
Protrusion 0 1 2 3
Left sounds
None Click Coarse crepitus Fine crepitus
Excursion right 0 1 2 3
Excursion left 0 1 2 3
Protrusion 0 1 2 3
Muscle and Joint Palpation

The examiner will be palpating (touching) different areas of your face, head, and neck. We would like you to
indicate if you do not feel pain or just feel pressure (0), or pain (1-3). Please rate how much pain you feel for
each of the palpations according to the scale below. Circle the number that corresponds to the amount of pain
you feel. We would like you to make a separate rating for both the right and left palpations.
0 = No Pain/pressure Only
1 = Mild Pain
2 = Moderate pain
3 = Severe pain
Extraoral Muscle Palpation

Right Left
Temporalis _______________ _______________
Temporalis (posterior) “Back of temple” 0 1 2 3 0 1 2 3
Temporalis (posterior) “Back of temple” 0 1 2 3 0 1 2 3
Temporalis (middle) “Middle of temple” 0 1 2 3 0 1 2 3
Temporalis (anterior) “Front of temple” 0 1 2 3 0 1 2 3
Masseter
Masseter (origin) “Cheek/under cheekbone” 0 1 2 3 0 1 2 3
Masseter (body) “Cheek/side of face” 0 1 2 3 0 1 2 3
Masseter (insertion) “Cheek/jaw line” 0 1 2 3 0 1 2 3
Posterior mandibular region
(stylohyoid / posterior digastric region) 0 1 2 3 0 1 2 3
“Jaw / throat region”
Submandibular region
(medial pterygoid / suprahyoid/ anterior
digastric region) “Under chin” 0 1 2 3 0 1 2 3
Joint Palpation
Right Left
_______________ _______________
Lateral Pole “Outside” 0 1 2 3 0 1 2 3
Posterior attachment “Inside ear” 0 1 2 3 0 1 2 3
Intraoral Muscle Palpation
Right Left
_______________ _______________
Lateral pterygoid area “Behind
upper molars” 0 1 2 3 0 1 2 3
Tendon of temporalis “Tendon” 0 1 2 3 0 1 2 3
INTERNAL DERANGEMENT
In 1814, the term internal derangement was whiplash injuries or iatrogenic injuries during
introduced by Hey as a general orthopedic term dental treatment. These conditions produce
for a localized mechanical fault in a joint. Internal bruising or joint tissue laceration that may lead
derangement is the most common temporoman- to an impaired function and eventually to an
dibular joint disorder, which is characterized by internal derangement.
a progressive displacement of disc relative to the
condyle. Microtrauma
According to the consensus meeting held by Microtrauma can occur from repetitive behaviors
the International Association of Oral and such as chronic clenching, bruxism, atypical
Maxillofacial Surgeons (IAOMS) in Buenos Aires chewing habits and nail biting.
1992 regarding TMJ-surgery, internal derange-
ment is defined as a localized mechanical fault Occlusal Factors
of the joint which interferes with its smooth
action. In simpler terms, internal derangement Occlusal factors such as class II, class II division
may be defined as the loss of spatial relationship II malocclusions, loss of molar support and
within the temporomandibular joint in which retentive phase in orthodontic treatment that
there is displacement of the disc (Fig. 4.10) from may deflect the condyle posteriorly have also
its normal anatomical and functional relationship been suggested as etiological factors.
with the mandibular condyle and the articular
fossa. CLINICAL STAGING
The most common TMJ disorder is the internal
ETIOLOGY
derangement, which is characterized by a
The three causes of internal derangement are progressive anterior disc displacement relative
macrotrauma, microtrauma, and occlusal factors. to the condyle. Traditionally, internal
derangement of the TMJ may be classified into
Macrotrauma
four consecutive clinical stages:
Macrotrauma to the temporomandibular joint 1. Stage I as disc displacement with reduction
can occur because of fractures, joint contusion, 2. Stage II as disc displacement with reduction
and transient locking
3. Stage III as disc displacement without
reduction (closed lock)
4. Stage IV as disc displacement without
reduction and with perforation of the disc
or posterior attachment tissue (degenerative
joint disease)
Stage I
Disc displacement with reduction is the Stage I
Fig. 4.10: Internal derangement of disc displacement. In Stage I, the displaced disc
returns to normal position on mouth opening. mouth opening less than 30 mm. Magnetic
Stage I is characterized by reciprocal clicking of resonance imaging shows anterior disc
the TMJ on opening and closing. The opening displacement in both centric occlusion and
click occurs when the condyle slides over the maximal mouth open positions. As the condition
posterior band of the disc. The closing click progresses, the condyle may steadily push the
reflects a reversal of this process, with the disc forward to achieve almost normal ranges of
condyle moving under the posterior band of the mouth opening, in spite of the presence of a non-
disc until it snaps off the disc and onto the reducing disc.
posterior disc attachment. Disc displacement
with reduction can occur without clicking. Stage IV
Therefore, the absence of joint sounds does not As the condyle steadily pushes the disc forward
indicate that the joint is normal. The clinical the posterior disc attachment slowly loses its
hallmark of disc displacement with reduction is elasticity, and the patient begins to regain some
limited mouth opening, usually accompanied by of the lost range of motion (translation). The
deviation of the mandible to the affected side, posterior disc attachment gradually remodels
until a click (reduction) occurs. After the click, with deposition of fibrous connective tissue
the mandible returns to midline position and the before it succumbs to thinning and perforation
patient is able to open the mouth fully. due to continuous stretching. Disk perforation
and bone-to-bone contact will elicit coarse
Stage II
crepitus upon opening and closing. Clinically,
Stage II features all the characteristics of Stage I, osteoarthrosis may be diagnosed because the
plus additional episodes of transient locking or remodelling often occurs unilaterally, the
joint locking, which can last for various lengths symptoms appear to worsen as the day goes on,
of time. Stage II begins when the disc is lodged and radiographic evidence is frequent (e.g.,
anteriorly in relation to the condyle, thereby flattening, sclerosis, osteophytes, erosion).
blocking translation and causing clinical locking.
Patients may describe it as “hitting an CLINICAL TEST TO DIAGNOSE DISC
obstruction” when opening is attempted. The DISPLACEMENT
“obstruction” may disappear spontaneously or
In order to diagnose disc displacement with
the patient may be able to manipulate the
reduction the patient is instructed to clench the
mandible beyond the interference. Repetitive
teeth in an intercuspal position. In a joint with a
locking and opening creates strain in the
reducing disc, the disc then becomes displaced.
posterior disc attachment, resulting in laxity.
The patient is instructed to open the mouth until
clicking occurs, indicating reduction of the disc,
Stage III
and from there to protrude the mandible and
Stage III is characterized by closed-lock (disc perform all jaw movements (opening, closing,
displacement without reduction).The clicking and lateral excursion). The patient is then is
noise disappears and the patient complains of instructed to let the mandible return to the
joint pain and limited mouth opening. Clinical normal intercuspal position. If clicking reoccurs
examination reveals preauricular tenderness, when the patient opens the mouth, the diagnosis
deviation of the mandible to the affected side and is disc displacement.
Treatment fluoromethane. Other commonly prescribed

methods include transcutaneous electric nerve
A majority of the patients with symptomatic
stimulation (TENS), ultrasound, soft laser, and
internal derangement can be successfully treated
acupuncture. In order to avoid hypomobility and
with non-surgical methods but in approximately
muscle atrophy because of pain the patient
5%, surgery is performed. According to Okeson,
should be instructed to perform different jaw
the four types of treatment that should be
exercises to improve muscular coordination,
considered for patients with painful internal
relax tense muscles, increase the range of motion
derangement are counseling, physical therapy,
of the mandible, and increase muscular strength.
pharmacological therapy, and occlusal therapy.
To achieve a favorable effect, the standard
Should these methods prove unsuccessful, they
program of jaw exercises must be performed for
are often followed by surgical methods such as
2 to 3 minutes at least 2 to 3 times a day, for a
meniscectomy, disc repositioning procedures,
minimum period of 2 to 3 months. The various
condylotomy, arthroscopy, and arthrocentesis.
jaw exercises are as follows:
1. Maximum mouth opening without
Counseling
resistance (Fig. 4.11)
Counseling includes patient education and 2. Mouth opening against resistance (Fig. 4.12)
reassurance and is an important part of the 3. Mouth closing against resistance (Fig. 4.13)
management. Patient education is important in 4. Excursion of the mandible to the right (Fig.
order to modify the patients behavior. It includes 4.14)
a brief description of the disorder, and an apt 5. Excursion of the mandible to the right
discussion about the treatment. A well-informed against resistance (Fig. 4.15)
patient could play a major role in the treatment
6. Excursion of the mandible to the left (Fig.
since the disorder is of biomechanical nature and
4.16)
therefore the patient should be instructed to eat
7. Excursion of the mandible to the left against
soft food in order to decrease joint loading.
resistance (Fig. 4.17)
Patient reassurance requires an understanding
8. Protrusion of the mandible (Fig. 4.18)
dentist. The patients should be told that their
9. Protrusion of the mandible against resistance
problem is commonly found in the population;
(Fig. 4.19)
that it is a benign disorder; that it is not life
threatening; and has a very good prognosis. Such 10. Stretching exercise (Fig. 4.20)
information, when conveyed by a confident
dentist has a powerful effect on the patients
concern and anxiety. Therefore, reassurance may
be the only treatment necessary for many
patients.
Physical Therapy
The aim of physical therapy is to reduce muscle-
joint pain and to improve the joint function.
Physical therapy may include application of
moist heat and coolant therapy in form of hot
moist towels, ice cubes, and different vapo-
coolant spray containing ethylchloride or Fig. 4.11: Maximum mouth opening without resistance
Fig. 4.15: Excursion of the mandible to the right against

Fig. 4.12: Mouth opening against resistance resistance
Fig. 4.13: Mouth closing against resistance Fig. 4.16: Excursion of the mandible to the left
Fig. 4.14: Excursion of the mandible to the right Fig. 4.17: Excursion of the mandible to the left against
resistance
If extra-force is needed or if the patient cannot

generate the necessary amount of force to open
the mouth, special devices such as therabite are
available to assist the patient in performing
stretching exercise.
Pharmacological Therapy
Since pain is the most common symptom in
temporomandibular joint disorder or TMD
disorder, pain relief is an important part of
treatment of TMD. The most common
medication used is nonsteroidal anti-
inflammatory drugs (NSAID). When muscle
Fig. 4.18: Protrusion of the mandible tension is a problem, a muscle relaxant and anti-
anxiety medications can be prescribed. Intra-
articular injections of corticosteroids (8 injections
a year with 6 to 8 weeks interval) and hyaluronic
acid may be administered. Intramuscular
injections of local anesthetics into tender areas
can relieve muscular pain.
Occlusal Therapy
There are mainly two types of occlusal appliances
for the treatment of internal derangement. The
stabilization appliance is prescribed more
frequently than any other occlusal appliance. It
is also known as full-coverage splint, flat splint,
and occlusal bite plane. The stabilization
Fig. 4.19: Protrusion of the mandible against resistance appliance reduces muscular hyperactivity. It
covers all teeth as well as areas without teeth and
gets its retention by letting the acrylic just pass
the prominence line of the teeth. In most patients,
a positive treatment effect can be achieved by
wearing the appliance only at night.
The other occlusal appliance for the treatment
of internal derangement is the mandibular
repositioning appliance. It is indicated for
patients with only disc displacement with
reduction. The mandibular repositioning
appliance puts the mandible in a forward
position so that the disc is recaptured to a correct
Fig. 4.20: Stretching exercise anatomical position.
BIBLIOGRAPHY Management; Medico Dental Media International

Inc; USA 2000.
1. Carlsson EG, Magnusson T. Management of 6. Hall HD. Intra-articular disc displacement Part
temporomandibular disorders in the general II: Its significant role in temporomandibular joint
dental Practice. Quintessence Publishing Co, Inc; pathology. J Oral Maxillofac Surg 1995;53:1073-
IL 1999. 9.
2. Dijkgraaf LC, Lambert GM, Boering G, Robert SB. 7. Isberg A. Temporomandibular Joint Dysfunction
Structure of the Normal synovial membrane of – A Practitioner’s Guide; Isis Medical Media Ltd;
the temporomandibular Joint: A review of the UK 2003.
literature. J Oral Maxillofacial Surg 1996;54:332- 8. McKay GS, Yemm R, Cadden SW. The structure
8. and function of the temporomandibular joint. Br.
3. Dolwick MF. Intra-articular disc displacement Dent J 1992;173:127-32.
9. Milam SB, Schmitz JP. Molecular biology of
Part I: Its questionable role in temporomandibular
temporomandibular joint disorders: Proposed
joint pathology. J Oral Maxillofac Surg
mechanisms of disease. J Oral Maxillofac Surg
1995;53:1069-72. 1995;53:1448-54.
4. Dworkin SF, LeResche L (Eds). Research 10. Schwartz HC, Kendrick RW. Internal
diagnostic criteria for temporomandibular derangements of the temporomandibular joint:
disorder: Review, criteria, examinations and Description clinical syndromes. Oral Surg
specifications, critique. J Craniomandib Disord 1984;58:24-9.
Facial Oral Pain 1992;6:301-26. 11. Solberg WK. Temporomandibular disorders:
5. Fricton JR, Kroening RJ, Hathaway KM. Fricton’s Management of internal derangement. Br Dent J
TMJ and Craniofacial Pain Diagnosis and 1986;160:379-85.
Chapter
Tobacco, Areca Nut
5 and Alcohol
INTRODUCTION
Tobacco (Nicotiana tabacum) is a member of the
Solanaceae family (Fig. 5.1). The generic name
of the tobacco plant, Nicotiana, is derived from
the name of the French Ambassador to Portugal,
Jean Nicot. Jean Nicot, introduced tobacco into
the French court in 1560 for medicinal purposes.
The tobacco leaves contain nicotine, a plant
alkaloid. Tobacco is native of North America.
Later, the plant came to be known by the name
of the device, as “tobacco.” The word tobacco was
originally used to denote a “Y” shaped piece of
cone or pipe called “tobago” or “tobaca” that was
used by Mexican-Indians. Mexican-Indians used
tobacco in number of ways:
1. Chewed the leaves to relieve hunger and
thirst
2. Inhaled powdered tobacco (snuff) to clear the
nasal passage
3. Smoked rolled up tobacco leaves, to relieve
fatigue
Fig. 5.1: Nicotiana tabacum

CHEMICALS IN TOBACCO
Cigarette smoke contains over 4000 chemicals. Nicotine
At least 50 of the chemicals in tobacco smoke are The most biologically active agent is the alkaloid,
known to cause cancer of the lung, throat, mouth, nicotine. Nicotine is a colorless, very hygroscopic,
bladder and kidneys. About 23 chemicals that volatile oily liquid that gives tobacco its smell. It
cause tumors have been isolated and identified turns brown when exposed to air or light. Its
in smokeless tobacco. formula is C10H14N2 and molecular weight is
Tobacco, Areca Nut and Alcohol 57
than the nicotine present in the cigarette smoke,

which is absorbed through the lungs and passes
directly into the blood stream without being first
inactivated in the liver.
Biologically nicotine resembles the neuro-
transmitter acetylcholine. Nicotine can combine
with acetylcholine receptors in the body.
Biological effects are largely due to this
resemblance. Nicotine can act as a stimulant or
as a depressant, depending upon the dosage. In
low doses, it acts like a stimulating agent, just
like acetylcholine, allowing impulses to pass
through the nerves. In large doses, it combines
and floods all receptors, blocking the passage of
all nerve impulses. An overdose of nicotine
(60 mg or more) causes a complete arrest of
respiration.
Biological Effects of Nicotine

1. Increases the motility of gastrointestinal
tract, followed by decrease in motility
resulting in constipation
2. Nicotine initially increases and then
Fig. 5.2: Structures of nicotine, cotinine
and acetylcholine chloride depresses the salivary and bronchial
secretion
3. Stimulates the adrenal medulla and
162.23 (Fig. 5.2). Free nicotine is highly lipid increases the release of catecholamines,
soluble and hence can easily penetrate into which in turn causes tachycardia and
tissues and cells, where it is readily absorbed. The increase in blood pressure
absorbed nicotine in the blood reaches and 4. In small doses, nicotine relieves anxiety,
accumulates in the brain within minutes, and produces exhilaration, and suppressing
exerts its psychological and pharmacological anger.
effects. It also enters various tissues, particularly
the liver, where it is metabolized into cotinine Carcinogenic Agents
and nicotine-N-oxide. Both these metabolites are A variety of carcinogens are found in tobacco.
biologically inactive. Cotinine is a useful They include volatile aldehydes, volatile
indicator of all kinds of smoking, including N-nitrosamines, radioactive isotopes, and other
passive smoking. Nicotine leaves the tissues toxic chemicals.
rapidly and is excreted in the urine. Nicotine
absorbed from chewing tobacco, passes through Volatile Aldehydes
the liver first, where it is partly metabolized into 1. Formaldehyde
inactive substances, and then reaches the blood 2. Acetaldehyde
stream. It is generally less active and less harmful 3. Crotonaldehyde
Volatile N-nitrosamines Radioactive Isotopes

The tobacco specific volatile N-nitrosamines are 1. Polonium–210
derivatives of alkaloids (nicotine, nornicotine, 2. Uranium–235 and 238
anabasine, and antabine). The alkaloids undergo Other Chemicals in Cigarette Smoke
nitrosation in the saliva, by using nitrites in the
1. Carbon monoxide
saliva and yield volatile N-nitrosamines
2. Carbon dioxide
(carcinogens). Nicotine gives rise to three potent
3. Carbonyl sulfide
carcinogens (Fig. 5.3). Of the three NNK is the 4. Benzene
most potent. The induction of oral cancers by 5. Toluene
NNN is considerably accelerated by the presence 6. Acrolein
of HSV-1 and HSV-2, which act as cocarcinogens. 7. Acetone
1. N-nitrosonornicotine (NNN) 8. Pyridine
2. 4-(N-nitrosomethlyamino)-1-(3-pyridyl) 9. Hydrogen cyanide
butanone (NNK) 10. Nitrogen oxides
11. Benz (a) anthracene
3. 4-(N-nitrosomethlyamino)-1-(3-pyridyl) – 1-
12. Benzo (a) pyrene
butanol (NNAL)
13. Cholesterol
14. Phenol
15. Cadmium
16. Nickel
17. Zinc
18. Benzoic acid
Tobacco Habits
Around 1600 A.D. Portuguese traders brought
tobacco, the pipe, and the cigar, into India.
Tobacco habits in India are practiced in various
different forms (Fig. 5.4) and (Fig. 5.5). Many of
the habits are specific to certain areas of India.
India is now the third largest producer of tobacco
in the world, after China and the U.S.A.
Tobacco Habits—Smoking
1. Bidi
2. Cigarette
3. Cigar
4. Chutta
5. Cheroot
6. Chilum
Fig. 5.3: Formation of N-nitrosamines
from tobacco alkaloids 7. Dhumti
8. Mawa
9. Mishri
10. Red tooth powder (lal dant manjan)
The Health Risks of Tobacco

Smoking (Fig. 5.6)
1. Angina pectoris
2. Asthma
3. Atherosclerosis
4. Bladder cancer
5. Cancer of the larynx
6. Cancer of the lungs
Fig. 5.4: Smoking habits in India 7. Cancer of the oesophagus
8. Cervical cancer
9. Chronic bronchitis
10. Emphysema
11. Hypertension
12. Impotency
13. Low birth weight baby
14. Myocardial infarction
15. Peptic ulcer
16. Pancreatic cancer
17. Stroke
Tobacco and Oral Health

1. Oral cancer
Fig. 5.5: Smoking habits in India 2. Precancerous lesions
a. Preleukoplakia
8. Hookah b. Leukoplakia
9. Hookli c. Erythroplakia
10. Reverse chutta smoking d. Smoker’s palate
11. Reverse dhumti
3. Tobacco-induced oral mucosal conditions
Tobacco Habits—Smokeless a. Leukoedema
b. Palatal erythema
1. Betel quid (pan) with tobacco c. Tobacco-lime user’s lesion
2. Bajjar d. Pan encrustation
3. Creamy snuff e. Snuff dipper lesion
4. Gudhaku f. Smoker’s melanosis
5. Gutkha 4. Tobacco-associated effects on the teeth and
6. Khaini (tobacco-lime preparation) supporting tissues
7. Mainpuri tobacco a. Premature tooth loss
Fig. 5.6: The health risks of tobacco smoking
b. Staining minimize the risk of oral cancer is to stop

c. Abrasion smoking. Dentists can play a vital role in smoking
d. Attrition cessation. Evidence indicates that smoking
e. Periodontal diseases cessation interventions are both effective and
f. Acute necrotizing ulcerative gingivitis cost-effective. Smoking cessation interventions
5. Other tobacco associated oral conditions result in significant health gain and, in the long
a. Calculus term, reduce smoking-related health-care costs.
b. Halitosis Giving up smoking is a difficult process made
c. Chronic hyperplastic candidiasis up of a series of steps rather than one event and
d. Median rhomboid glossitis dentists can help smokers at the varying stages
e. Black hairy tongue in the quitting process. Of utmost importance,
however, is to let smokers know that it is never
Smoking Cessation too late to stop smoking and that the sooner they
The most important step that smokers need to do, the greater the benefits will be to their long-
take in order to improve their oral health and term health.
The Four As Reasons for quitting will obviously vary for

different groups of smokers but might include
There are four essential features of smoking
the following:
cessation advice. These steps are recommended
1. Pregnant women: Increased risk of low
in the recently published evidence based Smoking
birth-weight and fetal death
Cessation Guidelines.
2. Long-term smokers: Increased risk of heart
1. Ask about smoking at every opportunity
disease, cancer, and stroke
2. Advice all smokers to stop
3. New smokers: Easier to stop now than later
3. Assist the smokers to stop
4. Any smoker: Save money and feel healthier
4. Arrange follow-up
Assist
Ask
If the smoker would like to stop, help should be
All patients should have their smoking status
offered. A few key points can be covered with
established and kept as up-to-date as possible,
the smoker in 5-10 minutes.
for example, following every visit. At the very
1. Set a date to quit smoking; stop smoking
least, this record should cover whether the
completely on that day
patient is a smoker, non-smoker, or recent ex- 2. Review past experience: what helped, what
smoker, and note any current interest in hindered?
stopping. Interest in stopping can be assessed 3. Provide self-help literature
with an open-ended question such as “Have you 4. Discuss the health benefits of quitting
ever tried to stop?” This can be followed by “Are 5. Tell family and friends to prepare the
you interested at all in stopping now?” environment (discard cigarettes)
Other types of questions can be asked:
1. How many cigarettes do you smoke? Arrange
2. How long have you been smoking? Arranging a follow-up is very important. Studies
3. When do you smoke? indicate that successful quit rates are high when
4. Have you ever tried to stop smoking? follow-up contact is routinely made with
From these questions, it is easy to identify what interested patients. Patients should be seen
might help the smoker make the decision to stop ideally 1-2 weeks after their quit date. Most
smoking. smokers make several attempts to stop before
finally succeeding (the average is around 3-4
Advice
attempts), so relapse is a normal part of the
Every smoker must be told of the value that process. To help smokers overcome nicotine
stopping smoking will have for them and of the cravings, dentists can recommend the following
risks to health that exist in continuing. Because the “Four Ds,” aimed at reducing the urge to
the needs and reasons for wanting to stop smoke:
smoking will be different for every smoker, it is 1. Delay: Do not open a pack or light a cigarette.
important to examine each individual situation After a few minutes, the urge to smoke
and give plain, precise, and personalized advice weakens and your resolve to quit will come
to them. This can include recommending aids to back
stopping smoking such as using Nicotine 2. Deep breaths: Take three deep, slow breaths
Replacement Therapy (NRT). in and out
3. Drink water: Sip it slowly and enjoy the taste those killed by smoking have lost 10 to 15 years
4. Do something else: Take your mind off of life.
smoking by doing some exercise, listening
to music or talking to a friend ARECA NUT
The areca nut resembles tobacco in some ways.
Aids to Cessation
Like tobacco, it also contains many alkaloids, of
Some people find it easier than others to stop which the most important is arecoline. These
smoking, and the degree of difficulty is not alkaloids like nicotine have stimulating effects
always related to tobacco consumption. Factors on the human body. They are also probably
such as maturity, the ability to cope with stress addictive, though to a lesser degree than nicotine.
or confidence of success are equally important. The nitrosation of areca nut alkaloids yields
carcinogenic N-nitrosamines, the most active
Nicotine Replacement Therapy (NRT) among them being 3-(methylnitrosamino)
propionitrile (MNPN). The areca nut is
Nicotine replacement therapy (NRT) is the most
composed of carbohydrates (50-75 %), proteins
widely used pharmaceutical aid to assist
(5-8 %), fats (14%), red tannins (15 %), alkaloids,
individuals in their attempts to stop smoking.
and other nitrogenous bases such as choline. The
Nicotine replacement therapy is available in the
alkaloids present in areca nut are arecoline,
form of a gum, patch, nasal spray, and inhalator.
arecaidine, guvacoline, and guvacine. Arecaidine
Nicotine replacement therapy is contraindicated
and guvacoline are isomers, containing one
in patients with diabetes mellitus,
methyl group less than arecoline. Both the methyl
hyperthyroidism, or pheochromocytoma, renal
groups of arecoline are absent in guvacine
or hepatic insufficiency, asthma, peptic ulcers,
(Fig. 5.7). Among these alkaloids, arecoline is by
contact dermatitis, generalized skin disorders,
far the most important, occuring to the extent of
nicotine allergy, depression, pregnancy, breast-
0.5-0.7 % in areca nut. Its molecular formula is
feeding, temporomandibular joint disease, and
C 8 H 13NO2 , and molecular weight is 155.19.
oral inflammation. Arecoline is an oily liquid; with a boiling point
of 209°C and a strong base, which is freely
Conclusion
miscible with water, alcohol, and ether. Arecoline
Stopping smoking prolongs life regardless of the mimics the action of acetylcholine, and stimulates
age at which a person stops. both the central and peripheral nervous system.
A smoker’s life span is shortened by about five The euphoric effect of areca nut is due to
minutes for each cigarette smoked. On average, arecoline. The cytotoxic properties of arecoline
Fig. 5.7: Areca nut alkaloids

and guvacoline are due to the presence of a 1. Raw or green (undried)

methylester group. The lower polarity and lower 2. Sun dried
degree of ionization of arecoline and guvacoline 3. Boiled
may facilitate their passage over biological Raw and sun dried areca nuts have higher
membranes. alkaloid and tannin content in comparison to
Nitrosation of the areca nut alkaloids takes boiled areca nuts. The areca nut chewers
place in the mouth through the nitrites in the generally swallow the saliva completely, thus
saliva. Nitrosation of arecoline yields four bathing the esophageal lining with the
N-nitroso compounds (Fig. 5.8), N-nitrosogu- genotoxins released during chewing. The
vacoline (NG), N-nitrosoguvacine (NGC), swallowing of saliva has been blamed for the
3-(methylnitrosamino) propionaldehyde increased rate of esophageal cancer. However,
(MNPA), and 3-(methylnitrosamino) propio- those who chew areca nut plus tobacco,
nitrile (MNPN). Among these N-nitroso expectorate the saliva periodically because of the
compounds, MNPN and MNPA are highly bitter taste of tobacco. Currently the habit of areca
genotoxic and carcinogenic. Areca nut produced nut chewing is recognized as the most important
in India, can be classified broadly under three etiologic agent in oral submucous fibrosis or OSF.
heads:
ALCOHOL
The main component of alcoholic beverages is
ethyl alcohol and water. According to Kabat and
Wynder, the main carcinogenic agent in alcoholic
beverages is ethyl alcohol or ethanol. In addition,
present in the alcoholic beverages are many
polycyclic aromatic hydrocarbons. The actions
of alcohol are local and systemic. Ethyl alcohol
is metabolized to acetaldehyde in the liver. In
the next step, acetaldehyde is converted to acetic
acid in the liver. These metabolic steps cause
damage to the hepatocytes because of acetic acid
and acetaldehyde. Thereby reducing the
absorption of nutrients from the intestine,
leading to nutritional deficiency and
immunodeficiency.
Local Action
Ethyl alcohol dissolves the lipid layer of epithelial
cells of the oral mucosa as a result it helps in the
penetration of carcinogens. Thus mainly acting
like a cocarcinogen. As a result, people who drink
and smoke at the same time are more prone to
Fig. 5.8: N-nitrosamines derived from areca nut alkaloids developing oral cancer.
BIBLIOGRAPHY 4. Sundqvist K, Liu Y, Nair J, Bartsch H, Arvidson

1. Mehta FS, Hammer JE, III. Tobacco-related Oral K, Grafström RC. Cytotoxic and genotoxic effects
Mucosal Lesions and Conditions in India; Basic of areca nut – Related compounds in cultured
Dental Research Unit, TIFR; Bombay 1993. human buccal epithelial cells. Cancer Research
2. Ogden GR, Wight AJ. Etiology of oral cancer: 1989;49:5294-8.
Alcohol. Br. J Oral and Maxillofacial Surg
5. Watt R, Robinson M. Helping Smokers to Stop: A
1998;36:247-51.
3. Sivaramakrishnan VM. Tobacco and Areca Nut; guide for the dental team; Health Education
Orient Longman; Hyderabad 2001. Authority; London 1999.
Chapter
Oral Precancer
6
INTRODUCTION 1. Oral leukoplakia
2. Erythroplakia
Oral cancer makes up approximately 3 % of all
3. Smokers palate
malignancies of the body, although in some parts
4. Actinic cheilitis
of the world, that percentage is much higher. The
majority of oral cancers consist of oral squamous
cell carcinoma. A number of such carcinomas PRECANCEROUS CONDITION
develop from preexisting pathologies, so called A generalized state associated with a
precancerous lesions and precancerous significantly increased risk of cancer. Examples
conditions. of precancerous conditions include:
The most common oral precancerous lesion 1. Oral submucous fibrosis
is a whitish change of the oral mucosa, an oral 2. Erosive lichen planus
leukoplakia. The development of oral cancer may 3. Syphilitic glossitis
also be promoted by certain precancerous 4. Sideropenic dysphagia
conditions such as oral submucous fibrosis, 5. Discoid lupus erythematosus
erosive lichen planus, syphilitic glossitis, 6. Dyskeratosis congentia
sideropenic dysphagia (Paterson-Kelly 7. Tylosis
syndrome, Plummer-Vinson syndrome), discoid
lupus erythematosus, tylosis (palmoplantar ORAL LEUKOPLAKIA
hyperkeratosis), and dyskeratosis congenita.
Sir James Paget had recognized the malignant
potential of oral leukoplakia and its relationship
PRECANCEROUS LESION
to pipe smoking, reporting on leukokeratosis and
A precancerous lesion is defined as a smoker’s patch as early as 1851. A quarter
morphologically altered tissue in which cancer century before Schwimmer from Budapest
is more likely to occur than in its apparently coined the term leukoplakia in 1877. One
normal counter part. Leukoplakia and hundred forty years later, oral leukoplakia is well
erythroplakia occurring separately or in established as one of the very best examples of
combination are the most common precancerous premalignancy in man.
oral lesions. Examples of precancerous lesions Leukoplakia is not only the most common oral
include: precancerous lesion, representing 85 % of such
lesions, but also the most common of all chronic clinical diagnosis of oral leukoplakia and a
lesions of the oral mucosa. The rate of malignant definitive one.
transformation of oral leukoplakia ranges from A provisional clinical diagnosis is made when
0.13 % to 6 %. a lesion at the initial clinical examination cannot
be clearly diagnosed as any other disease of the
Definition oral mucosa with a white appearance; a
The first recorded white oral plaque was an definitive clinical diagnosis of oral leukoplakia
icthyosis reported in 1818 by Alibert of Paris. is made as a result of the identification, and if
More than any other disease, oral leukoplakia possible elimination, of suspected etiological
has suffered from an excess of diagnostic terms factors and, in the case of persistent lesions (no
and definitions; at least 75 have been used so far. signs of regression within 2-4 weeks),
This lead to such confusion that many clinicians histopathological examination.
refuse to use any term beyond white patch.
Accordingly, whitish patches or plaques Epidemiology
associated with use of tobacco should be listed The prevalence of oral leukoplakia varies
as tobacco-associated oral leukoplakias. considerably when findings from various
The WHO in 1978 defined oral leukoplakia as countries are compared. These geographic
“A white patch or plaque that cannot be differences could probably be explained largely
characterized clinically or histopathologically, as by differences in tobacco habits and by the use
any other disease.” At the international seminar of different criteria. The onset of oral leukoplakia
held in 1983, the previous definition was changed usually takes place after the age of 30 years,
to: “Leukoplakia is a whitish patch or plaque that resulting in a peak incidence above the age of
cannot be characterized clinically or 50 years.
pathologically as any other disease and it is not Oral leukoplakias seems to most prevalent
associated with any physical or chemical among men, except for some areas in India,
causative agent except for the use of tobacco.” where certain tobacco habits are common among
Whitish patches or plaques related to local causes women. The most affected oral sites are the
other than tobacco usage should be listed commisures, buccal mucosa (60-90 %). Next are
according to the known cause and not be termed the lip (3.7 %), the alveolar ridge (3.0 %), the
leukoplakias. Examples of such lesions are tongue (1.4 %), the floor of the mouth (1.3%), the
frictional lesions, lesions associated with dental vestibular mucosa (1.1 %), and the palate (0.9%).
restorations, lesions associated with cheek biting Homogenous oral leukoplakias are much more
and glassblower’s lesion. prevalent than non-homogenous oral leuko-
In 1994, at another symposium on oral white plakias; while tobacco associated oral leuko-
lesions with special reference to precancerous plakias are more prevalent than idiopathic oral
and tobacco-related lesions the definition of oral leukoplakias.
leukoplakia was changed to: “Oral leukoplakia
is a predominantly white lesion of the oral
ETIOLOGY OF ORAL LEUKOPLAKIA
mucosa that cannot be characterized as any other
definable lesion; some oral leukoplakias will The etiology of oral leukoplakia remains
transform into cancer.” In that report, a unknown. Many physical agents have been
distinction was made between a provisional proposed, including tobacco, alcohol,
Oral Precancer 67
microorganisms, ultraviolet radiation, and carcinomas, has been shown to induce dysplasia
chronic friction. in squamous epithelium in a sterile in vitro
environment.
Tobacco Smoking
Ultraviolet Radiation
Tobacco smoking is by far the most accepted. The
evidence for a tobacco smoking etiology for oral Ultraviolet radiation is also an accepted etiologic
leukoplakia, however, is quite strong. Not only factor for oral leukoplakias, but only those
do 70% to 90% of oral leukoplakia patients have associated with actinic cheilitis or “farmer’s lip.”
such habit, but also 78% of lesions either Two-thirds of all lip vermilion carcinomas are
completely disappear or regress within 12 associated with oral leukoplakia.
months after smoking cessation. Ironically, oral
leukoplakias remaining after habit cessation or Chronic Friction
in persons who have never smoked may have a Chronic mechanical irritation is no longer
higher risk of malignant transformation than oral considered important to the production of oral
leukoplakias in smokers. leukoplakia. Such obvious traumatic lesions as
linea alba buccalis and chronic cheek bite have
Alcohol
never been reported to transform into
Alcohol as an independent etiological factor in malignancies. White lesions produced by
the development of oral leukoplakia is still mechanical irritation are best considered
questionable. frictional keratoses, which have no potential for
malignant transformation.
Microorganisms
Microorganisms have been implicated in the CLINICAL FEATURES
etiology of oral leukoplakia for more than a Oral leukoplakia has a varied clinical appearance
century, beginning with the classic dorsal and its appearance changes over time (Table 6.1).
leukoplakia of syphilitic glossitis. Today tertiary
syphilis is rare, but Candida albicans is so often Phase I — Preleukoplakia (Fig. 6.1)
found in Phase III and Phase IV lesions that the
terms candidal epithelial hyperplasia and Oral leukoplakias begin as thin, gray or gray-
candidal leukoplakia are commonly used to white plaques that may appear somewhat
describe them. It is not known whether this yeast translucent, are sometimes fissured or wrinkled,
produces dysplasia or secondarily infects and are typically soft and flat. They usually have
previously altered epithelium, but some oral sharply demarcated borders but occasionally
leukoplakias have disappeared or have become blend gradually into normal mucosa.
altered to a homogenous oral leukoplakia after
Phase II—Homogenous Leukoplakia
topical antifungal therapy.
(Fig. 6.2)
In recent years, the possible role human
papilloma virus type 16 in the pathogenesis of Phase I oral leukoplakias may disappear or
oral leukoplakia has also been discussed, continue unchanged, but as time progresses
particularly with regard to Phase III oral preleukoplakia may extend laterally and acquire
leukoplakia. However, human papilloma virus a distinctly white appearance due to thickening
type 16, demonstrated in oral leukoplakias and keratin layer. They may exhibit shallow cracks
Table 6.1: Various diagnostic descriptive terms used for Phase I to Phase IV leukoplakia subtypes
Phase Diagnostic Term Risk of Malignant Transformation
I Thin leukoplakia, Preleukoplakia, Homogeneous leukoplakia +/–
II Thick, smooth leukoplakia, Fissured leukoplakia,
Homogenous leukoplakia ++
III Granular leukoplakia, Verruciform leukoplakia, Rough leukoplakia,
Candidal epithelial hyperplasia, Homogenous leukoplakia +++
IV Erythroleukoplakia, Speckled leukoplakia, Candida leukoplakia,
Nonhomogenous leukoplakia ++++
Fig. 6.1: Preleukoplakia Fig. 6.2: Homogenous leukoplakia
and have a smooth, wrinkled, or corrugated scattered areas. Such areas presumably represent
surface with a consistent leathery texture sites in which epithelial cells are so immature that
throughout and are referred to as homogenous they are no longer able to produce keratin. These
oral leukoplakia. Homogenous oral leukoplakia intermixed red and white Phase IV lesions
remains indefinitely in this phase, but some (erythroleukoplakia, speckled leukoplakia, or
regress or disappear and a few become even nonhomogenous leukoplakia), are the most
more severe. worrisome form of the disease, and carry an
extremely high risk of malignant transformation.
Phase III—Verruciform Leukoplakia
(Fig. 6.3) LSCP CLASSIFICATION AND STAGING
Phase II oral leukoplakias begin to develop SYSTEM (Table 6.2)
surface irregularities and are referred to as In order to promote uniform reporting of various
granular or nodular oral leukoplakia. aspects of oral leukoplakia, there is a need for a
Occasionally, pointed projections develop on the classification and staging system in which the
surface and the resulting lesions are called site, the clinical subtype and the histopatho-
verruciform oral leukoplakia. logical features are taken into account. The
staging system (Stages I-IV) has not yet been
Phase IV—Speckled Leukoplakia (Fig. 6.4)
proven to be of value with regard to the
Phase III oral leukoplakias begin to develop management of the patient. A somewhat
multiple circular or oval patches of redness in debatable item that has been included in the
Oral Precancer 69
Fig. 6.3: Verruciform leukoplakia Fig. 6.4: Speckled leukoplakia
Table 6.2: LSCP-classification and staging system for oral leukoplakia

st
1 symbol (L) represents the size
L0 = No evidence of lesion
L1 = lesion < 2 cm
L2 = Lesion 2-4 cm
L3 = Lesion > 4 cm
LX = Not specified
2nd symbol (S) represents the site
S1 = All oral sites, except for the floor of the mouth and tongue
S2 = Floor of the mouth and tongue
SX = Not specified
rd
3 symbol (C) represents the clinical aspect
C1 = Homogenous
C2 = Nonhomogenous
CX = Not specified
th
4 symbol (P) represents the histopathological features
P1 = No dysplasia
P2 = Mild dysplasia
P3 = Moderate dysplasia
P4 = Severe dysplasia
PX = Not specified
Staging is only preformed in leukoplakias that have been examined histopathologically
Stage I = Any L, S1, C1, P1, or P2
Stage II = Any L, S1, C2, P1, or P2; any L, S2, C1, P1, or P2
Stage III = Any L, S2, C2, P1, or P2
Stage IV = Any L, any S, any C, P3, or P4
staging system is the assumption that there are, Histopathology

high-risk sites (tongue and floor of the mouth),
In order to arrive at a definitive diagnosis of oral
which may be true in certain parts of the world, leukoplakia it is mandatory that a biopsy should
e.g., North America and Europe, but not so in be taken and that a histopathological report is
other parts, e.g., India. available. If an oral precancerous lesion is
suspected clinically, the histopathological report
Differential Diagnosis should always include a statement on the
Differential diagnostic problems may arise presence or absence of epithelial dysplasia and,
clinically with candidosis, oral lichen planus, if present, an assessment of its severity.
discoid lupus erythematosus, and white sponge Individual cellular changes should be refered
nevus. The commonly used term “Candida- to as “atypia” and the general disturbance in the
associated oral leukoplakia” leaves the question epithelium as “dysplasia.” Regressive alterations
unsettled, whether one is dealing with oral in the cells such as alteration in their size, shape,
orientation, and functions are termed as
leukoplakia or with another disease entity, in
dysplasia.
particular candidosis. It is suggested, that those
Oral leukoplakias, which show epithelial
“Candida-associated oral leukoplakias” which,
dysplasia, carry an increased risk of malignancy.
after antimycotic treatment and cessation of
Dysplasia may be graded as mild, moderate,
smoking, disappear completely, should be
severe and carcinoma in situ.
termed as candidosis. In case of a residual lesion, 1. Mild: The dysplastic features are towards
the term oral leukoplakia should be maintained. lower third of the epithelium
2. Moderate: The dysplastic features occupy
Investigations two thirds
Although the experienced may be able to 3. Severe: The dysplastic features occupy more
diagnose and manage the majority of oral than two thirds of the epithelial thickness,
leukoplakias on clinical grounds only in general, but less than full
such practice should be discouraged, even in 4. Carcinoma in situ (intraepithelial
asymptomatic, homogenous leukoplakias. This carcinoma): All the features of dysplasia are
holds true while dealing with leukoplakic lesions present but the basement membrane is intact
in high risk sites such as the ventral aspect of the and there is no invasion
The World Health Organization collaborating
tongue and the floor of the mouth. Exfoliative
reference centre for oral precancerous lesions
cytology and application of toluidine blue are of
(1978) mentions the following changes as
limited value in the diagnosis of oral leukoplakia.
possibly occurring in epithelial dysplasia (Table
The most reliable information is provided by
6.3)
histopathological examination of biopsy. In
1. Drop-shaped rete pegs: The drop-shaped
lesions less than 1 cm in diameter, an excisional rete pegs are wider at their deeper aspect
biopsy can be carried out, while in lesions greater than the superficial aspect.
than 1 cm in diameter, an incisional biopsy 2. Disturbed nuclear polarity: The nuclei in the
should be taken which should be taken, which basal cell layer are irregularly disposed in
should include the most suspicious area as comparison to the nuclei in the basal cell
judged from clinical evaluation. In multiple oral layer of normal stratified squamous
leukoplakias, one may consider of taking epithelium where they are more or less in
multiple biopsies. the same position.
Oral Precancer 71
Table 6.3: Dysplastic features nucleus which may fill or almost fill an entire
Drop-shaped rete pegs keratinocyte.
Disturbed nuclear polarity
9. Cell crowding: Due to disturbed cellular
maturation, there is more number of cells in
Basal cell hyperplasia
a given area.
Disturbed epithelial cell maturation 10. Increased mitosis, superficial mitosis and
Pleomorphic cells and nuclei and anisocytosis abnormal mitosis may be found to different
Hyperchromatic nuclei extents in epithelial dysplasia.
Prominent nucleoli
11. Reduced cellular cohesion: Reduced cellular
cohesion is because their attachments are
Increased nucleocytoplasmic ratio
reduced or faulty.
Cell crowding 12. Keratinization below surface: Keratiniza-
Increased mitosis, superficial mitosis tion within the cytoplasm of individual cells
and abnormal mitosis is known as intraepithelial keratinization or
Reduced cellular cohesion it may occur in relation to a small cluster of
Keratinization below surface
cells.
TREATMENT
3. Disturbed epithelial maturation: Disturbed Management of oral leukoplakia includes
maturation of the epithelial cells may extend removing all etiological factors to determine the
for varying distances throughout the possibility of reversibility. The time required for
stratified squamous epithelium and may oral leukoplakia to regress after elimination of
even occur to its entire thickness. suspected etiological factors may vary from
4. Basal cell hyperplasia: Because of disturbed several weeks to months. When there are no signs
epithelial maturation, the basal cells do not of regression within 2-4 weeks after attempted
mature into typical polyhedral keratinocytes. elimination of etiological factors, surgical
Thus, the cells retain the morphology of the excision is the only established method of
basal cells. controlling oral leukoplakia.
5. Pleomorphic cells, nuclei, and anisocytosis: Treatment with carbon dioxide laser has been
There are cells and nuclei, which are of the most valuable approach based on the
different shapes, and sizes instead of biological effects of laser on oral tissues, ease of
demonstrating the regularity in found in operation, low incidence, and good control. The
normally maturing stratified squamous key is long-term follow-up after removal, because
epithelium. recurrences are frequent and additional oral
6. Hyperchromatic nuclei: The nuclei are more leukoplakias occur. Clinical evaluation every 6
basophilic than the normal keratinocytes. months is recommended; evaluation every 2 to
7. Prominent nucleoli: The nucleoli are 3 months is necessary for Phase IV lesions.
prominent and may be seen singly or in Treatment sites remaining disease free for 3 years
multiples in different nuclei. need no follow-up.
8. Increased nucleocytoplasmic ratio: Alternative approaches to control oral
Increased nucleocytoplasmic ratio observed leukoplakia include vitamin A, retinoic acid, and
in dysplasia is due to decrease in cytoplasmic β-carotene, which is the precursor of vitamin A.
volume and increase in the size of the Vitamin A, is not reproducibly effective, although
by mechanisms not understood, it will induce Definition

dekeratinization in some lesions. The role of The term erythroplakia (erythroplasia) was
antioxidant supplements is less certain and their coined to describe red lesions of the oral mucosa
use less predictive. in contrast to oral leukoplakia. Over the years,
several definitions of oral erythroplakia have
Prognosis
been suggested. The WHO in 1978 defined oral
Lesions of long duration have a greater risk of erythroplakia as “lesions of the oral mucosa that
malignant transformation than those of short present as bright red patches or plaques that
duration, and the older the oral leukoplakia, the cannot be characterized clinically or
worst is its prognosis. The risk of malignant pathologically as any other condition.” This
transformation of oral leukoplakia is more definition was confirmed during an International
common in women than in men. Homogenous seminar on oral leukoplakias and associated
oral leukoplakias carry lower risk of malignant lesions related to tobacco habits in 1983.
transformation, while nonhomogenous oral In 1994, at another symposium on oral white
leukoplakias carry a higher risk and the location lesions with special reference to precancerous
of the lesion is important, since apparently and tobacco-related lesions the definition of oral
similar lesions in different oral sites may carry erythroplakia was changed: “The term
different risks of malignant change. For example, erythroplakia is used analogously to leukoplakia
leukoplakia affecting the floor of the mouth or to designate lesions of the oral mucosa that
the ventral surface of the tongue appears to carry present as red areas and cannot be diagnosed as
a high risk. In general, it is assumed that any other definable lesion.” The same comments
approximately 5 % of all oral leukoplakias with apply in relation to provisional and definitive
an initially noncarcinomatous histologic picture diagnosis as for oral leukoplakias. In the second
will transform into malignancy in an average edition of ‘Histological typing of cancer and
period of five years. precancer of the oral mucosa’ erythroplakia was
defined as “A fiery red patch that cannot be
ERYTHROPLAKIA characterized clinically or pathologically as any
other definable lesion.” This definition is now
Historical Aspect
widely accepted, although it is based on the
In 1911, Queyrat described a sharply defined, principle of diagnosis per exclusion.
bright red, glistening velvety precancerous lesion
of the glans penis, which was termed Prevalence
“erythroplasie.” Queyrat used the term It is generally accepted that oral erythroplakia is
“erythroplasie” to designate a red area (plaque) less common than oral leukoplakia. Oral
by analogy to the French term “leucoplasie.” erythroplakia has range of prevalence between
Shear clearly pointed out that if the English word 0.02% and 0.83%.
leukoplakia is matched with “leucoplasie”, then
Queyrat’s “erythroplasie” should be translated
Clinical Features
into English “erythroplakia.” When exactly the Age: Oral erythroplakia mainly occurs in the
term “erythroplakia” was introduced to describe middle aged and the elderly.
a specific type of oral mucosal lesion is not well Gender: Recently it has been stated that oral
documented. erythroplakia occurs mostly in men. With the few
Oral Precancer 73
studies available indicating gender distribution Histopathology

this statement cannot be sustained.
Histopathologically, oral erythroplakia tends to
Location and size: The soft palate, the floor of show dysplasia, often in a distinctive pattern
the mouth, and the buccal mucosa are most with drop-shaped rete processes, marked nuclear
commonly affected by oral erythroplakia. The and cellular pleomorphism and minimal
typical lesion is less than 1.5 cm in diameter. keratinisation. Oral erythroplakia is typically
diagnosed microscopically as severe epithelial
ETIOLOGY dysplasia or carcinoma in situ.
Etiology and pathogenesis of oral erythroplakia
are poorly understood. Predisposing factors are Rate of Malignant Transformation
widely unknown, but it was suggested that
Oral erythroplakia has a high risk of malignant
tobacco and alcohol use are probably involved
transformation compared to all other oral
in most cases.
mucosal lesions (oral leukoplakia, erosive lichen
planus, and oral submucous fibrosis). The high
Clinical Appearance
risk of malignant transformation is because
The WHO Histological typing of cancer and histopathologically oral erythroplakia typically
precancer of the oral mucosa described the presents as severe epithelial dysplasia or
clinical features of oral erythroplakia as follows: carcinoma in situ. Generally, the rate of malignant
“Some erythroplakias are smooth and some are transformation in oral precancerous lesions
granular or nodular. Often there is a well-defined diagnosed histopathologically as severe
margin adjacent to mucosa of normal epithelial dysplasia or carcinoma in situ varies
appearance.” from 14 % to 50 %.
Shear elaborated on the different clinical
variants of oral erythroplakia: “Although
Differential Diagnosis
erythroplakic lesions may have a smooth velvety
surface, they may also be seen with other From the clinical point, diseases of the oral
morphological characteristics. They may have an mucosa with red (erythematous) changes should
irregular, red granular surface interspersed with be considered as differential diagnosis. Of the
white or yellow foci, which may be described as diseases with red (erythematous) changes,
granular erythroplakia. There may be numerous, atrophic candidosis, and erosive lichen planus
small irregular foci of leukoplakia dispersed in are the most important. Biopsy is mandatory in
the erythroplakic patch, and this has been called cases of doubt.
speckled leukoplakia.
Oral erythroplakia is soft to palpation and Treatment
does not become indurated or hard until Oral erythroplakia has a high risk of malignant
carcinoma develops in it. Oral erythroplakia, transformation and therefore early effective
while occasionally associated with oral treatment is compulsory. The recommended
leukoplakias and oral squamous cell carcinoma, treatment has been surgical excision of lesions
may also be observed in association with other with severe epithelial dysplasia or carcinoma in
mucosal diseases, in particular oral lichen planus. situ with regular follow-up.
Oral Submucous Fibrosis to tolerate spicy food and that the disease was
due to some form of hypersensitivity to capsaicin,
In 1952, Schwartz described a fibrosing condition
an irritant, which is present in chilies.
in the mouths of 5 Indian women from Kenya,
for which he called “atrophia idiopathica tropica Systemic Factors
mucosae oris.” Later it was termed oral It was also suggested that OSF was a mucosal
submucous fibrosis (OSF). OSF is an insidious, change secondary to chronic iron and / or
chronic disease affecting any part of the oral vitamin B-complex deficiency and is an Asian
cavity and sometimes the pharynx. analogue of Plummer-Vinson syndrome.
OSF is a precancerous condition with a high
risk of malignant transformation (7.6%). The Autoimmunity
estimated prevalence of OSF is 0.2 to 0.5% in the An autoimmune response to an antigenic
general Indian population. Unlike oral stimulus may manifest as chronic inflammation,
leukoplakia, OSF is not known to regress when which comes before the fibrotic changes in the
the person stops chewing areca nut. The oral mucosa. Human leukocyte antigens (HLA)
condition may remain unchanged or become are a series of proteins and their genes are located
severe. at a number of loci along the short arm of
chromosome 6. The main loci are designated A,
Synonyms B, C, DR (D-related). HLA antigens are detectable
Diffuse oral submucous fibrosis on the surface of most nucleated cells e.g., basal
Idiopathic scleroderma of the mouth cell layer of the epithelium. HLA-DR positive
Idiopathic palatal fibrosis cells in the basal cell layer of the epithelium may
Sclerosing stomatitis act as antigens, resulting in infiltration of HLA-
Juxta-epithelial fibrosis DR positive CD4 lymphocytes in the lamina
propria. Thus, the presence of HLA-DR positive
Geographic Distribution cells, Langerhans cells, and HLA-DR positive
CD4 lymphocytes in OSF tissues suggests that
There is no relationship between oral submucous there is a persistent antigenic challenge within
fibrosis and any community or religious group. the epithelium resulting in cellular immune
Oral submucous fibrosis predominantly occurs response. It is likely that this chronic
among Indians or Indians settled in other inflammation would enhance the permeability
countries. It occasionally occurs in other Asiatics of the epithelium to areca nut alkaloids,
and sporadically among non-Asians. flavanoids, and tannins, which could then alter
the synthesis and breakdown of the subepithelial
Etiology and Pathogenesis collagen.
The etiology of OSF is multifactorial and the Areca Nut
patients are genetically predisposed, which
However, currently the habit of areca nut
makes their oral mucosa susceptible to chronic
chewing is recognized as the most important
inflammatory changes if they chew areca nut.
etiologic agent. The fact that OSF is a permanent
condition, which does not resolve after the
Chilies
cessation of the areca nut habit, indicates a
The use of chilies was suggested as possible permanent cellular change in the affected
etiologic factor as patients with OSF were unable mucosa. As the amount of collagen in any tissue
Oral Precancer 75
is a result of the equilibrium between synthesis Table 6.4: Signs and symptoms of oral ulcer
and degradation, an increase in resistance to Oral Symptoms Oral Signs
collagenase would favor accumulation. The areca
Dryness of mouth Fibrous bands
nut alkaloids stimulate the fibroblasts to produce
collagen, inhibit the fibroblasts to produce Burning sensation Sensitivity to palpation
collagenase, inhibit the fibroblast phagocytosis, Altered taste Limitation of mouth opening
and may stimulate the fibroblasts to produce Referred pain in the
lysyl oxidase, which converts soluble monomers throat/ear region Blanching of oral mucosa
of collagen and elastin into insoluble fibers. The
Numbness in the mouth Atrophy of the tongue
tannins of areca nut may stabilize the collagen
Vesicles and ulcers
by forming cross-links between the peptide
chains rendering the cleavage sites inaccessible Dysphagia
to collagenase.
The bulk of connective tissue consists of cross- accumulation of inelastic fibrous tissue in the oral
linked insoluble Type 1 collagen. Collagen mucosa (Fig. 6.5). The buccal mucosa and lips
synthesis is due to excessive production by may be affected at an early stage. In the buccal
fibroblasts and not due to excessive proliferation mucosa, a mottled, marble-like appearance may
of fibroblasts. Hydroxy proline is an amino acid
be seen where the dense, pale, blanched, fibrosed
found only in collagen, and is incorporated in
areas alternate with pinker, more normal oral
the collagen as 4-hydroxy proline. This reaction
mucosa (Fig. 6.6). The blanching occurs due to
requires iron and ascorbic acid. The decreased
impairment of local vascularity. The oral mucosa
plasma ascorbate and iron concentrations may
is involved symmetrically and the fibrous bands
be due to their utilization in the fibrosis process.
in the buccal mucosa run in a vertical direction.
It is well-established that fibroblasts and
The fibrosis progresses into the posterior part of
proliferating basal cells of the epithelium
produce collagenase and that fibroblasts ingest the buccal mucosa, the anterior pillar of the
segments of collagen after its breakdown by fauces and the soft palate. The fibrous tissue is
collagenase. A characteristic feature of OSF is seen arching from the anterior pillars of the
atrophy of epithelium, which would decrease the fauces into the soft palate as a delicate reticulum
production of collagenase by the basal cells and of interlacing white strands, which later become
enhance the penetration of the tannins.
Therefore, a more likely explanation for
decreased collagen breakdown would be due to
interference with either collagenase production
or collagen degradation by cells or both.
Clinical Presentation
Patients may describe a sudden attack of burning
sensation in the mouth while consuming spicy
food, appearance of vesicles especially on the
palate, ulcerations of the oral mucosa, excessive
salivation, altered taste sensation, and
xerostomia (Table 6.4). The major presenting
complaint is inability to open the mouth due to Fig. 6.5: Inability to open the mouth
merged (Fig. 6.7). The uvula becomes small and

distorted. If the fibrosis extends into the
esophagus, the patient may experience
dysphagia, and reduced esophageal mobility.
The fibrosis leads to difficulty in opening the
mouth, difficulty in mastication, speech,
swallowing, blowing, whistling, and referred
pain in the throat, and ears.
As the disease progresses the floor of the
mouth becomes pale and thickened, there is
atrophy of the tongue papillae (Fig. 6.8),
impairment of tongue movements (Fig. 6.9) and Fig. 6.8: Atrophy of tongue
reduction in size of the tongue. Fibrous circular
palpable bands develop around the entire rima
Fig. 6.9: Impairement of tongue movements
oris. In advanced stages, the jaw may be

inseparable, and the inelastic mucosa is forced
Fig. 6.6: Blanching of buccal mucosa
against the buccal aspects of the teeth where
sharp edges or restorations may cause ulceration,
which becomes secondarily infected. At any
stage in the disease, the epithelium may become
the site of nonspecific ulceration, dysplastic
change, or malignant transformation.
Clinical Grading
Depending upon the clinical condition, OSF is
graded for the purpose of treatment as :
Grade I—Only blanching of oral mucosa without
symptoms
Grade II—Burning sensation, dryness of mouth,
Fig. 6.7: Impairement of tongue movements vesicles or ulcers in the mouth
Oral Precancer 77
Grade III—In addition to grade II, restriction of ridges. Epithelial atrophy is marked in advanced
mouth opening stages of the disease. The atrophic epithelium is
Grade IV—In addition to grade III, palpable one of the cardinal light microscopic features of
fibrous bands all over the mouth OSF and is more vulnerable to carcinogens,
Grade V—Grade IV and tongue is involved which in India are so often present in the form
Grade VI—OSF with histopathologically proven of tobacco. This atrophy of the oral epithelium
oral cancer may be of severe degree at focal sites resulting
in ulcerations with exposure of the underlying
HISTOPATHOLOGY connective tissue. The atrophic epithelium first
becomes hyperkeratotic (clinically leukoplakic),
Connective Tissue and later intercellular edema and basal cell
The connective tissue changes are always hyperplasia develop, eventually followed by
associated with chronic inflammatory reaction epithelial atypia with moderate epithelial
beneath the basement membrane (juxta- hyperplasia. From then on carcinoma may
epithelial). The chronic inflammatory cell develop any time.
infiltrate consists of lymphocytes, plasma cells,
monocytes, and macrophages. Disruption of the TREATMENT MODALITIES
basal cell layer of the epithelium by chronic Conservative
inflammatory cells is seen. The chronic
inflammatory reaction is followed by 1. Stoppage of the habit
accumulation of collagen beneath the basement 2. Biopsy to confirm the diagnosis and to reveal
any dysplasia
membrane, which undergoes fibroelastic
3. Treatment of any periapical and periodontal
transformation or hyalinization.
disease which may have aggravated or
Connective tissue exhibits thick, dense
caused restricted mouth opening
bundles of collagen fibers. Because of fibrosis of
4. Nutritional therapy (vitamin B-complex and
connective tissue, the blood vessels become
iron supplements, antioxidants)
narrow. The narrowing of the blood vessels
5. Topical application of anesthetics and
appears first in the upper connective tissue and
corticosteroids
spreads gradually downwards. A relative
6. Physiotherapy by the means of microwave
reduction in vascularity leads to atrophy of the
diathermy using microtone 200 unit
overlying epithelium. The bundles of collagen producing microwaves to relieve trismus.
fibers may extend downwards and involve the One sitting of 20 minutes a day for 15 days.
underlying striated musculature, which may 7. Inj hyaluronidase 1500 IU 0.5 ml injected
later undergo degeneration. intralesionally twice a week for 10 weeks
(hyaluronidase breaks down hyaluronic
Epithelium acid, lowers the viscosity of the intercellular
The epithelial changes are usually secondary to cement substances and decreases collagen
the connective tissue changes especially due to formation).
connective tissue fibrosis resulting in narrowing 8. Inj dexamethasoe 1.5 ml with 0.5 ml
of blood vessels. Histopathologically, OSF is lignocaine hydrochloride injected
associated with marked atrophy of the oral intralesionally twice a week for 5 weeks
epithelium (epithelium is thin) with loss of rete- (corticosteroids act as immunosuppressive
agents and anti-inflammatory agents, mouth opening exercises and nocturnal props are
thereby preventing fibrosis by decreasing required for a further 4 weeks.
fibroblasts proliferation and deposition of
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17. Miller RL, Simms BW, Gould AR. Toluidine blue
Pathol Med 1999;28:59-63.
staining for detection of oral premalignant lesions
27. Van Wyk CW, Grobler-Rabie AF, Martell RW,
and carcinomas J Oral Pathol 1988;17:73-8.
Hammond MG. HLA-antigens in oral submucous
18. Murti PR, Bhonsle RB, Gupta PC, Daftary DK,
fibrosis. J Oral Pathol Med; 1994;23:23-7.
Pindborg JJ, Mehta FS. Etiology of oral 28. Van Wyk CW, Olivire A, De Miranda CM, ven
submucous fibrosis with special reference to the der Bijl P, Grobler-Rabie AF. Observations on the
role of areca nut chewing J Oral Pathol Med effect of areca nut extracts on oral fibroblast
1995;24:145-52. proliferation J Oral Pathol Med 1994;23:145-8.
19. Pindborg JJ. Oral Cancer and Precancer; John 29. Van Wyk CW, Seedat HA, Phillips VM. Collagen
Wright and Sons Ltd Bristol 1980. in submucous fibrosis: An electron-microscopic
20. Rajendran R. Oral submucous fibrosis; Etiology study J Oral Pathol Med 1990;19:182-7.
pathogenesis and future research. Bulletin of 30. Wall van der I, Axell T. Oral leukoplakia: A
World Health Organization 1994;72:985-96. proposal for uniform reporting. Oral Oncology
21. Reichart PA, Philipsen AP. Oral erythroplakia: A 2002;38:521-6.
review. Oral Oncology 2005;41:551-61. 31. Wall van der I, Schepman KP, Meij van der EH,
22. Scutt A, Meghji S, Canniff JP, Harvey W. Smeele LE. Oral Leukoplakia: A clinicopatho-
Stabilization of collagen by betel nut polyphenols logical review. Oral Oncology 1997;33:291-301.
Chapter
Oral Cancer
7
INTRODUCTION upon the type of tobacco habits prevalent among
them. Oral cancer commonly occurs in the 6th
The word cancer was coined by Hippocrates. In
decade of life.
Latin, cancer means “Cancrum” denoting Crab,
thus reflecting the true nature of cancer since it
adheres to any part that it seizes upon in an GENETICS OF CANCER
obstinate manner like the crab (Fig. 7.1). The term Chromosomes
oral cancer is used to describe any malignancy
Each cell has a control center called a nucleus.
that arises from the oral tissues. Squamous cell
The nucleus contains information, which tells the
carcinoma is the most common, representing
cell what to do and when to grow and divide.
90-95% of all oral malignancies. The term oral
This information is contained in the
cancer is therefore used to imply squamous cell
chromosomes. In the nucleus of each human
carcinoma.
somatic cell (with the exception of sperm and egg
It is one of the 10 most common cancers across
cells), there are 23 pairs of chromosomes, for a
the globe. Generally, oral cancers are more
total of 46 (22 pairs of autosomes and one pair of
common among men than in women depending
sex chromosomes). Therefore, human somatic
cells are termed as diploid cells. However, the
gametes are haploid and have a total of 23
chromosomes. Chromosomes are passed from
parents to their children. One chromosome from
each pair is inherited from the mother, and the
other comes from the father. One of the
chromosome pairs consists of sex chromosomes.
In normal males, the sex chromosomes are a
Y chromosome inherited from the father and an
X chromosome inherited from the mother. Two
X chromosomes are found in normal females, one
inherited from each parent. This is why children
resemble their parents, both physically and in
Fig. 7.1: Crab their tendency to develop certain diseases.
Oral Cancer 81
Chromosomes are made up of long strands of parent and therefore exist in all cells of the body,
DNA (deoxyribonucleic acid). Within each including sperm and egg cells.
chromosome, there are about 30,000 to 40,000 The mutation can be passed from generation
genes. Genes are segments of DNA that tell the to generation and are called germline mutations,
cell make a protein. The normal gene consists of e.g., sickle cell anemia. Hereditary mutations
three exons and two introns. For example, certain cause a small percentage of cancers. An acquired
proteins help the cell divide into two cells, while mutation occurs when DNA in a cell changes
others prevent the cell from dividing too often. during the person’s life. This can be caused by
A cell uses its genes selectively, that is, it will exposure to radiation, chemicals, and biological
activate or “turn on” the gene it needs at the right agents. Acquired mutations do not exist in all
moment. Some genes stay active all the time to cells of the body, including sperm and egg cells
produce proteins needed for basic cell functions. and therefore cannot be passed from generation
Genes, serve two roles in cancer: some contribute to generation.
to the development of cancer and others protect It is important to realize that mutations occur
individuals from cancer. at all the time in our cells and are repaired. If the
mutation cannot be repaired, the cell begins a
Mutations process called apoptosis that leads to its death.
If the mutation occurs in a gene that controls cell
Carcinogens transform normal cells by causing division, it may lead to cancer or cancer may
changes in the cell’s DNA. These changes are occur if the mutation happens in a gene that
called mutations, and the carcinogen is thus said causes apoptosis. Cancer may also develop in
to be mutagenic. A mutated gene may tell the people who inherit genes that make them prone
cell to make an abnormal protein, which no to cancer along with acquired mutations.
longer functions normally. The mutated gene Therefore, some people may be more likely to
may not have any effect, or it may lead to a develop cancer than others simply due to their
disease, e.g., cancer. Mutations can be either genes. Mutations that have been found are point
hereditary or acquired. Hereditary mutations are mutation, gene amplifications, gene deletions,
gene changes (mutations) that come from a and chromosomal translocations (Table 7.1).
Table 7.1: Genetic changes that convert protooncogenes into oncogenes

Type of change Description and examples
Point mutation Point mutations results due to the substitution of one nucleotide for another, resulting in a
change in the amino acid sequence. Point mutations of Ras protein (glycine is replaced
by valine) can convert Ras genes into Ras oncogenes.
Gene amplification An abnormal increase in the copies of proto-oncogenes due to overreplication, resulting in
an increased amount of gene product, thereby including cell profileration. ErbB genes have
been amplified in squamous cell carcinomas.
Gene deletion Deletions of part of the coding region (exons) of a proto-oncogene can convert them into
oncogenes. The myc oncogene can arise from its myc proto-oncogene by deletion.
Chromosomal translocation A piece of chromosome may be translocated to another chromosome and affect the
expression of genes at the breakpoint site. In Burkitt’s lymphoma, a region of chromosome
8 is translocated to either chromosome 2, 14, or 22. The breakpoint in chromosome 8
causes the over expression of the myc gene.
The two main classes of genes that are now It may be helpful to think a cell as a car. The
recognized to play a role in cancer are oncogenes speed of the car is controlled by the brake. A
and tumor suppressor genes. proto-oncogene normally functions in a way that
is similar to the brake. An oncogene could be
Oncogenes compared to a brake that has failed, which causes
Oncogenes are mutated forms of genes that cause the cell to divide out of control. In the somatic
normal cells to grow out of control and become cells of the body, the cell cycle (Fig. 7.3) is
cancer cells. Oncogenes are a result of mutations regulated by different proteins. Scientists have
of certain normal genes of the cell called proto- divided these proteins into four different classes:
oncogenes. Proto-oncogenes are the genes that
normally control how often a cell divides and to
the degree, it differentiates. When a proto-
oncogene mutates (changes) into oncogene, it
becomes permanently activated or “turned on”
and the cell divides quickly, which can lead to
cancer (Figs 7.2A and B).
Fig. 7.2A: Proto-oncogene to oncogene
Fig. 7.3: Cell cycle regulation
1. Growth factors: The growth factors bind to

the cell surface growth factor receptors and
stimulate them. The best known of these is
called sis gene, which encodes platelet-
derived growth factor.
2. Growth factor receptors: The growth factor
receptors are present on the cell membrane.
These are normally turned “on” or “off” by
growth factors. The best known of these is
Fig. 7.2B: Proto-oncogene to oncogene
called erbB gene, which encodes epidermal
Oral Cancer 83
growth factor receptor. When the growth action of activated RAS protein by favoring
factor receptors are turned “on,” they hydrolysis of GTP to GDP. In cancer, the
stimulate the cell to grow. In cancer, they are mutant RAS protein can bind to GAPs, but
in a permanent “on” position (Fig. 7.4). their GTPase activity fails to be increased.
3. Signal transducers: These proteins are the Thus the mutant RAS protein is trapped in
intermediate pathways between the growth its activated form, which leads to continuous
factor receptors and the cell nucleus where stimulation of cells without any external
the signal is received. Like growth factor trigger (Fig. 7.5).
receptors, these can be turned “on” or “off.” 4. Transcription factors: These final proteins
The best known of these is called ras gene, tell the cell to divide. They act on the DNA.
which encodes RAS protein. When a normal The best known of these is called myc gene,
cell is stimulated through a growth factor which encodes transcription factor. In cancer,
receptor, inactive (GDP-bound) RAS is they are in a permanent “on” position.
activated to a GTP-bound state. Activated The oncogenes encode similar proteins that
RAS recruits RAF-1 and stimulates the regulate the cell cycle. These include growth
(mitogen-activated protein) MAP-kinase factors, growth factor receptors, signal
pathway to transmit growth-promoting
transducers, transcription factors.
signals to the nucleus. However, an excited
signal-transmitting state of RAS protein
Tumor Suppressor Genes
returns to a quiescent state because intrinsic
guanosine triphosphatase (GTPase) Tumor suppressor genes are normal genes that
hydrolysis GTP (guanosine triphosphate) to activate genes that promote DNA repair, activate
GDP (guanosine diphosphate). A family of genes that arrest cell division, and activate genes
GTPase-activating proteins (GAPs) acts as that promote apoptosis. An important difference
molecular brakes that prevent uncontrolled between oncogenes and tumor suppressor genes
Fig. 7.4: Growth factors and cancer

gene is “turned off” and the cells continue

to grow, and can eventually become
cancerous.
3. Genes that promote apoptosis: If there is too
much damage to a cell’s DNA, which cannot
be fixed by DNA repair genes, the p53 tumor
suppressor gene destroys the cell by
apoptosis or programmed cell death. If the
p53 gene is “turned off,” cells with DNA
damage continue to grow, and can
eventually become cancerous.
ETIOLOGY
Although oral cancer has a multifactorial
etiology, tobacco use and alcohol consumption
are widely considered its major risk factors.
Fig. 7.5: Action of RAS protein According to WHO, about 90% of oral cancer in
South-east Asia is attributable to tobacco use.
is that oncogenes develop from the activation
Carcinogens
(turning “on”) of proto-oncogene, whereas
tumor suppressor genes cause cancer when they Cancers can be induced in normal tissue by
are turned “off.” Another major difference is that exposure to one of the three classes of
while the oncogenes develop from mutations carcinogenic agents: chemicals, radiation and
during the life of the individual (acquired oncogenic viruses. Of the three, it appears that
mutations), whereas tumor suppressor genes can long-term exposure to chemical carcinogens is
be inherited as well as acquired. The p53 tumor responsible for most of the neoplasms arising in
suppressor gene plays a central role in all three humans. It appears in particular that oral
processes described below. Abnormalities of p53 mucosal carcinomas are caused predominantly
tumor suppressor gene can lead to head and neck by chemical carcinogens, although there is
evidence implicating viral and physical stimuli
cancers.
in the genesis of some oral neoplasms.
Types of Tumor Suppressor Genes Chemical Carcinogens
1. DNA repair genes: Every time a cell divides, Chemical carcinogens can be grouped into two
it must duplicate its DNA. This process is categories. Some are direct-acting and require no
not perfect, and copying errors occur chemical transformation to induce
sometimes. The copying errors are repaired carcinogenicity (e.g., alkylating agents). How-
by p53 tumor suppressor gene. In cancer, the ever, the most are indirectacting carcinogens or
p53 tumor suppressor gene is “turned off.” procarcinogens, which require chemical
2. Genes that arrest cell division: The p53 transformation to induce carcinogeni-city (e.g.,
tumor suppressor gene arrests the cell betel nuts). Most indirect-acting chemical carcin-
division. In cancer, the p53 tumor suppressor ogens are activated chiefly by the cytochrome P-
Oral Cancer 85
450 dependent enzymes (monooxygenases) those cells to proliferate. This process is known
located in the endoplasmic reticulum or in the as clonal expansion. With progression the tumor
nucleus. mass becomes enriched with tumor cell variants
(heterogeneity) i.e., they are nonantigenic,
Chemical Carcinogenesis invasive, metastatic, and require fewer growth
Chemical carcinogenesis is a multi-step process factors and are likely to be more aggressive.
involving two stages: initiation, and promotion.
Experimental results has led to the assumption Radiation
that oral cavity is more resistant to the effects of
The portion of the electromagnetic spectrum is
carcinogens than skin. This has been attributed
subdivided into ionizing radiation (X-rays,
to protective effects of saliva and the lack of
gamma rays, and cosmic rays) and non-ionizing
structures in the oral mucosa such as hair
radiation (ultraviolet rays). Ionizing radiations
follicles, and sebaceous glands, which might
are of high-energy, and are useful for medical
provide “portals of entry” in skin.
diagnosis because they penetrate the living
Initiation tissues for substantial distances. In the process,
these high-energy rays collide with molecules
All direct-acting and indirect-acting chemical (directly or indirectly) and cause the release of
carcinogens are highly reactive electrophiles (i.e., electrons, leaving positively charged free
have electron deficient atoms) that react with radicals. The free radicals in turn, collide with
electron rich atoms in DNA producing a other molecules and cause the release of
chemical-DNA adducts. If the chemical-DNA additional electrons and the cycle continues. The
adducts are not repaired by DNA repair genes, ionizing effects of X-rays are related to its
cell division takes place and the damaged DNA mutagenic effects. X-rays cause chromosomal
is transferred to the next generation of cells, each mutations or chromosomal aberrations e.g.,
of which carries the mutation (damaged chromosomal translocation, breakage of one or
DNA).Although any gene may be the target of both DNA strands (deletion), loss of a base (point
chemical carcinogens, ras gene and p53 gene
mutation), breakage of hydrogen bonds between
mutations are particularly common in several
DNA strands, and cross-linking of DNA strands
chemically induced cancers. Initiation is the first
with other DNA strands.
stage in carcinogenesis induced by chemical
The major effect of UV rays (non-ionizing
carcinogens.
radiation) is on the pyrimidines, where dimers
are formed, particularly between two thymine
Promotion
residues (Fig. 7.6). It is believed that thymine
Promotion is the next stage in chemical dimers distort the DNA conformation and inhibit
carcinogenesis. Promotion differs from initiation normal replication. The distortion of DNA strand
in that there is no DNA damage and that the caused by the thymine dimer is recognized and
promoting agents increase the ability of an the enzyme DNA photolyase binds to the
initiated cell to proliferate. The genetically thymine dimers and cleaves the phosphodiester
damaged cell proliferates; giving rise to a clone bonds. DNA polymerase I fills the gap by
of cells, each of which carries the same damaged inserting deoxyribonucleotides complementary
DNA. As the clones of cells divide rapidly to those on the intact strand. The joining enzyme
additional mutations occur, this further enhances DNA ligase seals the gap that remains at the end
of the last deoxyribonucleotide inserted, closing

the gap (Fig. 7.7). With extensive exposure to UV
light, this repair system is overwhelmed and skin
cancer develops.
Oncogenic Viruses
Both RNA containing and DNA containing
viruses have been identified as carcinogenic, both
in vitro and in vivo. There are two common
features in their mechanisms of neoplastic Fig. 7.6: Formation of a thymine dimer
induction. Firstly, these viruses incorporate their
genetic material (DNA or RNA) into the host
DNA, and secondly their genetic material must
be expressed in the form of proteins to maintain
the host cell in the transformed state.
Four DNA viruses have clearly demonstrated
their oncogenic potentials in animals and
humans: human papilloma virus (HPV), Epstein-
Barr virus (EBV), human herpes virus-8 (HHV-
8), and hepatitis B virus (HBV).
Two different types of oncogenic RNA or
retroviruses have been recognized based on their
ability to induce neoplasms; they include slow
transforming virus and acute transforming virus.
Most cancer-causing viruses are not very potent
at inducing cancer. An organism must be infected
for a long period of time before a tumor actually
develops.
A typical retrovirus requires three protein-
coding genes for the virus life cycle: gag, pol, and,
env (Chapter 11). In addition to the life-cycle
genes, some retroviruses also carry an oncogene
that gives them the ability to transform normal
cells into cancerous cells they infect; these are the
oncogenic retroviruses. Viral oncogenes (v-oncs)
are responsible for many different cancers. The
v-onc genes are named for the tumor that the
virus causes, with the prefix “v” to indicate that
the gene is of viral origin. Thus, the v-onc gene
of RSV or Rous sarcoma virus is v-src (sarcoma).
Further, most viruses are inefficient or unable
to transform normal cells into cancerous cells
grown in the laboratory, as they do not contain Fig. 7.7: DNA repair
Oral Cancer 87
v-onc. These are called slow transforming viruses

e.g., mouse mammary tumor virus. The slow
transforming viruses infect the cells but are
unable to produce progeny viruses because of
the absence of one or more genes needed for virus
reproduction. These defective slow transforming
viruses can produce progeny viral particles, if
the cell containing them is also infected with a
normal virus (helper virus) that can supply the
missing genes. This mechanism of
transformation is called insertional mutagenesis.
By comparison, some viruses rapidly induce
tumors in animals and efficiently transform cells
in culture, as they contain v-onc. These are called
acute transforming viruses e.g., Rous sarcoma
virus or Abelson leukemia virus.
The human T cell leukemia virus (HTLV-1) is
associated with a form of T-cell leukemia/
lymphoma that is endemic in certain parts of
Japan and the Caribbean islands. However, the
HTLV-1 does not contain v-onc. The genome of
HTLV-1 contains, in addition to the usual
retroviral genes, a unique region called pX. This
region encodes several proteins, including one
called TAX. Upon infecting may T cells the TAX
protein causes polyclonal proliferation of T cells
and suppresses the function of p53 tumor
suppression gene. Ultimately, a monoclonal
T-cell leukemia/lymphoma results when one
proliferating T cell suffers additional mutations.
METASTASIS
The mechanism of metastasis is best understood
by studying the normal epithelial–connective
tissue interface (Chapter 9). The basal lamina is
a formidable proteinaceous barrier to tumor cell
migration. Oral keratinocyte proliferation is
confined initially to the epithelial compartment.
Eventually, the proliferating keratinocytes ‘break
through’ the basal lamina and expand through
the underlying connective tissue to invade lymph
and blood vessels (Fig. 7.8), resulting in distant
spread (metastasis). For the purpose of Fig. 7.8: Metastatic cascade
discussion, the metastatic cascade can be called membrane type MMPs (MTMMPs) or
subdivided into two phases: invasion of mast cell chymase. The MMPs are a family of zinc
extracellular matrix and vascular dissemination containing endo-proteinases and the MMP
and homing of tumor cells. (matrix metalloproteinase) gene family encodes
more than 20 different MMPs. MMPs are
Invasion of Extracellular Matrix grouped by their substrate specificity:
1. Looseing of intercellular junctions i. The collagenases (MMP-1 and MMP-8)
cleave collagen I, II and III preferentially
The first step in metastasis is loosening of
ii. The stromelysins (MMP-3, MMP-10, and
intercellular junctions. E-cadherins act as
MMP-11) cleave laminin
intercellular glues, and their cytoplasmic
portions bind to β-catenin. E-cadherin molecules iii. The gelatinases (MMP-2 and MMP-9) cleave
keep the cells together, and transmit antigrowth type IV collagen
signals via β-catenin. E-cadherin function is lost Many other connective tissue proteins are
in oral squamous cell carcinoma, either by potential substrates of MMPs including elastin,
mutation of E-cadherin genes or by activation of proteoglycans (glycosaminoglycans e.g.,
β-catenin gene, which can activate transcription dermatan sulfate and heparan sulfate),
of growth factor genes by free β-catenin protein. hyaluronan, fibronectin, and integrins. MMP-1,
MMP-2, MMP-3, and MMP-9, are highly
2. Attachment expressed in oral cancers and the surrounding
The second step in metastasis is attachment of connective tissue (especially at the invading front
cancerous cells to the large cruciate glycoprotein, of the tumor) and high levels of MMPs
called laminin present in the lamina lucida and expression may indicate a poor prognosis.
fibronectin present in the lamina densa. Normal
4. Migration
epithelial cells have receptors at their basal
surface for laminin. In contrast, cancerous cells The fourth and final step in metastasis is
have more laminin receptors and these are migration of cancerous cells through the
distributed all around the cell membrane. degraded basal lamina and connective tissue.
Migration seems to be mediated by tumor cell-
3. Degradation derived protein called autocrine motility factor.
The third step in metastasis is local degradation Autocrine motility factor is a cytokine. Cytokines
of the basal lamina and connective tissue. are low molecular weight proteins, which induce
Cancerous cells penetrate the basal lamina barrier their effects in three ways:
and spread through the underlying connective i. They act on the same cell that produces them
tissue with the help of matrix protein degrading (autocrine effect)
enzymes called “matrix metalloproteinases’ ii. They effect other cells in their vicinity
(MMPs). The principal function of MMPs is the (paracrine effect)
proteolytic degradation of connective tissue iii. They effect cells systemically (endocrine
proteins. MMPs are produced by the cancerous effect)
cells themselves or the tumor may stimulate other
cells such as fibroblasts in the connective tissue 5. Vascular Dissemination and Homing of
to produce MMPs. Cancerous Cells
MMPs are secreted in an inactive form and Once in the circulation the cancerous cells are
are activated subsequently by other active MMPs prone to destruction by the host immune cells
Oral Cancer 89
(CD8+ T cells lymphocytes, NK cells, and

macrophages). However, most cancerous cells
evade the immune system by several escape
mechanisms, even in individuals who are
immunocompetent. Most cancerous cells
circulate as single cells. However, some
cancerous cells form embolus by aggregating and
adhering to platelets. Extravasation of cancerous
cells involves adhesion to the vascular
endothelium, followed by migration through the
basement membrane by mechanism similar to
that involved in invasion. The site of
extravasation and homing of the cancerous cells Fig. 7.9A: Exophytic squamous cell carcinoma
is dependent on the location of the primary

tumor and its vascular and lymphatic drainage.
CLINICAL APPEARANCE
Oral cancer has a varied clinical appearance.
Most of the lesions can be described as exophytic,
ulcerative and verrucous carcinoma.
Exophytic Cancer
The term exophytic is used to describe an
outwardly growing tumor. The exophytic lesion
(Figs 7.9 A and B) is fixed to the underlying
Fig. 7.9B: Exophytic cancer with palatal perforation in
tissues due to its spread. Exophytic cancers reverse chutta smoker
metastasize less frequently than the ulcerative
type.
Ulcerative
The ulcerative lesion (Fig. 7.10) burrows deep
into the mucosa with a breach in the surface.
Rolled (everted) margins and induration on
palpation, are indicative of a hard tumor mass
within the tissue. Ulcerative lesions metastasize
more frequently than exophytic cancers.
Verrucous
Verrucous carcinoma (Fig. 7.11) also known as
Ackerman’s tumor is a distinct clinico- Fig. 7.10: Ulcerative squamous cell carcinoma
lesion to therapy before obtaining a definitive

diagnosis. A definitive diagnosis requires a
biopsy. Screening for oral cancer should include
a thorough history and physical examination.
History
The first step in screening of oral cancer begins
with obtaining demographic data, history of
present illness, dental history, medical history,
and personal history including tobacco and
alcohol abuse. Patients over 40 years of age
Fig. 7.11: Verrucous squamous cell carcinoma should be considered at a higher risk for oral
cancer.
pathological variant of squamous cell carcinoma.
The term “verrucous” is used because of its fine,
Physical Examination
finger like surface projections. Verrucous
carcinoma represents up to 20% of all squamous The clinician should inspect and palpate the
cell carcinomas. The characteristic behavior of head, neck, oral, and pharyngeal regions.
this carcinoma is its slow growth and rarity to Forceful protraction of the tongue with gauze is
metastasize to the regional lymph nodes. necessary to visualize the posterior and lateral
Therefore, it has an excellent prognosis. aspect of the tongue. In addition, this procedure
involves digital palpation of head and neck
DIAGNOSIS lymph nodes (Fig. 7.12). A normal cervical lymph
node is not palpable on routine examination. In
Oral cancer, often presents as a clinical diagnostic general, tender, soft, enlarged, and freely
challenge to the clinician, particularly in its early movable nodes suggest acute infection. Non-
stages of development. The most effective way tender, hard, enlarged, and fixed nodes suggest
to control oral cancer is early diagnosis and chronic infection or malignancy (Fig. 7.13).
timely and appropriate treatment. The clinician’s The lymph nodes are fixed and non-mobile
challenge is to differentiate cancerous lesions due to perforation of the nodal capsule and
from a number of other red, white, or ulcerated invasion into the surrounding tissue. The
lesions that also occur in the oral cavity. Most lymphatics draining the various anatomical sites
oral lesions are benign, but may have an in head and neck are located in the specific
appearance that may be confused with a anatomical locations. To provide health care
malignant lesion. Conversely, some malignant professional with common terminology, the
lesions seen in the early stages may be mistaken lymph nodes of head and neck are described by
for a benign lesion. levels (Fig. 7.14).
Any oral lesion that does not regress
spontaneously or respond to the usual
DIAGNOSTIC AIDS
therapeutic measures should be considered
potentially malignant until proven histopatholo- Useful adjuncts include biopsy (Chapter 2), vital
gically. A period of 2-3 weeks is considered an staining, exfoliative cytology, fine needle
appropriate period to evaluate the response of a aspiration biopsy, and diagnostic imaging.
Oral Cancer 91
Fig. 7.12: Lymph nodes of head and neck (does not include all nodes)
Vital Staining
In 1963, Richart described an in vivo method of
staining for dysplasia and carcinoma in situ of
the cervix. This method has been used for many
years to help identify dysplastic or malignant
mucous membrane in oral cavity. The classic
reported technique involves, drying of the
mucosa with gauze and topical application of 1%
aqueous solution of tolonium chloride (Toluidine
blue) to the suspected lesion for 1 to 2 minutes.
A final 1 minute rinse with 1% acetic acid solution
for decolorization completes the sequence. If the
toluidine blue rinse is, retained malignancy or
dysplasia is suspected (Fig.7.15). Vital staining
is a useful adjunct in identification of the biopsy
site. The fact that false negative results occur in
a significant number of cases makes the method
Fig. 7.13: Non-tender, hard, enlarged and
fixed nodes in oral cancer unreliable as a diagnostic aid.
Fig. 7.14: Levels of cervical lymph nodes
the enlarged lymph node is prepared with iodine

and the needle is inserted into the mass. The
needle is moved up and down through the mass
while maintaining suction at the same time.
Suction is released and the needle is withdrawn.
One drop of fluid is expressed onto the
microscope slide and smeared using another
slide, and placed in the alcohol fixative. If there
is sufficient material, two or three slides can be
prepared. It should be remembered that a
negative result does not mean there is no cancer,
Fig. 7.15: Toluidine blue staining but a positive result is diagnostic.
Fine Needle Aspiration Biopsy Diagnostic Imaging

Fine needle aspiration biopsy is a quick, Diagnostic imaging consists of intraoral
inexpensive, accurate, and easy to perform radiographs, extraoral radiographs (Figs 7.16A
technique that can help in diagnosis of metastasis and B), magnetic resonance imaging,
in enlarged cervical lymph nodes in the patient computed tomography or optical coherence
with oral cancer. A 10 ml syringe, 22-gauge imaging. Computed tomography is superior in
needle, microscope slides, and 95% alcohol for detecting early bone invasion and lymph node
fixation are all that is required. The skin overlying metastasis, but magnetic resonance imaging is
Oral Cancer 93
Fig. 7.16A: Destruction of mandible due to oral cancer
Fig. 7.16B: Pathological fracture of mandibe due to oral cancer
preferred for assessing the extent of soft tissue carcinoma is the invasion of cancerous cells into
involvement and for providing a three- the underlying connective tissue, eroding the
dimensional display of the tumor. Magnetic lymphatic and blood vessel walls and being
resonance imaging is also the preferred technique transported to distant sites.
for imaging carcinoma of the nasopharynx or The potential to metastasize is related to the
lesions involving paranasal sinuses or the skull histopathological variation of oral squamous cell
base. carcinoma. The histopathological variation is
related to the degree of differentiation of the
HISTOPATHOLOGICAL FEATURES cancerous cells and their resemblance to the
Squamous cell carcinoma is diagnosed by normal stratified squamous epithelium. The
histopathological examination of the cancerous histopathological features of oral squamous cell
tissue. A common feature of oral squamous cell carcinoma are graded as, well-differentiated,
moderately differentiated, and poorly logically verrucous carcinoma is characterized by

differentiated. Most oral squamous cell large, keratinized clefts with bulbous rete pegs
carcinomas are moderately or well-differentiated. that project uniformly into the connective tissue.
The keratinized clefts contain parakeratin plugs.
Well-differentiated
Tumors that exhibit individual cell keratiniza- TREATMENT
tion, keratin pearls and bear resemblance to
The management of oral squamous cell
stratified squamous epithelium are considered
carcinoma depends on the tumor’s stage. At
as well-differentiated. The epithelial cells are
present, oral squamous cell carcinoma is
highly dysplastic. There is a break in the
primarily managed with surgery and radiation
basement membrane, and the dysplastic
therapy. Conventional staging uses the TNM
cancerous cells invade the underlying connective
system, in which T stands for tumor, N for nodes,
tissue, which has dense lymphocyte infiltration.
and M for metastasis. This system of staging has
The dysplastic cancerous cells have an
been suggested and revised by the International
architectural pattern and exhibit cohesiveness.
Union against Cancer (UICC, 1987). It has three
Moderately Differentiated main parameters: T, N, and M. T classification
(Table 7.2) is dependent on the size of the primary
Tumors that produce little or no keratin but in
tumor. N classification (Table 7.3) depends on
which the epithelium still is recognizable as
both the size and number of involved nodes. M
stratified squamous are considered as
classification (Table 7.4) is the simplest because
moderately differentiated. The epithelial cells are
tumors are classified as either M0 (i.e., show no
highly dysplastic. There is a break in the
evidence of metastasis) or M1 (i.e., show evidence
basement membrane, and the dysplastic
of distant metastasis). This classification is then
cancerous cells invade the underlying connective
used to divide the tumor into stages (Table 7.5)
tissue, which has moderate lymphocyte
which has prognostic significance.
infiltration. The dysplastic cancerous cells have
In stages I and II either surgery or radiation
an architectural pattern and exhibit cohesiveness.
therapy gives similar prognosis. Therefore,
Poorly Differentiated treatment depends on the patients choice, the
surgeon’s advice, or other factors, such as age,
Tumors that produce less keratin, and bear no
and general medical health. In general, radiation
resemblance to stratified squamous epithelium
therapy is usually recommended. If radiation
are considered as poorly differentiated. The
therapy fails patients can be saved by surgery.
epithelial cells are highly dysplastic. There is a
In stages III and IV, the best cure rates are
break in the basement membrane, and the
obtained with a combination of surgery and
dysplastic cancerous cells invade the underlying
radiation therapy. Most surgeons’s prefer to
connective tissue, which has minimal
administer radiation within 6 weeks after
lymphocyte infiltration. The dysplastic cancerous
surgery. Stage IV disease has the worst prognosis
cells have no architectural pattern and exhibit
and patients with distant metastasis die.
lack of cohesiveness.
Variants Complications of Radiotherapy

Rarely oral squamous cell carcinoma appears as Ionizing radiation delivered in doses that kill
a proliferation of spindle cells. This type of tumor rapidly dividing cancer cells induces
is known as spindle cell carcinoma. Histopatho- unavoidable changes in the surrounding normal
Oral Cancer 95
Table 7.2: TNM system: T classification Table 7.5: TNM system: Clinical staging
T Primary tumor Stage I T1 N0 M0
TX Primary tumor cannot be assessed Stage II T2 N0 M0
T0 No evidence of primary tumor Stage III T3 N0 M0
Tis Carcinoma in situ T1 N1 M0
T1 Tumor 2 cm or less T2 N1 M0
T3 N1 M0
T2 Tumor greater than 2 cm but not greater than 4 cm
Stage IV T4 N0, N1 M0
T3 Tumor greater than 4 cm
Any T N2, N3 M0
T4 Tumor invades adjacent structures (e.g., through
Any T Any N M1
cortical bone, into deep extrinsic muscle of tongue,
maxillary sinus, skin)
is short. During this period, oral care should be
Table 7.3: TNM system: N classification implemented to reduce complications during
N Regional lymph nodes and after radiotherapy.
NX Regional nodes cannot be assessed
Dental Treatment before Radiotherapy
N0 No regional lymph node metastasis
Oral care includes a radiographic survey of both
N1 Metastasis in a single ipsilateral lymph node, 3 cm
dentate and edentate patient. The resultant
or less
treatment plan should include the appropriate
N2
use of 0.2% chlorhexidine mouthwash, and
N2a Metastasis in a single ipsilateral lymph node, scaling. This will treat any periodontal diseases.
greater than 3 cm but not greater than 6 cm Decayed teeth should be restored preferably with
N2b Metastasis in multiple ipsilateral lymph nodes, none a permanent restorative material. Sharp teeth and
greater than 6 cm restorations should be reshaped since they can
N2c Metastasis in bilateral or contralateral lymph nodes, contribute to soft tissue damage and ulceration.
none greater than 6 cm Dentures should be examined and if ill-fitting
N3 Metastasis in a lymph node greater than 6 cm should be modified. Any necessary dental
extractions should be completed at least 10 days
Table 7.4: TNM system: M classification prior to commencement of radiotherapy. It
should be remembered that asymptomatic
MX Presence of distant metastasis cannot be
periapical lesions are unlikely to be aggravated
assessed
by radiotherapy.
M0 No distant metastasis
M1 Distant metastasis
SEQUELAE OF RADIOTHERAPY
Mucositis
tissues. The oral mucosa, the salivary glands, and
blood vessels can be damaged because of The acute oral mucosal reaction (mucositis) is
radiotherapy. As a result, patients experience secondary to radiation-induced death of the basal
unwanted oral effects during and after cells in the oral mucosa. Mucositis commences
radiotherapy. The period between diagnosis of within 12 to 15 days after radiotherapy starts. It
cancer and the commencement of radiotherapy is characterized by large areas of desquamation
and ulcerations. The patient needs to be complaint in patients receiving radiotherapy. A

constantly reassured that this condition is resultant weight loss tends to produce weakness,
temporary. inactivity, and susceptibility to infection.
Management of mucositis includes Therefore, close attention is given to food intake
application of topical anesthetics (2% lignocaine), and weight maintenance during and after
0.2% chlorhexidine mouthwash gargles, frequent therapy.
sipping of cold water, and holding of ice cubes
in the mouth. A short course of systemic Dental Caries
prednisolone (40 to 80 mg for not more than 1 Patients who have not shown any caries activity
week) may be helpful in reducing inflammation. for years may develop caries during
radiotherapy. The cervical areas are most
Loss of Taste
commonly affected. This condition appears due
Taste buds, which occur primarily in the to the lack of saliva as well as change’s in the
circumvallate and fungiform papillae, are very saliva’s chemical composition.
sensitive to radiation. Because of their location The 0.2% chlorhexidine mouthwash gargles
in the tongue, they are included in the beam of and daily applications of topical fluoride are
radiation for most oral cancers. Therefore, essential to prevent or at least minimize radiation
patients will develop a partial (hypoguesia) or caries. Food and beverages containing sucrose
complete (aguesia) loss of taste sensation during should be avoided. Restorations of the carious
radiotherapy. The cells of the taste buds usually teeth should take place immediately.
regenerate within 4 months after therapy.
Oral Candidosis
Xerostomia
Oral candidosis is commonly seen in patients
Exposure of the major salivary glands to ionizing who have been receiving radiotherapy. This
radiation induces fibrosis, fatty degeneration, condition appears due to the lack of saliva as well
acinar atrophy, and cellular necrosis within the as change’s in the saliva’s chemical composition.
glands. The serous acini appear to be more Management is accomplished with topical and
sensitive than the mucous acini. The saliva is systemic antifungal drugs.
thick, sticky, and bothersome. The duration of
depressed salivary function varies from patient Trismus
to patient. However, the depressed salivary
function may take upto 12 months. Ionizing radiation causes obliterative endarteritis
Management of xerostomia includes frequent resulting in tissue ischemia and fibrosis.
sipping of cold water, holding of ice cubes in the Obliterative endarteritis can contribute to the
mouth, chewing sugar-free gums, and development of trismus if the masticatory
lubrication with saliva substitutes. It is often muscles are within the beam of radiation.
difficult to sleep at night when the mouth is dry, Management of trismus can be very difficult. Jaw
butter wiped on lips and tongue prior to sleeping exercises using tongue blades may be helpful.
can be helpful.
Osteoradionecrosis
Nutrition Osteoradionecrosis or post-radiation osteoradi-
Because of mucositis, loss of taste, and onecrosis (PRON) is a painful and debilitating
xerostomia, the desire not to eat is a common serious complication of radiotherapy. Radiation
Oral Cancer 97
of the jaws in excess of 50 Gy kills bone cells and oxygen through a face mask in a large chamber
causes a progressive obliterative arteritis at 2 to 2.5 absolute atmospheres pressure for 1.5
(endarteritis, periarteritis, hyalinization, fibrosis, to 2 hours sessions or “dives” per day. Upto 80
and thrombosis of vessels), resulting in aseptic sessions have been recommended for severe
necrosis of the bone within the beam of radiation. cases but chambers are often small, and
Effective response to infection is reduced to a claustrophobic. HBO therapy causes an increase
great extent. It should be remembered that in arterial and venous oxygen tension; the
microorganisms are merely contaminants in additional oxygen is carried into the plasma.
osteoradionecrosis. Oxygen under increased tension enhances
Osteoradionecrosis is a radiation-induced healing by a direct bacteriostatic effect on
hypoxia, hypocellularity, and hypovascularity of microorganisms that renders them susceptible to
the bone forming cells. Pain and exposed bone lower antibiotic concentrations and phago-
(gray to yellow color) are the chief clinical cytosis. In addition, neoangiogenesis, fibroblastic
features of osteoradionecrosis of the jaws. Other proliferation, and collagen synthesis occur. There
clinical features of osteoradionecrosis include have been promising results recently with
trismus, halitosis, and pyrexia with extraoral and ultrasound at frequencies of 3 MHz pulsed 1 in
intraoral sinuses. Radiographic features include 4 at an intensity of 1 w/cm sq. applied to the
pathological fracture and formation of sequestra mandible.
or involucra.
The mandible is affected more commonly than CANCER CACHEXIA SYNDROME
the maxilla because most oral tumors are The term cachexia is derived from the Greek
perimandibular. Also, the absence of dense word kakos meaning “bad” and hexis meaning
cortical plates and the presence of extensive “condition.” Cancer cachexia syndrome is
vascular network in the maxilla decreases its characterized by anorexia (lack of desire to
probability of radiation necrosis compared with consume food), weight loss, marked muscle
the mandible. The risk is increased in dentate weakness, anemia of nonspecific type, impaired
patients if the teeth within the beam of radiation immune function due to increase nutritional
are removed after radiotherapy. Other risk demands of the tumor, increased energy
factors include mucosal ulcers, lacerations, expenditure of the cancer patient, and improper
scaling, fractures, periodontal disease, and use of nutrients by the cancer host. There is no
careless root canal therapy. satisfactory treatment for cancer cachexia
Extractions following radiotherapy should be syndrome other than removal of the underlying
done with minimal trauma along with soft tissue cause, i.e., the tumor.
closure. The use of 0.2% chlorhexidine mouth-
wash prior to extraction can reduce bacterial flora FUNCTIONAL REHABILITATION
and improve healing. In case of multiple
extractions, hyperbaric oxygen therapy is The cosmetic, functional, and psychosocial effects
recommended before and after extraction. of oral cancer treatment may combine to produce
Administration of antibiotics together with devastating effects on patients, especially if the
excision of necrosed bone and hyperbaric oxygen tumor is extensive or if the treatment is
(HBO) therapy may be helpful. Hyperbaric aggressive. Various functions are affected, which
oxygen therapy consists of breathing 100% include speech, mastication, and deglutition.
Functional rehabilitation is directly related to the 3. Mehta FS, Hammer JE, III. Tobacco-Related Oral
location and extent of the cancer and the type of Mucosal Lesions and Conditions in India; Basic
Dental Research Unit; TIFR; Bombay 1993.
surgery and radiation therapy used. Successful
4. Ogden GR, Wight AJ. Etiology of oral cancer:
functional rehabilitation and quality of life go Alcohol. Br. J Oral and Maxillofac Surg
hand in hand. 1998;36:247-51.
Functional rehabilitation is a multidisciplinary 5. Oral Cancer Foundation; CDC Oral Cancer
approach. Maxillofacial prosthetic rehabilitation Background Papers. Available: http://
is the basis to restore the patients oral functions www.oralcancerfoundation.org/cdc/index.htm.
and cosmetics following surgery. Other health 6. Ord RA, Blanchaert RH (Eds). Oral Cancer-The
Dentist’s Role in Diagnosis, Management,
care professionals including psychologist,
Rehabilitation, and Prevention; Quintessence
occupational therapist, physiotherapist, speech Publishing Co, Inc.; London 1999.
therapist, and dental hygienist are also members 7. Pindborg JJ. Oral Cancer and Precancer; John
of functional rehabilitation team. Wright & Sons Ltd; Bristol 1980.
The patient with a total maxillectomy is the 8. Puccio M, Nathanson L. The cancer cachexia
most difficult to treat prosthetically as well as Syndrome. Seminars in Oncology 1997;24:277-87.
emotionally. The fabricated prosthesis is usually 9. Scully C. Oncogenes, tumor suppressors and
less satisfactory to the patient. The patient with viruses in oral squamous carcinoma. J Oral Pathol
Med 1993;22:337-47.
a partial maxillectomy is much easier to treat.
10. Shaw MJ, Kumar NDK, Duggal M, Fiske J, Lewis
Generally, maxillofacial prosthodontists restore DA, Kinsella T, Nisbet T. Oral management of
maxillary resections with obturator prostheses. patients following oncology treatment: Literature
Patients with lesions involving the soft palate, review. Br J Oral Maxillofac Surg 2000;38:519-24.
which requires surgical excision, need an 11. Silverman S. Oral cancer: complications of
obturator with soft palate extension in order to therapy. Oral Surg Oral Med Oral Pathol Oral
restore speech. Radiol Endod; 1999;88:122-6.
12. Snustad, Simmons, Jenkins. Principles of
Genetics; John Wiley and Sons, Inc USA 1997.
BIBLIOGRAPHY 13. Topazian GR, Goldberg HM, Hupp RJ. Oral and
1. Boyd NM, Reade PC. Mechanisms of Maxillofacial Infections; Fourth edn.
carcinogenesis with particular reference to the W.B.Saunders Company; Pennsylvania 2002.
oral mucosa. J Oral Pathol 1988;17:193-201. 14. Vinay Kumar, Cotran RS, Robbins SL. Robbins
2. Klug WS, Cummings MR. Essentials of Genetics; Basic Pathology; Seventh edition; Saunders;
Macmillan Publishing Company; New York 1993. Philadelphia 2003.
Chapter
Oral Candidosis
8
HISTORY been isolated in high concentration from tissue
bearing surfaces of removable appliances. The
Hippocrates described oral candidosis in his
yeast candida can be inoculated in the mouth of
treatise (piece of writing) Epidemics, which was
newborn during birth, breast feeding, pacifiers
published in the 4 th century B.C. The first
and nurse’s hands. Audrey in 1887 described the
research on oral candidosis was carried out in
morphology of Candida. Morphologically Candida
the year 1786 in France. Berkhout in 1923
albicans exists in three forms Yeast form (blasto-
proposed the term candida that in Latin means spores), Pseudohypha and Chlamydospore (Fig.
toga candida referring to white robe worn by 8.1). It multiplies by division of blastospores.
Roman senates. Albicans also comes from Latin
word albicare, which means, “to whiten.” Rippon
has suggested that candidosis is European in
origin whereas candidiasis is basically American
in origin. However, according to Odds either
term is acceptable but candidosis is more
preferred term.
Microbiology
It is one of the most common fungal infections
of man. At least 90 genera and 90 species have
been isolated from the human beings few of them
are Candida tropicalis, Candida pseudotropicalis,
Candida albicans, and Candida glabrata. Candida Fig. 8.1: Morphology of Candida albicans
albicans is a normal commensal of the oral cavity
Predisposing Factors
and lives harmoniously with the other microbial
flora but when the immunity of the host is The various factors that predispose to an
suppressed or there are any predisposing factors individual oral candidosis are as follows:
it proliferates and penetrates the tissue to cause Palatal appliances: Local trauma from ill-fitting
candidosis. dentures and poor denture hygiene are
Candida albicans is most commonly found on important predisposing factors in the etiology of
the tongue, palate, and buccal mucosa. It has also oral candidosis.
Heavy smoking: In heavy smokers, the metabolic pathways thus predisposing the oral
phagocytosis and the bactericidal activity of mucosa to candidosis. For an organism like
PNML are impaired. Candida albicans, the most important thing is to
Xerostomia: Sjögren syndrome, medications adhere to epithelium or the denture. Recent
(e.g., anti-depressants), radiation therapy, studies have shown that this adherence is
surgical removal of salivary glands cause enhanced in the presence of carbohydrates like
xerostomia as a result of which the defense glucose and sucrose.
mechanism of saliva and the levels of salivary Uncontrolled diabetes mellitus: In diabetes
IgA is diminished or absent. mellitus there is defective PMNL function,
Steroid inhalers: Long-term use of steroid increased glucose in saliva and polyuria that
inhalers can induce oral candidosis because leads to xerostomia. All these are ideal
corticosteroids suppress the immunity. Hence, predisposing factors.
it is advisable to gargle after the use of steroid Acquired immune deficiency syndrome: The main
inhaler. cause of oral candidosis in AIDS is because of
Pregnancy: During pregnancy, there is decreased CD4 cell count, side effects such as
gestational diabetes mellitus, which may xerostomia due to didanosine (anti-retroviral
predispose the oral cavity to candidosis. Causes drug), and other antibiotics taken to treat or
of diabetes mellitus in pregnancy are as follows: prevent HIV-related conditions.
1. Increased absorption of glucose from Leukemia: Neutropenia and cancer chemo-
alimentary tract therapy predisposes to oral candidosis.
2. Inability of insulin to convert glucose into
glycogen Defense Mechanisms
3. Impaired tubular reabsorption of glucose The four important defense mechanisms that
which leads to glycosuria play a role against Candida albicans are:
The other predisposing factor during Secretory IgA: Minor salivary glands secrete
pregnancy is iron deficiency anemia. more IgA than major. Mechanism of action of
Broad spectrum antibiotic therapy: As the secretory IgA is that it prevents the adhesion of
normal flora are suppressed and destroyed Candida albicans to oral mucosa.
during treatment with broad spectrum Saliva: Major salivary glands secrete more saliva
antibiotics, the colonization of oral cavity with than minor salivary glands. Mechanism of action
Candida may be significantly increased. of saliva is that it dislodges microorganisms from
Nutritional factors: Deficiency of iron, folic acid, the surface of the mucosa and has the following
vitamin B12 and carbohydrate-rich diet can factors like lysozyme, lactoperoxidase, histatins,
predispose an individual to oral candidosis. The lactoferrin, and calprotectin, which inhibits the
various possible mechanisms by which iron growth of various Candida species in vitro.
deficiency can predispose to oral candidosis are Lactoferrin a chelating agent competes with the
as follows: Candida albicans and other microorganisms of the
1. Epithelial abnormalities because of iron oral cavity for free iron radicals that are
dependent enzyme systems apparently essential for bacterial and fungal
2. Depression of cellular immunity multiplication.
3. Inadequate antibody response PMNL and macrophages: PMNL and macro-
4. Deficient phagocytosis phages phagocytose and kill candida even in the
Vitamin deficiency usually affects the integrity absence of specific opsonizing antibodies, though
of the oral mucosa by altering the cellular their activity is enhanced when such antibodies
Oral Candidosis 101
are present. However, in heavy smokers, diabetes

mellitus, and Chediak-Higashi syndrome there
is defective PMNL function.
CLASSIFICATION
Acute
1. Pseudomembranous
2. Atrophic
Chronic
1. Atrophic
2. Hyperplastic Fig. 8.2: Acute pseudomembranous candidosis
Candida-associated Lesions
1. Angular cheilitis
during long-term antibiotic therapy. There are
2. Median rhomboid glossitis
no plaques in acute atrophic candidosis.
HIV-associated Candidosis However, there is severe burning sensation.
1. Erythematous
Chronic Atrophic Candidosis
2. Pseudomembranous
3. Mixed Chronic atrophic candidosis is also known as
denture sore mouth. It is the most common form
Chronic Mucocutaneous Candidosis of oral candidosis with a strong female
1. Localized (mucosa, nails, skins ) predilection. Patients who wear their appliances
2. Familial in day and night are prone to it. Classically the
3. 1. Endocrinopathy syndrome (hypopara lesions are seen on the denture bearing palatal
thyroidism, Addison’s disease, and hypothy- mucosa and are erythematous and asymp-
roidism) tomatic. The etiology of this lesion was not
known properly until mid 1960’s until Cawson’s
Acute Pseudomembranous Candidosis
studies. Prior to which it was thought that
Acute pseudomembranous candidosis is also etiology of chronic atrophic candidosis was due
known as thrush. It forms white plaques (Fig. to poor denture hygiene, mechanical irritation,
8.2) or flecks, which can be scrapped off. allergy to some component of the denture base
Scrapping these white plaques leaves a raw material, and irritation from leaching of
bleeding surface. These plaques are made up of monomer from an incompletely cured denture.
necrotic material composed of desquamated
epithelial cells. They often misguide the clinician Etiology
for a mistaken diagnosis of oral leukoplakia. Candida albicans adheres to the denture and
Angular cheilitis may or may not be associated. produces pyruvates and acetates, which decrease
It is seen in young, elderly, and debilitated the pH. These metabolites cause inflammation
patients. of the palatal mucosa.
Acute Atrophic Candidosis Classification
Acute atrophic candidosis is also known as Newton (1962) classified denture sore mouth into
antibiotic sore mouth because it frequently occurs three clinical types:
1. Localized simple inflammation CANDIDA ASSOCIATED LESIONS

2. Generalized simple inflammation
Angular Cheilitis
3. Inflammatory papillary hyperplasia (
involving hard palate and alveolar ridge) Angular cheilitis is also known as perleche or
angular stomatitis. The etiology is multifactorial
Treatment in origin and affects the angles of the mouth,
1. Avoid wearing the denture at night either unilaterally or bilaterally especially in
2. Wash the denture with soap and water denture wearers. Angular cheilitis can be present
3. Clean the denture with chlorhexidine in the absence or presence of oral candidosis. The
gluconate 0.20% solution various etiological factors that are associated with
4. Soak the denture in hypochlorite solution angular cheilitis are as follows:
1. Infection with Candia albicans and
Chronic Hyperplastic Candidosis Staphylococcus aureus
2. Iron deficiency anemia
Chronic hyperplastic candidosis was previously
3. Vitamin B12 deficiency
termed hyperplastic candidosis or candidal
4. Decreased vertical dimension resulting in
leukoplakia. It is most commonly observed on
skin creases at the angles of the mouth
the buccal mucosa, tongue, and palate. Speckled
leukoplakia accounts for 3-50% of all chronic
Treatment
hyperplastic candidosis and is symptomatic. The
risk of malignant transformation of chronic 1. Remove the underlying predisposing factors
hyperplastic candidosis is 9-40%, in comparison 2. When there is superadded candidal
to 2-6% risk of malignant transformation for infection, topical amphotericin (paste or
leukoplakias. When biopsy is taken and the ointment) or nystatin (ointment) should be
lesion examined, it shows parakeratinization, applied 4 times a day for 4 weeks
invasion of parakeratin by Candida albicans, 3. When Staphylococcus aureus is isolated from
varying dysplastic features, epithelial hyper- the angles, fusidic acid cream should be
plasia, neutrophilic microabscess (Munro applied 4 times a day for 4 weeks
abscess), and elongation of rete pegs. Whether
oral cancer will develop from chronic Median Rhomboid Glossitis
hyperplastic candidosis purely depends upon Median rhomboid glossitis is also known as
whether the lesion is speckled or homogenous. midline glossitis, glossal central papillary
atrophy. It is characterized by atrophy of central
Chronic Mucocutaneous Candidosis area of tongue (Fig. 8.3). The atrophy is found
The first case of chronic mucocutaneous anterior to circumvallate papillae (characteris-
candidosis or CMC was reported by Forbes in tically at the junction of the anterior two thirds
1909 in a three and half year old girl who had and posterior one-third of the tongue) and is
lesions of oral cavity and fingernails. CMC is rhomboid in shape. Initially median rhomboid
basically due to defective cell mediated immune glossitis was thought to be a developmental
response. Lesions of CMC involve skin, mucosa, disturbance (defective involution of tuberculum
and nails. There are reports of CMC associated impar). However, in 1965 Cerncea et al found
with endocrinopathies like hypoparathyroidism, that a high percentage of median rhomboid
hypothyroidism and Addison’s disease. glossitis has superficial Candida albicans.
Oral Candidosis 103
However, the debate continues as to whether anti-fungal therapy if necessary. Anti-fungal

Candida albicans causes median rhomboid drugs are mainly classified into two groups:
glossitis or is simply an opportunistic organism
that invades tissue that has been altered through Local
other mechanisms.
1. Clotrimazole 1% w/v –Candid Mouth paint
15 ml
2. Clotrimazole 1% w/v –Nifugal Mouth paint
15ml
3. Clotrimazole 1% w/v–Travoral Mouth paint
15 ml
4. Nystatin tablets–These tablets can be sucked
in the mouth and act locally
Systemic
1. Fluconazole tablets 50, 100, 150, 200 mg
2. Amphotericin B tablets 50, 100 mg
Fig. 8.3: Median rhomboid glossitis 3. Itraconazole tablets 100 mg
4. Frequent use of fluconazole leads to
Diagnosis resistance especially when treating HIV
To make a diagnosis of oral candidosis, one must patients
be able to see hyphae or pseudophyphae. The 5. When lesions are resistant to fluconazole the
most straightforward diagnostic approach is a drug of choice is itraconazole
tissue biopsy stained with periodic acid-Schiff 6. Itraconzole interacts with anticoagulants,
(PAS) stain. Alternatively a sterile cotton swab hypoglycemic drugs and is contraindicated
is used to scrape the lesion, following which the in pregnancy. Thus, it should be prescribed
swab can be streaked on the surface of a with care.
Sabouraud’s agar plate. Candida albicans will
grow as creamy-white colonies after 2 to 3 days BIBLIOGRAPHY
of incubation. 1. Challacombe SJ. Immunologic aspects of oral
candidiasis. Oral Surg Oral Med Oral Pathol
Differential Diagnosis 1994;78:202-10.
2. Greenspan D. Treatment of oral candidiasis in
1. Traumatic ulcers
HIV infection. Oral Surg Oral Med Oral Pathol
2. Chemical burns 1994;78:211-5.
3. Leukoplakia 3. Lynch D P. Oral candidiasis: History,
4. Mucous patches of syphilis classification, and clinical presentation. Oral Surg
5. Erosive lichen planus – (acute atrophic Oral Med Oral Pathol 1994;78:189-93.
candidosis) 4. Ohman SC, Dahlen G, Moller A, Ohman A.
Angular cheilitis: A clinical and microbial study.
Treatment J Oral Pathol 1986;15:213-7.
5. Samaranayake LP, Nair RG. Oral candida infections-
The main aim in the treatment of oral candidosis a review. Indian J Dent Res 1995;6:69-82.
is concerned is to primarily detect and remove 6. Samaranayake LP. Nutritional factors and oral
the predisposing factor or factors followed by candidosis. J Oral Pathol 1986;15:61-5.
Chapter
Vesiculobullous and
9 Ulcerative Lesions
INTRODUCTION PEMPHIGUS VULGARIS

The most common vesiculobullous conditions of Pemphigus vulgaris is a mucocutaneous
the oral and perioral soft tissues are viral autoimmune bullous disease. There are several
infections, especially herpes simplex, but also types of pemphigus (such as vulgaris, foliaceus,
varicella zoster (chicken pox or shingles). In vegetans, IgA pemphigus, herpetiform
normal immunocompetent patients, these self- pemphigus, and paraneoplastic pemphigus);
limiting conditions resolve spontaneously, however 80% of all patients have pemphigus
usually within days. vulgaris. Drug induced pemphigus vulgaris-like
Oral erythema multiforme is a mucocuta- lesions are known to be caused by D-
neous vesiculobullous disease that usually heals penicillamine, but similar lesions have also been
spontaneously within 2 to 3 weeks. Several reported for captopril, phenacetin, furosemide,
clinical forms occur, including major and minor penicillin, tiopronin and sulfones such as
types. The minor forms involve the skin, with dapsone.
characteristic “target” or “bull’s eye” lesions, and Before systemic corticosteroids were available,
the oral mucous membrane. The major types the disease was often fatal. Pemphigus vulgaris
include Stevens-Johnson syndrome, an acute affects the oral mucosa in nearly all cases and
form occurring in young individuals, and toxic more importantly, the oral mucosa is the site of
epidermal necrolysis both of which are the first lesion in the majority of cases. Two
characterized by large bulla formation. immune variants are recognized: the mucous
Some rare hereditary forms of vesiculobullous membrane predominant type (anti-desmoglein
diseases, such as epidermolysis bullosa, usually 3 only) and the mucocutaneous type (anti-
have onset in infancy. Bullous lichen planus is a desmoglein 1 and 3). In the mucocutaneous type,
rare vesiculobullous variant of lichen planus. oral ulcerative lesions are often seen before the
Other vesiculobullous conditions, such as contact disease affects the skin. The disease is less
or systemic allergic reactions, bullous common than mucous membrane pemphigoid
pemphigoid and linear IgA disease, more (MMP), occurring in about 0.1–0.5 patients per
commonly affect the skin. Pemphigus vulgaris 100,000 population a year.
and mucous membrane pemphigoid (MMP) are
the two most common mucocutaneous Normal Desmosomes
autoimmune bullous diseases that cause chronic The pathogenesis of pemphigus vulgaris can best
oral blistering. be understood by studying the structure of a
Vesiculobullous and Ulcerative Lesions 105
desmosome (Fig. 9.1). Adjacent keratinocytes Pathogenesis

share a number of attachment junctions
Serum from patients with pemphigus vulgaris
including tight junctions, gap junctions, and contain circulating autoantibodies (IgG) directed
desmosomes. Desmosomes constitute the against desmoglein 3. Circulating autoantibodies
primary attachment junctions between adjacent (IgG) are detectable in 80 to 90% of patients with
keratinocytes. The tonofilaments or intermediate pemphigus vulgaris, and the titer is generally
keratin filaments of each cell are inserted to correlated with severity of clinical disease.
specialized intracellular thickenings known as Pemphigus vulgaris is caused by type II
desmosomal or attachment plaque. The hypersensitivity reaction. It is likely that C1
attachment plaque contains proteins protein of complement system binds to antigen-
desmoplakin I, desmoplakin II, and plakogloblin. antibody complex (desmoglein 3-IgG) resulting
These proteins are linked to desmoglein 3 and in activation of classical complement pathway
desmocollin, which extend through the cell and formation of the (MAC) membrane attack
plasma membrane to a widened zone between complex (C5b, 6, 7, 8 (C9) n). The MAC is a
the two cells called the desmoglea. Within the cylindrical transmembrane channel which allows
desmoglea, the desmogleins 3 and desmocollins the influx of Na+ and H2O due to high internal
of adjacent keratinocytes join by homophilic colloid osmotic pressure, which eventually
binding to link the two cell membranes together. causes cytolysis of keratinocytes.
The expression of desmogleins varies between
oral epithelium and skin: oral epithelium Clinical Features
contains mostly desmoglein 3, whereas skin Pemphigus vulgaris affects both sexes equally
contains both desmoglein 3 and desmoglein 1. and is more common among Ashkenazic Jews.
Fig. 9.1: Structure of desmosome

Pemphigus vulgaris most commonly develops

during the 5th to 7th decade of life, although rare
pediatric cases have been reported.
Since the desmosome is the primary attachment
mechanism between keratinocytes, the
inflammatory destruction of desmosome leads
to the development of characteristic fluid filled
bullae. The bullae quickly rupture, leaving a
relatively nonspecific, shallow ulceration with an
irregular border (Figs. 9.2A to C).
Fig. 9.2A: Pemphigus vulgaris with multiple ulcers on the
Patients complain of painful, persistent ulcers right buccal mucosa
and sloughing, which may affect any part of the
oral cavity but is commonly seen first in the
buccal mucosa, palatal mucosa and lips. The
ulcerations may affect other mucous membranes,
including the conjunctiva, nasal mucosa,
pharynx, larynx, esophagus and genital mucosa,
as well as the skin where intact bullae are more
commonly seen.
When the epithelial attachment is destroyed,
even minor mucosal trauma may result in
acantholysis, and bullae formation. Therefore,
the formation of trauma-induced bullae is one
diagnostic tool (Nikolsky’s sign) used in assess-
Fig. 9.2B: Pemphigus vulgaris with large irregular shaped
ing the patient who has mucocutaneous bullous ulcer involving the right lateral surfa
disease such as pemphigus vulgaris or mucous
membrane pemphigoid. Bulla or ulcer formation
after gentle horizontal pressure is applied to the
oral mucosa is known as Nikolsky’s sign.
Diagnosis
The definitive diagnosis of pemphigus vulgaris
cannot be based solely on clinical examination,
as several other oral vesiculobullous lesions have
a similar appearance (bullous lichen planus,
pemphigoid and erythema multiforme). An
incisional biopsy containing normal intact
epithelium as well as tissue from the area of the Fig. 9.2C: Pemphigus vulgaris with
ulceration is required for a definitive diagnosis. ulceration of the tip of the tongue
The characteristic histopathological features of

pemphigus vulgaris include intraepithelial cleft,
acantholysis, and a dense mononuclear
lymphocytic infiltration in the underlying
connective tissue (Fig. 9.3). A simple smear taken
from a lesion can also be used to identify
acantholytic cells called Tzanck cells which are
indicative of pemphigus vulgaris. However,
Tzanck cells can also be found in diseases such
as herpes simplex, carcinoma, and transient
acantholytic dermatosis and therefore are not
diagnostic.
The autoantibodies can be detected in the
epithelium using direct immunofluorescent
Fig. 9.3: Intraepithelial cleft in pemphigus vulgaris
staining techniques. Direct immunofluorescent
staining technique reveals IgG deposits along the Mild localized lesions of oral mucous
cell membrane of kertinocytes, producing a
membrane pemphigus may be controlled with
characteristic “spider-web” or “chicken-wire” or
topical corticosteroid creams. Intralesional
“fish-net” pattern. When this technique is used,
triamcinolone acetonide may be used for
a special preservative medium is essential such
resistant local lesions of oral mucous membrane.
as Michel’s transport medium (pronounced mee-
However, patients with severe localized lesions
SHELL). Michel’s transport medium is used to of oral mucous membrane require systemic
transport specimens for immunofluorescence
corticosteroids, typically starting at 60–80 mg
studies. It is not a fixative, and is not suitable for
prednisolone a day. If no control is obtained in
any other use (particularly, it is not suitable for
the first week, the dose is increased to 120 mg a
transporting living cells for flow cytometry). It
day for a week, then up to 240 mg a day if
should be stored (refrigerated and not frozen)
necessary to prevent new bullae. Once control is
until use. Fixation in formalin will destroy the achieved, the dose is reduced by half, to 120 mg
antigen proteins and render the immuno-
a day for a week, and then to 80 mg a day for a
fluorescent staining technique useless.
week until a level of 40 mg a day is reached. The
dose is then decreased every 4 months. In most
Treatment
cases, low maintenance doses, usually every
Any patient diagnosed with pemphigus vulgaris other day, are needed for years.
or mucous membrane pemphigoid should High doses of corticosteroids may be delivered
undergo an ophthalmologic examination to for relapsing or resistant cases, either orally or
determine if there is any ocular disease. Both of intravenously (“pulse corticosteroid treatment”).
these diseases can result in severe corneal Pulse corticosteroid treatment refers to the
desquamation and conjunctival adhesions, or intravenous administration of 1 gm/day of
symblepharon, between bulbar and palpebral prednisolone, or its equivalent, over a period of
conjunctivae, thus causing functional blindness. 1–3 hours, for several consecutive days. The goal
The patient also should be evaluated for the of this approach is to quickly achieve the
presence of skin lesions by a dermatologist. immunosuppressive effects of corticosteroids,
while avoiding the long-term side effects hemorrhagic crustations. This condition is seen
associated with oral administration. It is well- in elderly patients who usually have a
tolerated in young and healthy patients, but may malignancy, typically a lymphoma or chronic
result in serious complications in those suffering lymphocytic leukemia.
from chronic disease. These include severe
electrolyte imbalances, hypertension, pancre- CHRONIC DESQUAMATIVE GINGIVITIS
atitis, seizures, and cardiac arrhythmias. Patients
Chronic desquamative gingivitis is a non-specific
often become cushingoid, and deaths are more
clinical term that is characterized by fiery red,
often attributed to side effects of corticosteroids
glazed, atrophic or eroded looking gingiva. There
than to the disease itself.
is loss of stippling and the gingiva may
Most patients with pemphigus vulgaris
desquamate easily with minimal trauma. In
receive a second immunosuppressant drug to
comparison to plaque induced gingivitis, chronic
achieve a complete remission. The most common
desquamative gingivitis is more common in
drug combination is prednisolone with
middle-aged to elderly females. Chronic
azathioprine, chlorambucil, cyclophosphamide,
desquamative gingivitis predominantly affects
cyclosporine, methotrexate, and mycophenolate
the buccal attached gingiva and sometimes
mofetil. These drugs not only provide additional
adjacent alveolar mucosa and frequently spares
immunoregulatory benefit, but also have steroid-
the marginal gingiva. Pemphigus, pemphigoid,
sparing properties that allow the dose of
erosive and atrophic lichen planus, lupus
prednisolone to be reduced significantly and
erythematosus, linear IgA disease, dermatitis
complete remission with fewer side effects. The
herpetiformis, chronic ulcerative stomatitis,
other therapeutic agents now being tried include:
graft-versus-host-disease, erythema multiforme,
Anti-inflammatory Drugs epidermolysis bullosa, plasma cell gingivitis,
1. Gold psoriasis, and Crohn’s disease are the entities that
2. Dapsone may be included under this heading. Its clinical
3. Nicotinamide appearance is not altered by traditional oral
4. Tetracycline hygiene measures or conventional periodontal
therapy.
Immunomodulatory Procedures
1. Plasmapheresis MUCOUS MEMBRANE PEMPHIGOID
2. Extracorporeal photopheresis
Mucocutaneous diseases, which are
3. Human intravenous immunoglobulin (IVIG)
characterized by separation of epithelium from
connective tissue, involve alterations in one or
PARANEOPLASTIC PEMPHIGUS
more of the anchoring proteins caused by genetic
Paraneoplastic pemphigus is a rare abnormalities (e.g., hereditary epidermolysis
vesiculobullous disease of sudden onset of the bullosa) or autoantibodies. MMP is the most
skin and mucous membranes and always affects common mucocutaneous autoimmune bullous
the oral mucosa. Oral lesions are very painful and disease to affects the oral cavity. In the past, MMP
consist of widespread, irregular shallow ulcers was known by several terms, including “benign
at multiple oral sites. Characteristically, they mucous membrane pemphigoid,” “cicatricial
extend on the vermilion border causing pemphigoid” and “ocular or oral–gingival
pemphigoid.” However, in the first international layer, called the lamina lucida and a deep,
consensus on mucous membrane pemphigoid, granular, electron-dense layer, called lamina
the term “mucous membrane pemphigoid” was densa.
recommended. MMP is defined as an oral disease The lamina lucida contains, the bullous
that rarely or perhaps never involves the skin. pemphigoid antigen 2 or BPAg2 (a180-kD
Orally, it primarily affects the gingiva (desqua- protein), and a large cruciate glycoproteins,
mative gingivitis) but may involve any area. called laminin 5 (epiligrin, kalinin, nicein,
uncein) and laminin 6. The lamina densa contains
Normal Epithelial-Connective Tissue proteins such as fibronectin and type IV collagen
Interface arranged in a chickenwire configuration. The
proteoglycan heparan sulfate coats both surfaces
The pathogenesis of MMP can best be of the lamina densa. Inserted into the lamina
understood by studying the normal epithelial- densa are small loops called anchoring fibrils,
connective tissue interface. The region where the which consists of type VII collagen. Collagen
connective tissue meets the overlying oral fibrils consisting of type I and type III collagen
epithelium is known as basement membrane run through these loops and are interlocked.
zone (BMZ). Ultrastructurally basement Intermediate keratin filaments are bound to
membrane zone is described as basal lamina and hemidesmosome plaque proteins, such as
is highly organized (Fig. 9.4). The basal lamina bullous pemphigoid antigen 1 or BPAg1 (a 230-
consists of a superficial, thin electronlucent zone kD protein), and plectin which are in turn
Fig. 9.4: Structure of hemidesmosome

connected to transmembrane proteins such as filled bullae. The bullae quickly rupture, leaving
BPAg2 and α6β4 integrin. In the lamina lucida, a relatively nonspecific, shallow ulceration with
these transmembranous proteins are linked to an irregular border. Scarring from gingival
laminins, which in turn are linked to underlying lesions is not seen, but may occur in other oral
lamina densa proteins such as type IV collagen areas, with associated reduced function. The
or fibronectin. Finally, the lamina densa proteins ulcerations may affect other mucous membranes,
are linked to type VII collagen anchoring fibrils. including the conjunctiva, nasal mucosa,
pharynx, larynx, esophagus and genital mucosa.
Pathogenesis The clinician must always rule out ocular and
Like pemphigus vulgaris, mucous membrane respiratory tract lesions.
pemphigoid is also caused by a type II
Diagnosis
hypersensitivity reaction, but the target antigens
are different. Autoantibodies (IgG or IgA or both) The definitive diagnosis of MMP cannot be based
attack one or more antigen sites present in the solely on clinical examination, as several other
basement membrane zone. The major antigens oral vesiculobullous lesions have a similar
involved in MMP are believed to be BPAg2, and appearance (bullous lichen planus, pemphigus
laminins. Consequently, the epithelium is poorly vulgaris and erythema multiforme). An
anchored to the underlying basal lamina and incisional biopsy containing normal intact
separates, allowing a subepithelial cleft to form. epithelium as well as tissue from the area of the
Circulating autoantibodies (IgG and IgA) against ulceration is required for a definitive diagnosis.
BPAg2 and laminins are usually found and the The characteristic histopathological features of
titer is generally correlated with severity of MMP include subepithelial cleft due to
clinical disease. detachment of the epithelium from the
underlying basal lamina and dense mononuclear
Clinical Features lymphocytic infiltration in the underlying
MMP is found in 2–5 people per 100,000 connective tissue (Fig. 9.5). Direct immuno-
population a year and is seen more often in fluorescence staining technique shows a linear
women. MMP most commonly develops during deposit of IgG, IgA, C3, or a combination of these
the 4th to 7th decade of life. in the BMZ.
Clinical Presentation Treatment

MMP usually appears suddenly, is painful, Patients with involvement of the conjunctiva and
waxes and wanes in severity and lasts for years pharyngeal, laryngeal, and genital mucosa
or may be active throughout the remainder of should be referred to appropriate medical
the patients life. Oral lesions are not life personnel for therapy. Patients who exhibit only
threatening, but may be associated with mild oral lesions may require no treatment, as
considerable morbidity in patients who do not the risk of therapeutic side effects outweighs the
respond to medication. Since the hemidesmo- benefit of the treatment. Many patients develop
some is the primary attachment mechanism a tolerance to the oral lesions and cease
between keratinocytes and the BMZ, the complaining about oral discomfort despite the
inflammatory destruction of hemidesmosome persistence of mild disease. The first line of
leads to the development of characteristic fluid treatment for those with only oral lesions is the
Fig. 9.5: Subepithelial cleft in mucous membrane pemphigoid
use of topical corticosteroids. However, this HERPES VIRUS INFECTIONS

treatment often fails. Systemic corticosteroids, General Characteristics of Viruses
such as prednisolone, may achieve success in
Viruses are infectious agents that are too small
some patients. Cyclophosphamide, azathioprine, to be seen with a light microscope and that are
and methotrexate are used in combination with not cells. They have no cell nucleus, organelles,
systemic corticosteroids. Patients resistant to or cytoplasm. Viruses differ from prokaryotic or
corticosteroid therapy may benefit from dapsone eukaryotic cells in important ways. Individual
(avlosulfone) therapy or combined tetracycline virus particles contain only one kind of nucleic
and nicotinamide therapy. Recently, topical acid-either DNA or RNA but never both, unlike
tacrolimus has been used experimentally with prokaryotic or eukaryotic cells, which contain
some success on a patient with genital lesions. both DNA and RNA.
Intravenous immunoglobulin (IVIG) has been Prokaryotic or eukaryotic cells grow and
tried with some success. Patients who do not divide, but viruses do neither. Viruses can
respond to any combination of treatments replicate, only inside a living host cell. Therefore,
continue to suffer intensely for decades. In all they are called obligate intracellular parasites.
cases involving the gingiva, excellent oral
hygiene is recommended in order to reduce Components of Viruses
plaque, despite the presence of desquamative The virus components are a nucleic acid core and
gingivitis. a surrounding protein coat called a capsid. In
addition, some viruses have a surrounding lipid As more was learned about the structure of
bilayer membrane called an envelope. A viruses at the molecular level, the viruses were
complete virus particle, including its envelope, classified by the type of nucleic acid they
is called a virion. contained.
As more viruses were discovered, conflictions
Host Range in classification systems resulted. The need for a
single, universal taxonomic scheme for viruses
The host range of a virus refers to the spectrum
led to the establishment of the International
of hosts that a virus can infect. The host range of
Committee on Taxonomy of Viruses (ICTV) in
Rhabdoviridae (rabies) virus is very extensive.
1996. This committee, which meets every four
However, most viruses are limited to only one
years, establishes the rules for classifying the
host and to only one specific cell of the host.
viruses.
Specificity of Viruses
Herpes Viruses
Viral specificity refers to the specific kind of cells
The herpes viruses (herpes, Greek for “creeping”)
or tissues a virus can infect. Therefore, viruses
are relatively large, icosahedral, enveloped
are grouped as dermotropic if they infect the skin,
viruses with linear (double stranded DNA)
neurotropic if they infect the nervous system,
dsDNA. The structure of the herpes virus is very
viscerotropic if they infect the digestive system,
complex (Fig. 9.6). The core consists of dsDNA.
pneumotropic if they infect the respiratory
The capsid surrounds the core. Surrounding the
system and lymphotropic if they infect the
capsid is the matrix or tegument, which contains
lymphocytes.
at least 15-20 proteins. On the outside is the
Viral specificity is determined mainly by three
envelope, which contains at least eight
factors:
glycoproteins. Herpes viruses are widely
1. Attachment: Attachment depends on the
distributed in nature, and most animals are
presence of specific receptors on the surfaces
infected with one or more of the 100 types
of host cells and specific attachment
discovered. At least, seven distinct human herpes
structures on viral capsids or envelopes.
viruses have been described each causing a
2. Host enzymes: Specificity also depends
characteristic disease (Table 9.1). An important
whether appropriate host enzymes and other
feature common to all the human herpes viruses
proteins the virus needs to replicate are
available inside the cell.
3. Release: Finally, specificity is affected by
whether replicated viruses can be released
from the cell to spread the infection to other
host cells.
Classification of Viruses
Viruses were first classified by the type of host
they infected. Thus, viruses have been classified
as bacterial viruses, plant viruses, and animal
viruses.
Fig. 9.6: Herpes simplex virus-1 structure
Table 9.1: Human herpes viruses

Genus Virus type Disease
Simplex virus Herpes simplex virus type 1 Oral herpes (sometimes genital)
Herpes simplex virus type 2 Genital herpes (sometimes oral)
Varicellovirus Varicella-zoster virus Chickenpox (Varicella); shingles (Herpes Zoster)
Cytomegalovirus Cytomegalovirus Infectious mononucleosis; Acute febrile illness;
(salivary gland inclusion virus) Kaposi’s sarcoma linked to AIDS; infections in
(human herpes virus 5) transplant recipients; birth defects
Roselovirus Roseola infantum Exanthema subitum (roseola infantum), a common
(formerly called herpes virus 6) disease seen in infants, featuring rash and fever
Lymphocryptovirus Epstein-Barr virus Infectious mononucleosis; Burkitt lymphoma;
(human herpes virus 4) Hodgkin disease; B-cell lymphomas; nasopharyngeal
cancer; Oral hairy leukoplakia linked to AIDS
Human herpes virus 8 Kaposi’s sarcoma virus Kaposi’s sarcoma linked to AIDS
is their ability to establish latency in the host. Both and tumor necrosis factor present on the host cell
herpes simplex virus type-1 (HSV-1) and herpes membrane. Fusion of the viral and host cell
simplex virus type-2 (HSV-2) are res-ponsible for membranes follows. This requires the action of
primary oral herpes simplex infections, with a number of viral glycoprotein’s including gB,
HSV-1 accounting for 75% to 90% of cases. gH, gI, and gL, which bind to corresponding
receptors on the host cell membrane.
Replication of Herpes Simplex Virus
Penetration
In general, viruses go through the following five
steps in their replication cycle to produce virions. Once inside the host cell, the viral capsid with
1. Adsorption (attachment of viruses to host cells) some tegument proteins migrates to the nuclear
2. Penetration (entry of genome into host cells) pore along microtubules utilizing cell transport
3. Synthesis (synthesis of viral dsDNA and machinery. The viral dsDNA is then injected
proteins) through the nuclear pore while the capsid
4. Maturation (assembly of the viral components) remains in the cytoplasm. Some tegument
5. Envelopment and release (acquiring envelope proteins, such as αTIF, also enter the nucleus with
and release of new virions from host cells) the viral dsDNA.
Adsorption Synthesis
For the initiation of infection the HSV dsDNA There are two main events in the replication of
must enter the host cell. The initial association is herpes simplex virus, designated as early and late
between proteoglycans of the host cell membrane transcription. Early transcription is subdivided
and glycoprotein gC present on the viral into two phases-immediate early and early. The
envelope. This is followed by interaction between early transcription takes place before the
HVEM (herpes virus entry mediators) and replication of dsDNA and results in the
glycoprotein gD present on the viral envelope. production of proteins necessary for viral dsDNA
The HVEM are receptors for nerve growth factor replication.
1. Immediate-early phase: In the immediate- on the rough endoplasmic reticulum are

early phase, α-mRNAs are transcribed, transported to the Golgi body in vesicles, which
which translate α4-proteins in the cytoplasm. are then transported in vesicles to modify the
2. Early phase: In the early phase, β-mRNAs host cell membrane. The cytoplasmic capsid then
are transcribed, which translate β-proteins associates itself with αTIF and vhs tegument
proteins and buds into an exocytotic vesicle. The
in the cytoplasm.
exocytotic vesicle migrates to virus modified cell
These proteins (α4-proteins and β-proteins)
membrane. Here it fuses with the virus modified
migrate back to the nucleus, and mediate the
cell membrane and acquires an envelope. The
replication of the viral dsDNA. The late events
new virion is released outside the cell. Release
occur in the nucleus after the replication of
of new virion results in lysis of keratinocytes.
dsDNA and result in transcription of structural
mRNAs and transcription of new structural
CLINICAL MANIFESTATIONS
proteins needed for building new capsids.
The structural proteins migrate back to the Primary HSV Infection
nucleus (scaffolding proteins and procapsid Primary HSV infections develop in people who
proteins), inserted into nuclear membrane (viral have not been previously exposed to the virus.
glycoproteins), inserted into host cell membrane Transmission occurs via direct contact
(viral glycoproteins), and float within the (thigmotaxis) with contaminated secretions from
cytoplasm (αTIF and vhs tegument proteins). an infected individual. Mucosal surfaces and skin
with cracks are highly susceptible. The most
Maturation commonly observed clinical manifestation of
Once an abundance of dsDNA and structural primary HSV infection is primary acute herpetic
proteins have been synthesized, they are gingivostomatitis (inflammation of gingiva and
assembled into new capsids. This step constitutes other intraoral mucosal surfaces). Primary acute
maturation. The scaffolding proteins (UL19, herpetic gingivostomatitis is most often seen in
UL26 and UL26.5) assemble and form children and adolescents. Most often, exposure
scaffolding. The procapsid proteins (UL18 and to HSV infection in children results in a
UL38) assemble around scaffolding following subclinical infection and the child may complain
which the scaffolding proteins are digested away. of mild flulike symptoms. Approximately 1% of
The empty capsid incorporates viral dsDNA by patients develop primary herpetic gingivosto-
means of the action of cleavage/packaging matitis. After an incubation period of 1 to 26 days,
proteins. Vesicles transport viral glycoproteins nonspecific signs and symptoms (prodromal)
that have been translated earlier (during such as fever, malaise, irritability, headache, and
synthesis) from structural mRNAs on the rough cervical lymphadenopathy occur. The prodromal
endoplasmic to the nuclear membrane. The signs and symptoms are followed by eruption
mature capsid migrates to the nuclear membrane of vesicles. The vesicles affect any intraoral
and buds into the lumen between the inner and mucosal surface (buccal mucosa, hard/soft
outer nuclear membrane. This capsid then enters palate, floor of the mouth, tongue, gingiva,
the cytoplasm as cytoplasmic capsid through tonsillar pillars, and pharynx). The vesicles
fusion with the outer nuclear membrane. rupture within a few days to produce painful,
small, round, shallow ulcers. Often, ulcers
Envelopment and Release coalesce to form larger irregular-shaped
Viral glycoproteins that have been translated ulcerations. Gradual healing, without scarring,
earlier (during synthesis) from structural mRNAs occurs within 1 to 2 weeks.
Recurrent HSV Infection systems respond and suppress it. It is not known
whether the reactivation involves the killing of
Approximately 30 to 40% of patients who have
one or more neurons, but evidence suggests that
been exposed to HSV will develop recurrent HSV
the frequency of reactivation decreases with time.
infections. Recurrent HSV infections can either
occur as recurrent herpes labialis (RHL) or
Recurrent Herpes Labialis
recurrent intraoral herpes (RIH). These recurrent
HSV infections represent reactivation and not Recurrent herpes labialis is the most
reinfection of HSV. During primary HSV predominant recurrent HSV infection. Prior to
infection, the virus is transported via retrograde RHL patients experience prodromal signs and
axonal transport to regional sensory ganglia symptoms such as burning, tingling, itching,
where it establishes latency in nerve cell bodies soreness or swelling at the site where the lesions
(Fig. 9.7). While latent, the virus exists in a will develop. Within hours, small vesicles
nonreplicating immunologically shielded state. develop along the vermilion border of the lips
The most frequent site of latency for HSV is the and other perioral sites such as the skin or ala of
trigeminal ganglion, but other potential sites the nose. The characteristic clinical appearance
include the nodosa ganglia of the vagus nerve, of RHL is focal clustering of vesicles (Fig. 9.8).
dorsal root ganglia, sympathetic ganglia, and The vesicles quickly rupture, resulting in ulcers
brain. Numerous well-documented triggering that coalesce to form the larger irregular-shaped
factors are associated with HSV recurrence. They ulcers with a crusted surface (Figs. 9.9 A and B).
include sunlight, trauma, menstruation, fever, In a healthy individual, the lesions heal without
immunosuppression, decompression of the scarring within 7 to 14 days.
trigeminal nerve, and irritation by dental
instruments. Once, reactivated the virus is Recurrent Intraoral Herpes
transported via anterograde transport to the RIH lesions occur less frequently than RHL. RIH
epithelium where it replicates, causing tissue lesions begin as clusters of tiny vesicles that
damage and recurrent HSV infection. The limited rupture quickly, resulting in erosions or ulcers
virus replication takes place until the host defense without crusting. The RIH lesions involve
Fig. 9.7: Herpes simplex virus-1 latency

keratinized mucosa (hard palate, attached

gingiva, and edentulous ridges) (Fig. 9.10).
However, in immunocompromised patients e.g.,
AIDS, the tongue can also be affected. The lesions
on the tongue exhibit mucosal erosions, each of
which is surrounded by a circinate, raised, yellow
border (Fig. 9.11). This border represents the
advancing margin of active viral destruction.
Intraoral recurrence follows a pattern of
presentation similar to that of RHL except the
lesions are intraoral, and crusting does not occur.
The pain associated with RIH may interfere with
Fig. 9.8: Focal clustering of vesicles
eating and speaking. In a healthy individual, the
lesions heal without scarring within 7 to 14 days.
Fig. 9.10: Recurrent intraoral herpes
B
Figs 9.9A and B: Recurrent herpes
labialis with crusted surface
Fig. 9.11: HIV-associated recurrent intraoral herpes

Recurrent herpetiform aphthous ulcers and RIH vesicle, and the base of the vesicle is gently
have similar clinical presentation except the scrapped on a glass slide. The scrapping is
recurrent herpetiform aphthous ulcers are seen allowed to dry in the air for couple of minutes
anywhere on the oral mucosa and patients do and then stained with Wright Giemsa stain for
not experience prodromal signs and symptoms. microscopic examination. Characteristic
multinucleated epithelial cells with intranuclear
Differential Diagnosis inclusions indicate a positive test.
Other diagnostic tests include tissue biopsy,
The diagnosis of RHL is based on their
viral culture, serology, and polymerase chain
characteristic clinical appearance of the lesions. reaction, but are not routinely used.
However, the diagnosis of RIH is based on the
clinical appearance of the lesions and their Dental Care
location. However, other oral mucocutaneous
The vesicular stage of recurrent HSV infection is
diseases should be considered in the differential
the most contagious. However, all stages of
diagnosis (Table 9.2) recurrent HSV infections are infectious until
complete re-epithelialization has occurred.
Table 9.2: Differential diagnosis of oral HSV infection Patients must be informed that recurrent HSV
Differential diagnosis Clinical appearance infections are extremely contagious and therefore
ANUG Fiery red gingiva, interproximal care must be taken to avoid autoinoculation of
crater formation other mucosal sites, as well as transmission to
others.
Erythema multiformae Oral ulcerations, target lesions on
Health care workers are highly susceptible to
skin
herpetic infection of the finger known as herpetic
Hand-foot-and- Multiple aphthouslike ulcerations whitlow (herpetic paronychia). Paronychia is the
mouth disease and lesions on hand and feet infection in the tissues adjacent to a nail on a
Herpangina Bandlike oral ulcerations affecting finger or toe. Herpetic whitlow often occurs as a
soft palate, uvula, tonsils, and result of failure to use gloves when the hand is
posterior pharyngeal wall in contact with the infected secretions such as
Intraoral shingles Oral ulcerations, skin lesions,
saliva because HSV is sloughed asymptoma-
tically in the saliva of patients during healing of
severe pain
RIH.
Pemphigus vulgaris Oral ulcerations, positive
Signs and symptoms of herpetic whitlow
Nikolsky’s sign include sudden onset of edema, erythema,
Recurrent herpetiform Recurrent, clustered, small, intense itching, and localized tenderness of the
aphthous ulcers shallow intraoral ulcers affecting infected finger. This is followed by eruption of
any part of oral mucosa, no vesicles and formation of pustules and is usually
prodrome of fever and malaise accompanied by fever and lymphadenopathy
(axillary lymph nodes). The vesicles and pustules
Diagnosis eventually rupture to become ulcers. The
duration of herpetic whitlow may be as long as
Tzanck Test (Mucosal Smear) 4 to 6 weeks. Recurrences may also occur with
The Tzanck test is a rapid and inexpensive this form of herpes infection and usually involve
diagnostic aid useful in the diagnosis of HSV the same site. Recurrent lesions may result in
infection. A sterile scalpel is used to unroof a paresthesia and permanent scarring.
To summarize health care workers should use Antiviral therapy for the immunocom-
gloves, face masks, and protective spectacles if promised patient should include systemic anti-
the patient infected with HSV is to be treated. viral therapy. Systemic acyclovir therapy, both
Because transmission occurs via direct contact parenteral and oral, accelerates viral shedding,
with contaminated saliva from an infected reduces pain, and reduces healing time. For
individual, care must be taken not to spread the intravenous administration, the regimen is
virus to the finger and other mucous membranes, 5 mg/kg (infused over 1 hour) every 8 hours for
such as eyes or nasal mucosa. For this reason, 5 to 10 days. A generally accepted oral regimen
air-water sprays should be avoided unless a is 400 mg taken 3 to 5 times per day for 10 days.
rubber dam is used. Trauma to the lesion must Acyclovir is a synthetic analogue of purine
be avoided so that healing will not be retarded. guanosine that inhibits viral DNA polymerase
and thereby inhibits viral dsDNA replication.
Management Acylovir is active only in virally infected cells
Therapy for HSV infection is dependent on the because only viral-encoded enzyme thymidine
clinician’s evaluation of both the clinical kinase converts acyclovir to acyclovir
presentation and patients overall health. For monophosphate. Cellular enzymes (cellular
example, the management of RHL affecting a kinase) then phosphorylate acyclovir
healthy patient will differ from the management monophosphate to acyclovir triphosphate, which
of RHL affecting an AIDS patient. Treatment of is the active form of the drug. Failure of acyclovir
HSV infection is symptomatic and has four major therapy is usually associated with HSV infections
goals: caused by thymidine kinase-deficient strains of
1. Ulcer management (to promote healing and HSV. It should be noted that these drugs such as
reduce duration) acyclovir act against the replicating virus and
2. Pain management (to reduce morbidity (the therefore they are ineffective against latent virus.
relative incidence of a particular disease) and to Foscarnet therapy should be initiated in
enhance function) immunocompromised patients who fail to
improve with acyclovir therapy. Foscarnet does
3. Nutritional management (to ensure
not require activation via phosphorylation by
adequate food and fluid intake)
viral thymidine kinase. Foscarnet is also active
4. Disease control (to prevent recurrence or
against HSV-1, HSV-2, VZV, cytomegalovirus
reduce frequency)
(CMV), influenza A and B, hepatitis B virus
Primary HSV Infection (HBV), and HIV. Foscarnet causes renal failure
The treatment of mild cases of primary herpetic and therefore adequate hydration is critical, as
gingivostomatitis is directed at relieving is proper monitoring and dose adjustment to
discomfort and improving the patients ability to minimize toxicity. Therapy consists of
eat and drink. The patient is instructed to intravenous foscarnet 40 mg/kg every 8 to
maintain adequate food and fluid intake, and 12 hours for 14 to 21 days.
maintain proper oral hygiene. A topical
Recurrent HSV Infection
anesthetic agent is prescribed which is to be used
for 2 minutes before each meal. Non-steroidal The treatment of RHL is primarily symptomatic
anti-inflammatory drugs can also be prescribed as in primary herpetic gingivostomatitis. Topical
to relieve fever and pain. antiviral ointments can be used as they accelerate
viral shedding, reduce pain, and reduce healing symptom may be odontalgia. This odontalgia is
time. Topical acyclovir 5% ointment applied a diagnostic challenge to the clinician who is not
during prodromal symptoms to the affected area familiar with shingles of the trigeminal nerve.
every 2 hours 6 times per day for 7 days until
resolution may be sufficient to control RHL. Varicella-zoster Virus
Topical penciclovir (1%) ointment applied during The varicella-zoster virus is responsible for two
prodromal symptoms to the affected area every common infectious diseases:
2 hours while awake for 4 days has been shown 1. Primary infection—chickenpox
to speed lesion healing and reduce pain. 2. Secondary infection—shingles
Recently, docosanol (10%) ointment became After the primary infection, the virus remains
available for the treatment of RHL. The dormant until there is reactivation that may occur
mechanism of action of docosanol is via alteration decades later. The subsequent reactivation is
of healthy cell membranes to prevent viral entry. shingles (Fig. 9.12)
Docosanol ointment applied during prodromal
symptoms to the affected area 5 times per day Reactivation
for 4 days may be sufficient to control RHL.
Because sunlight is a known triggering factor of Numerous well-documented triggering factors
RHL, prevention may be enhanced by using a are associated with reactivation of VZV. They
sunscreen lotion with a sun protection factor include neonates, nonimmune persons, pregnant
(SPF) 15 or greater. women, and immunocompromised patients.
However, immunocompromised patients fail
Transmission
to improve with topical antiviral therapy. In such
patients oral famciclovir is indicated. The Chickenpox and shingles are contagious and
recommended dosage is 500 mg twice daily for spread via direct contact with an infected person.
7 days, initiated at prodrome. In addition, the The transmission can also occur through
use of oral acyclovir has been shown to be ef- inhalation of airborne respiratory secretions. The
fective. For episodic therapy, the prompt (at the virus then infects the cells of the respiratory tract
first prodromal symptom) administration of oral or conjunctival epithelium and is transported
acyclovir, 400 mg 3 times per day for 10 days,
may be sufficient. For patients who have frequent
recurrences (more than six episodes per year),
chronic suppressive therapy with oral acyclovir,
400 mg 2 times per day, may prevent recurrence.
Foscarnet therapy should be initiated in
immunocompromised patients who fail to
improve with acyclovir therapy.
Shingles
Shingles of the trigeminal nerve is a disease that
falls within the diagnostic purview of all dentists
and dental specialists. During the prodromal
stage of this disease, the only presenting Fig. 9.12: Reactivation of varicella-zoster virus
through the body via blood and lymphatic

system. The virus then spreads from the
capillaries to the epidermis where it replicates
and destroys the basal cells. Following which the
virus migrates to the primary satellite cells of the
dorsal nerve root ganglia, where it establishes
latency in the nerve cell bodies (Fig. 9.13).
Shingles
Shingles may affect any sensory ganglia and its
cutaneous nerve. Most of the infections affect
dermatomes of T-3 to L-2 (Fig. 9.14). However,
in 13% of patients it involves any three branches
of the trigeminal nerve (Fig. 9.15). Ocular branch
(V1) involvement is the most common trigeminal
nerve infection (50% of all trigeminal
occurrences). Hutchins’ sign is pathognomonic,
when shingles involves the maxillary branch.
Hutchins’ sign is characterized by cutaneous
lesions of one side of the tip of the nose.
Diagnostic Stages
Patients with shingles usually progress through
three diagnostic stages (Fig. 9.16):
1. Prodromal stage
2. Active or acute stage
3. Chronic stage
Fig. 9.14: Dermatomes
Fig. 9.13: Transmission of varicella-zoster virus Fig. 9.15: Herpes-zoster involving mandibular nerve
Fig. 9.17: Perioral vesicles

Fig. 9.16: Diagnostic stages
Prodromal Stage
The prodromal stage presents with different
types of sensations occuring in the skin over the
affected nerve distribution they include.
1. Burning
2. Tingling
3. Itching
4. Boring
5. Prickly or knife-like
It is believed that these sensory changes are Fig. 9.18: Intraoral lesions
due to degeneration of nerve fibrils because of
viral infection. The sensory changes usually
precede (come before) the rash of the acute stage. severe cases, areas of epidermis and dermis may
The patient may present with odontalgia, which be lost. Intraoral lesions usually appear after the
may be the only prodromal symptom. cutaneous rash (Fig. 9.18). Pain and dysaesthesia
are minimal when the rash is active. However,
Acute Stage the pain returns during crust formation, but
The active stage is characterized by the subsides as the crusts clear off.
emergence of rash, which may be accompanied
by generalized malaise, headache, low-grade Chronic Stage
fever, and sometimes nausea. The rash The chronic stage is termed postherpetic
progresses from erythematous papules to neuralgia (PHN). PHN is pain lasting for 1 to
vesicles in 12 to 24 hours (Fig. 9.17). The vesicles 3 months after the skin lesions disappear but may
progress to pustules within 1 to 7 days. The in fact last for years and decades. PHN pain
pustules begin to dry and form crusts. These consists of three distinct components:
crusts fall off within 14 to 21 days, leaving 1. Constant, deep pain
erythematous macular lesions, which result in 2. Brief recurrent shooting or shocking tic-like
hyperpigmented or hypopigmented scarring. In pain
3. Sharp radiating dysaesthetic sensation Dental Complications

evoked by very light touching of the skin 1. Tooth neuralgia
2. Devitalization of teeth
Differential Diagnosis
3. Internal root resorption
The dental practitioner should be familiar with 4. Tooth exfoliation and osteonecrosis of
various diseases that can produce facial pain. The mandible (upon resolution of acute phase).
diagnosis of shingles is clear when the prodromal 5. The contralateral side of the patient’s jaw
symptoms and the rash are present. A diagnostic remains normal.
challenge is created when the vesicular rash does
not occur, as in zoster sine herpete (Herpes zoster Miscellaneous Complications of
without rash) of the trigeminal nerve and a Various Organs
culture may be required to confirm shingles. A 1. Skin
detailed and careful case history usually rules out 2. Heart
other pathologies such as: 3. Liver
1. Trigeminal neuralgia 4. Joints of the musculoskeletal system
2. Maxillary sinusitis 5. Urinary tract
3. Periodic migrainous neuralgia
Management
4. Myocardial pain
The recommended therapy for shingles should
5. Atypical facial pain
include:
6. Munchausen’s syndrome
1. Patient isolation
Complications 2. Management of skin lesions
3. Control and elimination of pain
The clinical presentations of shingles are variable
4. Antiviral drugs
and extend beyond the region of head and neck.
The complications can range from meningoen- 5. Management of PHN pain
cephalitis to superficial skin changes. It is Patient Isolation
important to remember that any part of CNS can Patients with shingles are contagious to persons
be affected. at high risk. They include neonates, nonimmune
Neurological Complications persons, pregnant women, and immuno-
compromised patients. Patients with shingles
1. Meningoencephalitis
remain contagious until crusting phase has taken
2. Horner’s syndrome place.
3. Ramsey-Hunt syndrome
Management of Skin Lesions
4. Guillian-Barre syndrome
Management of skin lesions includes, soaking of
Ocular Complications gauze is in cool water and applying to the rash
1. Ulcerations area for 30 minutes 3 to 6 times a day. Creams
and lotions may be used after the acute phase to
2. Hemorrhage
soften and remove adherent crusts. Creams and
3. Conjunctivitis lotions containing corticosteroids are not
4. Optic neuritis recommended.
Control and Elimination of Pain injury to the CNS and therefore is unlikely to
The acute pain of shingles during the prodromal respond to standard NSAID. The treatment of
and the acute phases can be reduced. Mild to PHN pain is varied. However, no single
moderately strong analgesics, such as treatment is universally effective for all PHN
acetaminophen and nonsteroidal anti- patients. The various treatment modalities of
inflammatory drugs (NSAID) are effective. PHN include.
1. Topical use of capsaicin cream (Capsain-P
Antiviral Drugs gel, 25 gm, which contains capsaicin 0.025
Once shingles is diagnosed, antiviral therapy w/w)
must be swift and precise. Acylovir has been the 2. Transcutaneous electric nerve stimulation
drug of choice for a number of years for many (TENS)
reasons. Recently newer forms of antiviral drugs 3. Topical anesthetics
have been developed specifically to manage 4. Injected local anesthetics
acute stage of shingles (famciclovir) and for use 5. Low dose tricyclic antidepressants such as
in immunocompromised patients (valacyclovir). amitriptyline, 10-25 mg 3 times a day, till
Antiviral drugs may help in limitation of the desired results are achieved
extent, duration, and severity of the disease.
Acylovir has been proven to decrease drastically ORAL LICHEN PLANUS
the duration and severity of shingles in the acute Lichen planus is a common mucocutaneous
phase, if administered within 48 hours of the disease, which was first described by Erasmus
onset of rash. Acylovir is less toxic than other Wilson in 1869. The condition can affect either
antiviral drugs. The dosages of various antiviral the skin or mucosa or both. Cutaneous lesions
drugs used in the management of shingles are typically present as small (2 mm) pruritic, white
listed in the Figure 9.19. to violaceous papules, which can increase in size
to 3 cm. They often occur bilaterally on the flexor
Management of PHN Pain surfaces of the extremities.
Standard NSAID are not effective in patients Oral lichen planus is a chronic disease that can
with PHN pain. The PHN pain is because of persist in some patients for a long time in contrast
to cutaneous lichen planus. It often does not
respond to treatment and complete remissions
are rare, particularly in patients with erosive
lesions. Exacerbations are unpredictable and
common. There is no cure and the treatment is
symptomatic.
Clinical Features
Oral lichen planus is a disease of adulthood and
children are rarely affected. It affects woman
more often than men and is usually observed in
nervous, “highly-strung” people.
Oral lichen planus may present anywhere in
Fig. 9.19: Antiviral drugs and dosages the oral cavity. The buccal mucosa, tongue and
gingiva are the most common sites, whereas

palatal lesions are uncommon. They are usually
symmetrical and bilateral lesions (mirror-image
lesions).
Clinical Variants
Oral lichen planus is divided into six types:
reticular, papular, plaquelike, erosive, atrophic
and bullous. The reticular, papular and plaque-
like forms are usually painless and appear
clinically as white keratotic lesions. The erosive,
atrophic and bullous forms are often associated Fig. 9.21: Papular lichen planus
with burning sensation and in many cases can
cause severe pain. the most common site. It is rarely seen and
because the lesions are small it is possible to
Reticular overlook them during a routine oral examination.
The most common type of oral lichen planus is Plaquelike
the reticular form. Characteristically, it presents
The plaquelike type of oral lichen planus
as a series of fine, radiant, white striae known as
resemble oral leukoplakia and occur as
“Wickham striae” (Fig. 9.20). The buccal mucosa
homogeneous white patches. The dorsum of the
is the most common site. The striae are typically
tongue and the buccal mucosa are the most
bilateral and symmetrical. They may also be seen
common sites. This form is much more common
on the lateral border of the tongue and less often
among tobacco smokers.
on the gingiva and the lips.
Erosive
The erosive type of oral lichen planus is the
second most common type. The lesions are
usually irregular in shape and covered with a
pseudomembrane (Fig. 9.22). The periphery of
the lesion is usually surrounded by fine, radiant,
white striae. The buccal mucosa is the most
common site. Gingival involvement in erosive
lichen planus produces chronic desquamative
gingivitis. Only the atrophic and erosive forms
of lichen planus undergo malignant change (Fig.
9.23), and this may be because of the atrophic
Fig. 9.20: Reticular lichen planus nature of the oral mucosa.
Papular Atrophic
The papular type of oral lichen planus presents The atrophic type of oral lichen planus presents
as small white pinpoint papules measuring about as diffuse, red lesion. The periphery of the lesion
0.5 mm in size (Fig. 9.21). The buccal mucosa is is usually surrounded by fine, radiant, white
Oral Lichen Planus and Pigmentation

The appearance of hyperpigmentation in
cutaneous lichen planus indicates the resolution
of the lesion. Hyperpigmentaion in cutaneous
lesions may result from melanin loss into the
dermis from the damaged basal cell layer.
However, no such conclusions can be made in
regard to oral lichen planus.
Etiopathogenesis
The cause of oral lichen planus remains unclear.
However, it is well-documented that oral lichen
Fig. 9.22: Erosive lichen planus
planus represents a chronic, cell-mediated
autoimmune disease process with the infiltrating
cell population composed of both CD4+ Tcells and
CD8+ T cells targeted against basal keratinocytes
of the oral mucosa in susceptible individuals.
Whether this chronic, cell-mediated auto-
immune disease process progresses to the
development of oral lichen planus, or is switched
off, probably depends on a number of factors,
which include:
1. The nature of the antigen
2. The ability of the individual to present the
Fig. 9.23: Malignant change in erosive lichen planus
antigen
3. The presence of T cells capable of recognizing
striae. The attached gingiva is often involved and the antigen
the condition is commonly referred to as chronic
4. Genetic susceptibility in the individual that
desquamative gingivitis.
promotes, rather than suppress, a cell-
Bullous mediated autoimmune disease response to
the antigen
The bullous type of oral lichen planus is rarer
than the other forms of oral lichen planus and Lymphocyte trafficking to the basal lamina –
appears as vesicles or bullae that tend to rupture basal keratinocyte interface is the hallmark of oral
easily and form ulcers. The bullous form is lichen planus. No specific oral lichen planus
commonly seen on the buccal mucosa, antigen has been detected but it seems that
particularly adjacent to the second and third various antigens are capable of inducing changes
molar teeth. The next most common site is the in the skin or oral mucosa. Some of the antigens
lateral margins of the tongue. The lesions are known to induce changes are:
rarely seen on the gingiva or inner aspect of the a. Dental restorative materials
lips. b. Cinnamon-flavoring agents used in foods
c. Medications (medications are known to of the draining lymph node. In the paracortical
induce oral lichenoid lesions that can be T cell zone the immature IDCs become mature
difficult to distinguish from oral lichen and interdigitate with the naive or virgin T cells
planus) and present the antigen with the help of MHC
d. Microbes class II molecules and costimulatory molecules
Peripheral immature dendritic cells IDCs e.g., such as B7 (Fig. 9.24). The naive T cells once
Langerhans cells bind to the basal keratinocytes primed with the antigen become activated T cells,
by expressing surface molecules such as which undergo clonal proliferation and
E-cadherin. The principle function of IDCs is to maturation (Fig. 9.25).
pick up the antigen, and process it. After The basal keratinocytes produce chemotactic
processing the antigen, under the influence of agents such as interleukin-1, interleukin-8,
tumor necrosis factor α (TNF-α), produced by interleukin-10, and leukotriene-B, and
surrounding basal keratinocytes or the transforming growth factor β. Production of
inflammatory infiltrate, these immature IDCs these chemotactic agents from the basal
loose their E-cadherin and produce collagenase, keratinocytes results in infiltration of T cells from
in order to facilitate their crossing through the the underlying blood vessels to the basal lamina-
basement membrane. basal keratinocyte interface.
They then travel as “veiled cells” via the This infiltration requires activation of integrins
afferent lymphatics to the paracortical T cell zone such as lymphocyte function associated antigen
Fig. 9.24: Migration pathway of Langerhans’ cell

Fig. 9.25: Clonal proliferation of T cells
(LFA-1) on the plasma membrane of T cells. Because both CD4+ T cell and CD8+
Integrins are normally expressed on T cell plasma T cell are present in oral lichen plans lesions, it
membranes but do not adhere to their has been speculated that CD8+ T cell may be
appropriate ligands until the T cells are activated responsible for the apoptosis of basal
by chemotactic agents. keratinocytes layer, particularly in erosive,
Upon activation the T cell integrins adhere to atrophic and bullous lichen planus.
their ligands (ICAM-1) and migrate towards the There are two main mechanisms by which
basal lamina-basal keratinocyte interface, which CD8+ T cell induce apoptosis in target cells such
is likely to be under the control of chemotactic as basal keratinocytes. Both require intimate
agents produced by the basal keratinocytes. contact between the CD8+ T cell and the basal
TNF-α and IFN-γ produced by the infiltrating keratinocyte.
T cells, induce the expression of adhesion 1. The first mechanism by which CD8+ T cell
molecules such as ICAM-1 (intercellular kill basal keratinocytes involves cross-linking
adhesion molecule) present on the lining of blood of the cell surface molecule Fas on the basal
vessels in the affected oral mucosa. keratinocyte by its ligand Fas-L expressed by
The activated T cells produce IFN-γ, which CD8+ T cell and NK cells. This triggers a
induces keratinocytes to express antigen with the cascade of intracellular enzymatic reactions
help of MHC class II molecules, increase their resulting in apoptosis of the target cell.
rate of differentiation (which results in 2. In the second mechanism, the CD8+ T cell
thickening of the epithelium and is clinically seen produces the molecule perforin that
as white lesion), and expression of intercellular polymerizes in the basal keratinocyte cell
adhesion molecule (ICAM-1) to which the membrane to form holes through which the
activated T cells adhere. In addition, these same CD8+ T cell secretes the enzyme granzyme
T cells express ICAM-1 and thereby allow B that initiates the breakdown of intracellular
lymphocyte to lymphocyte clustering. proteins.
TNF-α produced by CD8+ T cell may also histological features suggest a cell-mediated
promote apoptosis in oral lichen planus. It immune response.
induces differentiation and activation of CD8+
T cell, and NK cells. It is also anti-proliferative to Treatment
basal keratinocytes and cytotoxic to them at high Many patients with oral lichen planus have no
concentrations. Moreover, when produced symptoms. In such cases, no active treatment is
directly onto the surface of basal keratinocytes required except for reassurance. Most cases of
by adherent CD8+ T cell, it may directly induce asymptomatic lichen planus are detected during
apoptosis or further enhance Fas/Fas-L a routine check up. Patients who are not given
mediated apoptosis. any active treatment are advised to revisit every
six months for two years, or earlier if they get
Histopathology symptoms.
The histopathological features were first Corticosteroids
described by Dubreuill in 1906 and later by
The backbone of oral lichen planus treatment
Shklar. Shklar described the three classic
remains corticosteroids, which can be used
microscopic features of oral lichen planus as
topically, intralesionally or systemically.
overlying keratinization (hyperparakeratosis or
hyperorthokeratosis), a band like layer of chronic Topical Corticosteroids
inflammatory cells (T cells) within the underlying
Topical corticosteroids may be used when
connective tissue and liquefaction degeneration
systemic corticosteroids are contraindicated or
of the basal keratinocytes. The other features
if the patient refuses intralesional injections.
include acanthosis, thickening of the granular cell
Topical corticosteroids appear to be safe when
layer, separation of epithelium from the
applied to mucous membranes but prolonged
underlying connective tissue due to basal cell use requires careful frequent follow-up. Topical
destruction (typically seen in erosive forms), and betamethasone disodium phosphate applied
blunted rete ridges. Intimate comingling of basal orally may cause adrenal suppression and
cells and T cells obliterates the epithelial-stromal betamethasone valerate aerosol can be harmful
interface and results in loss of definition of the or fatal when applied to mucous membranes. In
stratum basale. In turn, this yields the jagged addition, topical corticosteroids may result in the
“candle dripping” or “saw tooth” appearance of development of secondary oral candidosis.
rete ridges. In cutaneous lichen planus the rete Therefore, adjunctive antifungal preparation
ridges have a jagged “candle dripping” or “saw should be considered. Triamcinolone acetonide
tooth” appearance. Colloid bodies (also termed ointment twice a day for two weeks and once a
cytoid, globular, hyaline, Civatte, and day for a further two weeks can be effective.
Sabouraud’s bodies) may be seen lying either in Alternative treatment is required for patients
the lower layers of the epithelium or within the whose symptoms do not respond to topical
upper layers of the connective tissue. They are treatment.
round, eosinophilic globules and are probably
degenerated epithelial cells or phagocytosed Intralesional Corticosteroids
epithelial cell remnants within macrophages. Intralesional injection of corticosteroids can
Direct immunofluorescence studies show that improve the symptoms. A 5% mixture in local
these bodies stain for IgA, IgG and IgM. These anesthetic has been recommended to lessen the
pain of the injections. Atrophy of tissue and and production of lymphokines. Adverse effects
secondary oral candidosis are possible local of cyclosporin include renal dysfunction due to
complications. It is difficult to inject sufficient prolonged use, and transient burning sensation
quantities into gingival lesions. Intralesional on the mucosal surface of the lesion. Treatment
triamcinolone acetonide 10 mg/ml repeated once of oral lichen planus by cyclosporin is expensive
or twice a week appear to be a practical so its use could be limited by cost.
supplement for the treatment of erosive-
ulcerative lesions. Retinoids
Systemic Corticosteroids Topical application of retinoids to asymptomatic,

white, reticulated oral lichen planus has given
Systemic corticosteroids should be reserved for
good results. The most readily available topical
acute exacerbations of symptoms, multiple
retinoid is 0.1% tretinoin. But it may cause
ulcerations, or widespread disease. Systemic
irritation and burning and lesions may relapse
corticosteroids are often used in combination
when it is withdrawn. The use of systemic
with topical corticosteroids. Prednisolone 30-
retinoids such as etretinate is limited because of
60 mg, depending on the severity of the disease,
their adverse effects including dry skin and hair
are given once daily for two to three weeks.
loss.
Adverse effects are common even after a course
as short as two weeks. The most common adverse
Dapsone
effects include gastrointestinal upset, mood
alteration, polyuria, and insomnia. Patients who Dapsone should be considered in resistant cases,
take systemic corticosteroids should be particularly in erosive-ulcerative lesions.
monitored regularly.
Photochemotherapy
Griseofulvin Topical and systemic psoralen (8-methoxy-
Griseofulvin is indicated for the treatment of psoralen) and long-wave ultraviolet-A (PUVA)
erosive-ulcerative lesions when corticosteroid is a common treatment for various dermatoses.
treatment is contraindicated or when lesions are PUVA without topical and systemic psoralen is
resistant to corticosteroids. When it is given orally also effective. One drawback of PUVA is the
or parenterally, it is distributed throughout the possible development of squamous cell
body and deposited in basal cells and carcinoma, particularly as oral lichen planus is
progressively reaches the stratum corneum as the regarded as a premalignant condition. As of now
cells mature. The mechanism of action is not these treatments should be considered
known. However, it is thought that it may experimental.
prevent desquamation of the stratum corneum,
and thereby prevent erosions. Surgery
Cryosurgery and carbon dioxide laser ablation
Cyclosporin have been suggested for the surgical treatment
Damage to the basement membrane in oral lichen of plaque-like oral lichen planus. However,
planus is due to the production of lymphokines surgical excision is contraindicated in erosive and
by CD8+ T cell. Cyclosporin is an immunosupp- atrophic lesions as oral lichen planus is a chronic
ressant and inhibits the proliferation, function inflammatory condition that will recur.
Moreover, operative trauma to the oral mucosa of administration of zidovudine and/or

may induce the formation of new lesions at these ketaconazole. Oral lichenoid lesions have also
sites. been described following ingestion of the street
drug, crystal methamphetamine. Hepatitis C is
Oral Lichenoid Lesions a systemic condition that has been implicated
The appearance of lesions having the clinical and with induction of oral lichenoid lesions.
histopathological features of oral lichen planus, Some of the drugs that have been shown to
but apparently induced by drugs, has been cause oral lichenoid lesions include anti-
recognized for some time but the importance was malarials (chloroquine), anti-arthritic drugs
emphasized by the large number of cases of oral (penicillamine), nonsteroidal antiinflammatory
lichenoid lesions that appeared in service drugs (NSAIDs), antihypertensive drugs (ACE
personnel receiving antimalarials in World War inhibitors), and antidiabetic drugs (tolbutamide,
II. chlorpropamide). However, associations
Oral lichenoid lesions (Fig. 9.26) may be between oral lichen planus and systemic diseases
triggered by mechanical trauma (Koebner may be co-incidental as oral lichen planus is
phenomenon) from calculus and plaque relatively common, it occurs predominantly in
deposits, friction from sharp cusps, rough dental older individuals, and drugs used in the
restorations, poorly fitting dental prostheses, treatment of systemic diseases trigger oral
tongue biting, lip biting or cheek biting lichenoid lesions. As an example, the oral
(morsicatio buccarum), and oral surgical lichenoid lesions in “Grinspan’s syndrome”
procedures. When these factors are removed or (triad of oral lichen planus, diabetes mellitus and
eliminated the lesions usually resolve. hypertension) may be a reaction to the drugs
used to treat diabetes mellitus or hypertension.
The clinical features of oral lichenoid lesions
are similar to that of oral lichen planus. The
diagnosis of oral lichen planus and oral lichenoid
lesions is made by histopathological
examination. Three characteristic features of oral
lichen planus are seen histopathologically:
1. Hyperparakeratosis or hyperorthokeratosis
2. A band like layer of chronic inflammatory
cells (T cells) within the underlying
connective tissue
Fig. 9.26: Lichenoid reaction 3. Liquefaction degeneration of the basal
keratinocytes
Contact allergy with allergens such as In comparison, oral lichenoid lesions cannot
cinnamon-flavoring agent, peppermint, dental always be distinguished from oral lichen planus
restorative materials (amalgam, mercury, copper, but may show a deep, as well as superficial
gold, nickel, and composites), and denture acrylic infiltrate of T cells, rather than the classic band
has been reported to cause oral lichenoid lesions. like infiltrate of oral lichen planus.
Oral lichenoid lesions have been found in Treatment of oral lichenoid lesions can be
HIV-positive individuals, apparently as a result variable. If the patient has been using flavoring
agents, they should be advised to discontinue the associated gingival erythema, and the RAU occur
use of such products. Unlike true lichen planus, almost exclusively on movable oral mucosa, such
drug-induced oral lichenoid lesions disappear as the buccal mucosa, labial mucosa, tongue, and
after drug withdrawal, removal or changing of soft palate. However, RAU are characterized by
the drug. Withdrawal, removal or changing of a prodrome of localized burning sensation for
the drug should be considered after consultation 24 to 48 hours that can precede the ulcers.
with the patients physician.
Some physicians may be reluctant to change Classification
a patients medication, particularly when that Recurrent aphthous ulcers have three clinical
drug has been proved beneficial in controlling presentations, which are as follows:
life threatening disease such as diabetes mellitus, 1. Minor RAU
and hypertension. 2. Major RAU
3. Herpetiform RAU
Recurrent Aphthous Ulcers
Minor Aphthous Ulcers
Recurrent aphthous ulcers (RAU) are a common
Minor aphthous ulcers (Mikulicz’s aphthae or
condition in which recurring round ulcers affect
mild aphthous ulcers) account for majority of all
the oral mucosa. Recurrent aphthous ulcers are
cases of recurrent aphthous ulcers. Minor
also called recurrent aphthous stomatitis or
aphthous ulcers can involve every non-
canker sores. It is one of the most painful oral
keratinized mucosa of the oral cavity. However,
mucosal inflammatory ulcerative conditions and
they usually involve the labial and buccal mucosa
can cause pain on eating, swallowing and
(Fig. 9.27), the floor of the mouth and the ventral
speaking.
or lateral surface of the tongue (Fig. 9.28). They
are smaller than 1 cm in diameter and tend to
Clinical Features heal slowly within 10 to 14 days without scarring.
Recurrent aphthous ulcers are more commonly
seen in young adults below 30 years of age. It
affects women more often than men.
The ulcers are painful, clearly defined, round or
oval, with a shallow necrotic center covered with
a yellow-grayish pseudomembrane and sur-
rounded by raised margins and erythematous
haloes. The pain lasts for three to four days
following which epithelialization can occur.
An important point to remember is that RAU
typically do not have a prodrome of fever, Fig. 9.27: Minor recurrent aphthous ulcer
malaise and vesicle formation, there is no involving the left buccal mucosa
Herpetiform Aphthous Ulcers

Herpetiform aphthous ulcers account for only 5
to 10% of all cases of recurrent aphthous ulcers.
Multiple (5 to 100) 1 to 3 mm small, rounded,
painful ulcers resembling ulcers of herpes
simplex are seen anywhere on the oral mucosa.
They tend to fuse and produce much larger ulcers
lasting for 10 to 14 days.
Etiology
The etiology is probably multifactorial, with
Fig. 9.28: Minor recurrent aphthous various predisposing factors (Table 9.3), which
ulcers involving the lateral border of tongue
provoke a cell-mediated immune response.
Major Aphthous Ulcers Table 9.3: Predisposing factors
Major aphthous ulcers (periadenitis mucosa • Trauma
necrotica recurrens, ulcerative stomatitis and • Stress
Sutton’s disease) account for 10 to 15% of all cases
• Foods
of recurrent aphthous ulcers. The prodromal
• Hormonal imbalance
symptoms are more intense than those of minor
aphthous ulcers. They are large solitary or
Genetic Basis
multiple, chronic, deep crater-like, painful
There is often a genetic basis for recurrent
ulcerations that extend through the epithelium
aphthous ulcers. The probability of recurrent
into the connective tissues and tend to involve
aphthous ulcers is 90% when both parents are
nonkeratinized oral mucosa (lips, soft palate, and
affected, but only 20% when neither parent has
throat) overlying the minor salivary glands but
recurrent aphthous ulcers. It is also likely to be
can present in any location (Fig. 9.29). They are more severe and tends to start at an earlier age
larger than 1 cm in diameter and can lasts for in patients with a positive family history than in
weeks or months and often leave a scar after those without a positive family history.
healing.
Immunopathogenesis
The immunopathogenesis of recurrent aphthous
ulcer is very much similar to that of oral lichen
planus, except the keratinocyte lysis occurs
throughout all strata and is not restricted to the
basal cell layer as seen in oral lichen planus. The
preulcerative stage is characterized by
lymphocytic infiltrate composed of CD8+ T cells
and natural killer (NK) cells in response to oral
keratinocyte-associated antigens. Tumor necrosis
factor released by CD8+ T lymphocytes results
in lysis of keratinocytes followed by a localized
Fig. 9.29: Major recurrent aphthous ulcer in HIV patient papular swelling surrounded by reactive
erythematous halo representing vasculitis. The

papule then ulcerates and is covered by a
fibrinous membrane. Finally, there is healing
with epithelial regeneration.
Diagnosis
The diagnosis of recurrent aphthous ulcers is
made on the basis of history and clinical
examination since there are no specific laboratory
tests available. Various laboratory tests should
be carried out, which include complete blood
picture, serum iron, folate, and vitamin B12.
Hemoglobin levels and red blood cell counts
are generally within normal range in patients
with recurrent aphthous ulcers. However,
patients with recurrent aphthous ulcers reveal
deficiency of serum iron, folate and vitamin B12.
A medical history should be taken to rule out
systemic disorders associated with recurrent
aphthous ulcers (Fig. 9.30). They include:
Fig. 9.30: Diagnosis of recurrent aphthous ulcers
1. Ulcerative colitis
2. Crohn’s disease of recurrent aphthous ulcers is symptomatic and
3. Reiter’s syndrome or Behcet’s disease has four major goals:
4. Sweet’s syndrome (acute febrile neutrophilic 1. Ulcer management (to promote healing and
dermatosis) reduce duration)
5. Periodic fever, aphthae, pharyngitis and 2. Pain management (to reduce morbidity and
adenitis syndrome (PFAPA syndrome) enhance function)
6. Neutropenia 3. Nutritional management (to ensure
7. HIV infection adequate food and fluid intake)
4. Disease control (to prevent recurrence or
Management reduce frequency)
There is no definitive treatment of recurrent In all patients with recurrent aphthous ulcers,
aphthous ulcers as the etiology is unknown. it is important to rule out predisposing factors
Some patients have mild outbreaks, whereas and treat them where possible, before
others have severe outbreaks. Some patients introducing specific therapy. In order to
present with single small ulcer, while others determine treatment strategies, the practitioner
present with multiple small ulcers. Some patients may classify recurrent aphthous ulcers into three
present with large ulcers, while others present clinical presentations:
with combination of small or large. In some
patients, the severity and frequency of outbreaks Type A
ease with the passing of years; in others, severity Recurrent aphthous ulcers last for only a few
and frequency worsen. Thus, therapy should be days and occur only few times a year. In this
tailored to each patient individually. Treatment condition, pain is tolerable. The clinician should
Table 9.4: Potential side effects of prednisolone and azathioprine

Prednisolone Insomnia, nervousness, increased appetite, indigestion, diabetes mellitus, hirsutism, joint pain,
and glaucoma
Azathioprine Thrombocytopenia, leukopenia, secondary infections, anemia, nausea, vomiting, anorexia,
diarrhea, and non-Hodgkin’s lymphoma
identify the predisposing factor that causes the (prednisolone, clobetasol, fluticasone or
ulcer and eliminate it. For example if trauma fluocinonide), and immunosuppressants
during tooth brushing has been identified, the (azathioprine or dapsone). Prednisolone, an anti-
clinician can suggest a softer tooth brush and inflammatory and an immunosuppressive agent,
gentle brushing. can be used in combination with topical
ointments and rinses. Systemic prednisolone
Type B
therapy should be started at 1.0 mg/kg a day as
Recurrent apphthous ulcers appear each month, a single dose in patients with severe RAS and
lasting three to ten days. In this condition, pain should be tapered after one to two weeks. Most
may or may not be tolerable and the patient may potential side effects of prednisolone are due to
have changed the diet and oral hygiene habits treatment that persists for more than 2 weeks.
because of the pain. The clinician should identify Prednisolone can be used in combination with
the predisposing factor that causes the ulcer and
another immunosuppressive agent, azathio-
eliminate it. It is essential to identify patients who
prine, to reduce the dosage of prednisolone.
use corticosteroids (if they are indicated for him
50 mg/kg per day for one week azathioprine can
or her) when they experience prodromal
be administered safely in combination with
symptoms. Treatment includes the use of
prednisolone (Table 9.4) shows the potential side
chlorhexidine gluconate 0.20% solution and a
effects of prednisolone and azathioprine.
short course of topical corticosteroid ointment
Recurrent aphthous ulcers can be prevented by
(triamcinolone acetonide) applied directly to the
thalidomide and pentoxifylline, which prevent
ulcers, four times a day. In patients with stubborn
the synthesis of TNF-α. Thalidomide therapy has
recurrent aphthous ulcers, a short course of
been thoroughly researched in HIV-positive
systemic corticosteroid therapy may be required.
Prednisolone, never exceeding more than 50 mg patients. One study concluded that HIV-positive
per day (preferably in the morning) for five days patients with recurrent aphthous ulcers benefited
is the ideal choice. If corticosteroids are used, from thalidomide therapy. Initial treatment in
patients should be monitored for superadded either HIV-positive or HIV-negative patients
oral candidosis. Oral prophylaxis should be should be 100 or 200 mg of thalidomide daily,
considered in patients with poor oral hygiene depending on the severity of the disease and the
due to altered oral hygiene habits once the ulcers patients tolerance. Once the lesion resolves,
heal. therapy must be stopped until remission occurs.
Other treatment modalities include the use of
Type C chemical cautery, electrocautery, or lasers to
Recurrent aphthous ulcer develops by the time convert the ulcer into a wound. Ultrasound has
one ulcer heals. Treatment includes the use of been suggested to provide a beneficial effect on
topical corticosteroids, systemic corticosteroids recurrent aphthous ulcers.
BIBLIOGRAPHY 17. Pedersen A, Klausen B. Glucocorticosteroids and

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3. Darling MR, Daley T. Blistering mucocutaneous Tenth edn. Blackwell Science Oxford, 2001
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J Oral Maxillofac Surg 2000;58:1278-85. Sarmadi M. Recurrent aphthous stomatitis.
6. Epstein JB, Wan LS, Gorsky M, Zhang L. Oral Quintessence Int 2000;31:95-112.
lichen planus: progress in understanding its 24. Siegel MA. Diagnosis and management of
malignant potential and the implications for recurrent herpes simplex infections. JADA
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Pathol Oral Radiol Endod 2003;96:32-7. 25. Sigurdsson A, Jacoway JR. Herpes zoster infection
7. Eversole LR. Immunopathology of oral mucosal presenting as an acute pulpitis. Oral Surg Oral
ulcerative, desquamative, and bullous disease: Med Oral Pathol Oral Radiol Endod 1995;80:92-
Selective review of the literature. Oral Surg Oral 5.
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pemphigus vulgaris. The Mount Sinai Journal of 2000;58:1286-8.
Medicine 2001;68:268-78.
27. Sirois D, Leigh JE, Sollecito TP. Oral pemphigus
9. Huber MA. Herpes simplex type-1 virus infection.
vulgaris preceding cutaneous lesions:
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10. Laskin DM, Giglio JA, Rippert ET. Differential
1160.
diagnosis of tongue lesions. Quintessence Int.
28. Stoopler ET, Sollecito TP, DeRossi SS.
(Indian Edition) 2003;3:15-26.
Desquamative gingivitis: early presenting
11. Lavelle CLB. Acyclovir: is it an effective virostatic
symptom of mucocutaneous disease.
agent for orofacial infections? J. Oral Pathol. Med
Quintessence Int 2003;3:74-8.
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12. McCreary CE, McCartan BE. Clinical 29. Tabaee A, Saltman B, Shutter J, Hibshoosh H,
management of oral lichen planus. Br. J Oral and Markowitz. Recurrent oral herpes simplex virus
Maxillofac Surg 1999;37:338-43. infection presenting as a tongue mass. Oral Surg
13. Meij van der EH, Schepman KP, Wall van der I. Oral Med Oral Pathol Oral Radiol Endod
The possible premalignant character of oral lichen 2004;97:376-80.
planus and oral lichenoid lesions: A prospective 30. Thornhill MH. Immune mechanisms in oral
study. Oral Surg Oral Med Oral Pathol Oral lichen planus. Acta Odontol Scand 2001;59:174-
Radiol Endod 2003;96:164-71. 7.
14. Mollaoglu N. Oral lichen planus: A review. Br. J 31. Tidwell E, Hutson B, Burkhart N, Gutmann JL,
Oral and Maxillofac Surg 2000;38:370-7. Ellis CD. Herpes zoster of the trigeminal nerve
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Oral Pathol 1994;77:116-20. 32. Vinay Kumar, Cotran RS, Robbins SL. Robbins
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Chapter
HIV/AIDS in Dental Care
10
CENTRE FOR DISEASE CONTROL AND the world, the AIDS epidemic claimed 3.1 million
PREVENTION (CDC) CASE DEFINITION lives in 2005; more than half a million (570 000)
were children.
CDC, in collaboration with Council of State and
The total number of people living with the
Territorial Epidemiologists (CSTE), has
human immunodeficiency virus (HIV) reached
expanded the AIDS surveillance case definition
its highest level: an estimated 40.3 million people
to include all HIV-infected persons with CD4+
(Fig. 10.1) are now living with HIV. Close to 5
T cell counts of less than 200 cells/μl. In addition
(4.9) million people were newly infected with the
to retaining the 23 clinical conditions in the
virus in 2005.
previous AIDS surveillance definition, the
expanded definition includes pulmonary National HIV infection levels in Asia are low
tuberculosis (TB), recurrent pneumonia, and compared with some other continents, notably
invasive cervical cancer. This expanded Africa. Diverse epidemics are underway in India,
definition for reporting cases to CDC became where an estimated 5.1 million Indians were
effective from January 1, 1993. living with HIV in 2003 (NACO, 2004a).
Although levels of HIV infection prevalence
Acronym (AIDS) appear to have stabilized in some states (such as
Tamil Nadu, Andhra Pradesh, Karnataka and
1. Acquired means you can acquire it Maharashtra), it is still increasing in at-risk
2. Immune deficiency means a weakness in the population groups in several other states. As a
body’s immune system to fight diseases result, overall HIV prevalence has continued to
3. Syndrome means a group of health problems rise.
that make up a disease In India, the National AIDS Control
Organization (NACO), established in 1992, is
Epidemiology
responsible for coordinating the overall health
Acquired Immunodeficiency Syndrome (AIDS) sector response to HIV/AIDS, supported by the
has killed more than 25 million people since it state AIDS control societies at the state level. The
was first recognized in 1981, making it one of National AIDS Control Programme, first
the most destructive epidemics in recorded launched in 1987, is now in its second phase of
history. Despite recent, improved access to anti- implementation (1999–2006). Its objective is to
retroviral treatment and care in many regions of reduce the transmission of HIV through a
HIV/AIDS in Dental Care 137
Fig. 10.1: Epidemiology
decentralized and comprehensive programme of Causative Organism

generating awareness, changing behavior,
targeting vulnerable groups with intervention AIDS is caused by a retrovirus called Human
and conducting research. Immune Deficiency Virus (HIV). It measures
about 90-100 nm in diameter and is lympho-
Historical Background tropic.
Dr. Luc Montagnier (1983) of Pasteur Institute, Structure of HIV (Fig. 10.2)
Paris, first identified and named it Lymphad-
enopathy Associated Virus. Dr. Roberto Gallo The HIV-1 virion is spherical in shape with an
identified it later at NIH Bethesda, Maryland, outer viral envelope with gp120 and gp41
U.S.A in 1984 and named it as Human T cell proteins. The viral core is surrounded by a matrix
Lymphotropic Virus. p17 protein. The viral core contains the capsid
Fig. 10.2: Structure of HIV

p24 protein, 2 copies of RNA, and 3 viral enzymes relate to HIV-1 and diseases caused by it, but are
(reverse transcriptase, protease, and integrase). generally applicable to HIV-2 as well. The strains
of HIV-1 can be classified into three groups:
HIV Genome 1. Major group designated as M: More than
90% of HIV-1 infections belong to HIV-1
The HIV genome contains gag, pol and env genes
group M. Within group M there are known
(Fig. 10.3), which encode various viral proteins:
to be at least nine genetically distinct
1. gag gene encodes—matrix protein p17 and
subtypes (clades). These are subtypes A, B,
capsid protein p24
C, D, E, F, G, H, J. The clades differ from each
2. pol gene encodes—reverse transcriptase,
other by their geographic distribution. For
protease and integrase
example, subtype C is largely predominant
3. env gene encodes—viral envelope proteins
in southern and eastern Africa, India, and
gp120 and gp41
Nepal
Classification of HIV 2. Outlier group designated as O: Group O
appears to be restricted to west-central Africa
HIV is a highly variable virus, which mutates 3. New group designated as N: Group N-
very readily, which means there are many discovered in 1998 in Cameroon is extremely
different strains of HIV, even within the body of rare
a single infected person. Based on genetic
similarities, the numerous virus strains may be Transmission of HIV (Fig. 10.4)
classified into types, groups, and subtypes. There
1. Sexual (homosexuals/heterosexuals)
are 2 genetically different types of HIV: HIV-1
2. Parenteral (intravenous drug abusers/
and HIV-2. Both types are transmitted by sexual
hemophiliacs)
contact, through blood, and from mother to child,
3. Mother to infant (vertical transmission)
and they cause AIDS.
a. Transplacental
However, it seems that HIV-2 is less easily
b. During delivery
transmitted, and the period between initial
c. HIV infected milk
infection and illness is longer in the case of HIV-2.
The relatively uncommon HIV-2 type is mostly HIV Is Not Transmitted Through
confined to West Africa and is rarely found 1. Saliva
elsewhere. Worldwide, the predominant virus is 2. Kissing
HIV-1, and in general when people refer to HIV 3. Mosquito bite
without specifying the type of virus they will be 4. Touching
referring to HIV-1. The rest of this chapter will 5. Sharing toilets
Fig. 10.3: HIV genome

Fig. 10.4: Routes of transmission of HIV
Saliva: Saliva contains a protein called “secretary 2. They should survive in the mosquito
leukocyte proteinase inhibitor” which inactivates 3. The feeding apparatus of a mosquito should
the HIV. Antibodies (IgA) are present in the be like a hypodermic needle
saliva against HIV.
Life Cycle of HIV (Fig. 10.5)
Mosquitoes: The first reason why mosquitoes do
not transmit HIV is that the virus is present at The target cells of HIV are the CD4 (where CD4
very low levels in the blood of HIV positive is cluster of differentiation or cluster designation)
individuals. The second reason is that even the cells, which include dendritic cells (Langerhans
HIV is digested along with the blood. The third cells) macrophages and CD4+ T cells (“master
reason is that the feeding apparatus of the cell”). CD4 is a docking molecule present on the
mosquito has two separate passages, one for the macrophages, Langerhans’ cells, and CD4+ T
saliva and the other for the blood. Thus, the cells and is a high-affinity receptor for HIV. This
mosquito delivers the saliva through one passage explains the tropism of the virus for the CD4+ T
and sucks the blood through the other in a cells, macrophages, and Langerhans’ cells.
unidirectional manner. However, binding to CD4 is not sufficient for
In order for a mosquito to transmit HIV from infection. The HIV envelope gp120 must also
an infected person to an uninfected, host: bind to coreceptors to enter the cell. There are
1. The levels of HIV in the circulating blood two coreceptors: CCR5 and CXCR4. The CCR5
should be high coreceptor is present on the macrophages,
Fig. 10.5: An overview of lifecycle of HIV
monocytes, and CD4+ T cells and the CXCR4 cDNA (complementary DNA), which is
coreceptor is present only on the CD4+ T cells. compatible with human DNA. This cDNA is
The life cycle of HIV can be divided into four transported to the nucleus, where it is integrated
stages: Entry, reverse transcription and into the human DNA by the enzyme integrase.
integration, transcription and translation, and Once integrated, the HIV DNA is known as a
assembly, budding and maturation. provirus.
Entry Transcription and Translation

The process typically begins when a HIV particle The provirus may remain dormant (non-
bumps into CD4+ T cell, a cell that carries on its transcribed) within a cell for a long time (months
surface a special docking molecule called CD4. or years) and the HIV infection becomes latent.
The gp120 on the surface of the virus particle It is important to note that although HIV can
binds to the CD4. This binding leads to infect resting CD4+ T cells, the transcription of
conformational change in the gp120 following provirus occurs only when the infected cell
which CD4 and gp120 bind to CCR5. The gp41 becomes activated by exposure to antigens (e.g.,
protein then binds and fuses with the cell microbes) or cytokines. Once the infected cell
membrane. After fusion, the contents of the HIV becomes activated, the provirus is transcribed
are then released into the cell, leaving the into messenger RNA (mRNA). The mRNA is
envelope behind. transported outside the nucleus into the
cytoplasm where it is translated to produce viral
Reverse Transcription and Integration RNA, viral proteins, and the enzyme protease.
Once inside the cell, the HIV enzyme reverse The viral RNA forms the genetic material for the
transcriptase converts the viral RNA into proviral next generation of viruses.
Assembly, Budding and Maturation arthralgia, skin rash, and sometimes aseptic
The viral RNA and viral proteins assemble at the meningitis.
cell membrane, following which the enzyme During this phase, HIV initially infects CD4+
protease chops up long strands of proteins into T cells and macrophages directly or is carried to
smaller pieces, which are used to construct regional lymph nodes by Langerhans cells where
mature viral cores. The viral core fuses with the these cells are present. Viral replication in the
cell membrane and buds out from the cell, taking regional lymph nodes leads to viremia (high
a bit of the cell membrane to form a new viral levels of viral particles in the blood) and
envelope. The newly matured HIV particles are widespread seeding of HIV in the lymphoid
ready to infect another CD4+ T cell and begin tissues (lymph nodes, spleen, and tonsils)
the replication process all over again. It has been resulting in reduction of CD4+ T cell count. The
estimated that 100 billion new viral particles are viremia is controlled by the development of
produced every day, and 1 to 2 billion CD4+ T antiHIV antibodies (usually within 3 to 12
cells die each day. weeks). As viremia dies away, CD4+ T cell count
returns to normal number.
Course of HIV Infection (Fig. 10.6)
Middle “Chronic” Phase
1. Early “acute” Phase The immune system is stable. Patients are usually
2. Middle “chronic” Phase asymptomatic or develop persistent lymph-
3. Final “crisis” Phase adenopathy, and many patients have minor
Early “Acute” Phase opportunistic infections such as oral candidosis
or shingles. The virus replicates in the CD4+ T
The early “acute” phase represents the initial
cells and macrophages present in the lymphoid
response of the immune system to HIV infection.
tissues for several years and gradually destroy
Clinically, this self-limiting illness develops in
the CD4+ T cells. However, when the CD4+ T
50 to 70% of adults 3 to 6 weeks after infection
cells that are destroyed cannot be replenished,
and is characterized by flu-like symptoms, which
the CD4+ T cell count decreases and the patient
include fever, malaise, generalized lymph-
enters the final crisis phase. The macrophages
adenopathy, pharyngitis, headache, myalgia,
are not destroyed by the virus replication and
they transport the virus to various tissues,
particularly the brain.
Final “Crisis” Phase

This phase is characterized by the appearance of
opportunistic infections and specific conditions
as outlined by CDC (Table 10.1). Approximately
90% of patients with untreated AIDS die from
opportunistic infections. Patients with AIDS
often have generalized lymphadenopathy,
severe weight loss, fatigue, chronic diarrhea,
chronic fever, and night sweats. Laboratory tests
reveal increased viral load (suggestive of
Fig. 10.6: Course of HIV infection viremia), altered CD4/CD8 ratio, and decrease
in CD4+ T cell count. The number of CD4+ T 5. Depletion of CD4+ T cell precursor cells,
cells decrease from a normal range of 1500 to 200 either by direct infection of thymus cells or
cells/mm3. The normal CD4+ T cell/CD8+ T cell by infection of cells that secrete cytokines
ratio is about 2. In AIDS patients, it is < 0. 5 and essential for CD4+ T cell differentiation
therefore the ratio is an important measure of
the disease progression. Thus, as the disease Consequences of CD4+ T-cell
progresses the number of CD4+ T cells decrease (“Master Cell”) Destruction
and CD8+ T cells increase. The marked reduction 1. Decreased antigen presentation by
of CD4+ T cells explains the lack of immune macrophages
response and is most likely related to the increase 2. Decreased antibody production by plasma
in malignant disease associated with AIDS. cells in response to antigen
3. Decreased killing of tumor cells by Natural
Causes for Decreased CD4+T-lymphocyte
Killer (NK) cells
Count
4. Decreased CD8+ T cell cytotoxicity
1. Because of HIV infection. 5. Decreased response to antigen and
2. Killing of infected CD4+ T cells by CD8+ T decreased cytokine production by CD4+ T
cells cells
3. Formation of syncytia (giant cells) by fusion
of infected CD4+ T cells and uninfected Oral Manifestations
CD4+ T cells Oral lesions are frequently associated with HIV
4. Uninfected CD4+ T cell may bind to free infection. Oral lesions associated with HIV
gp120 resulting in apoptosis infection, also occur in other conditions
Table 10.1: Diagnostic criteria for AIDS

AIDS is diagnosed when an individual with HIV develops at least one of these conditions:
1. CD4+ T cell count drops below 200 cells/mm3
2. Development of one of the following opportunistic infections:
• Fungal: Candidosis of bronchi, trachea, lungs, or esophagus; Pneumocystis carinii pneumonia; histoplasmosis
(disseminated or extrapulmonary)
• Viral: Cytomegalovirus disease (other than liver, spleen, or nodes); cytomegalovirus retinitis (with loss of vision);
herpes simplex with chronic ulcers (greater than 1 month’s duration), or bronchitis, pneumonitis, or esophagitis;
progressive multifocal leukoencephalopathy; extrapulmonary cryptococcosis
• Protozoal: Coccidioidomycosis (disseminated or extrapulmonary), toxoplasmosis of brain; chronic intestinal
isosporiasis (greater than 1 month’s duration); chronic intestinal cryptosporidiosis (greater than 1 month’s duration)
• Bacterial: Mycobacterium tuberculosis any site (pulmonary or extrapulmonary); Mycobacterium avium complex or
Mycobacterium kansasii (disseminated or extrapulmonary); recurrent pneumonia; Recurrent salmonella septicemia
3. Development of one of the following opportunistic cancers:
• Invasive cervical cancer; Kaposi’s sarcoma; Burkitt lymphoma; lymphoma immunoblastic; lymphoma primary of
the brain
4. Wasting syndrome occurs: Defined as loss of 10% or more of ideal body mass
5. Dementia
characterized by immunosuppression. Many prophylaxis). There is no evidence to suggest that

HIV related oral lesions occur early in HIV this entity will proceed to the far more
infection. Thus, early detection of associated oral destructive necrotizing periodontitis.
lesions should, in many cases, result in earlier Histological examination fails to reveal any
diagnosis of HIV infection. HIV related oral significant inflammatory response, suggesting
lesions could be broadly classified into four that the lesions represent an incomplete (aborted)
categories: infections (bacterial fungal and viral), inflammatory response, principally with only
neoplasms, immune-mediated, and others hyperemia present. Treatment includes intensive
(xerostomia, pain syndromes, and nutritional) daily oral hygiene, oral rinsing with chlorhe-
(Table 10.2). xidine gluconate 0.20% solution, scaling and root
planing (if necessary) with 10% betadine solution
Table 10.2: Oral lesions associated with AIDS irrigation, and careful follow-up and mainte-
Bacterial infections: Linear erythematous gingivitis; nance.
necrotizing ulcerative periodontitis; necrotizing stomatitis;
actinomycosis; bacillary epitheloid angiomatosis Nectrotizing Ulcerative Periodontitis (NUP)
Fungal infections: Oral candidosis; angular cheilitis or This unique periodontal lesion is characterized
angular cheilosis; cryptococcosis; histoplasmosis; by pain, generalized gingival erythema that is
aspergillosis; mucormycosis; geotrichosis often associated with spontaneous bleeding,
Viral infections: Herpes simplex virus infection; shingles; interproximal gingival necrosis, cratered soft
oral hairy leukoplakia; oral warts; focal epithelial tissues, deep osseous pain in the jaws, and
hyperplasia; condyloma acuminatum rapidly progressive destruction of the
Neoplasms: Squamous cell carcinoma; Kaposi’s
periodontal attachment and bone (Fig. 10.7).
sarcoma; non-Hodgkin lymphoma
Destruction of the periodontal attachment and
bone can be extremely rapid and extensive and
Others: Bell’s palsy; recurrent aphthous ulcers;
may result in as much as 90% bone loss around
xerostomia; parotid gland enlargement ; pain syndromes;
isolated teeth in as few as 12 weeks. If left
immune thrombocytopenic purpura; melanotic
untreated, NUP may extend into the adjacent
pigmentation; trigeminal neuropathy
tissues and expose the alveolar or palatal bone
Linear Eythematous Gingivitis and the condition has been called necrotizing
Linear erythematous gingivitis or linear gingival

erythema appears as an erythematous distinctive
linear band (1-3 mm wide) at the free gingival
margin, often with petechiae. It is typically
associated with no symptoms and in most cases,
gentle probing produces bleeding. Unlike
conventional gingivitis, linear erythematous
gingivitis is not significantly associated with
plaque and can be seen in patients with excellent
oral hygiene. Therefore, linear gingival erythema
usually does not respond and persists following
conventional periodontal therapy (dental Fig. 10.7: Necrotizing ulcerative periodontitis
stomatitis. NUP adversely affects oral intake of indicators for initiating and continuing
food, resulting in significant and rapid weight prophylaxis for Pneumocystis carinii pneumonia.
loss. The diagnosis of NUP should be made based Diagnosis of oral candidosis should be made by
on distinctive clinical characteristics. identification of clinically distinctive lesions, by
Treatment includes oral rinsing with microscopic examination of cytological smears
chlorhexidine gluconate 0.20% solution, or biopsy tissue, or by response to antifungal
intrasulcular lavage or irrigation with 10% therapy.
betadine solution, antibiotic regimen of 250 mg Treatment of oral candidosis is determined by
metronidazole 3 times per day for 5 to 7 days, the clinical type, distribution, and severity of
often combined with 250 mg amoxicillin- infection. Clotrimazole 1% w/v–(Candid
clavulanate potassium 3 times a day for 5 to mouthpaint 15 ml) is effective for limited and
7 days. As systemic antibiotics increase the accessible lesions. Patients should be instructed
patients risk of developing oral candidosis, to maintain proper oral hygiene in order to
concurrent administration of an antifungal agent prevent caries that may result from the high
should be considered. Careful follow-up or sugar content in nystatin and clotrimazole. The
frequent appointments are appropriate and use of topical fluoride therapy should be
recommen-ded in the acute and healing stages considered for patients taking such medication
of NUP to perform the necessary periodontal for extended periods. When oropharyngeal
therapies (e.g., scaling and root planing), to assess candidosis cannot be controlled with topical
tissue response, and to monitor the patients oral medication alone, systemic antifungal therapy
hygiene performance. should be initiated.
Systemic antifungal therapy for oral
Oral Candidosis candidosis involves the use of ketoconazole,
The most common HIV-related soft-tissue lesion fluconazole, and itraconazole antifungal
is acute pseudomembranous oral candidosis medications. Fluconazole (100 mg tablet, 1 tablet
(reported in approximately 75% of cases), a day) is an excellent systemic antifungal
predominantly due to Candida albicans, a normal medication with a favorable therapeutic index,
inhabitant of the oral cavity in healthy making it the preferred systemic antifungal
individuals. The following forms of oral medication. A typical antifungal treatment
candidosis have been frequently associated with course should be for 10 to 14 days, with use of
HIV infection: acute pseudomembranous, acute the antifungal agent continued even after clinical
erythematous and angular cheilitis. Angular signs and symptoms of oral candidosis have been
cheilitis, though prevalent in HIV-infected resolved. Because patients with reduced salivary
individuals, is also seen in individuals who do flow are more susceptible to developing oral
not have HIV infection. Chronic hyperplastic candidosis, salivary flow should be stimulated
type has been described, but this finding is rare. to help reduce the incidence and severity of oral
In individuals infected with HIV, the candidosis. Chewing sugarless gum in the mouth
development of oral candidosis may be an can accomplish salivary flow stimulation.
indication of immune deterioration and has
prognostic significance for the development of Herpes Simplex Infection
AIDS. Oral candidosis may precede other signs In immunocompetent patients, oral ulcers caused
of immune deficiency and is one of the clinical by the herpes simplex virus (HSV) occur in
primary infection form (primary herpetic These ulcers do not have a characteristic
gingivostomatitis) and recurrent forms clinical appearance and may appear to be similar
(recurrent herpes labialis and recurrent intraoral to ulcers caused by other agents or circumstances.
herpes). The primary infection most commonly These ulcers differ from herpes simplex
occurs in children but also may occur in adults. ulceration in immunocompetent individuals in
Recurrent HSV infection represents that they are larger, can occur anywhere in the
reactivation of latent virus and not reinfection oral cavity, present for longer periods, and are
of HSV. Recurrent HSV infections can either non-responsive to routine therapy. The pain
occur as recurrent herpes labialis (RHL) or associated with persistent herpetic ulceration can
recurrent intraoral herpes (RIH). The result in reduced oral intake of food and
characteristic clinical appearance of RHL is focal significant weight loss.
clustering of vesicles. The vesicles quickly As atypical herpetic ulcers may be the first
rupture, resulting in ulcers that coalesce to form sign of immunosuppression, patients with these
the larger irregular-shaped ulcers with a crusted ulcers who are not known to be HIV infected
surface. In a healthy individual, the lesions heal should be referred for HIV counseling and
without scarring within 7 to 14 days. testing.
Recurrent intraoral herpes (RIH) lesions begin Diagnosis of typical herpes simplex infection
as clusters of tiny vesicles that rupture quickly, includes Tzanck test (mucosal smear), tissue
resulting in erosions or ulcers without crusting. biopsy, viral culture, serology, polymerase chain
The RIH lesions involve keratinized mucosa reaction and response to acyclovir are
(hard palate, attached gingiva, and edentulous recommended options to accurately diagnose the
ridges). However, in immunocompromised ulcers.
patients e.g., AIDS, the tongue can also be Intraoral HSV infection responds well to
affected. The lesions on the tongue exhibit systemic acyclovir, (200 mg capsules, 1-2
mucosal erosions, each of which is surrounded capsules, 5 times a day for 10 days). However,
by a circinate, raised, yellow border. This border the incidence of acyclovir-resistant HSV has
represents the advancing margin of active viral increased among patients with HIV infection. For
destruction. Intraoral recurrence follows a pat- most of these cases, oral famciclovir and
tern of presentation similar to that of RHL except valacyclovir and intravenous foscarnet alone or
the lesions are intraoral, and crusting does not in combination are effective.
occur. The pain associated with RIH may
interfere with eating and speaking. In a healthy Oral Hairy Leukoplakia (Greenspan lesion)
individual, the lesions heal without scarring
within 7 to 14 days. The term “oral hairy leukoplakia” is unfortunate
In patients with HIV infection who have for several reasons. First of all, oral hairy
marked immune deficiency, ulcers caused by leukoplakia is a definable lesion as per WHO
herpes simplex infection tend to be persistent, Collaborating Centre on oral manifestations of
superficial (infecting the epithelium and not the immunodeficiency virus (1993). Furthermore,
connective tissue), and painful. Persistent the lesion is not a premalignant one. Therefore,
herpetic lesions in HIV infected patients that do the use of the term oral hairy leukoplakia should
not resolve after 4 weeks fulfill the Centers for be abandoned. As an alternative, the term
Disease Control and Prevention (CDC) criteria “Greenspan lesion” has been suggested by Waal
for a diagnosis of AIDS. van der I (1996).
It appears as an asymptomatic adherent white Sutton’s disease) account for 10 to 15% of all cases
patch with vertical corrugations, most commonly of recurrent aphthous ulcers. The prodromal
on the lateral borders of the tongue. It may be symptoms are more intense than those of minor
confused with chronic hyperplastic oral aphthous ulcers. They are large solitary or
candidosis and is predominantly found in multiple, chronic, deep crater-like, painful
homosexual males. Oral hairy leukoplakia (Fig. ulcerations that extend through the epithelium
10.8) has since been shown to be associated with into the connective tissue. As in non-HIV-
a localized Epstein-Barr virus (EBV) infection and infected patients, these ulcers generally occur on
occurs most commonly in individuals whose nonkeratinized oral mucosa (lips, soft palate, and
CD4+ T cell count is less than 200/mm3. throat) overlying the minor salivary glands but
can present in any location.
They are larger than 1 cm in diameter and can
lasts for weeks or months and often leave a scar
after healing. Major aphthous ulcers are the most
common immune-mediated HIV-related soft-
tissue oral lesions, with a prevalence of
approximately 2–3% (Fig. 10.9).
Fig. 10.8: Oral hairy leukoplakia
As in all patients, when an HIV infected

patient presents with a white lesion on the lateral
border of the tongue that cannot be diagnosed
because of its clinical appearance, biopsy and
microscopic examination should be considered.
Oral hairy leukoplakia generally does not require
treatment. Fig. 10.9: Major aphthous ulcer
Oral Warts Diagnosis of aphthous ulcers should be based

on the characteristic clinical appearance of
In some patients with HIV infection, human painful, round to oval, yellow to white ulcers
papilloma virus causes a focal epithelial and surrounded by a halo of erythema. They often
connective tissue hyperplasia, forming an oral last much longer and are less responsive to
wart. Diagnosis of human papilloma virus therapy.
lesions should be made by routine biopsy and The management of aphthous ulcers should
histological examination. include the use of topical corticosteroids;
however, caution should be taken because
Major Aphthous Ulcers
steroid use may result in oral candidosis,
Major aphthous ulcers (periadenitis mucosa therefore, concurrent administration of an
necrotica recurrens, ulcerative stomatitis, antifungal agent should be considered.
Treatment requires the use of a potent topical large numbers of specimens on a daily basis, e.g.,
corticosteroid when the lesion is accessible or blood donations and the most widely used
corticosteroid steroid mouthwash confirmatory test is the Western Blot. The key
(dexamethasone 3 times daily, rinse for 45 points in the diagnosis of HIV are as follows:
seconds and expectorate) when the lesion is 1. HIV disease is diagnosed by the presence of
inaccessible. clinical signs and symptoms and specific
When multiple ulcers are present or response laboratory tests
to topical treatment is incomplete, systemic 2. The ELISA (enzyme-linked immunosorbent
corticosteroid therapy is required (1-2 mg/kg a assay) is the screening test used to diagnose
day divided in 4 doses) may be necessary. HIV infection
Systemic corticosteroid therapy should be given 3. The Western blot and PCR (polymerase
for 5-7 days, with gradual tapering of the dose chain reaction) tests help to confirm HIV
over 2 weeks. infection
Thalidomide has been shown to be effective 4. Maternal antibodies are present in an infant’s
for the treatment of non-resolving aphthous blood for up to 18 months after birth, making
ulcers in HIV-positive patients Because of severe it difficult to establish the diagnosis of HIV
side effects, thalidomide should only be used by ELISA and Western blot
when all other options have been exhausted. In 5. The CDC has established a staging system
adolescent and adult women capable of bearing for HIV disease in infants and children based
children, thalidomide should only be used when on the CD4+ T cell count and clinical signs
the woman is known not to be pregnant and is and symptoms
using effective methods of birth control. 6. The WHO clinical diagnostic system is based
However, if the ulcers are thought to be drug on dividing signs and symptoms into major
induced, the medication should be temporarily and minor criteria
discontinued or dose reduced. Medications that 7. Diagnosing HIV follows the same principles
can cause aphthous ulcers include zidovudine, in adults as in children.
and foscarnet.
Diagnostic Tests
Diagnosis ELISA
The diagnosis of HIV infection is usually made One screening test used to diagnose HIV is the
on the basis of the detection of antiHIV ELISA (enzyme-linked immunosorbent assay),
antibodies. Serological tests for detecting antiHIV which is an enzyme immunoassay (EIA). When
antibodies are generally classified as screening this test is performed on a patients serum or
tests (initial tests) or confirmatory tests blood, it identifies antiHIV antibodies. ELISA
(supplemental tests). tests are highly sensitive but not always specific.
Screening tests help in the likely identification This means that other illnesses besides HIV can
of antiHIV antibodies, and confirmatory tests are cause a positive test. Among these illnesses are
used to confirm whether the antiHIV antibodies autoimmune diseases, certain viral infections,
found are reactive with proteins specific to syphilis, and hematological malignancies.
antiHIV antibodies. Pregnancy may also cause a false-positive ELISA.
The most widely used screening test is the As maternal antibodies are present in an infant’s
ELISA as it is most appropriate for screening blood for up to 18 months after birth, the ELISA
is accurate only in children over 18 months of of the protein bands are seen, the western blot is
age. Further, because the test is based on the positive. The western blot test can be
detection of antiHIV antibodies, an infected inconclusive. In the event that an inconclusive
patient may have a negative ELISA during a test result is found, the test should be repeated
“window period”. on the same serum sample and then repeated
again in two weeks. If the inconclusive pattern
Window Period
persists, the western blot needs to be repeated
The window period is the time between initial
periodically for the next six months. If the pattern
infection with HIV and the development of
persists after six months, the person is most likely
enough antiHIV antibodies to be detected
not infected with HIV.
through testing. In general, 3 to 3 months (12
weeks) is required after infection. A recently
Rapid Tests
infected individual, therefore, may not test
positive for HIV but could still transmit HIV to Rapid HIV screening tests, first approved in 1996,
others. can be performed in an average of 10 minutes.
The virus is not latent during the window Several rapid tests detect antiHIV antibodies,
period. Viral replication in the regional lymph much like the ELISA and are as accurate as
nodes leads to viremia (high levels of viral ELISA. The results are available in just a few
particles in the blood) and widespread seeding minutes to hours. Most rapid tests can be
of HIV in the lymphoid tissues (lymph nodes, performed on blood obtained from a finger stick
spleen, and tonsils) resulting in reduction of and performing them requires little training.
CD4+ T cell count. In fact, the viral load (number Many different commercial rapid tests are
of HIV RNA copies per mL of blood plasma) is available, and most are 99-100% sensitive and
higher after initial infection than any period until specific. Rapid test methods include “dot blot”
advanced HIV disease. Understanding the or “immunoblot” assays that produce a colored
window period is important for recommen- dot on the solid phase surface. Some rapid tests
dations regarding for risk prevention and further can use saliva or urine samples instead of blood
testing as mentioned below: samples.
1. Persons should be counseled to take For positive-tests, however, a confirmatory
precautions to prevent transmission of HIV ELISA and Western blot is still required to
during the window period
eliminate false-positives. Like the ELISA, these
2. A recently exposed person should be advised
rapid tests are accurate only in children over 18
to return for antiHIV antibody testing within
months of age and usually give a negative result
3 weeks after the exposure incident
during the window period.
3. It is important to ensure that persons
receiving pre-HIV test counseling and post- DNA/RNA PCR
HIV test counseling understand the window
period concept. Finally, polymerase chain reactions (PCR) for the
DNA or RNA of the HIV virus can be performed.
Western Blot These tests are highly sensitive and specific for
A western blot is a polyacrylamide gel HIV infection. They are often used if the results
electrophoresis that detects bands of proteins of other diagnostic tests are unclear. DNA PCR
specific to antiHIV antibodies. If no bands are is most commonly utilized to diagnose HIV
seen, the western blot is negative. If most or all infection in children under the age of 18 months.
Test Counseling 7. Discuss the terminology of HIV and AIDS,

concepts like CD4 cell and viral load, signs
Pretest Counseling
and symptoms of HIV-related illness
The pretest counseling consists of a process 8. Encourage to undergo regular medical
starting with asking history of exposure to risk check-up and to have appropriate lab tests
factors and an explanation of preventive (including PPD skin test for TB and
measures. Information about the test, including pregnancy test, if indicated)
an explanation about what the test can and 9. Provide educational materials, as
cannot determine is also necessary. However, appropriate
pretests require consent prior to testing because
of the emotional, physical, and social Disclosure in Health Care Settings
implications of having a diagnosis of HIV
infection. Disclosure of HIV infection to others is a serious
and sensitive issue. Informed consent must be
Post-test Counseling obtained for any disclosure. Health care workers
Post-test counseling should be performed with have legal and ethical responsibilities to maintain
all patients who return for test results. the confidentiality of patient status and
treatment.
Seronegative post-test counseling should include: Despite this, patients should be encouraged
1. Reinforce to avoid risk factors for the to disclose a diagnosis of HIV infection to all
prevention of HIV transmission health care workers so that appropriate treat-
2. Confirm whether the last possible exposure ments can be provided.
was not within the last six months. If it was, However, most of the times, patients will not
encourage retesting 3 weeks to 3 months after disclose as they do not feel safe. It is essential
the most recent exposure that all health care workers, including the
3. Provide information on community support paramedical staff, be oriented to the responsi-
services bility of maintaining confidentiality and mana-
4. Provide information on psychosocial ging clinic records appropriately.
support, if appropriate
Seropositive post-test counseling should include: Antiretroviral Therapy (ART)
1. Assess the individual for mental distress Antiretroviral (ART) therapy refers to the use of
2. Assess the availability of personal support pharmacologic agents that have specific
(friends, family, etc.) inhibitory effects on HIV replication. These
3. Discuss plan for partner notification agents belong to four distinct classes of drugs:
4. Persons should be counseled for eliminating Nucleoside reverse transcriptase inhibitors
or reducing the risk of transmission to others (NRTIs), non-nucleoside reverse transcriptase
5. Review basic principles of good health such inhibitors (NNRTIs), protease inhibitors (PIs) and
as nutrition, stress reduction, sleep and the fusion inhibitors (FIs). The current standard
exercise, and good dental care for formulating a highly active antiretroviral
6. Discuss the importance of avoiding therapy (HAART) regimen recommends the use
additional infections that will stress the of either PIs or NNRTIs in combination with two
immune system e.g., candidosis nucleoside reverse transcriptase inhibitors.
Classification of Antiretroviral Drugs Protease Inhibitors: They act by binding to the

(Fig. 10.10) viral protease, in this way preventing the correct
cleavage of viral proteins. Thus, they prevent
1. Nucleoside reverse transcriptase inhibitors
HIV from being successfully assembled and
2. Non-nucleoside reverse transcriptase
released from the infected cells. Examples:
inhibitors
indinavir (IDV), nelfinavir (NFV), ritonavir
3. Protease inhibitors
(RTV), saquinavir (SQV), amprenavir (AMP).
4. Fusion inhibitors.
Fusion Inhibitors: Fusion inhibitors work by
blocking HIV entry into cells. Example:
Enfuvirtide (T-20).
Indications for Antiretroviral Therapy

1. Symptomatic AIDS
2. Asymptomatic, AIDS - (CD4+ T cell count <
350 cells/mm3and plasma HIV RNA any
value)
3. Asymptomatic - (CD4+ T cell count > 350
cells/mm3 and plasma HIV RNA > 100,000
copies/ml (RT-PCR or bDNA)
4. Asymptomatic - (CD4+ T cell count > 350
Fig. 10.10: Antiretroviral drugs
cells/mm3 and plasma HIV RNA < 100,000
copies/ml (RT-PCR or bDNA)
Mode of Action
Post-exposure Prophylaxis
Nucleoside Reverse Transcriptase Inhibitors:
Nucleoside reverse transcriptase inhibitors are Health Canada’s Laboratory Center for Disease
faulty versions of building blocks that HIV needs Control, in cooperation with the U.S. Centers for
Disease Control and Prevention (CDC), issues
to make more copies of itself. They act by
recommendations on a variety of health concerns
incorporating themselves into the RNA of the
for the general population and for health care
virus (competing with natural nucleotides),
settings. One such recommendation, which has
thereby stopping the building process of
been modified relatively recently, is a protocol
transcription from RNA to DNA. The resulting
for post-exposure prophylaxis (PEP) of percuta-
DNA is incomplete and cannot create a new
neous injury with known HIV contaminated
virus. Examples: zidovudine (ZDV), lamivudine
blood.
(3TC), stavudine (d4T) and didanosine (ddL). Healthcare personnel are at risk for
Non-nucleoside Reverse Transcriptase occupational exposure to blood borne pathogens,
Inhibitors: They act by stopping HIV production including human immunodeficiency virus or
by binding directly onto reverse transcriptase (non- HIV. Exposures occur through needle sticks or
competitively) and preventing the conversion of cuts from sharp instruments contaminated with
RNA to DNA. Examples: efavirenz (EFV), an infected patients blood. Several clinical studies
nevirapine (NVP), and delavirdine (DLV). have demonstrated that HIV transmission
following occupational exposure can be 3. Splash of blood to a mucosal surface (mouth,

significantly reduced by administration of nose, or eyes)
antiretroviral agents or ARV. Therefore, post- 4. A nonintact skin exposure to blood (e.g.,
exposure prophylaxis or PEP is an integral dermatitis).
component of a complete program to prevent
infection after an occupational exposure to blood. Risk of HIV Infection after Occupational
Exposure among HCW
Implementing PEP
The average risk of HIV infection after
PEP should be initiated as soon as possible,
percutaneous exposure is only 0.3%. The average
ideally within 2 hours and generally no later than
36 hours post-exposure. PEP provides a risk of HIV infection after exposure of eye, nose,
“window of opportunity” in limiting and and mouth to HIV infected blood is estimated to
preventing viral replication following exposure be 0.1%. The average risk of HIV infection after
to blood. The prescribing provider should ensure exposure of non-intact skin to HIV-infected blood
that the health care worker or HCW has access is estimated to be less than 0.1%.
to the full course of ARV drugs. According to CDC National Surveillance
System for Healthcare Workers, June 1995
PEP Indications through August 2001, injuries occurred most
PEP is indicated under the following circum- frequently with small hollow bore needle (34%),
stances: followed by burs (13%), suture needles (11%),
1. Break in the skin by a sharp object that is surgical scalpels (7%), scalers (6%), explorers
contaminated with blood (5%), and wires (4%); “other sharp objects”
2. Bite from a HIV infected patient with visible accounted for 20% (Fig. 10.11).
bleeding in the mouth that causes bleeding Injuries with other sharp objects, involved
in the health care worker with large hollow bore needle (< 23-gauge) used
Fig. 10.11: Devices causing injuries

for blood collection, and another involved a exposed person should be reevaluated within
needle used to deliver intravenous fluids. 72 hours and monitored for drug toxicity for at
After an occupational blood exposure, induce least two weeks. If the source patient is
bleeding from the wound by squeezing the injury determined to be HIV-negative, PEP should be
site and holding it under warm, running water, discontinued. Perform HIV-antibody testing for
thoroughly wash the wound several times with at least six months postexposure and perform
an antimicrobial hand wash, primary closure of HIV-antibody testing if illness with early “acute”
the wound, if necessary, should be performed, phase occurs. Advice exposed persons to use
and report the exposure to the infection control precautions to prevent secondary transmission
department responsible for managing exposures. during the follow-up period. Because most
occupational blood exposures do not result in
Treatment of Exposure Site, Exposure transmission of HIV, the decision to recommend
Report and Evaluation of the Exposure PEP must be based on the type of exposure,
Each occupational blood exposure should be information about the infectious status of the
evaluated individually. This evaluation is based source and side effects of PEP. When possible,
on the following: the regimens should be implemented in
consultation with persons who have expertise in
1. The amount of blood involved
antiretroviral treatment and HIV transmission.
2. The details of the procedure being
According to CDC a basic regimen using two
performed, including where and how the
nucleoside reverse transcriptase inhibitors
exposure occurred, type of device involved
(NRTIs) is recommended if the source is Class 1.
(e.g., small hollow bore needle), and when
An expanded PEP regimen, which adds non-
during its handling the exposure occurred
nucleoside reverse transcriptase inhibitors
3. The type of exposure (e.g., percutaneous
(NNRTIs) or a protease inhibitor (PIs) is
injury, contact with mucous membrane,
recommended if the source is Class 2. The
contact with non-intact skin, bites resulting
addition of a third drug should be considered
in blood exposure)
for exposures that pose an increased risk for
4. The infectious status of the source
transmission.
Infection Status of the Source In most cases, if the HIV status is unknown,
no PEP is recommended. However, for source
The infection status of the source according to
with HIV risk factors or in settings where they
CDC is classified as:
are likely to be HIV-positive, a basic two regimen
1. Class 1: Asymptomatic HIV infection or
using two nucleoside reverse transcriptase
patient has a known viral load of < 1500 RNA
inhibitors is recommended.
copies/milliliter
1. Class 1: Zidovudine (ZDV) + lamivudine
2. Class 2: Symptomatic HIV infection, full
(3TC); lamivudine (3TC) + stavudine (d4T);
blown AIDS or patient with known viral load
stavudine (d4T) + didanosine (ddL).
of > 1500 RNA copies/milliliter
2. Class 2: Zidovudine + lamivudine +
3. Unknown HIV Status: The HIV status of the
indinavir or nelfinavir or efavirenz;
patient is unknown
lamivudine + stavudine + indinavir or
nelfinavir or efavirenz.
PEP for Occupational Exposure
3. Unknown HIV status: Zidovudine +
If PEP is indicated, it should start as soon as lamivudine; lamivudine + stavudine;
possible (within hours rather than days). The stavudine + didanosine.
The possible contributing factors which may 6 months after exposure to prevent HIV
result in failure of PEP include resistant HIV transmission and potential drug toxicities.
strain, high viral titer, delayed initiation of PEP,
PEP of short duration, and decreased cellular Preventing Needlestick Injuries
immunity. Prevention of occupational infections with HIV
Avoiding occupational blood exposures is the includes:
primary way to prevent transmission of 1. Appropriate uses of barriers such as face
bloodborne pathogens in health care settings. mask, eye glasses, gloves, and drape.
Reducing injuries can be accomplished through 2. Safely handling needles and other sharp
appropriate use of barriers such as gown, gloves objects
and eye protection, safely handling needles and 3. Using devices with safety features
other sharp instruments, and using devices with
safety features as recommended by OSHA or
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Chapter
Pregnancy and
11 Dental Care
Terminology
1. Nullipara: Who has never completed a term
of pregnancy
2. Nulligravida: Who has never become
pregnant
3. Primipara: Who has delivered one viable
child
4. Primigravida: Who is pregnant for the first
time
5. Multigravida: Who has been previously
pregnant
6. Multipara: Who has delivered two or more
children
7. Parturient: Who is in labour
8. Puerpera: Who has just given birth
Pregnancy Fetal Development

First Trimester
INTRODUCTION
The duration of the first trimester is first 12 weeks
Management of a pregnant dental patient poses (84 days). The first 12 days from conception to
a unique challenge to the dentist, as he or she is implantation is the preimplantation period.
solely responsible for providing safe and effective Exposure to harmful drugs during preimplan-
care to the mother and the developing fetus. tation period can kill the embryo. From the 13th
There are number of anatomical and physio- day, there is organogenesis and the fetus is
logical, maternal changes during pregnancy. A susceptible to abortion and teratogenicity
sound knowledge of these changes will help the
dental surgeon in careful management of the Second Trimester
pregnant dental patient. Apart from these The duration of the second trimester is from
changes, various complications of pregnancy 13 weeks to 28 weeks (112 days). It is the optimal
may complicate the dental treatment. trimester for dental care.
Third Trimester Anatomical and Physiological Changes

during Pregnancy
The duration of the third trimester is from
29 weeks to 40 weeks (84 days). Dental care is Due to increasing demands of the fetus, there are
not advisable during this period as the fetus is various anatomical, physiological, endocrinal,
mature and there is an increased risk of supine and metabolic changes during pregnancy (Tables
hypotension, hypertension, and preeclampsia. 11.1 to 11.4).
Table 11.1: Anatomical changes during pregnancy
Genital organs Anatomical changes
Ovaries Growth of corpus luteum
Fallopian tubes Tubes are congested
Uterus Increase in size
increase in vascularity
Increase in weight due to hypertrophy of the muscles
Frequent changes in shape
Position is altered and it lies on the bladder
Cervix Hypertrophy and hyperplasia of the epithelium and connective tissue
Hypertrophy and hyperplasia of the mucous glands
Increase in vascularity
Cervix becomes soft (Goodell’s sign)
Increased mucus secretion, which forms a mucosal plug that seals the cervical canal
Vagina Increase in size
The mucosa is violet in colour due to increase in vascularity (Jacqumier’s sign)
pH becomes acidic due to conversion of glycogen into lactic acid by Lactobacillus acidophilus
because of high estrogen level
Breasts Increase in size due to hypertrophy and hyperplasia of ducts and alveoli
Hypertrophy and hyperplasia of the connective tissue stroma
Increase in vascularity
Increase in size of the nipples
Pigmentation of the nipple and areola
Skin Pigmentation of face (chloasma gravidarum or pregnancy mask)
Pigmentation of the abdomen
Striae gravidarum (stretch marks)
Vascular spider
Loss of hair
Brittle nails
Table 11.2: Physiological changes during pregnancy

Systems Physiological changes
Hematological changes Due to increase in the blood volume and plasma volume there is hemodilution which results in
fall of total hemoglobin concentration though there is an increase in total hemoglobin which
indicates that hematological changes are only quantitative and not qualitative
Contd...
Pregnancy and Dental Care 157
Contd...
Increase in concentration of coagulation factors
Increase in plasma fibrinogen level
ESR is increased but has no significance
Cardiovascular system Increased cardiac output due to increase in blood volume
Blood pressure is normal in spite of increased cardiac output because of reduced peripheral
resistance due to high level of progesterone
Pulse rate is increased
Heart is pushed upwards and outwards with a slight rotation to the left because of elevation of
diaphragm due to enlarged fetus
Palpitations due to displaced heart
Apex beat is shifted to fourth intercostal space
Systolic murmurs
No hypertrophy or cardiac dilatation
Respiratory system Breathlessness due to the action of progesterone on the respiratory centre and its increased
sensitivity to arterial carbon dioxide
Digestive system Decreased motility of gastrointestinal tract due to high level of progesterone
Relaxed cardiac sphincter (sphincter of the esophagogastric junction) which leads to
regurgitation of acid into esophagus causing heart burn
Excretory system Increased renal blood flow
Increased glomerular filtration rate
Polyuria due to pressure applied on the bladder by the enlarged and displaced uterus
Nervous system Mental irritability
Sleeplessness
Generalized neuritis due to vitamin B1 (thiamine) deficiency
Compression of lumbosacral trunk by the fetus may lead to paralysis of some leg muscles
Table 11.3: Endocrinal changes during pregnancy

Endocrine glands Endocrinal changes
Pituitary gland Hyperplasia of the pituitary gland
Bitemporal hemianopia due to impingent on the optic chiasma by the hyperplastic pituitary gland
Increased secretion of growth hormone
Increased secretion of thyroid stimulating hormone
Increased secretion of adrenocorticotrophic hormone
Increased secretion of antidiuretic hormone
Increased secretion of oxytocin
Thyroid gland Hyperplasia of the thyroid gland
Increased secretion of thyroxine
Increased basal metabolic rate
Parathyroid gland Hyperplasia of the parathyroid glands
Increased secretion of parathyroid hormone
Contd...
Contd...
Adrenal cortex Hyperplasia of the adrenal cortex especially zona fasiculata
Increased secretion of glucocorticoids
Absence of Cushing’s syndrome with such plasma levels of glucocorticoids indicate that the
tissue receptors are insensitive
Pancreas Hyperplasia of the pancreas
Increased secretion of glucagon
Increased secretion of insulin (see anti-insulin factors)
Placenta Progesterone and oestrogens (estriol, estradiol and estrone)
Human chorionic gondaotrophin
Human chorionic somatomammotrophin (placental lactogen)
Human chorionic thyrotrophin
Human chorionic corticotrophin
TRH
GnRH
Table 11.4: Metabolic changes during pregnancy

Metabolic changes
Carbohydrate metabolism Glycogenolysis
Gluconeogenesis
Maternal fasting hypoglycemia due to increased consumption of glucose by the fetus
Postprandial hyperglycemia
Altered insulin sensitivity due to tissue resistance, placental insulinase (which degrades
the insulin), human placental lactogen(anti-insulin effect), increased secretion of growth
hormone, glucagons and glucocorticoids
Protein metabolism Increased protein synthesis
Positive nitrogen balance
Fat metabolism Increased free fatty acid level because of breakdown of fats and increased absorption of
fats
Deposition of fats in the abdominal walls, breasts, hips and thighs
Iron metabolism The total iron requirement during pregnancy is 1000 mg thus there is increased absorption
of iron from the duodenum and jejunum which is then transported across the placenta to
the fetus
Calcium metabolism Due to increase in calcium demand by the fetus, there is an increase in absorption of
calcium from the gut and kidneys due to the action of parathyroid hormone
Physiology of Female Sex Hormones

of women (Table 11.5). Progesterone is primarily
Oestrogens (estriol, estradiol and estrone) and a hormone of pregnancy and most of its actions
progesterone are female sex hormones secreted in nongravid women are to prepare the female
by the ovaries, which play a major role in the life reproductive system for gestation.
Table 11.5: Physiology of female sex hormones

Actions estradiol progesterone
Female reproductive tract Enlargement of vagina
Enlargement of external genitalia
Secondary sexual characteristics Widening of pelvic girdle
Deposition of subcutaneous fat
especially in the buttocks, thighs,
and breasts
Mammary gland Growth of ducts Growth of alveoli and lobules
Uterus. Increases blood supply, which causes Increases blood supply to uterine
proliferation of uterine endometrium endometrium
Increases contraction of myometrium Decreases contraction of myometrium
Decreases the viscosity of mucus by Increases secretion of glands
increasing its water content Increases the viscosity of mucus thereby
forming mucus plug
Oviducts Increases muscular contractions Decreases muscular contractions
Increases secretion of glands
Endothelium Proliferation Proliferation
Glycosaminoglycans Reduce synthesis Reduce synthesis
Physiology of Placental Hormones Progesterone Metabolism

During pregnancy, the placenta produces Some hormones like testosterone become
varieties of hormones of which steroid and biologically active after metabolization, while
protein hormones are important (Table 11.6). The progesterone becomes biologically inactive after
placenta produces estriol rather than estradiol metabolization. In healthy human gingiva, rate
as secreted by the ovaries. of progesterone metabolization is low, which
may indicate the presence of high amounts of
Table 11.6: Physiology of placental hormones
biologically active progesterone. However, in
Steroids Progesterone
inflamed gingiva, the metabolism of
Estrogens (estriol, estradiol and estrone)
progesterone is two to three times greater than
in healthy gingiva. This may mean that there is
Proteins Human chorionic gondaotrophin
a very low or negligible amount of biologically
Human chorionic somatomammotrophin
active progesterone in the inflamed tissue.
(placental lactogen)
The reason as to why progesterone is not
Human chorionic thyrotrophin
metabolized in an inflamed gingiva of pregnant
Human chorionic corticotrophin
patient is difficult to explain. However,
Peptides TRH progesterone may be responsible for the
GnRH increased permeability of gingival vessels during
pregnancy. It is a well-known fact that proges- feature in hyperemesis gravidarum is erosions

terone concentrations in the maternal circulation of the palatal surfaces of upper anterior teeth.
are sufficient to cause immunosupression and
Hemorrhage
that progesterone functions as an immuno-
suppressant in the placenta and other tissues The causes of hemorrhage in pregnancy may be
during pregnancy. Thus, coexistence of these two related or unrelated to pregnancy.
important factors prevents acute-type of tissue
Hemorrhage Related to Pregnancy
reaction (which would keep the tissues clinically
healthy) to plaque, which would otherwise keep 1. Miscarriage
the tissues healthy, but allows an increased 2. Ectopic pregnancy
chronic-type of tissue reaction, resulting in an 3. Hydatidiform mole
exaggerated inflammatory clinical appearance. Hemorrhage Unrelated to Pregnancy
1. Polyps
Complications of Pregnancy
2. Vascular erosions
The dentist should be aware of the complications 3. Ruptured varicose veins
that complicate the pregnancy because any 4. Malignancy
dental treatment may be looked upon as a
causative factor for the complication especially Anemia
abortion. Thus, a detailed case history prior to Anemia is the most common hematological
any dental procedure is of immense value as it disorder that may occur during pregnancy.
rules out any complication. According to WHO, anemia during pregnancy
is present when the hemoglobin concentration
Vomiting in the peripheral blood is < to 11 gm/100 ml. The
total iron requirement in pregnancy is
Vomiting is a symptom, which may be related
approximately 1000 mg (placenta = 300 mg,
or unrelated to pregnancy.
fetus = 600 mg, and expanded red cell
Vomiting Related to Pregnancy volume = 300 mg).
The iron present in the placenta and fetus is
1. Simple vomiting permanently lost along with iron present in
2. Hyperemesis gravidarum expanded red cell volume, which is partially lost
during delivery. Anemia in pregnancy may be
Vomiting Unrelated to Pregnancy
due to the following reasons:
1. Urinary tract infection 1. Preexisting anemic state
2. Hepatitis 2. Decreased intake
3. Diabetic ketoacidodsis 3. Faulty diet
4. Peptic ulcer 4. Multiple pregnancies
Simple vomiting is common during 5. Increased demand for iron by the developing
pregnancy and is a symptom. The pregnant fetus
patient complains of nausea and sickness on 6. Polymorphism (polymorphism is a condition
waking up in the morning. Hyperemesis in pregnancy that tends to interfere with
gravidarum is a severe type of vomiting which erythropoiesis by competing for the available
has deleterious effects on the health of mother raw materials such as iron, folic acid, vitamin
and incapacitates day-to-day life. A common B12, and proteins.
Jaundice Screening for gestational diabetes mellitus is

between 24 and 28 weeks. However, after
If the serum bilirubin level exceeds 2 mg/100 ml
parturition the blood glucose levels return to
(normal = 0.5-1.0 mg/100 ml) visible yellow
normal. The various mechanisms that lead to
staining of the tissues and mucous membranes.
The causes of jaundice during pregnancy may gestational diabetes are:
be related or unrelated to pregnancy. 1. Increased absorption of glucose from
alimentary tract
Jaundice Related to Pregnancy 2. Inability of insulin to convert glucose into
1. Preeclampsia glycogen
2. Eclampsia 3. Impaired tubular reabsorption of glucose
3. Hyperemesis gravidarum which leads to glycosuria
Jaundice Unrelated to Pregnancy Hypertension

1. Viral hepatitis Hypertension is one of the common complica-
2. Gallstones (obstructive jaundice) tions in pregnancy. It is a sign of underlying
3. Mismatched blood transfusion (hemolytic
pathology, which may be preexisting or
jaundice)
appearing for the first time during pregnancy.
The causes of hypertension in pregnancy may
Acute Abdominal Pain
be related or unrelated to pregnancy.
Some amount of abdominal discomfort is
common during pregnancy. However, severe Hypertension Related to Pregnancy
abdominal pain and discomfort is indicative of 1. Preeclampsia
underlying pathology. Few of the causes of acute 2. Eclampsia
abdominal pain are ectopic pregnancy, abortion, Preeclampsia: Preeclampsia is a multisystem
preterm labour, labour pains, hydatidiform mole, disorder of unknown etiology, induced during
ruptured uterus, polyhydraminos, acute pregnancy after the 20th week and characterized
appendicitis, cystitis, and pyeliytis. by development of hypertension to the extent of
140/90 mmHg or more with proteinuria.
Asthma
Eclampsia: In Greek, eclampsia means “like a flash
During pregnancy, some amount of of lightning.” Eclampsia may occur quite
breathlessness is common due to the action of abruptly, without any warning manifestations.
progesterone on the respiratory centre and its Usually features of severe preeclampsia precede
increased sensitivity to arterial carbon dioxide. eclampsia.
Incidence of asthma is about 1% in all pregnant
women. The course of asthma during pregnancy Hypertension Unrelated To Pregnancy
is unpredictable. It may improve, deteriorate or 1. Thyrotoxicosis
may remain unchanged. 2. Coarcation of aorta
3. Pheochromocytoma
Gestational Diabetes Mellitus
4. Essential hypertension
Gestational diabetes is present in the late second 5. Renovascular hypertension
and during third trimester of pregnancy. 6. Systemic lupus erythematosus
Supine Hypotension or third trimester. Histologically pregnancy

tumor is identical to pyogenic granuloma.
During pregnancy, the gravid uterus compresses
Recurrence of the excised lesion is common
the inferior vena cava when the patient is in a
supine position, which results in opening of the during pregnancy. Partial or complete regression
collateral circulation by means of paravertebral of the lesion is common after childbirth.
and azygos veins. In 10% of the cases, the Pathogenesis
collateral circulation fails to open up which
There is an increased frequency of pregnancy
results in supine hypotension, tachycardia, and
tumor during pregnancy. The three major
syncope. By turning the patient to a lateral
hormones produced by the placenta are
position, the normal blood pressure is restored.
progesterone, oestrogens (estriol, estradiol and
estrone), and human chorionic gondaotrophin.
ORAL MANIFESTATIONS OF PREGNANCY
Human chorionic gondaotrophin is in large
The oral manifestations of pregnancy are: amounts during the first 10 weeks of pregnancy,
1. Pregnancy tumor (pregnancy granuloma, after which levels fall dramatically. Therefore, it
epulis gravidarum) seems unlikely that this hormone plays a role in
the pathogenesis of pregnancy tumor. On the
2. Pregnancy gingivitis (gingivitis gravidarum)
other hand, the concentrations of progesterone
3. Erosions of hard tissues and oestrogens rise steadily until childbirth. By
the end of 40th week of pregnancy, the oestrogen
Pregnancy Tumor production is 100 times more than the oestrogen
Pyogenic granuloma is a benign inflammatory levels of the nonpregnant female. This indicates
lesion composed of proliferating capillaries and that there is an increased incidence of pregnancy
tumor as pregnancy progresses.
endothelial cells (exuberant granulation tissue)
The gingiva is subjected to higher levels of
in a lobular pattern, accompanied by mixed
these hormones not only through the
inflammatory cell infiltrate. Pyogenic granuloma
bloodstream but also from saliva. This additive
is well-known in dermatology and the term
effect explains why so many pregnancy tumors
“lobular capillary hemagioma” is gaining favor
occur in the oral cavity. Many authors stress the
in the dermatologic literature. Pyogenic
importance of some form of chronic low-grade
granuloma commonly occurs in the gingiva but
irritation (plaque, calculus, irregular dental
may be present on the tongue, lips, or buccal
restorations) as the inciting factor, with the
mucosa. response enhanced by female sex hormones
Pyogenic granuloma of the gingiva is (Fig.11.1). For a lesion to respond to oestrogen
“pregnancy tumor.” Pregnancy tumor is a and progesterone, the vascular endothelial cells
clinical term used to describe a red or reddish must exhibit receptors for these hormones.
purple, often nodular, and/or ulcerated localized However, very low concentrations of estrogen
tumor that bleeds easily. Pregnancy tumor is a and progesterone receptors are present in
clinical diagnosis for a red swelling, usually an gingival vessels. It is a well-known fact that
epulis, in pregnant women. It is single but may oestrogen induces neovascularity of the
be multiple and may grow rapidly. The clinical endometrium in the proliferative phase of the
onset of pregnancy tumor is around the second menstrual cycle.
Fig. 11.1: Pathogenesis of pregnancy tumor
Treatment Protocol for Pregnancy Tumor gingiva is due to increased levels of estradiol (E2)
Surgical excision is not required for lesions that and progesterone as they reduce the synthesis
do not cause significant functional or esthetic of glycosaminoglycans, which are hydrophilic.
problems as they may recur. However, surgical Pregnancy gingivitis is more common at the
excision is required for lesions, which do not incisor region than the premolar and molar
resolve after pregnancy. region.
Pregnancy Gingivitis Pharmacological Considerations

The gingiva in pregnancy is oedematous and Administration of drugs to pregnant patients is
characterized by marked tendency towards of significant concern because of the teratogenic,
bleeding and histologically has no specific feature toxic, or otherwise harmful effects of drugs on
distinguishing it from normally inflamed the developing fetus. The placenta does not
gingiva. The oedematous appearance of the strictly constitute a barrier and any drug can cross
it to a greater or lesser extent. The embryo is one pharmacokinetics lead to changes in drug
of the most dynamic biological systems and in absorption, distribution, excretion, and
contrast, to adults, drug effects are often metabolism.
irreversible.
Teratogenicity refers to capacity of a drug to
Drug Absorption
cause fetal abnormalities when administered to Because of high levels of progesterone the
the pregnant mother. The teratogens disturb gastrointestinal motility is decreased which
organogenesis in the developing embryo so that results in slower drug absorption. Thus, in order
defects in one or more structures are produced. to obtain a quick response parenteral drug
If the defects are incompatible with life, fetal administration is preferred.
death, or spontaneous abortion ensues and if they
Drug Distribution
are less severe, the result is a malformed child.
The teratogenic potential of drugs became The albumin binding capacity of drugs is
evident during 1960-1962 when women to relieve decreased during pregnancy due to
morning sickness used an extremely safe hemodilution as a result; freer drug is available
sedative—hypnotic drug by the name for placental transfer.
thalidomide. This was followed by thalidomide
Drug Excretion
disaster characterized by infants born with
phocomelia, or “seal limb” malformation of the During pregnancy, the renal blood flow increases
arms and legs. Other defects produced by by 25-50% and the glomerular filtration rate by
thalidomide were absence of external ears, 50%. Therefore, drugs are rapidly eliminated
cranial nerve dysfunction, and anorectal stenosis. which depend on the kidney.
Surprisingly thalidomide has made a comeback
Drug Metabolism
as a treatment option for Behcet’s syndrome, and
The level of hepatic drug metabolizing enzymes
recurrent aphthous ulceration in patients infected
is high probably due to high levels of proges-
with HIV.
terone. This leads to rapid metabolic degradation
The clinician should understand the
of lipid soluble drugs.
interaction between drugs and pregnancy in
order to avoid disastrous consequences.
FDA Pregnancy Risk Categories
Although pregnant women do not differ
qualitatively from the nongravid women in their The Food and Drug Administration (FDA) has
response to drugs, certain quantitative classified drugs with respect to their toxic
differences do occur because of physiological potential during pregnancy (Table 11.7). Drugs
changes during pregnancy. These physiological in categories D, X, and in some cases C, may pose
changes and the consequent alterations in similar risk.
Table 11.7: FDA pregnancy risk categories

Category Definition
A Adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of
pregnancy and there is no evidence of risk in later trimesters.
B Adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of
pregnancy and there is no evidence of risk in later trimesters, but animal reproduction studies have shown
an adverse effect on the fetus or human studies are lacking, but animal studies have failed to demonstrate a
risk to the fetus.
C No adequate and well-controlled studies have been performed in pregnant women, but animal reproduction
studies are lacking or have shown an adverse effect on the fetus. Potential benefit may warrant use of the
drug in pregnant women despite potential risk.
D Positive evidence exists of human fetal risk based on adverse reaction data from investigational or marketing
experience or studies in humans. Potential benefit may warrant use of the drug in pregnant women despite
potential risk.
X Studies in animals and humans have demonstrated fetal abnormalities, and/or there is positive evidence of
human fetal risk based on adverse reaction data from investigational or marketing experience, and the
potential risk of the drug in pregnant women clearly outweighs the potential benefit.
Drug Considerations in Pregnant Patient
Maternal medication Category first trimester Category second trimester Category third trimester
Local Anesthetics
Lignocaine B B B
Mepivacaine C C C
Nonopioid Analgesics
Aspirin C C D
Celecoxib C C D
Diclofenac sodium B B D
Ibuprofen B B D
Mefenamic acid C C D
Nimesulide X X X
Paracetamol B B B
Valdecoxib C C C
Antimicrobials
Acyclovir B B B
Amoxycillin B B B
Ampicillin B B B
Amphotericin B B B B
Cefazolin B B B
Cefotaxime B B B
Contd...
Contd...
Cefalexin B B B
Chloramphenicol C C C
Clindamycin B B B
Clotrimazole B B B
Cloxacillin B B B
Co-trimoxazole C C D
Erythromycin B B B
Fluconazole C C C
Ketoconazole C C C
Metronidazole B B B
Nystatin C C C
Ofloxacin D C C
Streptomycin D D D
Tetracycline D D D
Corticosteroids
Betamethasone D C C
Dexamethasone D C C
Prednisolone D C C
Triamcinolone D C C
Sedatives
Alprazolam D D D
Clonazepam D D D
Diazepam D D D
Lorazepam D D D
Antiallergic
Chlorpheniramine maleate B B B
Antiepileptic
Carbamazepine D D D
Dental Management 2. A detailed case history should be

undertaken, which should include history of
The main objective is to protect the developing
previous pregnancy or pregnancies and
fetus and the expecting mother and the important
complications
points to consider in management of a pregnant
dental patient are: 3. The approach of the dentist in management
1. A written consent from gynecologist is of a pregnant dental patient should be
required because any dental treatment may conservative
be looked upon as a causative factor for 4. The importance of oral hygiene must be
abortion stressed and dietary instructions given
5. Avoid elective dental care in first and third 2. Dutta DC. Text Book of Obstetrics including
trimester Perinatology and Contraception; Sixth edition;
6. Only emergency procedures are New Central Book Agency (P) LTD; Calcutta 2004.
3. Kumbhare SP, Dr. Birangane RS. Drug
accomplished during the first trimester and
considerations in pregnant dental patient; JIDA
late third trimester 2000;71:192-3.
7. The optimal trimester for dental care is 4. Ojanotko-Herri AO, Harri MP, Hurttia HM,
second trimester Sewon LA. Altered tissue metabolism of
8. The duration of the treatment procedure progesterone in pregnancy gingivitis and
should be short granuloma. J Clin Periodontal 1991;18:262-6.
9. At the beginning of second and third 5. Raber-Durlacher JE, van Steenbergen TJM, van
der Velden U, Graaff J de., Abraham-inpijn L.
trimester, oral prophylaxsis should be
Experimental gingivitis during pregnancy and
undertaken postpartum: Clinical, endocrinological, and
10. In order to prevent supine hypotension microbiological aspects. J Clin Periodontal
during third trimester the patient should be 1994;21:549-58.
in a sitting position rather than lying down 6. Sooriyamoorthy M, Gower DB. Hormonal
11. Elective radiography is contraindicated but influences on gingival tissue: relationship to
when taken lead apron is mandatory periodontal disease. J Clin Periodontal
1989;16:201-8.
7. Whitaker SB, Bouquot JE, Alimario AE, Whitaker
BIBLIOGRAPHY
TJ. Identification and semiquantification of
1. Daley TD, Wysocki GP. Pregnancy tumor: An estrogen and progesterone receptors in pyogenic
analysis. Oral Surg Oral Med Oral Pathol Oral granulomas of pregnancy. Oral Surg Oral Med
Radiol Endod 1991;72:196-9. Oral Pathol Oral Radiol Endod 1994;78:755-60.
Chapter
Systemic Diseases and
12 Dental Care
I. ORAL HEALTH AND HEART HEALTH

BASIC CARDIOLOGY
HEART STRUCTURE The heart is composed of three layers of tissue:

pericardium, myocardium, and endocardium.
External Structure of the Heart
The heart is a roughly cone-shaped hollow Pericardium
muscular organ, measures about 10 cm long and
The pericardium is made up of two sacs the outer
about the size of the owner’s fist. Its approximate
fibrous and the inner serous. The outer fibrous
weight is 225 g in women and 310 g in men.
sac is continuous with the tunica adventitia of
The heart lies obliquely in the thoracic cavity the great blood vessels above and is adherent to
in the mediastinum between the lungs, is rotated the diaphragm below. Its inelastic and fibrous
to the left than the right, and presents a base nature prevents the overexpansion of the heart.
above, and apex below. The inner serous sac is composed of two
The apex is about 9 cm to the left of the midline layers, an outer parietal pericardium and an
at the level of the fifth intercostal space, i.e., a inner visceral pericardium or epicardium. The
little below the nipple and slightly near the outer parietal pericardium lines the outer fibrous
midline. The base extends to the level of the sac. The inner visceral pericardium lines the
second rib. The various organs associated with myocardium.
the heart are: The space between the outer parietal
1. Superiorly: The great blood vessels (superior pericardium and inner visceral pericardium is
vena cava, arch of aorta, pulmonary artery, known as pericardial space. The pericardial space
and pulmonary veins) is lined by flattened epithelial cells that secrete
2. Inferiorly: The diaphragm the serous pericardial fluid. The serous
3. Anteriorly: The sternum, ribs, and pericardial fluid allows smooth movement
intercostal muscles between outer parietal pericardium and inner
4. Posteriorly: The trachea, right and left visceral pericardium when the heart beats.
bronchus, esophagus, descending aorta, and Normally the outer parietal pericardium and
inferior vena cava inner visceral pericardium are in close
5. Laterally: The lungs, with the left lung association with only thin film of serous
overlapping the left side of the heart pericardial fluid.
Systemic Diseases and Dental Care 169
Myocardium Endocardium
The myocardium is composed of specialized The endocardium lines the myocardium and the
muscle found only in heart. Unlike skeletal heart valves. It is a thin, smooth, shining
muscle it is not under voluntary control. Each membrane, which permits smooth flow of blood
cardiac muscle cell (fiber) has a nucleus and one inside the heart. It consists of flattened epithelial
or more branches. The ends of each cardiac cells, which are continuous with the endothelium
muscle cell are in very close contact with the ends that lines the great blood vessels.
of the adjacent cardiac muscle cell via intercalated
discs. Internal Structure of the Heart (Fig.12.1)
The intercalated discs are actually cell Internally the heart is divided into right and left
membranes that separate individual cardiac side by a septum consisting of myocardium lined
muscle cells from one another and are seen as by endocardium. Each side is divided by an
dark lines under the microscope. Because of atrioventricular valve into an upper chamber, the
connectivity between the individual cardiac atrium and a lower chamber, the ventricle. The
muscle cells, each cell does not need to have atrioventricular valves consist of myocardium
separate nerve innervation. Thus, when an lined by endocardium. The right atrioventricular
impulse is initiated it spreads from cell to cell valve (tricuspid valve) has three flaps or cusps
causing contraction of the myocardium. and the left atrioventricular valve (mitral valve)
The myocardium is thickest at the apex has two flaps or cusps.
especially the left ventricle and thins out towards The valves between the atria and ventricles
the base. This reflects the amount of work each open and close passively according to pressure
chamber contributes to the pumping of blood. changes within the chambers. They open when
Fig. 12.1: Internal structure of heart

the pressure in the atria is greater than that in Blood Supply to the Heart
ventricles (atrial systole) and close when pressure
The heart is supplied with arterial blood by the
in the ventricles is greater than that in atria
right and left coronary arteries, which branch,
(ventricular systole). The valves are prevented
from the aorta immediately distal to the aortic
from opening upwards into the atria by
valve. The right and left coronary arteries receive
tendinous cords, called chordae tendineae. The
about 5% of the blood pumped from the heart.
chordae tendineae extend from the inferior
The right coronary artery travels in the coronary
surface of the cusps to little projections of the
sulcus to reach the posterior surface of the heart
myocardium lined by endocardium, called
where it anastomoses with the circumflex left
papillary muscles.
coronary artery. Early in its course, it gives off
the SA node artery, AV node artery, marginal
Flow of Blood through the Heart
branch, and a posterior descending branch in the
The two largest veins of the body, the superior interventricular groove, which anastomoses with
and inferior vena cava empty the blood into the the anterior descending left coronary artery. The
right atrium. This blood passes via the right left coronary artery divides into circumflex left
atrioventricular valve into the right ventricle coronary artery, and anterior descending left
from where it is pumped into the pulmonary coronary artery in the interventricular groove.
artery (the only artery in the body that carries The right and left coronary arteries traverse
deoxygenated blood). The opening of the (cross) the heart and form a vast network of
pulmonary artery is guarded by pulmonary capillaries.
valve, formed by three semilunar cusps. The
pulmonary valve prevents the backward flow of Venous Drainage of the Heart
blood into the right ventricle when the ventricles
The deoxygenated blood is collected by the
relax.
oblique vein of the left atrium, small cardiac vein,
After leaving the heart, the pulmonary artery
middle cardiac vein, and the great cardiac vein.
divides into right and left branches, which carry
These veins join to form the coronary sinus,
the deoxygenated blood to the lungs where
which opens into the right atrium between the
carbon dioxide is excreted and oxygen is
opening of inferior vena cava and the right
absorbed. Two pulmonary veins from each lung
atrioventricular valve. A semicircular valve
carry oxygenated blood back to the left atrium.
guards the opening of coronary sinus.
The oxygenated blood passes via the left
atrioventricular valve into the left ventricle from Conducting System of the Heart
where it is pumped into the aorta (first artery of
circulation). The opening of the aorta is guarded The conducting system of the heart is composed
by aortic valve, formed by three semilunar cusps. of specialized neuromuscular tissue in the
The aortic valve prevents the backward flow of myocardium, which initiates and conducts
the blood into the left ventricle when the ventricle impulses causing coordinated (operating as a
relaxes. It should be noted that the right and left unit) and synchronized (operating at the same
atria contract at the same time and this is time) contraction of the myocardium.
followed by the simultaneous contraction of right The conducting system of the heart is not
and left ventricles. dependent on the innervation from the brain.
However, the conducting system can be ventricular myocardium. The AV bundle, bundle
stimulated or depressed by nerve impulses branches, and Purkinje fibers conduct impulses
initiated in the brain and by the circulating from the AV node to the apex of the myocardium.
chemicals and hormones. From the apex of the myocardium, the wave of
ventricular contraction begins, which sweeps
Sinoatrial Node (SA Node) upwards and outwards, pumping blood into the
The sinoatrial node is a small, flattened, ellipsoid pulmonary artery and the aorta.
mass of specialized neuromuscular tissue that is
Innervation to the Heart
situated in the posterosuperior lateral wall of the
right atrium immediately below and slightly The heart is innervated by the sympathetic and
lateral to the opening of the superior vena cava. parasympathetic nerves.
The SA node is the “pacemaker” of the heart
because it initiates the cardiac muscle contraction Sympathetic
and determines the heart rate. The cell bodies of the preganglionic sympathetic
nerve fibers are located in the lateral column of
Atrioventricular Node (AV node) grey matter in the spinal cord between the levels
of T1 and L3 and are known as spinal
Three internodal fibers (anterior internodal fibers
sympathetic centers. The spinal sympathetic
of Bachman, middle internodal fibers of
centers are not independent centers. They are
Wenckebach, and posterior internodal fibers
under the control of vasomotor center present in
Thorel) conduct the impulses from SA node to
the ventrolateral medulla. The vasomotor center
the AV node (i.e., they converge towards the AV
is controlled by the higher centers (cerebral cortex
node and interdigitate with fibers of AV node).
and hypothalamus), nucleus of the tractus
The AV node is a small, oval or elliptical mass of
solitarus, and is sensitive to oxygen tension and
specialized neuromuscular tissue that is situated
pH of the arterial blood. The preganglionic
in the wall of interatrial septum near the
sympathetic nerve fibers leave the spinal cord
atrioventricular valves in the triangle of Koch.
via the anterior root and terminate in the lateral
Normally the AV node is stimulated by the
chain of sympathetic ganglia. The preganglionic
impulses originating in the SA node. However,
sympathetic nerve fibers release the
the AV node is capable of initiating impulses that
neurotransmitter acetylcholine.
cause contraction but at a slower rate than the
The postganglionic sympathetic nerve fibers
SA node.
have their cell bodies in the lateral chain of
Atrioventricular Bundle (AV bundle sympathetic ganglia. The postganglionic
or bundle of His) sympathetic nerve fibers release the
neurotransmitter noradrenaline and innervate
The AV bundle is a mass of specialized the tissues or the target organs e.g., salivary
neuromuscular tissue that originates from the glands, heart, arterioles, capillaries, veins,
AV. At the upper end of interventricular septum coronary arteries, and skeletal blood vessels. The
the AV bundle divides into right and left bundle postganglionic sympathetic nerve fibers raise the
branches. These bundle branches run on either total peripheral resistance and blood pressure by
side of the interventricular septum and give of vasoconstriction of the arterioles, capillaries, and
fine fibers called the Purkinje fibers within the veins. Under normal conditions the
postganglionic sympathetic nerve fibers exert a preganglionic parasympathetic nerve fibers leads
continuous discharge on the arterioles, to decrease in heart rate (negative chronotropic
capillaries, and veins all over the body and effect), and decrease in force of contraction
maintain a partial state of vasoconstriction, called (negative ionotropic effect). The preganglionic
vasomotor tone. However, the postganglionic parasympathetic nerve fibers that innervate the
sympathetic nerve fibers that innervate the heart exert a continuous discharge which keeps
coronary arteries and blood vessels supplying the the heart rate within normal limits (vagal tone)
skeletal muscle cause vasodilatation. even at rest. The heart rate of healthy adults at
The cell bodies of the preganglionic rest is usually between 60-75 beats/minute. In
sympathetic nerve fibers that innervate the heart fetus, the heart rate is about 140 beats/minute.
are located in the lateral column of grey matter After delivery the heart rate of the newborn
in the spinal cord between the levels of T1 and decreases, but is on the higher side in comparison
T4. The postganglionic sympathetic nerve fibers to adults. The adult heart rate is achieved at the
innervate the SA node, AV node, and the age of 18 years. The heart rate decreases in
myocardium of atria and ventricles. Stimulation middle age and increases again in old age.
of postganglionic sympathetic nerve fibers leads
to increase in heart rate (positive chronotropic Blood Pressure
effect), and increase in force of contraction Definition
(positive ionotropic effect).
Arterial blood pressure is the lateral pressure
Parasympathetic exerted by the contained column of blood on the
The parasympathetic nerve cell bodies of the wall of arteries (Fig.12.2). The pressure is exerted
vagus nerve (visceral motor component of vagus when the blood flows through the arterioles. The
nerve) are located in the dorsal motor nucleus of two main factors that determine the blood
the vagus. The parasympathetic nerve cell bodies pressure are cardiac output and peripheral
are influenced by inputs from the hypothalamus, resistance. Two terms that express arterial blood
the olfactory system, the reticular formation, and pressure are:
the nucleus of the tractus solitarius. The dorsal
motor nucleus of the vagus is located in the floor
of the fourth ventricle (vagal trigone) and in the
central grey matter of the medulla. Preganglionic
parasympathetic nerve fibers arise from dorsal
motor nucleus of the vagus traverse the spinal
nucleus of the trigeminal nerve and emerge from
the lateral surface of the medulla, and travel in
the vagus nerve. Within the thorax, the
preganglionic parasympathetic nerve fibers of
vagus nerve innervate the heart through the right
and left cardiac branches.
The preganglionic parasympathetic nerve
fibers innervate mainly the SA node, AV node,
Fig. 12.2: Blood pressure
and the myocardium of atria. Stimulation of
1. Systolic pressure: Systolic pressure is the nerve (Hering’s nerve) and vagus nerve present
maximum pressure exerted in the arteries in the baroreceptors are stimulated and the
during the systole of heart impulses are transmitted via these peripheral
2. Diastolic pressure: Diastolic pressure is the processes whose cell bodies are located in the
minimum pressure in the arteries during the inferior ganglion.
diastole of the heart From the inferior ganglion, the impulses are
transmitted via the central processes, which enter
Regulation of Normal Blood Pressure the medulla and descend in the tractus solitarius
The arterial blood pressure varies even under to enter the caudal part of the nucleus of the
normal physiological conditions. However, tractus solitarius. The nucleus of the tractus
immediately it is brought back to normal level solitarius sends inhibitory impulses to the
because of well-organized regulatory mecha- vasomotor center (C1) via the inhibitory
nisms. The various regulatory mechanisms are: interneurons. The vasomotor center in turn sends
1. Neural regulation or short-term inhibitory impulses to the spinal sympathetic
2. Renal regulation or long-term center via the bulbospinal pathway. Inhibition of
the spinal sympathetic center results in
Neural Regulation or Short-term vasodilatation of the arterioles and veins,
The baroreceptors are stretch receptors present decrease in heart rate, and decrease in blood
in the walls of the atria, pulmonary veins, wall pressure.
of the left ventricle, wall of the aortic arch, and
carotid sinuses. The carotid sinuses are slight Renal Regulation or Long-term
dilatations present in the wall of each internal The renin-angiotensin system (Fig.12.3) plays an
carotid artery slightly above the common carotid important role in the regulation of arterial blood
artery bifurcation. When there is a rise in the pressure. Renin is small protein enzyme
arterial blood pressure, the nerve endings of the synthesized and stored in an inactive form called
peripheral processes of the glossopharyngeal prorenin in the juxtaglomerular cells (JG cells).
Fig. 12.3: The renin-angiotensin mechanism

The JG cells are modified smooth muscle cells The renin enters the renal blood and then
located in the wall of afferent arteriole passes out of the kidneys to circulate throughout
immediately proximal to the glomerulus. When the body. Renin is not a vasoactive substance but
there is a fall in arterial blood pressure, the a protein enzyme that acts on circulating
prorenin molecules split and the JG cells release α2-globulin, called angiotensinogen, or renin
renin. substrate to release angiotensin I. The
Fig. 12.4: The effects of Angiotensin II

angiotensin I has mild vasoconstrictor properties 1. Vasoconstriction: Vasoconstriction of

but it is not effective to cause any functional arterioles increases the total peripheral
changes in the circulation. Within a few seconds resistance thereby increasing the arterial
after the formation of the angiotensin I, two blood pressure. It also causes vasoconstric-
additional amino acids are split from the tion of veins including the splanchnic veins
angiotensin I to form 8-amino acid peptide thereby increasing the venous return to the
heart.
angiotensin II.
2. Direct action on the kidneys: The
This conversion occurs entirely in the lungs
angiotensin II stimulates zona glomerulosa
and is catalyzed by angiotensin converting
of the adrenal glands to secrete aldosterone.
enzyme (ACE) that is present in the endothelium The aldosterone increases sodium and water
of the lung blood vessels. Angiotensin II persists reabsorption from the distal convoluted
in the blood for 1 to 2 minutes because multiple tubules and collecting tubules. Sodium and
blood and tissue enzymes collectively called water reabsorption increases the blood
angiotensinase rapidly metabolize it. During its sodium levels and blood volume, which in
presence in the blood angiotensin II has two turn increases the venous return, and the
effects (Fig.12.4) that can elevate the arterial cardiac output. Thereby increasing the blood
blood pressure. The two effects are: pressure.
HYPERTENSION
Persistent increase in systemic arterial pressure peripheral resistance) that control blood pressure
is known as hypertension. Clinically when the in the genetically predisposed patients. Essential
systolic blood pressure rises above 140 mm Hg hypertension accounts for 85-90% of all cases and
and diastolic pressure rises above 90 mm Hg, it is subdivided as benign and malignant according
is considered as hypertension. If there is increase to the rate at which the disease progresses.
only in systolic blood pressure, it is called systolic 1. Benign (chronic) hypertension: In benign
hypertension. hypertension, the blood pressure rises slowly
Depending on the cause hypertension may be over many years and is compatible with long
described as essential (primary or idiopathic) or life, unless there are complications like
secondary (secondary to other disease). myocardial infarction, cerebrovascular
However, irrespective of the cause, hypertension accident, or congestive cardiac failure.
commonly affects the kidneys. Occasionally the rate of progress of blood
pressure increases and hypertension
Types of Hypertension becomes malignant.
Essential 2. Malignant (accelerated) hypertension: In
Essential hypertension is a complex multifac- malignant hypertension, the blood pressure
torial disorder the cause of which is unknown continues to rise rapidly. Diastolic pressure
(idiopathic). Various environmental factors in excess of 120 mm Hg is common. The
(heavy consumption of salt, sedentary life style, effects are serious and quickly become
obesity, excessive intake of alcohol, and cigarette apparent, e.g., retinal hemorrhages,
smoking) affect the variables (cardiac output and papilledema (edema around the optic disc),
encephalopathy (cerebral edema), and renal 1. Decreased renal sodium excretion:

failure. Malignant hypertension, if left Decreased renal sodium excretion leads to
untreated, leads to death within 1 to 2 years. increase in the ECF and blood volume,
increase in the venous return, increase in the
cardiac output and vasoconstriction, thereby
Mechanism of Essential Hypertension elevating the blood pressure
Essential hypertension occurs when the 2. Functional vasoconstriction: Functional
vasoconstriction increases the peripheral
environmental factors affect the variables that
resistance and blood pressure. Moreover,
control blood pressure in the genetically chronic or repeated vasoconstriction causes
predisposed patients. The various genetic factors thickening of arterioles (resistance vessels)
are decreased renal sodium excretion and and subsequent increase in peripheral
functional vasoconstriction (Fig.12.5). resistance and blood pressure
Fig. 12.5: Mechanism of essential hyertension

Secondary Table 12.2: Complication of hypertension

Systems Complications
Secondary hypertension is secondary to other
diseases and accounts for 10-15% of all cases. The Heart Right ventricular hypertrophy
Left ventricular hypertrophy
various causes of secondary hypertension are
Cardiac failure
given in Table 12.1
Ischemic heart disease
Complications of Hypertension Blood vessels Atherosclerosis

Aneurysms
The effects of long standing and progressively Lungs Pulmonary congestion
rising blood pressure are serious (Table 12.2). Eye Retinal hemorrhages
Papilledema (edema around the optic
Treatment disc)
The management of hypertension includes Brain Stroke (secondary to cerebral
modification of lifestyle and drug therapy hemorrhage)
(Table 12.3). Death (secondary to rupture of large
vessel)
Encephalopathy (cerebral edema)
Kidneys Renal failure
Proteinuria (secondary to renal
vasculature damage)
Table 12.1: Causes of secondary hypertension

Systems Pathology
Renal Acute glomerulonephritis
Renal artery stenosis
Renal vasculitis
Renin producing tumors
Endocrine Acromegaly
Hypothyroidism
Hyperthyroidism
Cushing’s syndrome
Conn’s syndrome
Pregnancy-induced
Pheochromocytoma
Exogenous hormones ( contraceptives, glucocorticoids, and MAO inhibitors)
Cardiovascular Increased cardiac output
Coarcation of aorta
Rigidity of aorta
Increased intravascular volume
Polyarteritis nodosa
Neurologic Acute stress
Psychogenic
Table 12.3: Management of hypertension cardiovascular disease may be at greater risk of

Lifestyle modifications experiencing massive endogenous adrenaline
release secondary to poor local anesthesia than
• Regular moderate exercise
they are from the small amount of vasocons-
• Reducing alcohol intake
trictor used in local anesthetics.
• Restricting salt intake
Most human studies examining hemody-
• Good nutrition
namics (blood pressure, heart rate, heart rhythm,
• Giving up smoking cardiac output, and myocardial oxygen
Drug Therapy requirement) after dental injection of 1.8 to 5.4
• Diuretics ml of 2% lidocaine with adrenaline (1:80,000)
• β-blockers have found no significant changes in blood
• ACE inhibitors
pressure or heart rate in healthy patients or in
those with mild to moderate cardiovascular
• Angiotension II receptor antagonists
disease. Therefore, it is recommended that
• Calcium antagonists
patients with mild to moderate cardiovascular
disease receive the smallest amount of local
Dental Considerations
anesthetic with vasoconstrictor needed to
The use of local anesthetic agents with provide profound anesthesia, with aspiration
vasoconstrictors in patients with cardiovascular performed to prevent intravascular injection.
disease remains controversial. The most Exogenous vasoconstrictors may be contrain-
commonly used vasoconstrictor is adrenaline. dicated in patients with:
Vasoconstrictor restricts the spread and systemic 1. Hypersensitivity
side effects (e.g., dizziness, drowsiness, 2. Unstable angina
lightheadedness, blurred vision, slurred speech, 3. Recent myocardial infarction or coronary
muscle twitching, bradycardia, and hypotension) artery bypass surgery
of lidocaine. Vasoconstrictor also prolongs the 4. Uncontrolled dysrhythmias
anesthetic effect of lidocaine. 5. Severe hypertension
Normal adrenaline release from the adrenal 6. Severe congestive cardiac failure
medulla can increase 20 to 40 fold during stress. 7. Hyperthyroidism
Such stress may be induced by pain during 8. Pregnancy
dental treatment. Patients receiving local Intraligamentary injection of local anesthetics
anesthetic without vasoconstrictor often have with vasoconstrictor is generally contraindicated
significantly impaired pain control compared in patients with severe cardiovascular disease,
with those receiving local anesthetic with since the hemodynamics is similar to those
adrenaline. For this reason, patients with observed after intravenous adrenaline injection.
ISCHEMIC HEART DISEASE

The most common cause of ischemic heart ATHEROSCLEROSIS
disease is atherosclerosis of the coronary arteries,
and hence ischemic heart disease is often termed Atherosclerosis is a progressive disease
as coronary heart disease or coronary artery characterized by lesions (atheromas or fibrofatty
disease. The other causes of ischemic heart plaques) in the tunica intima of elastic arteries
disease are coronary heart thrombosis and (e.g., aorta, carotid, and iliac arteries) and large
coronary artery vasospasm. to medium sized muscular arteries (e.g., coronary
and popliteal arteries). The impact of atherosc- with infectious agents such as Sterptococcus
lerosis on overall health is staggering. In some sanguis, Chlamydia pneumonae, Helicobacter pylori,
developing countries, atherosclerosis accounts Porphyromonas gingivalis, Prevotella intermedia,
for about 50% of deaths. Bacteroides forsythus, and herpes virus is
These atheromas consist of lipids primarily associated with atherosclerosis. People with
cholesterol and cholesterol esters, proliferating severe periodontitis are highly predisposed to
smooth muscle cells, and fat filled macrophages atherosclerosis as they have the greatest amounts
(monocytes) known as foam cells. The atheromas of pathogenic bacteria, which may contribute to
are covered with a fibrous capsule. As atheromas inflammatory response. The infectious agents
grow they spread along the artery wall forming can activate the inflammatory response, either
swellings that protrude into the lumen and via direct or indirect mechanisms.
obstruct it. Critical stenosis is occlusion of the 1. Direct: The infectious agents may cause
lumen of one or more coronary arteries to 75% direct injury to the endothelium by
or more by an atheroma. recruitment and stimulation of proinfla-
mmatory (in favor of inflammation)
Risk Factors cytokines (interleukin-1, prostaglandin E2
The four major risk factors are hyperlipidemia and tumor necrosis factor-α) and tissue
(increased low density lipoprotein (LDL) growth factors in the arterial wall and by
cholesterol levels), hypertension, cigarette enhancing the accumulation of LDL
smoking, and diabetes mellitus. Increased LDL cholesterol through stimulation of LDL
cholesterol levels are due to consumption of egg receptors.
yolk, animal fats, and dairy products (e.g., 2. Indirect: The infectious agents cause indirect
butter). The other risk factors for atherosclerosis injury to the endothelium by accelerating the
are as follows: inflammatory response caused by another
1. Alcohol use agent e.g., hypertension. The indirect injury
2. Genetic predisposition can either be due to release of endotoxin into
3. Infection the circulation by the infectious agents,
4. Lower educational status which may indirectly damage the vascular
5. Males endothelium or by systemic cytokine, which
6. Obesity could predispose the arterial environment to
7. Older age group (60 years in men and 70 procoagulant (in favor of coagulation) state,
years in women) resulting in thrombus formation on a
8. Periodontitis preexistent unstable plaque.
9. Poverty level
Pathogenesis
10. Sedentary life style
11. Socially isolated and divorced people Considerable evidence has identified
atherosclerosis as an inflammatory disease. This
Infection hypothesis, known as the Ross “Response to
Sir William Osler in 1908 proposed that Injury Hypothesis” explains how inflammation
atherosclerosis itself was an infection. Infection is related to atherosclerosis. Ross hypothesis
is now recognized as one of the risk factor for suggests that injury to the endothelium causes
atherosclerosis. There is evidence that infection the initial lesion, leading to a chronic arterial
inflammatory process. The various risk factors of vasodilators (nitric oxide and prostacyclin) by
that cause injury to the endothelium have been the endothelial cells.
mentioned earlier. During this inflammatory
process, monocytes and platelets adhere to the Ischemic Heart Diseases
endothelium and migrate between endothelial Depending upon the severity of coronary artery
cells into the tunica intima. This is followed by narrowing and myocardial response, ischemic
release of growth factors, including platelet heart diseases are classified as:
derived growth factor (PDGF), which leads to
1. Angina pectoris
smooth muscle migration from tunica media into
2. Myocardial infarction
the tunica intima. The macrophages and smooth
If the coronary artery is completely occluded
muscle cells engulf LDL (cholesterol and
by an atheroma or thrombus, acute myocardial
cholesterol esters), to become foam cells. The LDL
infarction occurs. In contrast, if the coronary
are derived from the blood vessel lumen,
artery is partially occluded by an atheroma or
particularly in the presence of hyperlipidemia
thrombus, the patient may develop unstable
and from degenerating foam cells. The smooth
angina (Fig.12.6).
muscle cells produce large amounts of
extracellular matrix, including collagen and
Angina Pectoris
proteoglycans forming atheroma or fibrofatty
plaque. Typical or stable angina pectoris
With progression the atheroma becomes Typical or stable angina pectoris refers to
prominent on the intimal aspect, producing a episodic chest pain associated with exertion or
fibrous cap. The occlusion of small arteries by some other form of stress. The pain is classically
an atheroma leads to ischemia (decreased blood described as a crushing or squeezing retrosternal
supply) and infarction of the tissues. The focal sensation, which may radiate down to the left
rupture of the fibrous cap may result in thrombus arm, mandible, shoulder, and neck. Stable angina
formation. pectoris is usually associated with a fixed
occlusion (75% or more) of one or more coronary
Coronary Heart Thrombosis arteries by fixed atheroma. With this degree of
occlusion, the myocardial oxygen demand may
Focal rupture of an atheroma involving the be adequate under normal conditions but is not
coronary artery exposes the underlying sufficient to meet the increased requirements
thrombogenic lipids, and subendothelial imposed by exercise or other conditions that
collagen which initiate platelet aggregation, stress the heart.
thrombin generation, and ultimately thrombus The pain is usually relieved by rest or by
formation. The platelet aggregates release administration of sublingual glyceryl trinitrate.
vasospastic mediators such as thromboxane A2, The main action of sublingual glyceryl trinitrate
causing vasospasm. is to cause dilatation of the capacitance vessels
as a result of which there is decreased venous
Coronary Artery Vasospasm
return and decreased cardiac output
Coronary artery vasospasm is probably due to In large doses sublingual glyceryl trinitrate
release of vasospastic mediators such as may increase the blood supply to the
thromboxane A2, by platelet aggregates after the myocardium by causing vasodilatation of the
rupture of an atheroma and reduced synthesis coronary arteries.
Fig. 12.6: Angina pectoris and myocardial infarction
Prinzmetal angina Unstable angina pectoris

Prinzmetal Angina or variant angina refers to Unstable angina pectoris or crescendo angina is
angina that occurs at rest or in some cases, characterized by the increased frequency of
awakens the patient from sleep. Angiographic anginal pain, which is precipitated by less
exertion. The attack is more intense and often
studies have shown that prinzmetal angina is
lasts longer than stable angina pectoris. Unstable
associated with coronary artery vasospasm. The
angina pectoris is usually associated with
cause of vasospasm is not clear but exposure to
incomplete luminal occlusion by the thrombus.
cold weather and emotional stress may
Unstable angina pectoris is sometimes referred
precipitate the secretion of endogenous
to as preinfarction angina as it may develop into
adrenaline and noradrenaline, which increases acute myocardial infarction.
the vascular tone of coronary blood vessels
causing vasoconstriction. Although the Acute Myocardial Infarction
vasospasm usually occurs near an atherosclerotic An infarct is an area of necrotic tissue that has
plaque, it may affect a normal blood vessel. died because of lack of oxygenated blood. When
a branch of coronary artery is completely ventricle, and posterior one third of interventri-
occluded by a thrombus, overlying the ruptured cular septum. Occlusion of the anterior descen-
atheroma, acute myocardial infarction occurs ding left coronary artery causes infarction in the
because of lack of oxygenated blood to the anterior and apical areas of the left ventricle, and
myocardium. Acute myocardial infarction is also anterior two thirds of the interventricular
known as “heart attack”. The risk of acute septum. Occlusion of circumflex left coronary
myocardial infarction increases progressively artery causes infarction of lateral wall of the left
throughout life. Between ages of 45 and 54, men ventricle. If the thrombus occludes proximal
are 4 to 5 times as likely to develop acute segments (situated near to the point of origin) of
myocardial infarction as women. However, after the coronary arteries, the size of the infarct is
80 years the risk factor is same in both sexes. large. If the thrombus occludes distal segments
(situated far from the point of origin) of the
Pathogenesis coronary arteries, the size of the infarct is small.
Angiographic studies indicate that most acute
myocardial infarctions are caused by coronary Types of Acute Myocardial Infarction
artery thrombosis. Infarction of the myocardium When the myocardial infarct involves most of the
begins within 20 to 30 minutes of the coronary thickness of the ventricular wall, they are refered
artery occlusion. The subendocardial region of to as transmural infarcts, while those restricted
the myocardium is the most poorly perfused to inner subendocardial region (the inner one
region because it is the last area to receive blood third of the myocardium) are designated as
supply from branches of the coronary arteries. subendocardial infarcts.
The high intramural pressure further
compromises the blood flow to the subendo- Clinical Features
cardium Because of this the subendocardium is
vulnerable to ischemic injury and the infarction Acute myocardial infarction is usually
typically begins in the subendocardial region. accompanied by severe, crushing retrosternal
Although infarction proceeds from the pain, which may radiate to the neck, jaw,
subendocardium to epicardium, a very narrow epigastrium, shoulder, or left arm. The pain
zone of myocardium immediately beneath the associated with acute myocardial infarction
endocardium is spared from infarction because typically lasts for several hours to days and is
it can be oxygenated by diffusion from the not relieved by sublingual glyceryl trinitrate. The
ventricle. The infarct usually reaches its full size other clinical features are weak and rapid pulse,
within 3 to 6 hours. During this period, lysis of dyspnoea (pulmonary congestion and edema
the thrombus by the administration of due to impaired contraction of ischemic
thrombolytic agents (alteplase or streptokinase) myocardium).
may limit the size of the infarct.
Electrocardiographic (ECG)
The location of myocardial infarction is
Abnormalities
determined by the site of the vascular occlusion
and by the anatomy of the coronary circulation. When the blood supply to the myocardium is
Occlusion of the right coronary artery causes interrupted, there are irreversible changes
infarction of the posterior wall of the left (ischemia and necrosis) in the myocardium that
produce various ECG abnormalities. The ECG Management of Acute Myocardial

abnormalities associated with acute myocardial Infarction (Figs.12.7, Table 12.4 and 12.5)
infarction are deep Q wave, loss of R wave,
elevation and depression of ST segment,
elevation and depression of T wave. Thus, the
ECG is very useful in diagnosing and locating
areas of infarction.
Laboratory Evaluation
Laboratory evaluation is an integral part in the
diagnosis of acute myocardial infarction. A
number of enzymes and proteins are released
into the circulation by the dying myocardial cells.
Measurement of the level of some of these
enzymes or proteins in the serum is helpful in
the diagnosis of acute myocardial infarction.
Increased serum creatinine kinase within
72 hours of acute myocardial infarction is
suggestive of acute myocardial infarction.
Increased levels of troponins within 7 days after
attack of acute myocardial infarction are
suggestive of acute myocardial infarction. Fig. 12.7: Management of acute myocardial infarction
Complications Dental Considerations
1. Dysrhythmias or arrhythmias The medications most commonly used to treat

2. Heart block (impaired conduction of patients with stable angina include glyceryl
impulses) due infarction of the myocardium trinitrate, β1 receptor blocking agents, and
calcium channel blockers (e.g., amlodipine). It is
3. Congestive cardiac failure due to impaired
clear from the literature that psychological or
contraction of the myocardium
physiological stress may exacerbate ischemic
4. Rupture of ventricular wall usually within
symptoms. Therefore, use of a stress reduction
2 weeks of original episode protocol and profound (heavy) anesthesia is an
5. Mural thrombi, which develop on the integral part of dental treatment for such patients.
endocardial surface overlying the infarct, are Dental treatment planning may be altered in
potential sources for pulmonary embolism, these patients. The duration of the treatment
and cerebral embolism. should be short, small amount of local anesthetic
6. Pericarditis with vasoconstrictor should be used, and if
7. Angina pectoris indicated preoperative or intraoperative
8. Recurrence conscious sedation should be performed.
Table 12.4: Early management of anginal attack are 100% oxygen and sublingual
acute myocardial infarction glyceryl trinitrate (300-600 mcg repeated three
Provide facilities for defibrillation times within 15 minutes if necessary). The patient
Immediate measures
should be instructed to bring his or her own
glyceryl trinitrate tablets for each appointment,
• 100% oxygen
and the dentist should have glyceryl trinitrate
• i.v. analgesics (e.g., morphine sulphate) and
tablets in the emergency medical kit.
antiemetics (e.g., meclozine); analgesics and
Patients with unstable angina generally are
antiemetics should not be administered intramuscularly
not candidates for elective dental therapy, and
because of delay in clinical effect due to poor skeletal
consultation with the patients physician usually
muscle perfusion is indicated. If emergency dental care is needed,
• ECG monitoring preoperative anxiolytic agents may be indicated
Reperfusion of the myocardium for stress reduction and to minimize endogenous
• Thrombolytic agents such as alteplase or adrenaline release. The dentist should closely
streptokinase; thrombolytic agents cause coronary monitor the patients hemodynamic status and
artery thrombolysis and help restore coronary patency oxygen saturation before and during treatment.
• Primary percutaneous coronary intervention (PCI) of It is commonly recommend that patients not
affected coronary artery; It is a safe and effective receive routine dental care for at least 6 months
alternative to thrombolytic therapy after experiencing a myocardial infarction. This
recommendation is based on the fact that the
Detection and management of complications
peak mortality rate (death rate) following
• Dysrhythmias
myocardial infarction occurs during the first
• Left ventricular failure
year, primarily resulting from the increased
• Cardiac failure
electrical instability of the myocardium after the
infarction. After the six-month post-myocardial
Table 12.5: Late management of
infarction period, most patients may be treated
acute myocardial infarction
with techniques similar to those used for the
Life style modification
patient with stable angina, including relatively
• Stop smoking short appointments and a stress-reduction
• Regular exercise protocol where indicated.
• Diet (weight control, lowering of LDL levels)
Secondary prevention drug therapy
Anticoagulant Therapy
• Antiplatelet therapy e.g., aspirin or warfarin Patients with history of valvular heart disease,
• β1 receptor blocking agents e.g., atenolol myocardial infarction, and cerebrovascular
• ACE inhibitors e.g., captopril accident frequently receive anticoagulant
• Atorvastatin (reduces the LDL level) therapy consisting of aspirin or warfarin.
• Additional therapy for diabetes and hypertension Therefore, the dentist should consult with the
patients physician before the dental treatment (as
Rehabilitation
it may induce bleeding) to determine whether
modification of anticoagulant therapy is
Supplemental oxygen delivered via a nasal indicated.
canal may help prevent intraoperative anginal Aspirin, an inhibitor of platelet aggregation,
attacks. The drugs of choice for treating an acute often is used to prevent thrombosis formation.
Because of its irreversible binding to platelets, time significantly at this dose. However, higher
the effect of aspirin lasts at least 4 to 7 days. doses may increase bleeding time and predispose
Aspirin is generally used in small doses of 75 mg the patient to develop postoperative bleeding.
(150-300 mg loading dose followed by 150 mg For these patients, aspirin therapy should be
daily for the 1st month and then 75 mg daily modified or discontinued for several days before
thereafter) and usually will not alter bleeding the dental procedure.
VALVULAR HEART DISEASES

The heart valves prevent backflow of the blood by fibrous scar tissue resulting in defective
in the heart during the cardiac cycle. Distinctive closure and regurgitation.
heart sounds are produced during the cardiac
cycle when the valves close. Damaged valves Rheumatic Fever
generate abnormal heart sounds called murmurs. Rheumatic fever is an autoimmune disease in
The most common causes of valve defects are which the heart valves are likely to be damaged
rheumatic fever, infective endocarditis, and or destroyed. The fact that symptoms typically
congenital abnormalities. The mitral and aortic do not develop until 2 to 3 weeks after infection
valves are subjected to high pressure stresses and that the streptococci are absent from the
than the tricuspid valves and the pulmonary lesions supports the concept that rheumatic fever
valve. Therefore, the mitral and aortic valves are results from an immune response against
commonly affected, the tricuspid valve streptococci.
sometimes and the pulmonary valve rarely.
1. Stenosis: Stenosis is defined as pathological Etiology
narrowing of the cardiac valve orifice e.g.,
Rheumatic fever occurs 2 to 4 weeks after a
narrowing of the aortic valve orifice. Stenosis
preliminary infection (pharyngitis, scarlet fever,
occurs when there is deposition of
or middle ear infection) caused by Sterptococcus
vegetations (a clot composed blood platelets,
pyogenes (group A β-hemolytic streptococci).
fibrin, and bacteria adherent to the heart
Streptococcus pyogenes produces numerous
valve) on the cusps along their line of closure,
virulence factors. One of the most important
which results in adherence of the valve
virulence factor is the antiphagocytic cell wall
edges. These vegetations tend to become
organized, resulting in the formation of M protein. Sterptococcus pyogenes also elaborates
fibrous scar tissue. The fibrous scar tissue 20 extracellular products, which include
shrinks as it ages and distorts the shape of enzymes such as streptolysins, hyaluronidase,
the cusps and causes stenosis, incompetence, streptokinase, deoxyribonucleases (DNases),
and regurgitation. nicotinamide adenine dinucleotidase (NADase),
2. Incompetence: Incompetence is defined as and pyrogenic toxin (erythrosine). Neither
defective closure of the cardiac valve e.g., streptolysins (streptolysin O and streptolysin S)
defective closure of the aortic valve has a proven role in the pathogenesis of human
permitting backward flow of blood disease. Streptokinase promotes fibrinolytic
(regurgitation) into the left ventricle during activity by converting plasminogen to plasmin,
ventricular diastole. Incompetence occurs and hyaluronidase may enhance the spread of
when the edges of the valves are destroyed organism through the connective tissue. The
pathogenic significance of DNases and NADase fibrous thickening of the pericardium.

is unknown. The pyrogenic action of erythrosine Because of fibrous thickening of pericardium
is due to direct action on the hypothalamus. the heart may not be able to expand fully
during systole, leading to reduced cardiac
Pathogenesis output, generalized venous congestion and
edema.
The pathogenesis of rheumatic fever is not fully
2. Myocardium: The hallmark of rheumatic
understood. It has been proposed that
fever is the presence of multiple foci of
preliminary infection caused specifically by
inflammation within the myocardium, called
Sterptococcus pyogenes evokes an autoimmune Aschoff bodies. The Aschoff’s bodies consist
response. This preliminary infection is followed of central area of necrotic collagen
by production of antibodies against antipha- surrounded by a zone of inflammatory cells
gocytic cell wall M protein of Sterptococcus polymorphs, macrophages, and Aschoff’s
pyogenes, which then cross react with normal giant cells. The Aschoff’s giant cells or
proteins present in the heart (cardiac myosin and Anitschkow cells are large macrophages
sarcolemmal membrane protein), joints, and with multiple vesicular nuclei (upto 4) and
other tissues. These reactions take place as long abundant eosinophilic cytoplasm. The
as the antibodies persist in the blood (i.e., for 1 Aschoff bodies ultimately undergo fibrosis.
year or more). Rheumatic fever causes damage 3. Endocardium: Valvulitis (inflammation of
to many parts of the body especially the heart, the heart valves) is common in rheumatic
joints, and skin. fever when the endocardium is involved and
is the most important lesion of rheumatic
Heart fever. The degree of heart valve damage is
directly correlated with the antibody titer
Rheumatic pancarditis is characterized by
and the persistence of these antibodies.
inflammatory changes in all three layers of heart
Valvulitis is most pronounced in mitral and
i.e., pancarditis (Table 12.6).
aortic valves than tricuspid and pulmonary
1. Pericardium: Inflammation of the
valves. Valvulitis is characterized by
pericardium leads to the accumulation of
deposition of small vegetations on the cusps
serous exudates in the pericardial space.
along their line of closure. These vegetations
Healing is accompanied by obliteration of
tend to become organized, resulting in the
pericardial space due to fusion of outer
formation of fibrous scar tissue. The fibrous
parietal and inner visceral pericardium and
scar tissue shrinks as it ages and distorts the
shape of the cusps and causes stenosis,
Table 12.6: Features of pancarditis
incompetence, and regurgitation. The mitral
• Dyspnoea (due to pericarditis or congestive cardiac
valve orifice looks stenotic, appearing as
failure)
pinhole, sometimes designated as “fish-
• Chest pain (due to pericarditis)
mouth deformity.”
• Pericardial rub (due to pericarditis)
• Carey Coombs murmur (a soft mid diastolic murmur Joints
due to valvulitis) The joints are red, swollen, and tender. Migrating
• Heart block (due to fibrosis of the myocardium) polyarthritis typically involves the ankles, knees,
• Congestive cardiac failure due to impaired contraction elbows, and wrists sequentially (consecutively).
of myocardium The pain characteristically responds to aspirin.
Skin hemolytic properties of streptolysins can be

Skin changes take the form of erythema assessed. Serological evidence of recent
marginatum. Clinically erythema marginatum streptococcal infection may be helpful (Table
appears as a maculopapular rash mainly on the 12.8).
trunk and proximal extremities but not on the
face. Microscopically, erythema marginatum Table 12.7: Jones criteria for diagnosis
appears as large Aschoff’s bodies. of rheumatic fever
Major manifestations
Sydenham’s Chorea (St Vitus dance)
• Pancarditis
Sydenham’s chorea named after English • Migratory polyarthritis
physician, Thomas Sydenham, is commonly
• Erythema marginatum
associated with streptococcal throat infection,
• Sydenham’s chorea (St Vitus dance)
rheumatic fever and infective endocarditis and
is characterized by rapid uncoordinated, Minor manifestations
involuntary muscle movements. In mild cases, • Fever
recovery takes place within 4 weeks and in some • Arthralgia
cases recovery may be followed by recurrences. • History of previous rheumatic fever
• Leucocytosis
Clinical Features
• Raised ESR
Rheumatic fever is a disease of childhood and
• First or second degree heart block
affects those between 5 and 15 years of age. It
typically occurs 2 to 4 weeks after the preliminary Evidence of recent streptococcal infection
infection. It is interesting to note that rheumatic • Increased titre of antistreptolysin O antibody titre or
fever rarely follows infections by Streptococci antibodies against antiphagocytic cell wall M protein;
pyogenes at other sites, such as the skin. positive throat swab culture
Rheumatic fever is characterized by fever,
N.B. Evidence of recent streptococcal infection is
pancarditis, migrating polyarthritis, erythema
marginatum, and Sydenham’s chorea. particularly important if there is only one major manifestation
While most of the other lesions of rheumatic
fever undergo resolution, those of the valves do Table 12.8: Investigations in acute rheumatic fever
not and tend to progress to a state of chronic Evidence of systemic illness (Nonspecific)
inflammation where the valves become fibrosed • Leucocytosis
and distorted. Damaged valves predispose the • Raised ESR
patients to infective endocarditis.
• Raised C-reactive protein
Diagnosis Evidence of recent streptococcal infection (Specific)
The diagnosis according to the revised Jones Throat swab culture: Group A β-hemolytic streptococci
criteria (Table 12.7) is based upon two or more Increased titres of antistreptolysin O antibodies: > 200
major manifestations, or one major and two or units (adults) or > 300 units (children)
more minor manifestations; evidence of Evidence of pancarditis
preceding streptococcal infection is also required.
Chest radiograph: Cardiomegaly; pulmonary congestion
When diagnosing rheumatic fever, only 25% of
patients with have positive culture for group A ECG: First and second degree heart block; features of
β-hemolytic streptococci because there is a latent pericarditis; T wave inversion; reduction in QRS voltages
period between infection and presentation. Blood Echocardiography: Cardiac dilation and valve
or chocolate agar is preferred because the abnormalities
Management endocarditis, acute and subacute. Bacteremia

may result due to infection elsewhere in the body
Management of rheumatic fever includes bed
e.g., periodontitis, dental treatment procedures,
rest (due to which the joint pain is minimized,
mastication, brushing of teeth, surgical
and cardiac output is reduced in patients with
procedures, and urinary catheterization.
pancarditis), and administration of antibiotics
Infection occurs when microorganisms are
e.g., benzathine penicillin G or sulphadiazine or
erythromycin (if allergic to benzathine implanted on the endocardial surface during
penicillin G or sulphadiazine), analgesics, and episodes of bacteremia.
corticosteroids (indicated in cases with Bacteria causing infective endocarditis have
pancarditis and severe arthritis). been subdivided into two groups: high virulence
and moderate to low virulence. Coagulase
Infective Endocarditis positive Staphylococcus aureus is highly virulent
and is a common cause of acute endocarditis. The
Infective endocarditis is a condition in which the viridans groups of streptococci (Streptococcus
heart valves are invaded by microorganisms, mitis, Streptococcus sanguis, and α hemolytic
usually bacteria and hence the name “bacterial streptococci) are low virulent commensals in the
endocarditis.” However, apart from bacteria, oral cavity and are common causes of subacute
other microorganisms like fungi and viruses are
endocarditis.
capable of causing this condition and hence the
name “infective endocarditis.” Risk Factors
The hallmark of infective endocarditis is the
Factors that increase the risk of infective
presence of large friable (light) vegetations on the
endocarditis can be subdivided into four
heart valves. The vegetations consisting of
categories.
platelets and fibrin surround the microorganisms
1. Previous cardiac abnormalities: Any cardiac
and seem to protect them from normal body
abnormality that increases the hemodynamic
defenses and antibiotics. The vegetations may be
trauma to the endocardial surface such as
single or multiple and may involve more than
high pressure shunts within the heart (e.g.,
one valve. The appearance of the vegetations is
ventricular septal defect) or chronic valvular
influenced by the type of microorganism
diseases (e.g., rheumatic fever) increase the
responsible for the infection, the degree of host
risk of infective endocarditis.
immune response to the infection, and previous
2. Prosthetic heart valves: Prosthetic valves are
antibiotic therapy for e.g., Candida albicans tends
of two types: mechanical and bioprosthetic
to cause larger vegetations than bacterial
valves (derived from bovine or porcine
infection. The aortic and mitral valves are the
tissues). Prosthetic heart valves undergo
most commonly affected, although the tricuspid
some degree of stiffening after implantation
valve may also be involved particularly in
causing stenosis, which may predispose to
intravenous drug abusers.
infective endocarditis. Infective endocarditis
in prosthetic heart valve patients is caused
Etiology by coagulase negative Staphylococcus
Virtually any type of microorganism is capable epidermis.
of causing infective endocarditis, although most 3. Intravenous drug abusers: Intravenous drug
cases are caused by bacteria. Bloodborne bacteria abusers are at high risk for development of
(bacteremia) are the requirements for infective infective endocarditis because they inject
contaminated material directly into the organisms. When the vegetations break off
blood. Infective endocarditis in intravenous and embolize the microorganisms are
drug abusers occurs on previously normal exposed to the bactericidal action of the
valves, often involving the tricuspid valve. blood resulting in the formation of antigen-
The causative organism of infective antibody complexes.
endocarditis in intravenous drug abusers is 2. Subacute Endocarditis: Subacute endocardi-
Staphylococcus aureus, which is commonly tis is typically caused by moderate to low
found in the skin. virulent organisms most frequently
4. Immunosupression: Immunosupression Streptococcus viridans, but sometimes other
enables low virulence microorganisms such microorganisms e.g., Candida albicans are
as α-hemolytic streptococci, fungi, and responsible. During the course of bacteremia,
viruses to become established and cause the streptococci may invade the previously
infection. injured or abnormal heart valves to produce
subacute endocarditis, which is
Classification
characterized by the deposition of small
Infective endocarditis has been traditionally friable vegetations on the valve surface, and
subdivided into acute and subacute endocarditis. may embolize with less frequent
1. Acute Endocarditis: Acute endocarditis is complications. The vegetations of subacute
typically caused by highly virulent endocarditis are distinguished from those of
organisms (e.g., Staphylococcus aureus) but acute endocarditis by the presence of
sometimes other microorganisms (e.g., granulation tissue, which attaches the
Streptococcus pneumoniae and Neisseria vegetations to the valves.
gonorrhoeae) are responsible. During the
course of bacteremia, the staphylococci may Clinical Features
invade the previously normal heart valves
1. Acute endocarditis: Acute endocarditis
and produce endocarditis, which is
typically presents as rapidly developing
characterized by the deposition of large
friable vegetations on the valve surface. The fever with rigors, malaise, weight loss,
vegetations in acute endocarditis begin as petechiae (due to microemboli or antigen-
small excrescences (protrusions) but as the antibody complexes), and changing cardiac
microorganisms proliferate, the vegetations murmurs. The larger vegetations often cause
enlarge and eventually become large and embolic complications and there frequently
friable that may obstruct the valve orifice. is splenomegaly. Cardiac failure and renal
The vegetations may cause rapid destruction failure develop rapidly. Even with treatment,
of the valves, chordae tendineae, and death occurs in days to weeks in 50 to 60%
papillary muscle resulting in cardiac failure. of the patients.
The infection may eventually extend into the 2. Subacute endocarditis: Subacute endocardi-
adjacent myocardium to produce abscess tis should be suspected when the patient is
often known as ring abscess. The vegetations known to have any previous cardiac
are large, and friable, and tend to break off abnormalities such as ventricular septal
and embolize to spleen, kidneys, heart, and defect, mitral valve prolapse, and rheumatic
brain resulting in infarction and metastatic fever. It typically has an insidious onset with
infection (abscesses) because the embolic low grade fever, malaise, weight loss, and
fragments contain large number of virulent flu-like syndrome. Other features include
subconjuctival hemorrhages, petechiae on Dental Considerations

the skin and mucous membranes, splincter The most important goal of dental treatment in
hemorrhages under the finger or toe nails, patients with valvular heart disease is to prevent
Osler’s nodules at the finger tips due to infective endocarditis. The dental treatment
vasculitis, digital clubbing, splenomegaly, procedures known to induce gingival or mucosal
and hematouria. bleeding may often cause transient bacteremia
that rarely lasts longer than 15 minutes.
Clinical Complications However, within these 15 minutes the bacteria
may lodge (stick) themselves on previously
1. Direct injury to the heart valves injured or abnormal heart valves, which may
2. Formation of ring abscess result in infective endocarditis. Although
bacteremia is common following many invasive
3. The vegetations are large, and friable, and
procedures, only certain bacteria usually cause
tend to break off and embolize to spleen,
infective endocarditis. It is not always possible
kidneys, heart, and brain resulting in
to predict which patients will develop this
metastatic infection and infarction. infection or which particular procedure will be
responsible.
Diagnosis The percentage of patients with infective
Diagnosis is confirmed by blood culture. endocarditis who received recent dental
However, if the clinical picture suggests treatment procedures varies from 3 to 40%. Most
endocarditis, treatment should begin without cases of infective endocarditis involving oral
waiting for pathological confirmation. microorganisms are not likely to be caused by
Echocardiography is helpful in detecting dental treatment procedures, but by dental
diseases, mastication, and brushing of teeth.
vegetations and ring abscess. Urine examination
Certain cardiac conditions are associated with
reveals microscopic hematouria. ECG may show
infective endocarditis more often than others.
abnormalities due to ring abscess formation.
Antibiotic prophylaxis is recommended in
individuals who have a high risk of developing
Treatment infective endocarditis. The patients with
Treatment consists of multidisciplinary approach cardiovascular diseases, who are associated with
between physician, surgeon, and microbiologist. infective endocarditis, are grouped into:
The treatment regimen consists of removing the 1. Negligible-risk category: The low-risk
source of infection (e.g., periodontitis) and category includes patients with implanted
antimicrobial treatment consisting of intravenous cardiac pacemakers (intravascular and
epicardial), automatic defibrillators, and a
administration of benzylpenicillin or
previous history of coronary artery bypass
vancomycin in patients who are allergic to
surgery.
penicillin.
2. Moderate-risk category: The moderate-risk
Vancomycin plus gentamycin is recommen- category includes patients with patent
ded for staphylococcal endocarditis. Cardiac ductus arteriosus, atrial septal defect,
surgery is advisable when there are large ventricular septal defect, coarctation of the
vegetations (increased risk of systemic aorta, bicuspid aortic valve, acquired
embolization), heart failure due to valve damage, valvular dysfunction (e.g., due to rheumatic
failure of antibiotic therapy, and the presence of heart fever or collagen vascular disease), and
ring abscesses. hypertrophic cardiomyopathy.
3. High-risk category: The high-risk category (e.g., dental extractions, periodontal surgery,
includes patients with prosthetic heart valves dental implant surgery, intraligamentary local
(mechanical and bioprosthetic), a previous anesthetic injection, initial placement of
history of infective endocarditis, complex orthodontic bands, and periapical surgery)
cyanotic congenital heart disease (e.g., known to induce gingival or mucosal bleeding.
Fallot’s tetralogy), and surgically constructed In order to reduce microbial resistance and
systemic pulmonary shunts. potential side affects, it is important that the
The antibiotic prophylaxis for infective antibiotic prophylaxis should be initiated one
endocarditis should consider: hour before the procedure and should not be
1. The degree to which the patients underlying continued for more than 6 to 8 hours.
condition creates a risk of endocarditis Alternatively, numerous dental treatment
procedures may be accomplished at the same
2. The apparent risk of bacteremia with the
appointment, and if possible as a local accessory
procedure
to systemic antibiotic prophylaxis, a
3. The potential side effects of the prophylactic chlorhexidine gluconate 0.20% solution mouth
antibiotic rinse can be used before dental treatment
4. The cost-benefit aspects of the recommended procedures. In case of delayed healing, it may
prophylactic antibiotic regimen. be necessary to provide additional doses of
Failure to consider all of these factors may lead antibiotics for treatment. It is advisable to
to overuse, excessive cost and risk of adverse administer antimicrobial prophylaxis before a
drug reactions. The American Heart Association dental treatment procedure that involves
(AHA) recommends antibiotic prophylaxis infected tissues. Prophylaxis should be directed
(Table 12.9) prior to dental treatment procedures at the most likely pathogen causing the infection.
Table 12.9: Antibiotic prophylaxis against subacute endocarditis

Situation agent† regimen‡
Standard prophylaxis Amoxycillin Adults, 2.0 grams; children, 50 mg/kg orally 1 hour before
procedure
Unable to take oral medications Ampicillin Adults, 2.0 g IM†† or IV§; ; children, 50 mg/kg IM†† or
IV§ within 30 minutes before procedure
Allergic to penicillin Clindamycin Adults, 600 mg; children, 20 mg/kg orally 1 hour before
procedure
Cefalexin or cefadroxil Adults, 2.0 g; children, 50 mg/kg orally 1 hour before
procedure
Azithromycin or Adults, 500 mg; children, 15 mg/kg orally 1 hour before
clarithromycin procedure
Allergic to penicillin and Clindamycin Adults, 600 mg; children, 20 mg/kg IV§ 1hour before
unable to take oral medications procedure
Cefazolin Adults, 1.0 g; children, 25 mg/kg IM†† or IV§ within 30
minutes before procedure
† Cephalosporins should not be used in patients with immediate-type hypersensitivity reaction (urticaria,
angioedeman or anaphylaxis) to penicillins
‡ Total children’s dose should not exceed adult dose
†† IM: intramuscular
§ IV: intravenous
CEREBROVASCULAR ACCIDENT AND DYSRHYTHMIAS
Stroke stroke. Therefore, a stroke can cause impairment

of body functions such as speech, memory, and
A stroke results from sudden interruption of
movement that are controlled by the affected
blood flow to the brain, which deprives it of portion of the brain. The risk factors include
oxygen. When the blood vessel that delivers smoking, hypertension and diabetes mellitus.
oxygen and nutrients to the brain is obstructed
by atherosclerosis or embolus, the condition is Oral Manifestations
called ischemic stroke or cerebral ischemia Dysphasia (lack of coordination in speech) may
(Fig.12.8). Hemorrhagic stroke occurs when a be present in the patient with stroke and can
blood vessel supplying the brain ruptures and cause changes in diet, mastication, nutrition, and
causes bleeding into the brain. In any form of body weight. Inability to completely clear food
stroke, the nerve cells of the brain are deprived in the mouth may result in halitosis, caries,
of oxygen and die within minutes of onset of the gingivitis and periodontitis.
Fig. 12.8: Stroke

Dental Considerations Pacemakers and automatic defibrillators

present a low risk of infective endocarditis and
1. Patients with stroke are frequently treated
do not require prophylactic antibiotic coverage
with oral anticoagulants therefore; the
before dental therapy. Older pacemakers were
dentist should consult the concerned
unipolar and were affected by equipment that
physician before treatment to determine
generates an electromagnetic field, such as
whether anticoagulant therapy should be
ultrasonic scalers and electrocautery units. Most
modified
pacemakers placed within the last 30 years are
2. To prevent a subsequent stroke, clinicians
bipolar and generally are not affected by the
must treat active infections aggressively,
small electromagnetic fields created by dental
since even minor infection may alter blood
equipment.
coagulation and trigger thrombus formation
Automatic defibrillators are often activated-
ensuing in cerebral infarction
without warning, which may cause sudden
3. Weakness of the facial area or paralysis of
movement and endanger the patient in the dental
extremities may make oral hygiene
chair. The dentist must be aware of this potential
procedures extremely difficult; therefore, the
problem during treatment, and should stabilize
dentist in consultation with an occupational
the operating field through use of a bite-block
therapist may modify oral hygiene
with floss (for easy retrieval) and rubber dam.
instruments for ease of use
4. The patients head position should be
SUMMARY
adjusted, while constant evacuation will
prevent aspiration of foreign matter Dental Management of Patients with
5. The gag reflex may be diminished after a Cardiovascular Disease
stroke, which may require particular The primary goal in the management of a patient
attention during dental therapy with cardiovascular disease during dental
6. The dentist should counsel the patient about treatment is to minimize any alterations in
the importance of oral hygiene and may hemodynamics during treatment (i.e., by
initiate a long-term regimen of chlorhexidine maintaining the patients blood pressure, heart
gluconate 0.20% solution to help in plaque rate, heart rhythm, cardiac output and
control myocardial oxygen requirement). Psychological
and physiological stress during dental treatment
DYSRHYTHMIAS has the potential to alter the hemodynamics
significantly. Therefore, a stress-reduction
Dental Considerations
protocol is frequently suggested for patients with
Many of the antidysrhythmic drugs have side significant cardiovascular compromise, which
effects such as gingival overgrowth or includes the following:
xerostomia. The use of local anesthetics with 1. Shorter appointments, preferably in the
vasoconstrictors may be contraindicated in morning when the patient is well-rested and
patients with uncontrolled dysrhythmias; dental has a additional physical energy
treatment may best be accomplished in a hospital 2. Use of profound local anesthesia to minimize
setting with careful cardiac monitoring. Some discomfort
dysrhythmias are treated with implanted cardiac 3. Preoperative or intraoperative (during the
pacemakers or automatic defibrillators in procedure) conscious sedation or both
addition to drug therapy. 4. Postoperative analgesia
II. ASTHMA AND DENTAL CARE
Respiratory problems such as asthma affect 2. Middle layer: The middle layer consists of
many aspects of dental treatment. Extracting a cartilage and bands of smooth muscle. There
proper history from the patient with asthma will is some areolar tissue, containing blood and
help prevent serious problems and alert the lymph vessels and autonomic nerves
dentist to orofacial conditions e.g., oro- 3. Inner layer: The inner layer or the lumen of
pharyngeal candidosis, which may result from the trachea is lined by pseudostratified
the use of appropriate medication (corticosteroid ciliated columnar epithelium intermingled
inhalers). Patients with severe persistent asthma with goblet cells
or status asthmaticus are best treated in the
hospital setting. Blood Supply
NORMAL ANATOMY OF THE The blood supply to the trachea is through the
RESPIRATORY TRACT inferior thyroid and bronchial arteries and the
venous return is by the inferior thyroid veins.
Trachea
The trachea (windpipe) is a continuation of the Innervation
larynx and extends downwards to about the level The trachea is innervated by the parasympathetic
of the 5th thoracic vertebra where it divides at and sympathetic nerves. Parasympathetic
the carnia into right and left bronchi, one innervation is by the recurrent laryngeal nerve.
bronchus going to each lung. Structures The sympathetic innervation is by nerves of the
associated with the trachea are: sympathetic ganglia.
1. Superiorly: The larynx
2. Inferiorly: The right and left bronchi Lymphatic Drainage
3. Anteriorly: The isthmus of the thyroid gland
4. Posteriorly: The esophagus, which separates The lymph from the trachea passes through the
the trachea from the vertebral column. lymphatic vessels to the lymph nodes situated
5. Laterally: The apex of the lungs and the lobes around the trachea and in the carnia, the area
of the thyroid gland where it divides into two bronchi.
Structure Bronchi and Bronchioles
The trachea is composed of 16 to 20 incomplete The trachea divides into two branches: the right
C-shaped rings of hyaline cartilages lying one bronchus and the left bronchus. The right
above the other. The cartilages are incomplete bronchus divides into three branches, one to each
posteriorly. Connective tissue and involuntary lobe, after entering the right lung at the hilum.
muscle join the cartilages and form the posterior The left bronchus divides into two branches, one
wall where they are incomplete. The soft tissue to each lobe, after entering the left lung at the
posterior wall is in contact with the esophagus. hilum.
The trachea is composed of three layers of tissue: After entering the lobe each bronchus
1. Outer layer: The outer layer consists of progressively subdivides into bronchioles,
fibrous and elastic tissue and encloses the terminal bronchioles, respiratory bronchioles,
cartilage. alveolar ducts, and finally alveoli. The bronchi
are composed of the same tissues as the trachea. the left side and right lymphatic duct on the right
They are lined with pseudostratified ciliated side.
columnar epithelium intermingled with goblet
cells. Lungs
Towards the distal end of the bronchi the There are two lungs, lying on each side of the
cartilages become irregular in shape and are midline in the thoracic cavity. They are cone
absent at bronchiolar level. In the absence of shaped and have an apex, a base, costal surface,
cartilage the smooth muscles in the walls of the and medial surface.
bronchioles become thicker and are responsive
1. Apex: The apex is round and rises above the
to autonomic nerve stimulation. As the bronchus
level of the middle third of the clavicle. The
subdivides the pseudostratified ciliated
structures associated with it are the first rib,
columnar epithelium changes gradually to non-
and the blood vessels and nerves in the root
ciliated squamous cells in the alveoli.
of the neck
Interspersed between the squamous cells are
2. Base: The base is concave and semilunar in
type II alveolar cells (pneumocytes) that secrete
shape and is closely associated with the
surfactant, a phospholipid fluid, which reduces
thoracic surface of the diaphragm
surface tension of the fluid lining the alveoli and
3. Costal Surface: The costal surface is convex
prevents the alveolar walls from collapsing
and is closely associated with the costal
during expiration. In addition, surfactant
cartilages, the ribs, and the intercostal
prevents the alveoli from drying out.
muscles
Blood Supply 4. Medial Surface: The medial surface is
concave and has a roughly triangular shaped
The blood supply to the bronchi and bronchioles area, called the hilum at the level of the 5th,
is through branches of the right and left bronchial 6th, and 7th thoracic vertebrae. Structures
arteries and the venous return is by the right and which enter and leave the lung at the hilum
left bronchial veins. include the primary bronchus, the
pulmonary artery supplying the lung, the
Innervation
two pulmonary veins draining it, the
The bronchi and bronchioles are innervated by bronchial artery, the bronchial veins, the
the parasympathetic and sympathetic nerves. lymph vessels, and parasympathetic and
Parasympathetic innervation is by the vagus sympathetic nerves. The area between the
nerve. The vagus nerve stimulates the lungs is the mediastinum. It is occupied by
contraction of the smooth muscles in the the heart, great vessels (inferior vena cava
bronchial tree, causing bronchoconstriction, and and aorta), trachea, esophagus, right and left
sympathetic stimulation causes broncho- bronchi, lymph vessels, lymph nodes, and
dilatation. nerves.
Lymphatic Drainage Organization of the Lungs

The lymph from the bronchi and bronchioles The right lung is divided into three distinct lobes:
passes through the lymphatic vessels to the superior, middle, and inferior. The left lung is
lymph nodes situated around the trachea and smaller in comparison to the right lung as the
bronchial tree and then into the thoracic duct on heart is situated left to the midline. It is divided
into two lobes: superior, and inferior. Each lobe The walls of the alveoli and those of the
is made up of large number of lobules. capillaries consist of only one layer of flattened
epithelial cells. The exchange of gases between
Pleura and Pleural Cavity air in the alveoli and blood in the capillaries takes
The pleura consist of a closed sac one for each place across these two thin membranes.
lung, which contains a small amount of serous The pulmonary capillaries eventually form
fluid. The pleura have two layers: one adheres two pulmonary veins in each lung. They leave
to the lung, and the other to the wall of the the lungs at the hilum and carry oxygenated
thoracic cavity. blood to the left atrium of the heart. The
1. Visceral Pleura: The visceral pleura is innumerable blood capillaries and blood vessels
adherent to the lung, covering each lobe and in the lungs are supported by connective tissue.
passing into the fissures which separate
them. ASTHMA
2. Parietal Pleura: The parietal pleura is
Asthma is an inflammatory disease of the
adherent to the thoracic cavity and the
bronchioles in which the mucous membranes
thoracic surface of the diaphragm. It is
and muscle layers of the bronchioles become
continuous with the visceral pleura at the
thickened and the mucous glands present in the
hilum.
submucosa enlarge, reducing airflow in the lower
Pleural Cavity respiratory tract. The airway is obstructed during
The visceral pleura and the parietal pleura are an asthmatic attack due to spasmodic contraction
separated by a space, the pleural cavity. The of bronchial muscles (bronchospasm) and
pleural cavity consists of thin film of serous fluid, excessive secretion of mucous.
which allows the visceral and the parietal pleura An attack of asthma is characterized by severe
to glide over each other, thereby preventing dyspnoea and wheezing (soft whistling sound
friction between them during respiration. during expiration). Inspiration is normal but only
The two layers of pleura, with the serous fluid partial expiration is achieved, resulting in
between them, behave in the same way as two hyperinflation of the lungs due to air trapped
pieces of glass separated by a thin film of water. distal to the bronchi, where the bronchioles are
They glide over each other easily but can be constricted and filled with mucous and debris.
pulled apart only with difficulty, because of the The duration of attacks usually varies from a
surface tension between the two glass layers and few minutes to hours, and very occasionally,
the water. If either pleura are punctured, the days (status asthmaticus). In severe acute attacks
underlying lung collapses due to its inherent the bronchioles may be obstructed by mucous
elastic property. plugs, leading to hypoxia, hypercapnia (high
level of carbon dioxide in the circulating blood),
Blood Supply acidosis, and possibly death.
The pulmonary artery divides into two branches, With good management the symptoms may
each carrying deoxygenated blood to each lung. diminish and even disappear, allowing the
Within the lungs each pulmonary artery divides patient to lead a normal professional and social
into many branches, which eventually end in a life. Asthma is most commonly found in children,
dense capillary network around the walls of the with about half of all cases developing before the
alveoli. age of 10 years. However, up to 70 percent of
children with asthma undergo remission by the Pathogenesis

age of 20 years.
An understanding of the mechanism by which
Definition asthma develops provides the basis for the
methods of treatment currently proposed for its
The definition of asthma proposed by the
management. Asthma is considered to be caused
International Consensus and by the “Global
by many factors in individuals who often have a
Strategy for Asthma Management and
genetic tendency towards the disease.
Prevention” is as follows:
The pathogenesis of extrinsic asthma is readily
“Asthma is a chronic, inflammatory disorder
explained by type 1 hypersensitivity reaction.
of the airways in which many cells and cellular
However, the pathogenesis of intrinsic asthma
elements play a role. The chronic inflammation
is non-immune and is unknown or poorly
causes an associated increase in airway
defined.
hyperresponsiveness that leads to recurrent
Inhalation of allergens stimulates the
episodes of wheezing, breathlessness, chest
production of immunoglobulin E (IgE)
tightness and coughing, particularly at night or
antibodies that bind to the surface of mast cells
in the early morning. These episodes are usually
in the airways (bronchioles). When the allergen
associated with widespread but variable airflow
is encountered again, the antigen and antibody
obstruction that is often reversible either
reaction results in the release of histamine and
spontaneously or with treatment.”
other mediators (leukotrienes, prostaglandins,
Risk Factors platelet activating factor, and mast cell tryptase)
from the mast cells, that open tight junctions
The risk factors, which may trigger an asthmatic
between pseudostratified columnar ciliated cells.
attack include:
Antigen then enters the submucosa to activate
1. Hereditary: Heredity is also a predisposing
more mast cells and eosinophils, which in turn
factor in asthma, and a family history of
release chemical mediators which induce
asthma is common among asthma patients.
bronchoconstriction, bronchospasm (Fig.12.9),
2. Allergy: Allergy is the most important
vasodilatation, increased vascular permeability,
predisposing factor in asthma. It is reflected
and increased mucous production.
in the tendency to produce abnormally high
levels of immunoglobulin E (IgE) in response
Classification
to exposure to allergens in the environment.
Some of the allergens include dust mites, Asthma is commonly classified as extrinsic and
animals (cats, dogs, rats, cockroaches etc.), intrinsic. However, both give rise to identical
moulds (a fungus that produces a superficial symptoms and are treated in the same way.
growth on various kinds of damp or Important differences include age of onset and
decaying organic matter), pollen, and food. contribution of allergens. The distinction
3. Environmental: Environmental factors between these two types of asthma is largely
include dust, tobacco smoke, cold air, air academic, because in clinical practice, many
pollution, upper respiratory tract infection, patients do not fit into either category but instead
stress, and strenuous exercise. fall into a mixed group with features of each.
Fig. 12.9: Structure of lungs and asthmatic bronchiole
Extrinsic Asthma (Childhood Onset, Allergic, Clinical Symptoms

Atopic Asthma)
The principal clinical symptoms of asthma are:
The extrinsic asthma occurs in children and
1. Wheezing
young adults who are atopic, that is, they readily
2. Chest tightness
develop IgE antibodies against allergens (Type I
hypersensitivity). Attacks tend to become less 3. Dyspnea (breathlessness)
frequent and less severe with age. 4. Cough
However, none of these clinical symptoms is
Intrinsic Asthma (Adult Onset, Late Onset, specific for asthma, and may occur with other
Cryptogenic Asthma) chest conditions. As a result, asthma is often
The intrinsic asthma occurs later in adult life and misdiagnosed and therefore poorly treated, or
there is no history of childhood allergic reactions. even not treated at all. Asthma must always be
These patients are said to have a predisposition considered in case of the following:
to asthma (asthmatic diathesis). In intrinsic 1. Episodes of breathlessness occur mainly at
asthma, the factors responsible for attacks are nights that wake up the patient, especially
unknown or poorly defined. However, some of in the early hours of the morning
the factors responsible for attacks include: 2. Breathlessness compels the patient to sit up
aspirin, penicillin, nasal polyps, chronic
in bed to relieve the symptoms
bronchitis, cold, psychological stress, exercise,
3. The patient has a history of coughing spells
and inhaled irritants such as ozone, nitrogen
dioxide, and sulfur dioxide. Attacks tend to 4. The symptoms appear in recurrent attacks
increase in severity and there may be irreversible 5. The symptoms disappear either
damage to the lungs. Eventually impaired lung spontaneously or after taking asthma
function (ventilation) leads to hypoxia, medication (bronchodilator)
pulmonary hypertension, and right-sided heart 6. The patient has a personal or family history
failure. of allergic reactions
7. Symptoms are brought on by a variety of presence of crackles is suggestive of other

factors such as dust, cold air or strenuous conditions. Nevertheless, the absence of wheeze
exercise or stress does not exclude asthma, as during symptom
free periods there is no evident abnormality and
Diagnosis the auscultation is normal.
Before treating a patient for asthma, it is
Chest Radiograph
necessary to:
1. Establish the diagnosis of asthma and Although chest radiograph has no place in the
identify the possible causal and trigger diagnosis of asthma, it is, nevertheless, used:
factors 1. If conditions other than asthma are suspected
2. Determine the degree of severity of the that are likely to cause the symptoms
disease mentioned by the patient
If the patient has already been examined 2. If a complication of asthma is suspected, such
during an attack, the diagnosis is obvious. as pneumothorax or pneumonia
Diagnosis is more difficult if the patient presents
during symptom free period. Lung Function Tests
Lung function tests should be conducted for all
History
persons suspected of having asthma. The
Case history taking is the key to diagnosis. In diagnosis is confirmed by measurement of peak
taking the history it is important to use simple expiratory flow (PEF) using a simple peak flow
words, in a manner that is easy for the patient to meter or spirometry.
understand (or the family, if the patient is a
child). Open questions are asked to allow the Peak Flow Meter
patient or family to provide information about The peak flow meter is a tool that is reliable,
the history of the disease, and specific questions robust, practical and cheap, used to detect airflow
to obtain information about the respiratory limitation. The degree of airflow limitation can
symptoms, time of attacks, variability be evaluated by comparing the patient’s PEF
(recurrence) of attacks, trigger factors, as well as level with the ‘normal’ value of PEF expected.
factors that improve the symptoms. Recurrent Predicted or ‘normal’ values of PEF are given in
attacks of breathlessness, mainly at night, with tables by age, sex and height for adults and by
wheezing, that wake the patient and compels the height only for children.
patient to sit up to be able to breathe, are the
symptoms most characteristic of asthma. Spirometry
Spirometry is another method used to test lung
Clinical Examination
function and for both diagnosis and assessment
If the patient presents during a symptom free of progress. Spirometry is the method of choice
period, the results of the clinical examination as measurement of PEF by peak flow meter has
often do not lead to a diagnosis of asthma. The significant limitations, but in most low or middle
presence of wheezing is consistent with asthma; income countries it is only available in large
however, wheezing is not specific for asthma, hospitals and some specialized referral centers.
and may occur with other chest conditions. The The aim of spirometry is to:
1. Diagnose airflow obstruction i. Clinical and functional improvement

2. Measure the degree of airflow obstruction ii. Trying to obtain the best results
3. Monitor the effects of treatment possible with the minimum of side
4. Demonstrate the presence of airflow effects
obstruction to the patient 4. Preventive Measures
5. Demonstrate the presence of reversibility of Preventive measures consist of avoiding or
airflow obstruction to the patient controlling the risk factors of asthma and
6. Provide objective feedback to the patient parents of children with asthma should be
about the presence and severity of asthma informed that it is harmful to expose their
child to passive smoking
Treatment
Objectives of Treatment ESSENTIAL DRUGS FOR TREATMENT OF
The treatment objectives should be explained to ASTHMA
the patient and/or the patient’s family from the To manage asthma patients, the drugs must
start of treatment. It should also be explained that always be available. A limited number of drugs
treatment is long term and that it is impossible are necessary for long-term treatment of asthma
to determine immediately how long it will take and are included in the WHO list of essential
to attain these objectives. Asthma is under control drugs (Table 12.10).
when the following objectives are reached:
1. Clinical Objectives Corticosteroids
a. Reduction and even total disappearance
Inhaled Corticosteroids (beclomethasone)
of symptoms, particularly nocturnal
b. Absence of visits to the physician Because of its effectiveness and low rate of side
c. No limitation of day-to-day activities effects, inhaled beclomethasone in high doses, is
2. Functional Objective the treatment of choice for cases of persistent
Peak expiratory flow (PEF) normal or > 80% asthma. Due to its anti-inflammatory action, it
of PEF predicted progressively reduces bronchial inflammation
3. Treatment Objective and thereby the symptoms of asthma.
a. No need or only occasional need to use Local side effects include hoarseness, mild
bronchodilator sore throat, and oropharyngeal candidal
b. In the most severe and persistent cases, infection, if daily treatment consists of doses
these objectives may not be achieved due >1000 μg. These side effects can be avoided by
to irreversible inflammatory changes of advising patients to use a large volume spacer
the bronchial mucosa. The objectives of and to rinse and gargle with water after use of
treatment are modest: their inhaler.
Table 12.10: Essential drugs for asthma treatment

Type of drug Generic name Mode of administration and dosage
Corticosteroids Beclomethasone Aerosol (inhaler): 250 µg per puff
Prednisolone Tablets: 4-5 mg
Bronchodilator Salbutamol Aerosol (inhaler): 100 µg per puff
Systemic Corticosteroids (Oral induced asthma. Short acting β2-agonists initiate

prednisolone) a bronchodilator effect within 15-19 minutes and
These can be used in short or long-term can be maintained for up to 6 hours. They are
treatment: well-tolerated and systemic side effects
1. Short-term: They are used to treat acute (tachycardia, tremors, and hypokalaemia), which
attacks for a short period, and then stopped. may result from large doses is rare. Salbutamol
In this case they have few or no harmful side is one of the best short-acting β 2 -agonist.
effects. Administration is preferably by inhalation, due
2. Long-term: Due to their harmful effects, they to the following reasons:
should only be used for severe persistent 1. Small doses
asthma or status asthmaticus, which do not 2. Rapid action (attaining its maximum action
respond to other treatments. Harmful effects in a few seconds)
of long-term corticosteroids include 3. Almost total absence of side effects
infections (in particular tuberculosis), β2-agonists such as salbutamol and terbutaline
diabetes mellitus, hypertension, and can produce xerostomia, dysgeusia, and
osteoporosis. Furthermore, acute adrenal discoloration of the teeth. Dry mouth may
insufficiency can occur if long-term oral increase incidence of dental caries and thus a
corticosteroids are suddenly interrupted. prophylactic regimen is important. If the dry
mouth is severe, lubrication with saliva
Bronchodilators substitutes may be indicated. The hypokalaemia
which may result from large doses of β2-agonists
These drugs aim to reduce bronchospasm caused
may be aggravated by high doses of cortico-
by an allergen-induced immune response. Three
steroids and by adrenaline in used in dental local
groups of drugs are included:
anesthetics.
1. β2-agonists (drugs that can combine with a
receptors on a cell to produce a physiological
Muscarinic Receptor Antagonists
reaction)
2. Muscarinic receptor antagonists (drugs that Muscarinic receptor antagonists (anti-
neutralizes or counteracts the effects of cholinergic) to reverse the effects of acetylcholine
another drug) released from vagus nerve. The aim of
3. Methylxanthines muscarinic receptor antagonists is to cause
bronchodilatation by acting as antagonists of
β2-agonists acetylcholine for muscarinic receptors
β 2 -agonists are the most powerful (macaronis M 2- M5 subtypes) located in smooth
bronchodilators. They relax the bronchial smooth muscle cells of bronchioles.
muscle and assist in clearing the mucus The two examples of muscarinic receptor
secretions present in the bronchial airways. β2- antagonists used to treat airway
agonists are broadly classified as short acting and hyperresponsiveness are ipratropium and
long acting. The long acting β2-agonists such as oxitropium bromide. It has additive
salmeterol and formoterol exert an effect within bronchodilator effect with theophylline and
10-20 minutes and can be maintained for up to therefore is more effective in chronic obstructive
12 hours. pulmonary disease (COPD) than in bronchial
Short acting β2-agonists are the drugs of choice asthma. Transient side effects include
for asthma attacks and for preventing exercise xerostomia, dysguesia, blurred vision, and
urinary retention. Systemic side effects are rare 7. Nonsteroidal anti-inflammatory drugs
because of poor absorption from lungs. should not be prescribed as many asthmatic
patients are allergic to these analgesics.
Methylxanthines Similarly, sulphite-containing compounds
The two drugs that are commonly used in this (such as preservatives in some adrenaline
group are theophylline and aminophylline and containing local anesthetics) can produce
they produce actions similar to that of caffeine. allergy in asthmatic patients.
Theophylline and aminophylline are the second 8. A severe asthmatic attack can be life
most common drugs used in the treatment of threatening and stress during dental
asthma. treatment procedures may contribute to the
beginning of such a condition and therefore
Dental Considerations the dentist should have the equipment to
deal with such an emergency. In case of an
1. Effort should be made to relieve anxiety as
emergency:
far as possible.
a. A salbutamol inhaler or nebulised
2. Treatment should not be carried out if the
salbutamol is useful.
patient has not brought their normal
medication and if such medication is b. Intravenous aminophylline (250-500 mg
unavailable. by slow IV injection over 20 min) is
3. Patients may not be comfortable in the reserved for patients who do not respond
supine position. quickly to nebulised salbutamol.
4. If possible, asthmatic patients should be c. Intramuscular or intravenous prednis-
treated using local anesthesia. onlone (4-60 mg) should be administered
5. General anesthesia using nitrous oxide and to all severely ill patients.
oxygen is preferred to intravenous sedation d. Intramuscular chlorpheniramine maleate
since the former can be rapidly controlled. (10-20 mg) or intravenous chlorphenir-
6. General anesthesia can be complicated by amine maleate (10-20 mg slow IV
hypoxia and increased carbon dioxide which injection over 1 min) or should be
can lead to pulmonary oedema even if administered for the management of
cardiac function is normal. anaphylactic shock.
III. DIABETES MELLITUS AND DENTAL CARE

Diabetes mellitus is a chronic metabolic disorder directly into the blood. The different cells types
characterized by disorders of carbohydrate, are as follows:
protein and lipid metabolism, resulting in 1. α cells which secrete glucagon
hyperglycemia. 2. β cells which secrete insulin and amylin
Islets of Langerhans 3. δ cells which secrete somatostatin
The pancreas consist groups of cells called islets 4. PP cells which secrete pancreatic
of Langerhans which secrete their hormones polypeptide
Classification Type 2 Diabetes Mellitus

Type 1 or insulin dependent diabetes mellitus It accounts for 95% of all cases of diabetes
(IDDM) or juvenile mellitus and usually affects people who are
1. Type 2 or non-insulin dependent diabetes above 40 years when the basal metabolic rate is
mellitus (NIDDM) or maturity onset low. But there is a recent trend which shows that
2. Gestational diabetes mellitus type 2 diabetes mellitus also affects people who
3. Drug induced diabetes mellitus are in the age group of 20 years, which is related
4. Diabetes mellitus due to infections to truncal obesity and lack of exercise. Obesity
5. Diabetes mellitus associated with syndromes increases insulin levels and decreases the
concentration and sensitivity of insulin receptors.
Normal Glucose Metabolism Therefore glucose uptake is very minimal at the
In a normal person the blood glucose level is cellular level resulting in hyperglycemia.
< 110 mg/dl. But after consumption of meals it However, exercise and modified lifestyle
increases to 120-140 mg/dl. The blood glucose increases the concentration and sensitivity of
level returns to normal within 2 hours, this is insulin receptors.
achieved by secretion of insulin by the β cells of
Clinical Features
islets of Langerhans. To carry out its effects
insulin first binds with its receptor and activates The classical clinical features of diabetes mellitus
the cell membrane, facilitating the entry of (Fig.12.11) are as follows:
glucose into cell. The insulin receptor consists of 1. Polyuria (increased diuresis)
four subunits (two α subunits and two 2. Polyphagia (increased appetite)
β subunits) held together by disulfide bonds. 3. Polydipsia (increased thirst)
Most of the receptors are present in the muscle 4. Asthenia (weakness due to loss of muscle
tissue. When the blood glucose level decreases, mass)
α cells of islets of Langerhans secrete glucagon
which breakdowns the liver and muscle Gestational Diabetes Mellitus
glycogen (glycogenolysis) and proteins During the third trimester of pregnancy there is
(gluconeogenesis) to increase the blood glucose diabetes mellitus. However, after parturition the
levels. blood glucose levels return to normal. The
various mechanisms that lead to gestational
Type 1 Diabetes Mellitus diabetes are:
It comprises approximately 3-5% of all cases of 1. Increased absorption of glucose from
diabetes mellitus and is usually seen in people gastrointestinal tract
below 40 years. The various etiological factors of 2. Inability of insulin to convert glucose into
type 1 diabetes mellitus are: glycogen
1. Autoimmune related destruction of â cells 3. Impaired tubular reabsorption of glucose,
of islets of Langerhans (Fig.12.10) leading to which leads to glycosuria
deficiency in insulin and increased blood
glucose levels Drug or chemically Induced Diabetes
2. Genetics (HLA–DR3) also plays an Mellitus
important role in the development of type 1 There are many drugs or chemicals that induce
diabetes mellitus diabetes mellitus few of them are:
Fig. 12.10: IDDM diabetes mellitus
Fig. 12.11: Clinical features of diabetes mellitus

1. Thyroxine or T4 wound site).

2. Thiazide diuretic e.g., chlorothiazide The accumulation of AGEs in the tissues of
3. Glucocorticoids patients with diabetes mellitus also increases the
4. Phenytoin sodium intensity of the inflammatory response to
5. α-interferon periodontal pathogens, because inflammatory
cells such as monocytes and macrophages have
Diabetes Mellitus due to Infections receptors for AGEs. Interactions between AGEs
1. Congenital rubella and their receptors (RAGEs) on inflammatory
2. Cytomegalovirus virus cells result in the increased production of matrix
metalloproteinases, proinflammatory cytokines
Diabetes Associated with Syndromes such as IL-1β, IL-6, and mediators such as TNF-
1. Down’s syndrome α. This interaction may be the cause of increased
2. Turner’s syndrome levels of IL-1β, IL-6, and TNF-α in the gingival
3. Klinefelter’s syndrome crevicular fluid and may magnify the
4. Grinspan syndrome inflammatory response, alter wound healing,
and induce connective tissue damage, and bone
COMPLICATIONS resorption.
Increased Susceptibility to Infection Diabetic Microangiopathy
Diabetics are prone to bacterial, viral and fungal Diabetics have a predisposition to develop
infections because of: vascular lesions of the small blood vessels
1. Hyperglycemia (arterioles, capillaries, and venules). Diabetic
2. Diabetic microangiopathy microangiopathy is characterized by deposition
of proteins at the basement membrane, which
Hyperglycemia
ultimately leads to thickening of the basement
A consequence of hyperglycemia in diabetes membrane and finally vascular occlusion.
mellitus is the alteration of circulating and Diabetic microangiopathy affects several organ
immobilized proteins. When proteins such as systems and the lesions are seen in the retina
collagen, or lipids, are exposed to aldose sugars, (retinopathy), kidneys (nephropathy), and
they undergo nonenzymatic glycosylation or peripheral nerves (neuropathy). Diabetic
glycation. Initially the nonenzymatic microangiopathy interferes with the delivery of
glycosylation of proteins is reversible, but nutrients and adherence, chemotaxis, and
eventually the nonenzymatic glycosylation of phagocytosis of PMNL to the tissues, resulting
proteins becomes irreversible and irreversible in decreased oxygen supply and elimination of
glycosylated proteins are formed. metabolic waste, contributing to altered wound
These irreversible glycosylated proteins are healing and periodontitis. The vascular changes
called advanced glycosylation end products worsen with poor metabolic control and longer
(AGEs). The AGEs accumulate in high levels in duration of the disease.
the tissues, including the periodontium. AGEs
induce marked changes in the cells (fibroblasts) Altered Wound Healing
and extracellular matrix components Altered wound healing is a common problem in
(glycosylation of existing collagen at the wound diabetics due to diabetic microangiopathy,
margins results in delayed remodelling at the improper function of primary reparative cell
(fibroblast) due to hyperglycemia, and degrada- Diabetic Neuropathy

tion of collagen by matrix metalloproteinase Diabetic neuropathy is characterized by
enzymes, the production of which is elevated in segmental demyelinization, and injury to
diabetes mellitus. Thus, periodontal wound Schwann cells.
healing in response to chronic microbial insult
may be altered in uncontrolled diabetes mellitus, Diabetic Retinopathy
resulting in increased bone loss and attachment
Diabetic retinopathy is due to diabetic
loss.
microangiopathy and is the leading cause of
Metabolic Ketoacidosis blindness in diabetes mellitus.
As blood glucose is not utilized by the cells due Diabetic Nephropathy
to severe deficiency of insulin, large amounts of
Kidneys are commonly involved in diabetes
adipose tissue is broken down (lipolysis) for
mellitus and the various types of lesions
release of energy leading to circulation of free
associated with diabetic nephropathy are:
fatty acids in the blood and resultant metabolic
ketoacidosis or diabetic ketoacidosis (DKA). 1. Diffuse glomerulosclerosis: Thickening of
Also, the inhibitory effect of lipase is withdrawn basement membrane of glomerular vessels
due to severe insulin deficiency. The signs and 2. Nodular glomerulosclerosis: Focal
symptoms of metabolic ketoacidosis include deposition of hyaline in the lobule of
nausea, disorientation, abdominal cramps, and glomerulus (Kimmelsteil-Wilson lesions)
fatigue.
Diagnosis
Hypoglycemic Shock
An International Expert Medical Committee was
Hypoglycemia is characterized by sweating
established in May 1995 to renew the scientific
(diaphoresis), confusion, tremors, tachycardia,
literature since 1979 and to decide the changes
and permanent brain damage. Hypoglycemic
to the classification and diagnosis of diabetes
signs and symptoms are likely to occur if the
mellitus if needed.
blood glucose level falls below <60 mg/dl. The
The International Expert Medical Committee
most common causes of hypoglycemia include: recommended the new revised diagnostic criteria
1. Injection of excess insulin for diabetes mellitus from those recommended
2. No caloric intake with the usual dose of by National Diabetes Data Group (NDDG) and
insulin WHO, which was based on type of pharmaco-
3. Increasing exercise without adjusting insulin logical treatment used in the management of
dose (exercise reduces the requirement of diabetes mellitus.
insulin)
4. Alcohol intake (alcohol inhibits gluconeo- Criteria for the Diagnosis of Diabetes
genesis)
Mellitus
1. Classical symptoms (polyuria, polyphagia,
Atherosclerosis Leading to Myocardial polydipsia, and asthenia)
Infarction 2. Casual plasma glucose concentration > 200
The cause of atherosclerosis in Type 1 and 2 mg/dl (casual means anytime of the day
diabetes mellitus is due to hyperlipidemia. without regard to time since last meal)
3. Fasting plasma glucose (FPG) > 126 mg/dl Urine Analysis

(fasting is defined as no caloric intake for at 1. Benedicts test
least 8 hours) 2. Diastix reagent strips for urine glucose
4. Two hours postprandial glucose > 200 mg/ monitoring
dl during an oral glucose tolerance test 3. Keto-diastix reagent strips for diagnosis of
(OGTT). According to WHO this test has to ketone bodies and glucose in urine
be performed by giving 75 gm anhydrous
glucose dissolved in water Oral Glucose Tolerance Test
5. In absence of any hyperglycemia these tests • Two hours postprandial glucose test.
have to be carried out on different day.
The expert committee has recognized an Monitoring Diabetes Mellitus
intermediate group of subjects whose glucose Glycosylated Hemoglobin Assay
levels are not meeting the criteria for diabetes
Glycosylated or glycated hemoglobin assays
mellitus. The glucose levels of this intermediate
have emerged as the “gold standard” for long
group of subjects are too high to be considered
term glycemic control. It assesses the glycemic
normal but too less to be considered as diabetes
control and has a prognostic value as it was
mellitus. This intermediate group of subjects
have impaired fasting plasma glucose (IFG) shown in the diabetes control and complications
levels > 110 mg/dl but < 126 mg/dl. The trial in 1993. Glycosylated hemoglobin assay
categories of FPG are as follows: cannot be influenced by recent caloric intake.
1. FPG < 110 mg/dl = Normal fasting plasma Glycosylation or glycation is the nonenzymatic
glucose reaction of glucose with the hemoglobin A
2. FPG > 110 and < 126 mg/dl = Impaired molecule within the circulating erythrocytes
fasting plasma glucose (IFG). resulting in the formation of glycosylated
3. FPG > 126 mg/dl = Provisional diagnosis of hemoglobin (HbA1C). This test measures the
diabetes mellitus glucose that binds to hemoglobin A molecule
The corresponding categories when OGTT is within the circulating erythrocytes and remains
used are as follows: attached for the life span of the RBC (120 days).
1. Two hours postprandial glucose < 140 mg/ Therefore, the levels of glycosylated hemoglobin
dl = Normal glucose tolerance test indicate the glycemic state over a period of 8 to
2. Two hours post-prandial glucose > 140 mg/ 12 weeks. Reduced glycosylated hemoglobin
dl and < 200 mg/dl = Impaired glucose levels decreases the incidence of diabetic mellitus
tolerance test (IGT) complications. The normal value of glycosylated
3. 2 hours post prandial glucose > 200 mg/dl hemoglobin is less than 6%. Glycosylated
= Provisional diagnosis of diabetes mellitus. hemoglobin levels above 8% indicate the
existence of higher levels of plasma glucose.
Diagnostic Tests
Blood Analysis Fructosamine Test
1. Casual blood glucose (casual means anytime The principle behind this test is that glucose
of the day) reacts with serum proteins to produce fructosyl
2. Fasting blood glucose derivative called fructosamine. The concentra-
3. Gluostix reagent strips for blood glucose tion of fructosamine increases over a period of
monitoring time and is helpful in controlling diabetes
mellitus. Fructosamine test is a marker of tuned glucose control program. The insulin
glycemia over the preceding 2 to 3 weeks. pump can deliver incremental doses as low as
0.1 unit of insulin/hour. The lowest dose that a
Treatment of Diabetes Mellitus patient can deliver with accuracy through a
Type 1 traditional syringe is 1.0 unit.
However, if there is mechanical disruption of
Type 1 diabetic patients need exogenous source
this finely tuned glucose control program,
of insulin. Insulin was first discovered by Banting
counter regulatory hormones to insulin, such as
and Best. The most common complication of
adrenaline (increases glycogenolysis) and
insulin therapy is hypoglycemia. The various
glucocorticosteroids (increases gluconeogenesis)
types of insulin are as follows:
cause hyperglycemia. Metabolic ketoacidosis is
1. Short acting: Regular insulin
another risk associated with insulin pump,
2. Rapid acting: Insulin aspart, lispro
therefore patients using insulin pump generally
3. Intermediate acting: Neutral protamine
carry back-up supplies of insulin and insulin
hagedron (NPH) and lente (most effective
syringes in case there is a mechanical problem
treatment)
with the insulin pump.
4. Long acting: Ultralente and new developed
suspension free insulin (glargine) Type 2
Insulin can be administered using a traditional Most of the patients suffering from Type 2
insulin syringe, an insulin pen or a subcutaneous diabetes mellitus can control hyperglycemia by
insulin pump or SCII. reducing weight either by diet control or exercise.
Insulin pump Exercise increases the concentration and
It is a battery powered device that delivers sensitivity of insulin receptors and reduces the
phosphate-buffered rapid or short acting insulin requirements of exogenous insulin. Most of the
stored in a reservoir syringe that is located within oral hypoglycemics cause hypoglycemia. Oral
the plastic pump and is replaceable. If the insulin hypoglycemics are of no use in Type 1 diabetes
is not buffered, then it may precipitate (separate mellitus. The oral hypoglycemic agents are
as a fine suspension of solid particles) inside the classified as follows:
system, resulting in occlusions that can stop the 1. α-glucosidase inhibitors: Acarbose, miglitol
flow of the insulin. (block the absorption of carbohydrate in
Insulin is delivered from the device by means small intestine leading to hypoglycemia)
of an infusion set. The infusion set consists of a 2. Sulfonylureas: (increase the secretion of
plastic tube (the catheter) with a plastic or insulin from the β cells)
metallic needle. The needle is inserted
a. First generation—Tolbutamide, chlorpro-
subcutaneously into upper arm, abdomen or
pamide
thigh. Patient has to replace the infusion set every
48 hours to avoid infection at the site of insulin b. Second generation—Gilbenclamide,
delivery. Glipizide
The major risk associated with the insulin 3. Biguanides: Metformin and phenformin
pump is the rapid development of severe (enhance binding of insulin to its receptors)
hyperglycemia and metabolic ketoacidosis, 4. Thiazolidin-ediones: Rosiglitazone,
leading to diabetic coma. The insulin pump pioglitazone (increase tissue sensitivity to
controls the blood glucose levels through a finely insulin, especially in muscle)
5. Benzoic acid derivatives: Repaglinide, 2. Treatment should be done under antibiotic

nateglinide (increase the secretion of insulin coverage.
from the â cells) 3. Physician’s approval whether the diabetic is
fit for treatment.
ACE Inhibitors 4. Dentist should keep a glucometer with him
It was recently found out that angiotensin and check the blood glucose level prior to
converting enzyme inhibitor ramipril decreases the treatment.
the incidence of diabetes mellitus related 5. The dentist must be aware of the signs and
complications. Ramipril is an antihypertensive symptoms of hyperglycemia and metabolic
drug. The side effect of ramipril includes sudden ketoacidosis. He should ensure that the
swelling of lips, tongue, face and laryngeal plastic tube from the insulin pump is not
tissues leading to asphyxia. Adrenaline 1:1000 compressed by the dental chair because this
can be administered to overcome this side effect. will block the flow of insulin.
6. The treatment should not be stressful.
Oral Manifestations of Diabetes Mellitus
7. Just prior to treatment the dentist should
Oral manifestations of diabetes mellitus are due check the blood glucose level with a
to: glucometer.
1. Hyperglycemia a. If the glucometer shows blood glucose
2. Diabetic microangiopathy levels below 80 to 120 mg/dl then a
3. Polyuria leading to xerostomia
glucose or fruit juice can be administered.
Oral Manifestations Also dissolved sugar placed sublingually
may reverse hypoglycemia as the
1. Xerostomia
dissolved sugar is rapidly absorbed from
2. Dental caries
the sublingual site. However, if the
3. Gingivitis
patient is sedated then 25 to 30 ml of 10%
4. Periodontitis
dextrose or 1 mg of glucagon can be
5. Dysphagia
administered intravenously, intramus-
6. Candidosis
cularly, or subcutaneously. Glucagon
7. Recurrent aphthous ulcers
causes glycogenolysis and reverses
8. Lichen planus
hypoglycemia usually within 15 minutes.
9. Burning mouth syndrome
10. Glossodynia b. However, if the glucometer shows severe
11. Dysesthesia (impairment of sensation short hyperglycemia (> 400 mg/dl) the dentist
of anesthesia) should call upon the physician
12. Dysguesia (impairment in the sense of taste) immediately. The physician may instruct
the dentist to administer rapid acting
Dental Management insulin with an insulin syringe. In a
To avoid complications in a dental chair the patient using insulin pump, the insulin
following precautions are to be taken by the injection is administered after
dental surgeon prior to starting of the treatment: disconnecting the insulin pump. Finally
1. The dentist should know the time, dose and the dentist should call an ambulance or
type of insulin the patient has taken, which refer the patient for immediate medical
is possible through a detailed case history. care.
IV. BELL’S PALSY

The Motor Pathway components of the facial nerve are: (i) Branchial
motor, (ii) Visceral motor, (iii) General sensory
The motor pathway comprises two major
and (iv) Special sensory. The branchial motor
neurons: upper motor neuron and lower motor
component constitutes the largest part of the
neuron (Fig.12.12).
facial nerve fibers. The remaining fibers (visceral
Upper Motor Neuron motor, general sensory and special sensory) are
The cell bodies of this neuron are usually located bound in a distinct fascial sheath and are referred
in the cerebral cortex. Its axon projects caudally to as nervus intermedius. The functions of
and bilaterally to contact the cell bodies of the various components of facial nerve are as follows:
lower motor neurons in the brain stem (pons). 1. Branchial motor: To innervate the stapedius,
stylohyoid, posterior belly of digastric,
Lower Motor Neuron occipitalis, muscles of facial expression, and
The cell bodies of this neuron are usually located platysma.
in the brain stem. The cell bodies of the lower 2. Visceral motor: For stimulation of lacrimal,
motor neurons form motor group of cranial nerve sub-mandibular, and sublingual glands as
nuclei. Axons that leave these nuclei make up well as mucous glands in the nasal mucosa,
the lower motor neurons. hard and soft palate
3. General sensory: To innervate the skin of the
Facial Nerve
concha of the auricle, and a small area behind
Knowledge of the anatomy of the facial nerve is the ear
important in understanding the pathophysiology 4. Special sensory: To carry taste sensation
and management of Bell’s palsy. The various (salty, sweet, sour, and bitter) from taste buds
Fig. 12.12: The motor pathway

on the lateral border of the anterior two-third canal. Therefore, the meatal foramen constitutes
of the tongue a “physiologic bottleneck” in the presence of
The corticobulbar axons (upper motor neural edema. The facial nerve is without
neurons) that arise from the motor cortex of the epineurium in the meatal foramen and is instead
cerebral hemispheres carry signals for voluntary ensheathed by periosteum.
movement of the facial muscles. The The labyrinthine segment of the facial nerve,
corticobulbar axons then travel through the encased within the meatal foramen of the facial
posterior limb of the internal capsule, to reach canal courses 2-4 mm laterally and takes an acute
the ipsilateral and contralateral motor nuclei of turn to enter the middle ear. This acute turn is
the facial nerve present in the brainstem called the genu and is thickened by the presence
(Fig.12.13). of the geniculate ganglion (Fig.12.15). The
Fibers that project to the part of the nucleus geniculate ganglion is so called because it lies on
that innervates the upper muscles of facial the genu.
expression project bilaterally. Fibers that project
to the part of the nucleus that
innervates the lower facial muscles
of facial expression project only
contralaterally (Fig.12.14).
The lower motor neuron (facial
nerve) courses dorsally towards the
floor of the fourth ventricle and
loops around the abducens nucleus
to form a slight bulge, the facial
colliculus. The loop around the
abducens nucleus is the internal
genu of the facial nerve. The facial
nerve then turns ventrally to
emerge from the ventrolateral
aspect of the pons, to enter the
temporal bone via internal auditory
meatus along with vestibuloco-
chlear nerve (Fig.12.14). The
segment of the facial nerve within
the internal auditory meatus is the
meatal segment.
The meatal segment of the facial
nerve remains in the internal
auditory meatus and enters the
facial canal or fallopian canal at the
meatal foramen. The meatal
foramen (mean diameter 0.68 mm)
is the narrowest part of the facial Fig. 12.13: Bilateral and contralateral nerve projection
Fig. 12.14: Facial motor nucleus in the pons
After emerging from the stylomastoid

foramen it gives off the stylohyoid nerve, nerve
to posterior belly of digastric, and posterior
auricular nerve to innervate the occipitalis
muscle. The facial nerve then pierces and lies
within the substance the parotid gland. At this
point the facial nerve divides into five branches
(Fig.12.16) which are as follows:
Fig. 12.15: Course of facial nerve in facial canal
The tympanic segment (horizontal segment)

of facial nerve runs backwards in relation to the
medial wall of the middle ear and turns gradually
(pyramidal turn) to continue downwards as
mastoid segment (vertical segment) along the
junction of medial wall and posterior wall of the
middle ear to give off the nerve to stapedius. The
remaining branchial motor fibers reach the Fig. 12.16: Muscles innervated by branchial motor
stylomastoid foramen. component of facial nerve
1. Temporal branch His contributions to the medical field were

2. Zygomatic branch rewarded with a knighthood in 1831, by King
3. Buccal branch George IV. Some speculate that the enigmatic
4. Mandibular branch and curious smile of Mona Lisa (la Giaconda)
5. Cervical branch might be the result of Bell’s palsy. Careful
examination of her portrait reveals a subtle
Upper Motor Neuron Lesion (UMNL)
asymmetrical smile—perhaps a clue about her
Damage to any part of the upper motor neuron
medical history (Fig.12.20).
in the cortex results in upper motor neuron lesion
Bell’s palsy is a common and cosmetically
(Fig.12.17). Voluntary control of lower muscles
devastating cranial neuropathy. It accounts for
of facial expression is lost contralateral to the
lesion. Upper muscles of facial expression about half of all cases of paralysis affecting the
continue to function, because the part of the facial face. Bell’s palsy is defined as an idiopathic,
nucleus that innervates them still receives input unilateral, lower motor neuron facial paresis
from the ipsilateral cortex. The most common (partial loss of movement), or paralysis (complete
upper motor neuron lesion that involves facial loss of movement) of acute onset in which no
nerve is cerebrovascular accident that damages other etiology, such as infection, neoplasm or
the upper motor neurons in the cortex. trauma, can be identified. Incidence of Bell’s
palsy is approximately 15 to 40 cases per 100,000
Lower Motor Neuron Lesion (LMNL) people per year, with a recurrence rate up to 10%.
Damage to any part of the lower motor neuron
anywhere along its course results in lower motor Etiology
neuron lesion (Fig.12.18). All the muscles of facial
expression (upper and lower) innervated by the Since, by definition Bell’s palsy is idiopathic; its
lower motor neurons are paralyzed ipsilateral to exact cause is unknown. However, recent studies
the lesion. Bell’s palsy is a lower motor neuron suggest that HSV-1 may play a role. PCR assays
lesion. have identified HSV-1 in the endoneurial fluid
and saliva in patients with Bell’s palsy.
Bell’s Palsy
Therefore, idiopathic Bell’s palsy may actually
Bell’s palsy was named after the British be a reactivation of the latent HSV-1 in the
neurosurgeon, neuroanatomist and artist, Sir geniculate ganglion. Reactivation of the latent
Charles Bell (Fig.12.19). As his services were
HSV-1 may in response to stress, fever, dental
required during the “Battle of Waterloo” he got
extraction, menstruation, or immunosupression.
a unique opportunity to study the anatomy and
Reactivation of HSV-1 causes acute
musculature of the face as a result of facial
inflammation and edema of the facial nerve in
gunshot injuries. Battlefield experiences
combined with animal experiments done in his the narrow facial canal especially at the meatal
laboratory led to his conclusion that the seventh foramen. Acute inflammation and edema of the
cranial nerve controlled facial expression. He facial nerve, leads to compression ischemia and
named the seventh cranial nerve “the respiratory conduction block of nerve signal. Due to
nerve of the face” and described its functions. conduction block of nerve signal, all actions of
“In all the exhilarating emotions, the eyebrows, the facial muscles are affected, and there is
eyelids, the nostrils and angle of the mouth are raised. atrophy of the facial muscles. This results in
In the depressing passions it is reverse.” marked facial asymmetry.
Fig. 12.17: Upper motor neuron lesion
Fig. 12.18: Lower motor neuron lesion

Clinical Features
Age: Most cases occur among people between
40-44 years, but it can affect all age groups,
including children. Incidences of Bell’s palsy are
(Fig.12.21):
1. Lowest in children under 10 years
2. Increases from the ages of 10 to 29
3. Remains stable at the ages of 30 to 69
4. Highest in people over the age of 70
Sex: Men and women are equally affected i.e.,
with no gender bias.
Anatomical location: The left and right sides of
the face are involved with equal frequency. In
less than 1% of all cases, Bell’s palsy may affect
both sides of the face at once. Bilateral facial palsy
(diplegia) should remind of Mobius syndrome,
and myasthenia gravis.
Genetics: About 10% of patients with Bell’s palsy
Fig. 12.19: Sir Charles Bell (1774-1842) have a family history.
Predisposing factors: Those at high risk include
pregnant women and people with diabetes
mellitus. Most often in the third trimester of
pregnancy, the risk of Bell’s palsy increases by
3:3 times, especially with concurrent pre-
eclampsia. Pre-eclampsia is an abnormal state of
pregnancy characterized by hypertension, fluid
retention and albuminuria, which can lead to
eclampsia if untreated. Eclampsia is charac-
terized by convulsions and possibly coma during
or immediately after pregnancy.
Clinical Presentation (Fig.12.22 and

12.23A and B)
1. Sudden pain especially below the ear
probably due to neuritis of the facial nerve
in the mastoid segment
2. Abrupt onset with complete, unilateral facial
weakness at 24 to 72 hours
3. Facial asymmetry
Fig. 12.20: Mona Lisa
4. Loss of wrinkling on forehead
Fig. 12.21: Incidence of Bell's palsy
5. Unable to elevate eyebrow

6. Drooping of the eyelid (ptosis)
7. Incomplete eyelid closure (lagophthalmos)
8. Flattened nasolabial fold
9. Frozen ala nasi
10. Asymmetrical smile
11. Difficulty in eating and speaking
12. Drooling of liquids from angle of mouth
13. Xerostomia and dryness of eyes is (present
in 15 to 17% of patients) due to involvement
of the visceral motor component
14. Ageusia on the lateral border of the anterior
Fig. 12.22: Clinical presentation of Bell's palsy two-third of the tongue due to involvement
of special sensory component. However,
Fig. 12. 23A: Facial asymmetry in patient with Fig. 12.23B: Bell’ s phenomenon in patient
Bell’s palsy of the left side of face with Bell’s palsy of the left side of the face
there is no loss of general sensation as the Wallerian degeneration does not take place. The
tongue is innervated by the lingual branch results during this time will be near normal.
of the mandibular nerve Because of this limitation, the prognosis cannot
15. The function of the stapedius muscle is to be established until 4th or 5th day. However, there
dampen the vibrations of the ear ossicles. is a steady decline in electrical activity from the
Hyperacusis results from paralysis of the 4th or 5th day onwards as Wallerian degeneration
stapedius muscle, causing sounds to be of damaged nerve fibers takes place. If there is
abnormally loud on the affected side 90% or greater reduction in the amplitude of
(hypersensitivity to sounds). There is no ENoG waveform on the affected side, the
hearing loss prognosis worsens.
16. The practitioner should test for Bell’s
phenomenon. This is done by asking the Sequelae
patient to close his eyes. On the affected side
the upper eyelid is pulled upwards, causing Sequelae of Bell’s palsy are characterized as
an upward movement of eyeball with only minor and major (Fig. 12.24).
the scleral rim being exposed. 1. Aguesia: Ageusia is defined as loss or
absence of taste sensation
Prognosis 2. Dysacusis: Dysacusis is defined as difficulty
The spontaneous course of Bell’s palsy includes: in processing details of sound due to paresis
paresis or incomplete paralysis and complete of the stapedius muscle
paralysis. Majority of the patients with paresis 3. Epiphora: Epiphora is defined as an
have an excellent prognosis of recovery of facial overflow of tears upon the cheek, due to
nerve function without any sequelae (any imperfect drainage by the tear-conducting
abnormality resulting from a disease or injury passages
or treatment) within a six-week period. 4. Synkinesis: During regeneration (reproduc-
However, some patients who develop tion) and reinnervation (restoration of
complete facial nerve paralysis show recovery innnervation), some nerves grow along
of facial nerve function (House-Brackmann grade aberrant (different) pathways resulting in
I and II) within three weeks. Patients with synkinesis. Synkinesis is defined as
complete facial paralysis, who do not show any
signs of recovery over three months after the
onset of Bell’s palsy, are left with various
permanent sequelae (House-Brackmann grade
III to V). These patients may benefit the most
from medical or surgical treatment.
Electrodiagnostic Testing
The tests used to establish prognosis in Bell’s
palsy include the NET (nerve excitability test),
MST (maximum stimulation test), ENoG
(electroneurography), and EMG (electromyo-
graphy).
With the first three days after the onset of facial
palsy, electrical studies reveal no changes as Fig. 12.24: Minor and major sequelae of Bell's plasy
involuntary movement of facial muscles 2. Hearing loss

accompanying voluntary facial movement 3. Ringing of the ears (tinnitus)
e.g., Many patients with Bell’s palsy develop 4. Vertigo due to extension of viral infection to
“jaw winking” which is closure of the eye involve vestibulocochlear nerve
when attempting to smile Some of the other causes of facial nerve
5. Gustatory lacrimation: Crocodile tears paralysis are (alphabetical order):
syndrome, also called gustatory lacrimation, 1. Acoustic neuroma
gustolacrimal reflex, paroxysmal lacrimation 2. AIDS
and Bogorad’s syndrome. It is one of the rare 3. Alcoholic neuropathy
complications of Bell’s palsy and was 4. Altitude paralysis (barotrauma)
described by a Russian neuropathologist in 5. Amyloidosis
1913. After Wallerian degeneration, 6. Eosinophilic granuloma
regenerating preganglionic parasympathetic 7. Facial injuries
fibers of the chorda tympani (visceral motor 8. Forceps delivery
component of facial nerve) that project to the 9. Hemangioma
submandibular ganglion may regrow 10. Hypertension
(misdirected) through the greater petrosal 11. Hyperthyroidism
foramen to stimulate the lacrimal gland 12. Inferior alveolar nerve anesthesia
secretion (lacrimal fluid) on the same side 13. Leprosy
when the patient eats or drinks. The 14. Malaria
syndrome may also occur following acoustic 15. Mastoiditis
neuroma surgery, maxillofacial trauma, and 16. Mobius syndrome (facial diplegia associated
Paget’s disease. with other cranial nerve deficits)
17. Multiple sclerosis
Differential Diagnosis 18. Mumps
Bell’s palsy is a common cause of facial nerve 19. Paget’s disease
paralysis. Before making a diagnosis of Bell’s 20. Parotitis
palsy, other specific causes of facial nerve
paralysis should be considered. The differential
diagnosis of Bell’s palsy is broad. Some of the
common conditions that cause facial nerve
paralysis include: Ramsay-Hunt syndrome,
Lyme disease, malignancies of parotid gland,
diabetes mellitus, and Melkersson-Rosenthal
syndrome (Fig.12.25).
One of the most common causes of facial nerve
paralysis is Ramsay-Hunt syndrome, or herpes
zoster oticus, caused by the varcicella zoster
virus. Ramsay-Hunt syndrome is characterized
by:
1. Vesicular lesions in the preauricular skin, Fig. 12.25: Common conditions causing facial nerve
external auditory canal, or the soft palate paralysis
21. Sarcoidosis loss, rash, or progressive facial weakness over

22. Scuba diving (barotrauma) more than 4 weeks. A number of tests may be
23. Syphilis helpful:
24. Tuberculosis 1. CBP and differential count–Leukemia
25. von Recklinghausen’s disease 2. Blood glucose–Diabetes mellitus
3. Serum antibodies against VZV–Ramsay-
Diagnosis Hunt syndrome
4. Serum antibodies against Borrelia burgdoferi
Case history and physical examination provide –Lyme disease
information key to the diagnosis of Bell’s palsy. 5. Serum calcium and angiotensin-converting
Most patients do not require any laboratory enzyme levels–Sarcoidosis
testing or imaging studies. However, patient’s
who have persistent facial weakness without Hearing Testing
significant improvement, require further If hearing loss is suspected, then audiometry
investigations. Diagnosis of Bell’s palsy includes: should be performed to measure hearing loss and
1. Case history and physical examination to help rule out facial nerve tumors e.g., acoustic
2. Laboratory examination neuroma and involvement of vestibulocochlear
3. Hearing testing nerve.
4. Imaging
Imaging
Case History and Physical Examination Computed tomography (CT) or magnetic
Physical examination helps rule out other resonance imaging (MRI) is indicated in the
conditions and narrow the differential diagnosis following cases:
of Bell’s palsy. Things to observe are: 1. No improvement in facial paralysis after one
1. Whether it is UMNL or LMNL? month
2. Hearing loss
Facial weakness is best demonstrated by the
3. Multiple cranial nerve deficits
patient’s response to the requests “close your
4. Signs of limb paresis or sensory loss
eyes” (for testing the upper facial area) and “show
me your teeth (for testing the lower facial area.”
Treatment
In an UMNL, the patient is unable to close
the eyes on the affected side due to Most patients with Bell’s palsy recover
denervation of the orbicularis oculi muscle. completely and achieve normal function within
In an LMNL, the patient is unable to show a few months. Though treatment of Bell’s palsy
the teeth and close the eyes on the affected is still controversial, evidence suggests that oral
side due to denervation of the risorius and steroids and antiviral medications shorten the
orbicularis oculi muscles. disease course. However, there is only limited
a. Is Bell’s phenomenon present? evidence to show that these treatments are
b. Assess the facial nerve damage using effective. Surgical decompression of the facial
“House-Brackmann facial nerve grading nerve is controversial and should be considered
system.” for patients who have a poor clinical outcome.
Laboratory Examination Oral Steroids

Laboratory testing is necessary if the patient has Oral steroids have been shown to limit
signs of systemic disease, such as fever, weight denervation (to cut off the innervation), within the
first 24 hours or so after the onset of the Recurrence

symptoms. Oral steroids have been used to
Bell’s palsy rarely recurs. Approximately 7-12%
control the inflammation and edema which
of patients develop recurrent Bell’s palsy. Usually
results in facial nerve entrapment. Patients
the second attack affects the opposite side.
treated with oral steroids have fewer incidents
Recurrence is more likely seen in patients with a
of synkinesis. The most commonly used oral
steroid regimen is 10-day course of oral family history, pregnancy, and in those with
prednisolone (60 mg a day orally for 5 days, diabetes mellitus.
tapered by 10 mg a day for 5 days).
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Glossary
Abscess: A localized accumulation of pus or Administration: How a drug or therapy is

purulent material in a cavity formed by tissue introduced into the body. Systemic
disintegration, e.g., periapical abscess. administration means that the drug goes
Acantholysis: Loss of cohesion between the cells throughout the body (usually carried in the
in the spinous layer. bloodstream), and includes oral (by mouth),
Acanthosis: Increased thickness of spinous layer intravenous or parenteral (injection into the vein,
or stratum Malphigii. IV), intralesional (injection into the lesion),
intramuscular (injection into a muscle, IM),
Active immunity: Protection from a disease as a
intraarticular (injection within the joint space),
result of previous exposure to the disease-causing
intrathecal (injection into the spinal canal),
infectious agent or antigen. The protection can
subcutaneous (injection beneath the skin, SQ),
be a result of having had the disease or having
and rectal administrations. Local administration
received a vaccine to prevent getting the disease.
means that the drug is applied or introduced into
Acute: Phenomenon characterized by a quick,
the specific area affected by the disease, such as
fast course, as opposed to chronic.
application directly onto the affected skin surface
Acute inflammation: A traumatic or pathologic (topical administration). The effects of most
phenomenon or process having a short and therapies depend upon the ability of the drug to
relatively severe course. In contrast to chronic reach the affected area; thus the route of
inflammation, the host immune response quickly administration and consequent distribution of a
overwhelms the injurious agent, which is drug in the body are important determinants of
followed by the resolution of pathologic process its effectiveness.
and recovery or death of the patient.
Adverse reaction: An unwanted effect caused
Acupuncture: A Chinese medical treatment by the administration of drugs. Onset may be
involving the insertion of very fine sterile needles
sudden or develop over time.
into the body at specific points according to a
mapping of “energy pathways.” Adenopathy: Any disease involving or causing
enlargement of glandular tissues, especially one
Abrasion: It is the pathologic wearing away of
involving the lymph nodes.
the tooth substance due to abnormal mechanical
process and usually occurs on the exposed root Adjuvant: An ingredient added to a prescription
surfaces of the teeth (cervical region). Frequently or solution that facilitates or modifies the action
caused by abrasive dentrifice, improper brushing of the principal ingredient.
technique, improper use of dental floss and tooth Aerobes: Microorganisms that can live and grow
picks (interproximal abrasion), and habitual in the presence of oxygen, e.g., Mycobacterium
opening of bobby pins (incisal abrasion). tuberculosis.
Agammaglobulinemia: A nearly total absence Allodynia: Pain without noxious stimuli.

of immunoglobulin’s resulting in the loss of Alopecia: Loss of hair that frequently occurs in
ability to produce immune antibodies. patients undergoing chemotherapy for cancer or
Agenesis: It is defined as failure of an organ to suffering from other diseases, such as AIDS,
develop, e.g., anodontia due to agenesis of where cell-killing or cytotoxic drugs are used.
enamel organ. Ambidextrous: Able to use either hand (right or
Agonists: Drugs that can combine with receptors left) equally well e.g., ambidextrous latex gloves.
present on cell membrane to produce a Amino acid: Amino acids are the building blocks
physiological reaction. of proteins.
Aguesia: Ageusia is defined as loss or absence Anachoresis: The accumulation of particulate
of taste sensation. material or microorganisms from the circulating
AIDS: The most severe manifestation of infection blood in certain sites in the tissues.
with the Human Immunodeficiency Virus (HIV). Anaerobes: Microorganisms that can live and
The Centers for Disease Control and Prevention grow in partial or complete absence of oxygen,
(CDC) lists numerous opportunistic infections e.g., Bacteroides forsythus.
and cancers that, in the presence of HIV infection, Analgesia: Absence of sensibility to pain.
constitute an AIDS diagnosis. In 1993, CDC Anaphylactic shock: A life-threatening allergic
expanded the criteria for an AIDS diagnosis in reaction characterized by a swelling of body
adults and adolescents to include CD4+ T cell tissues (including the throat) and a sudden
count at or below 200 cells per microliter in the decline in blood pressure. Symptoms include
presence of HIV infection. In persons (age 5 and difficulty breathing, violent coughing, and chest
older) with normally functioning immune constriction.
systems, CD4+ T cell counts usually range from Anaplasia: When the normal cells undergo
500–1,500 cells per microliter. Persons living with differentiation to resemble embryonic tissue.
AIDS often have infections of the lungs, brain, Anemia: Anemia is a term indicating that the
eyes, and other organs, and frequently suffer concentration of hemoglobin or the number of
debilitating weight loss, diarrhea, and a type of red blood cells is below the accepted normal
cancer called Kaposi’s sarcoma. value with respect to age and sex.
AIDS wasting syndrome: The involuntary Anesthesia: Absence of all sensation.
weight loss of 10 percent of baseline body weight Angiogenesis: The process of forming new blood
plus either chronic diarrhea (two loose stools per vessels. Angiogenesis is essential for the growth
day for more than 30 days) or chronic weakness of tumors, especially Kaposi’s sarcoma.
and documented fever (for 30 days or more, Anorexia: The lack or loss of appetite that leads
intermittent or constant) in the absence of a to significant decline in weight.
concurrent illness or condition other than HIV Antagonists: Drugs that neutralizes or
infection that would explain the findings. counteracts the effects of another drug.
Allergen: A substance capable of producing an Antenatal: Occurring before birth.
allergic response. Common allergens are pollens, Antibiotic: A natural or synthetic substance that
dust, drugs or foods. inhibits the growth of microorganisms such as
Allergy: A hypersensitive reaction (antigen- bacteria or fungi. Some antibiotics are used to
antibody reaction) of the body to an allergen. treat infectious diseases.
Glossary 225
Antibodies: Protein formed and secreted by B Arterioles: A minute arterial branch proximal to
cells derived plasma cells to an antigenic a capillary.
stimulus. Arthralgia: Pain in a joint or joints.
Antifungal: A substance that kills or inhibits the Arthritis: Inflammation of joint or joints.
growth of a fungus. Artifact: Tissue that has been altered physically
Antigen: A protein that often stimulates the from its natural state by processing.
production of antibodies. Asepsis: Without infection or free of viable
Antigen presentation: The event of providing pathogenic microorganisms.
fragments of foreign proteins, including viruses Ataxia: Lack of muscular coordination.
and bacteria, to the helper CD4+ and CD8+ T Attrition: It is the pathologic wearing away of
cells. the occlusal surface of tooth as a result of tooth-
Antigen presenting cell (APCs): APCs are the to-tooth contact. Frequent causes are bruxism,
cells, which process the antigen and present it to and chewing tobacco.
the T cell receptor present on CD4+ T cells in Atrophy: It is defined as decreased in size of an
combination with MHC class II molecules or organ or tissue due to decrease in number of cells,
CD8+ T cells in combination with MHC class I e.g., atrophic epithelium in oral sub mucous
molecules. Examples of APCs are macrophages, fibrosis.
B cells, and Langerhans cells (dendritic cells). Autoantibodies: Antibodies produced against
Antioxidants: Agents that inhibits oxidation and one’s own antigens.
thus prevents the deterioration of other materials Autoimmunity: Autoimmunity is a condition in
through oxidative processes. which there is immune response to one’s own
Antiviral: A substance that kills or inhibits the tissues. Most of the vesiculo-bullous diseases are
growth of a virion. autoimmune. Autoimmune diseases have a
Anxiety Mental disorder characterized by female predilection, increased serum autoanti-
increased muscle tension, perspiration, bodies, and hypergammaglobulinemia.
movements of hand and feet. He/She frequently Avulsion: The sudden tearing out of tissue as a
seeks assurance and asks number of questions. result of trauma e.g., avulsion of a tooth.
Apical periodontitis: Inflammation of the Bacteremia: The presence of viable bacteria in
periodontal ligament at the apical region of the the blood.
tooth, as sequelae of pulpitis. Bacteria: Single-celled spherical (coccus), spiral
Apical scar: A radiolucent area at the periapex (spirillum), rod-shaped (bacillus), comma-
of a tooth characterized histologically by dense shaped (vibrio), and corkscrew-shaped
fibrous connective tissue. (spirochete) organisms lacking chlorophyll that
Aplasia: When the hypoplasia is very severe it reproduce by fission; important as pathogens and
is called aplasia, e.g., aplastic anemia. for biochemical properties.
Apoptosis: Derived from Greek meaning Bactericidal: Capable of killing bacteria.
“dropping off,” this means programmed cell Bacteriostatic: Capable of inhibiting reproduc-
death occurring in normal tissues or pathologic tion of bacteria.
tissues. B lymphocytes: A short-lived, nonthymus
Artery: A blood vessel through which the blood dependent form of lymphocytes that synthesize
passes from the heart to the various structures antibodies. They are the precursors of plasma
of the body. cells.
Basophil: A type of granulocyte, which has Bronchospasm: A spasmodic contraction of the

coarse granules and a bent lobed nucleus found muscular walls of the bronchi.
in the blood and resembles the tissue mast cell. Bulla: Elevated, fluid-filled blister measuring
bid: Twice a day dosing instructions. greater than 0.5 cm in diameter, e.g., mucous
Biopsy: Surgical removal of pathologic tissue membrane pemphigoid.
from a living being for histopathological Calculus: A concretion composed of calcium
examination. phosphate, calcium carbonate, magnesium
Blister: Common term used for vesicle or bulla. phosphate, and other elements within an organic
Blood: A red colored fluid circulating through matrix composed of desquamated epithelial cells,
the heart, arteries, capillaries, and veins and mucin, microorganisms, and other debris.
carries nutrients and oxygen to body tissues. Cancer: The word cancer was coined by Hippo-
Blood clot: A coagulum formed of blood of a crates. In Latin, cancer means “Cancrum” deno-
semisolidified nature. ting crab.
Blood pressure: The lateral pressure exerted on Cancerophobia: Fear of cancer.
the arterial walls by the blood. Cachexia: General ill health and malnutrition,
Bone marrow: Soft tissue located in the cavities marked by weakness and emaciation, usually
of the bones where blood cells such as associated with serious disease.
erythrocytes, leukocytes, and platelets are Capillaries: The terminal vessels uniting the
formed. arterial with the venous systems of the body.
Brachy: Meaning short. Carcinoma: A malignant tumor arising from
Brachycephalic: Broad, round head. epithelial cells, e.g., squamous cell carcinoma.
Brachychilia: Abnormally short lips. Carcinogen: Any cancer-producing substance.
Brachyglossal: Abnormally short tongue. Case history: A detailed and concise compilation
of all demographic, personal, medical, physical,
Brachytherapy (internal radiation therapy):
and dental factors relative to diagnosis, prognosis
Brachytherapy uses radiation that is placed very
and treatment.
close to or inside the tumor. The radiation source
is usually sealed in a small holder called an Causalgia: Post-extraction localized pain, usually
implant. Implants may be in the form of thin characterized by a continuous burning sensation.
wires, plastic tubes called catheters, ribbons, CD4: Cell surface glycoprotein usually on helper
capsules, or seeds. The implant is put directly T cells.
into the body. Internal radiation therapy may CD8: Cell surface glycoprotein usually on
require a hospital stay. is usually delivered in one cytotoxic T cells.
of two ways: interstitial radiation therapy and Central lesion: A pathology present within the
intracavitary or intraluminal radiation therapy. bone causing enlargement, loss of function and
Bronchoconstriction: The reduction in the caliber loss of continuity.
of the bronchi. Cell: According to the cell, doctrine cells are the
Bronchodilation: The increase in the caliber of a fundamental units of both structure and function
bronchus. in all living things.
Bronchodilator: A drug that dilates or expands Cellulitis: A diffuse red, tender inflammatory
the diameter of the bronchi by relaxing the process that spreads along fascial planes and
muscular walls. through tissue spaces without gross suppuration.
Glossary 227
Chemotaxis: A response involving movement phalanges of the fingers. It is usually acquired

that is positive (toward) or negative (away) to a and may be associated with certain cardiac and
chemical stimulus e.g., phagocytic activity of pulmonary diseases.
neutrophils and monocytes. Collagen: Derived from a Greek word meaning
Chemotherapy: In general, it is the use of to produce glue. Collagen is the most abundant
medications to treat cancer. protein, which is found in skin, tendons,
Chemoprophylaxis: The use of a drug or ligaments, muscles, teeth (dentine), and mucosa.
chemical to prevent a disease. Corticosteroids: Compounds that resemble
Chief complaint: This is the reason, usually a cholesterol chemically and also contain
symptom or cluster of symptoms, why the hydrogenated cyclopentanoperhydrophenan-
patient seeks treatment. threne ring system e.g., hydrocortisone secreted
Chronic: Phenomenon characterized by a long, by adrenal corticosteroids. Endoge-nously
slow course, as opposed to acute. cortisone is probably a metabolite of hydrocor-
Chronic inflammation: A traumatic or tisone. When exogenous cortisone is given, it
pathologic phenomenon or process, which is a exhibits no biological activity until it is converted
slow, insidious, event that persists for several to hydrocortisone (cortisol).
months to years. Chronic inflammation results Combination therapy: Two or more drugs or
when the injuring agent persists in the lesion, and treatments used together to achieve optimum
the host’s immunity responds in a manner that results against a disease e.g., AIDS.
is not sufficient to overcome the effects of the Complement: A group of serum proteins
injurious agent. involved in inflammation, phagocytosis, and cell
Chromosomes: Darkly staining bodies present lysis.
in the nucleus that are observed in cells during Concomitant drugs: Drugs that are taken
division. Each chromosome carries genes in a together.
linear order.
Connective tissue (lamina propria): The binding
Civatte bodies: Apoptotic cells.
and supportive tissue of the body; derived from
Clade: Also called a subtype. A clade is a group the mesoderm and is composed of fibroblasts,
of related HIV isolates classified according to primitive mesenchymal cells, collagen fibers,
their degree of genetic similarity (such as the elastic fibers with associated blood vessels,
percentage of identity within their envelope lymphatic vessels, and nerve fibres embedded
genes). in a ground substance.
Clinical: Pertaining to or founded on observation
Convulsion: A violent spasm.
and treatment of patients, as distinguished from
theoretical or basic science. Crepitus (coarse): Coarse grating noise
suggestive of gross bone-on-bone contact.
Clinical latency: The period of time a virus or
bacteria or other organism is living or developing Crepitus (fine): Fine grating noise suggestive of
in the body without causing symptoms. mild bone-on-bone contact.
Cloacae: Penetration of involucrum by channels Crust: Desiccated contents of ruptured vesicle.
(cloacae) through which pus escapes to an Cryotherapy: The use of liquid nitrogen to freeze
epithelial surface. and destroy a lesion or growth, sometimes used
Clubbing (pulmonary osteoarthropathy): to induce scar formation and healing to prevent
Deforming enlargement of the terminal further spread of a condition.
Cyanosis: A characteristic bluish tinge or color Desmosome: Structure that attaches cells,
of the skin and mucous membranes associated especially in stratified squamous epithelium of
with reduction in hemoglobin brought about by the skin and mucosa.
inadequate respiratory change. Dolichocephalic: Long and narrow head.
Cyst: “A cyst is a pathological cavity having fluid, Drug-drug interaction: A modification of the
semi fluid or gaseous contents and which is not effect of a drug when administered with another
created by the accumulation of pus” (Kramer, drug. The effect may be an increase or a decrease
1974). in the action of either substance, or it may be an
Cytotoxic T lymphocyte: CD8+ T cells which kill adverse effect that is not normally associated
target cells. with either drug.
Cytokines: Low molecular weight proteins that Diagnose: To make a diagnosis.
stimulate or inhibit the differentiation,
Diagnosis: Diagnosis is an assessment of the
proliferation, or function of immune cells.
clinical findings, which may help in identifying
Cytotoxic: An agent or process that is toxic or a specific disease.
destructive to cells.
Diagnostic: Relating to or aiding in diagnosis.
Data gathering: Comprehensive collection of
Diagnostician: One who is experienced in
information about the patient through case
making diagnosis.
history and examination.
Definitive (final diagnosis): Diagnosis derived Diapedesis: The passage of blood or any of its
after using differential diagnosis is the definitive formed elements (cells), through the intact walls
or final diagnosis. of the blood vessels.
Dental caries: An infectious disease of the tooth Differential diagnosis: It is a process of
with progressive destruction of tooth substance, identifying a specific disease from other diseases
beginning on the external surface by deminera- that may produce similar signs and symptoms.
lization of enamel or exposed cementum. Diffusion: The random movement of free
Dementia: Chronic intellectual impairment (i.e., molecules or ions or small particles in solution
loss of mental capacity) with organic origins that or suspension under the influence of Brownian
affects a person’s ability to function in a social or (thermal) motion toward a uniform distribution
occupational setting. throughout the available volume.
Demyelination: Destruction, removal, or loss of Diplegia (double hemiplegia): Paralysis of
the myelin sheath of a nerve or nerves. corresponding parts on both sides of the body.
de novo: Arising anew, afresh, once more, from DNA: Deoxyribonucleic acid is the genetic
the beginning. material of the cells and many viruses, e.g.,
Depression: Mental disorder characterized by Herpes simplex virus-1.
gloominess, sadness, lack of motivation and Drug: A substance used in the prevention, cure,
interest. or alleviation of pain or disease.
Desensitization: Gradually increasing the dose Drug resistance: The ability of some disease
of a medicine in order to overcome severe causing microorganisms, such as bacteria,
reactions. viruses, and fungi, to adapt themselves, to
Desmoplasia: Formation and development of multiply, and to grow even in the presence of
fibrous tissue. drugs that usually kill them.
Glossary 229
Dys: Prefix which means bad or difficult. granules, which contain toxic cationic proteins.
Dysacusis: Impairment in the sense of hearing Epidemic: A disease that spreads rapidly
(difficulty in processing details of sound). through a demographic segment of the human
Dysaphia: Impairment in the sense of touch. population, such as everyone in a given
geographic area. Epidemic diseases can be
Dysesthesia: Impairment of sensation short of
spread from person to person or from a
anesthesia (unpleasant sensation).
contaminated source such as food or water.
Dysguesia: Impairment in the sense of taste.
Epidemiology: The branch of medical science
Dysphagia: Difficulty in swallowing. that deals with the study of incidence and
Dysphasia: Lack of coordination in speech. distribution and control of a disease in a
Dysplasia: Abnormal tissue development e.g., population.
epithelial dysplasia in precancerous lesions. Epiphora: Epiphora is defined as an overflow of
Dyspnea: Difficult or labored breathing. tears upon the cheek, due to imperfect drainage
Dystrophy: It is defined as a congenital disorder by the tear-conducting passages.
of the structure or function of an organ or tissue Epistaxis: Bleeding from the nose.
e.g., craniocarpotarsal dystrophy (ulnar Erosion: It is the loss of tooth substance caused
deviation of hands, frontal bone defects, protru- by chemical process that does not involve
sion of lips, sunken eyes with hypertelorism) or bacteria and usually involves the palatal aspect
muscular dystrophy (congenital abnormality of of upper anterior teeth. Frequent causes are
muscle associated with dysfunction and anorexia nervosa, simple vomiting, hyperemesis
ultimately deterioration). gravidarum (chronic vomiting in pregnant
Ecchymosis: Discoloration of mucous membrane women), and consumption of acidic fruit
caused by diffuse extravasations of blood. beverages malic acid (apples), tartaric acid
Frequently called a bruise. (grapes), and citric acid (citrus fruits).
Erosion: Partial loss of the epithelium without
Ectoderm: The outermost layer of the embryo.
the exposure of underlying connective tissue e.g.,
The ectoderm gives rise to the nervous system,
erosive lichen planus or pathologic loss of tooth
the organs of the special senses, the epidermis,
substance seen on the palatal surface of maxillary
and epidermal tissues such as fingernails, hair
anteriors due to chemicals and involving
and sebaceous glands.
bacteria.
Embolus: A blood clot, mass of bacteria, or other
Erythema: Redness or inflammation of the skin
foreign body that travels in the blood vessels and
or mucous membranes.
then deposits in a vessel to obstruct circulation.
Erythrocyte sedimentation rate: The rate at
Endoderm: The innermost layer of the embryo. which red blood cells of unclotted blood settle in
The endoderm gives rise to the epithelial lining a pipette, measured in millimeters per hour. It is
of the primitive gut tract, its glands, and the used as an index for infection.
epithelial component of structures arising from Erythroplakia: Oral erythroplakia is a
the gut. predominantly red lesion of the oral mucosa that
Endogenous: Relating to or produced by the cannot be characterized as any other definable
body. lesion.
Endotoxin: A toxin present inside a bacterial cell. Etiology: The study or theory of the factors that
Eosinophils: A leukocyte that has coarse cause disease.
Exogenous: Developed or originating outside the invasion, and subsequent putrefaction e.g.,
body. gangrene of the pulp is total death and necrosis
Exophthalmos: An abnormal protrusion of the of the pulp.
eyeball, it is characteristic of toxic (exophthalmic) Ganglion: A mass of nervous tissue composed
goiter. principally of nerve-cell bodies, usually lying
Exotoxin: A toxic substance, made by bacteria outside the central nervous system.
released outside the bacterial cell. Gene: A unit of DNA that carries information
Extravasation: The escape of a body fluid out of for the biosynthesis of a specific product in the
its proper place e.g., extravasation of blood into cell. Genes are arranged along the length of, the
the surrounding tissues after trauma. chromosome. Alteration of either gene number
Exudate: A tissue fluid that has high protein or arrangement can result in mutation.
content in comparison to transudate. Genome: The complete set of genes in the
Fascicle: A bundle. chromosomes of each cell of a particular
Fibroblast: Connective tissue cell that produces organism.
collagen and plays an important role in wound Gene therapy: Any experimental treatment in
healing. which cell genes are altered.
Fibrosis: The process of forming fibrous tissue Genetic engineering: The technique by which
e.g., oral submucous fibrosis. genetic material from one organism is inserted
Final diagnosis: The diagnosis arrived after into a foreign cell in order to produce the protein
collecting, analyzing, and subjecting the data to encoded by the inserted genes.
logical thought. Giant cell: An abnormally large tissue cell. It
Fistula: Abnormal tract connecting two cavities often contains more than one nucleus and may
and may or may not be lined by epithelium, e.g., appear as a merger of several normal cells e.g.,
oro-antral fistula. Langhans’ giant cell, Tzanck cells, Touton giant
Fixative: Any substance used to preserve gross cell, Foreign body giant cell, Reed-Sternberg
or histological specimens of tissue for later giant cells, Anitschkow cells, giant cell, Syncytia
examination e.g., 10 % neutral buffered formalin. of CD4+ T cells in HIV, gigantoblast (abnormally
Follicle: A small anatomical sac, cavity, or deep large erythroblast), gigantocyte (abnormally
narrow mouthed depression e.g., hair follicle. large erythrocyte).
Fracture: Break of a part. In the oral and maxillo- Gingivitis: Inflammation of the gingiva.
facial region, fracture is most frequently seen in Glossodynia: When the symptoms of the
teeth and bones. burning mouth are limited to the tongue the term
Fulguration: The destruction of soft tissue by an glossodynia is preferred.
electric spark that jumps the gap from an Gluconeogenesis: The formation of blood
electrode tip to the soft tissue without the glucose from proteins.
electrode tip touching the tissue e.g., fulguration Glycogenesis: The formation of liver and muscle
artifact in LASER biopsy. glycogen from blood glucose.
Fungus: A plantlike organism feeding on organic Glycogenolysis: The formation of blood glucose
matter, such as mushrooms, yeasts (Candida from liver and muscle glycogen.
albicans), and molds. Glycoprotein: A conjugated protein in which the
Gangrene: The death of a tissue en masse, usually nonprotein group is a carbohydrate (i.e., a sugar
as a result of loss of blood supply, bacterial molecule) also called glucoprotein.
Glossary 231
Gram-positive: Microorganisms that appear Half-life: The time required for half the amount
violet colour after being stained with Gram’s of a drug to be eliminated from the body.
stain. Headache (cephalagia, cerebralgia, cephalo-
Gram-negative: Microorganisms that appear dyia): Diffuse pain in various parts of the head
rose pink after being stained with Gram’s stain. resulting from intracranial, extracranial and
Granuloma: Localized mass of granulation tissue psychogenic causes.
characterized by an accumulation of giant cells, Hematotoxic: Poisonous to the blood or bone
epithelioid cells, macrophages and lymphocytes, marrow.
e.g., tuberculosis.
Hemidesmosome: Structure that attaches basal
Granulation tissue: Pink tissue formed during cells of the stratified squamous epithelium of the
the wound healing process, mainly composed of skin and mucosa with the basal lamina.
proliferating capillaries and plump fibroblasts.
Hemiplegia: Paralysis of one side of the body.
Overgrowth of granulation tissue is called
“Proud Flesh”. Hemoglobin: The component of red blood cells
that carries oxygen.
Growth: An increase in size.
Ground substance: The ground substance Hemolysis: The rupture of red blood cells.
supports the connective tissue and its various Hemorrhage: Excessive bleeding or loss of large
elements (see connective tissue) and consists of amount of blood from the blood vessels within a
protein-carbohydrate complexes, which are short period of time.
permeable to tissue fluid. Chemically the protein- Helper T cell: CD4+ T cells responsible for cell–
carbohydrate complexes can be subdivided into mediated immunity.
two distinct groups, proteoglycans, and Histological basis of red lesions:
glycoproteins. The proteoglycans consist of long 1. Atrophy of epithelium
polypeptide chain to which numerous hexose
2. Increased blood supply
and hyaluronic acid residues are attached. The
3. Dilated blood vessels
hyaluronic acid residues are responsible for the
4. Hemorrhage
water binding capacity of the connective tissue.
In comparison, the glycoproteins consist of Histological basis of white lesions:
branched polypeptide chain to which only a few 1. Increased thickness of epithelium
simple hexoses are attached. 2. Development of surface fungal colonies
Haematoma: Collection of a mass of extravasated (Candida albicans)
blood in the tissues due to rupture of blood 3. Decreased blood supply
vessels because of trauma; usually bluish-purple 4. Increased keratin production
in colour.
HLA: Human leukocyte antigens (HLA) are a
Hamartomata: Tumor like malformations of oral
series of proteins and their genes are located at a
tissues, developmental in origin, with the tissue
number of loci along the short arm of
being native to the site, e.g., odontoma (complex
chromosome 6. The main loci are designated A,
and compound), dens invaginatus, dens
B, C, DR (D-related). HLA antigens are detectable
evaginatus, talon’s cusp, enameloma, heman-
on the surface of most nucleated cells e.g., basal
gioma, lymphangioma, glomus tumor, torus
cell layer of the epithelium.
palatinus, torus mandibularis, pigmented
cellular nevus, Epstein’s pearls, and oral Hormone: Chemical messengers secreted into
melanotic macule. the blood vessel from ductless glands (endocrine
glands). The hormone (e.g., growth hormone) is outflow of the blood from a tissue e.g., physical
formed in one gland (e.g., pituitary gland) and obstruction or pressure from a tumor).
carried in the blood vessel to another tissue (e.g., Hyperglycemia: An increase in the concentration
bone) where it influences cellular activity, of sugar in the blood and is a feature of diabetes
especially growth and metabolism. mellitus.
Hyalin: A clear, eosinophilic, homogenous Hyperkalemia: An increase in the amount of
substance occuring in degeneration e.g., juxta- potassium in the blood. Causes include advanced
epithelial hyalinization of lamina propria in OSF. dehydration, shock, renal failure, and Addison’s
Hyaline: Glassy, homogenous, translucent disease.
appearance. The term refers to characteristic Hypernatremia: An increase in the amount of
gross and microscopic appearance and not a sodium in the blood. Causes include nephrosis,
specific chemical substance. congestive cardiac failure, after administration
Hyalinization: The formation of hyalin. of ACTH, and Cushing’s syndrome.
Hyaluronic acid: A mucopolysaccharide made Hyperostosis: Excessive growth of bone as in
up of alternating residues of glucuronic acid and infantile cortical hyperostosis.
N-acetylglucosamine, forming a gelatinous Hyperpigmentation: An unusual darkening of
material in connective tissue spaces, and as an the skin. Causes include heredity, exposure to
intercellular cementing substance. sun, drugs, pregnancy, and endocrinal
disturbances.
Hyperalgia: An increased sensitivity to pain that
may result from a pain stimulus or decreased Hyperplasia: Increase in size of an organ or tissue
pain threshold. due to increase in number of its cells, e.g., fibroma
arising from the gingiva.
Hyperacusis: Hypersensitivity to normal
Hypersalivation (sialorrhea, ptyalism):
environmental sounds.
Increased secretion of saliva. Causes include
Hypercalcemia: An increase in the amount of
acute stomatitis, ill-fitting dentures, pregnancy,
calcium in the blood. Causes include primary
teething, alcoholism, malnutrition, mental
hyperparathyroidism, sarcoidosis, multiple
retardation, neurological disorders, and cystic
myeloma, malignant neoplasms, prolonged
fibrosis.
androgen therapy, and massive doses of vitamin
Hypersensitivity (allergy): Abnormal or
D.
excessive sensitivity to an antigen. The
Hypercapnia: An increase in the amount of hypersensitivity reactions are traditionally
carbon dioxide in the blood resulting from
subdivided into four types, three are antibody
increase of carbon dioxide in the inspired air or
mediated injuries (Type I, Type II, Type III),
a decrease in elimination.
whereas the fourth is cell mediated (Type IV).
Hypercementosis: An excessive formation of Hypertelorism: Increased distance between
cementum on the root/roots of one or more teeth. paired organs as in Greig’s (ocular hyperte-
Hyperesthesia: Increased sensitivity to lorism) syndrome.
stimulation. Hypertension: Abnormal elevation of systolic
Hyperemia: An increase in the amount of blood and/or diastolic arterial pressure.
in a tissue. The hyperemia can be active Hypertrichosis: Excessive growth of hair on the
(increased blood flow due to dilatation of body e.g., hirsutism due to excessive adreno-
arterioles and capillaries) or passive (decreased cortical function.
Glossary 233
Hypertrophy: Increase in size of an organ or Hypoxia: Reduction of oxygen supply to tissues.

tissue due to increase in size of its cells, e.g., Hypothesis: A supposition or assumption
hypertrophy in muscles due to mechanical advanced as a basis for reasoning or argument,
stimulus. or as a guide to experimental investigation.
Hypervolemia: Increased blood volume. Icterus (jaundice): A condition characterized by
Hypoalgesia: A decreased sensitivity to pain that an abnormal accumulation of bilirubin in the
results from an increased pain threshold. blood and manifested by the yellowish discolo-
Hypocalcemia: A decrease in the amount of ration of the skin, mucous membranes, and skin.
calcium in the blood e.g., hypoparathyroidism, Idiopathic: Without a known cause.
rickets, osteomalacia. Immunity: A natural or acquired resistance to a
Hypocapnia: A decrease in the amount of carbon specific disease. Immunity may be partial or
dioxide in the blood. complete, long lasting, or temporary.
Hypoesthesia: Decreased sensitivity to Immune complex: Clusters formed when
stimulation. antigens and antibodies bind together.
Hypoguesia: Decreased sense of taste. Immune deficiency: Breakdown in immuno-
Hypoglycemia: A decrease in the concentration competence, when certain parts of the immune
of sugar in the blood. Common causes include system no longer function. This condition makes
fasting, and following injection of insulin. a person more susceptible to certain diseases.
Hypokalemia: A decrease in the amount of Immune response: The activity of the immune
potassium in the blood. Hypokalemia may occur system against foreign substances.
in chronic diarrhea, metabolic acidosis, Immune system: The body’s complicated natural
Cushing’s syndrome, excessive use of ACTH, defense against disruption caused by invading
and primary aldosteronism. foreign agents (e.g., microbes, viruses). There are
Hyponatremia: A decrease in the amount of two aspects of the immune system’s response to
sodium in the blood. Hyponatremia may develop disease: innate and acquired. The innate part of
in extreme sweating, chronic renal failure, and the response is mobilized very quickly in
adrenocortical insufficiency. response to infection and does not depend on
Hypoplasia: Condition in which there is small recognizing specific proteins or antigens foreign
under developed organ. to an individual’s normal tissue. It includes
complements, macrophages, dendritic cells, and
Hyposalivation (xerostomia): Dryness of the
granulocytes. The acquired, or learned, immune
mouth (decreased or absence of saliva) resulting
response arises when dendritic cells and
from functional or organic disturbances of the
macrophages present pieces of antigen to
salivary glands.
lymphocytes, which are genetically programmed
Hypotension: Low systolic and/or diastolic to recognize very specific amino acid sequences.
arterial pressure. The ultimate result is the creation of cloned
Hypotrichosis: A less than normal amount of populations of antibody-producing B cells and
hair on the body. cytotoxic T lymphocytes primed to respond to a
Hyperkeratosis: Condition characterized by unique pathogen.
hyperkeratinization of keratinized mucosa. Immunocompetent: 1. Capable of developing an
Hypoesthesia: Decreased sensitivity to immune response. 2. Possessing a normal
stimulation. immune system.
Immunocompromised: Refers to an immune used in experimental research to study a disease

system in which the ability to resist or fight off or process.
infections and tumors is subnormal. In vivo: From the Latin, meaning “within the
Immunofluorescence: The use of fluorescein– living organism”; studies conducted within
labeled antibodies to identify bacterial, viral, or living organisms (e.g., animal or human studies).
other antigenic material specific for the labeled Ionizing radiation: Radiation which causes
antibody. Immunofluorescence tests are either removal of orbital electrons from atoms in the
direct or indirect. irradiated matter and converting those atoms to
Immunotherapy: Treatment aimed at electrically charged atoms or free radicals e.g.,
reconstituting an impaired immune system. X-rays.
Incidence: The number of new cases (e.g., of a Ischemia: A focal deficiency of blood to a part of
disease) occurring in a given population over a the body (in simple terms a local anemia). It
certain period of time. results from impingement of the lumen of a blood
Incompetence: Incompetence is defined as defec- vessel supplying the affected area. Causes of
tive closure of the cardiac valve e.g., defective impingement are allergic hypersensitivity,
closure of the aortic valve permitting backward atherosclerosis, inflammation, physical pressure,
flow of blood into the left ventricle during pharmacological or toxic agents, and neurogenic
ventricular diastole. disorders.
Induration: Abnormal hardening of soft tissue Keratosis: Condition characterized by
because of influx of exudate or fibrous tissue hyperkeratinization of nonkeratinized mucosa.
elements. Ketogenesis: The formation of ketone bodies
Inflammation: Body’s reaction to injury and is from adipose tissue.
characterized by five cardinal signs namely LASER: “Laser” is an acronym for “light
rubor, calor, tumor, dolor, and functio laesa. amplification by simulated emission of radiation.”
Infarct: An infarct is an area of necrotic tissue Basically, a laser beam is generated when an
that has died because of lack of oxygenated external power source stimulates a chamber
blood. containing laser medium-solid, liquid or gas.
Infarction: The death of a tissue caused by partial Lesion: A general term to describe an area of
occlusion of a vessel or vessels supplying the altered tissue (e.g., the infected patch or sore in a
area. skin disease).
Infection: An invasion of tissues by disease Leukemia: Progressive proliferation of abnormal
producing microorganisms and the reaction of leukocytes found in hemopoietic tissues, other
these tissues to the microorganisms and/or their organs, and usually in the blood in abnormal
toxins. The mere presence of microorganisms numbers.
without reaction is not an evidence of infection. Leukoplakia: Oral leukoplakia is a predomi-
Innervation: The supply of nerve fibers. nantly white lesion of the oral mucosa that cannot
In situ: From the Latin, meaning in the original be characterized as any other definable lesion.
place. Locus: Position of a gene on the chromosome.
In vitro: From the Latin, meaning “within the Lower motor neuron: Neuron located in the
glass”; an artificial environment created outside brain stem is lower motor neuron. Its cell bodies
a living organism (e.g., a test tube or culture plate) are located in brain stem and axons leave this
Glossary 235
nucleus makes up the motor component of Macule: Flat circumscribed discolored nonele-
cranial nerves. vated area of oral mucosa or skin.
Luxation: Dislocation or displacement of a tooth Malaise: A generalized, nonspecific feeling of
from the socket or the temporomandibular joint discomfort.
from the articular fossa. Manometer: An instrument used to indicate
Lymph: Lymph is a clear watery fluid, which pressure of gases or vapor, or the tension of the
originates in organs and tissues of the body. It is blood.
similar in composition to plasma, with the Manometry: Measurement of pressure of gases
exception of plasma proteins. Lymph transports or vapor, or the tension of the blood by means of
the plasma proteins that seep out of the capillary manometer.
bed back to the blood vessels. It also carries away Macroglossia: Abnormally large tongue.
bacteria and cell debris from damaged tissues,
Mast cells: A connective tissue cells whose
which can then be filtered out and destroyed in
specific physiological function remains
the lymph nodes. unknown; capable of elaborating (expanding)
Lymphadenitis: An inflammation of a lymph basophilic, metachromatic, cytoplasmic granules
node or nodes characterized by swelling, pain, that contain histamine.
and redness.
Meiosis: It is a special process of cell division
Lymphadenopathy: Enlargement (localized or that produces four reproductive cells in sexually
generalized) of a lymph node or nodes resulting reproducing organisms; the nucleus divides into
from a disease. four nuclei each containing half the chromosome
Lymphatics: The lymphatic system consists of a number leading to gametes (ova and sperm) in
series of lymph vessels, which begin as blind- animals and spores in plants).
end tubes in the spaces between the blood Mesocephalic: Head size between dolichocep-
capillaries and tissue cells. The lymphatic system halic and brachycephalic.
consists of lymph capillaries, thin lymph vessels, Mesoderm: The middle of the three cell layers
large lymph vessels. The large lymph vessels of the developing embryo. It lies between the
eventually join together to form 2 large ducts, ectoderm and endoderm. The mesoderm gives
the thoracic duct and right lymphatic duct, which rise to bone, connective tissue, muscle, blood,
empty the lymph into the subclavian veins. vascular and lymphatic tissue, the pleurae of the
Lymphoma: Neoplasm made up of lymphoid pericardium and peritoneum.
tissue e.g., B cell lymphoma, T cell lymphoma, Metaplasia: Condition in which the cells/tissue
Burkitt lymphoma, non-Hodgkin lymphoma, undergoes differentiation to another type of
Hodgkin lymphoma. similar cells/tissue e.g., stratified squamous
Lymphokines: Cytokine produced by epithelium undergoing metaplasia to pseudo-
lymphocytes. stratified columnar epithelium, mucous cells, and
Lymph nodes: Lymph nodes are small oval or sebaceous cells in dentigerous cyst.
bean-shaped organs of the immune system, Metastasis: The spread of a disease (e.g., cancer)
which lie in groups, along the length of lymph from an original site to other sites in the body.
vessels. MHC (major histocompatibility complex): A
Macrophages: Any phagocytic cell of the genetic region encoding proteins involved in
reticuloendothelial system including specialized antigen presentation to T cells. Class I MHC
Kupffer’s cells in the liver and spleen, and molecules are present on virtually all nucleated
histocytes in loose connective tissue. cells and are encoded mainly by the HLA-A, B,
and C in man while Class II MHC molecules are Nausea: A sensation of leading to the urge to
expressed on APC (primarily macrophages, B vomit.
cells, Langerhans cells) and are encoded by HLA- Neonatal: Concerning the first 6 weeks of life
DR, DQ, and DP in man. after birth.
Migraine: A vascular type of headache, typically Neoplasm (tumor): “A neoplasm is an abnormal
unilateral in the temporal, frontal, and mass of tissue, the growth of which exceeds and
retroorbital area, but may occur in the midfacial is uncoordinated with that of the normal tissue
region. It is described as throbbing, burning, and persists in the same excessive manner after
pulsating, exploding, or pressure and may cessation of the stimuli which evoked the change
become generalized and persist for hours or days. (Sir Rupert Willis).
Onset of pain is usually preceded by prodromal Neuralgia: Neurogenous pain that is felt along
symptoms that may include visual disturbances, the pathway of peripheral nerve.
nausea, and vomiting. Neurosis: Mental disorder characterized by
Mitosis: Division of the cell that produces two inability to cope with frustrations and is milder
daughter cells exactly like the parent cell. than psychosis.
Morbidity: The relative incidence of a particular Neutrophils: The major circulating phagocytic
disease. polymorphonuclear granular leukocyte. Enters
Mortality: The ratio of deaths in an area to the tissues early in an inflammatory response and is
population of that area; expressed per 1000 per also able to mediate (in-between) antibody-
year. dependent cellular cytotoxicity.
Nodule: Solid lesion located within the
Mucosa: A membrane composed of epithelium
subcutaneous tissue.
and lamina propria that lines the oral cavity and
other canals and cavities of the body that Non-reproducible click: Present on opening or
communicate with external air. in laterotrusion but not repeatable.
NK (natural killer) cells: Large granular
Mucous: The viscous, slippery secretions of
lymphocyte which does not rearrange nor
mucous membranes and glands, containing
express either immunoglobulin or T cell receptor
mucin, white blood cells, water, inorganic salts,
genes but is able to recognize and destroy certain
and exfoliated cells.
tumor and virally infected cells in an MHC and
Mutagen (carcinogen): An environmental agent,
antibody-independent manner.
physical, chemical or biological, that is capable
NSAID: A classification of drugs called
of inducing mutations.
nonsteroidal anti-inflammatory drugs. NSAIDs
Mutation: The process by which a mutagen reduce inflammation and are used to treat
produces an alteration in DNA or chromosome. arthritis and mild to moderate pain.
Myalgia: Pain felt in the muscles. od: Once a day dosing instructions.
Myopathy: Progressive muscle weakness. Odontalgia: Pain felt in the tooth.
Necrosis: The local death of cell or group of cells Oncogene: Oncogenes are mutated forms of
resulting from, loss of blood supply, bacterial genes that cause normal cells to grow out of
toxins, or physical and chemical agents. control and become cancer cells or a gene that
Examples include caseous (tuberculosis), causes cancer.
exanthematous (noma), gingival (ANUG), Oral cancer: Malignancy that arises from oral
ischemic (trauma of the pulp), and radiation. tissues, e.g., squamous cell carcinoma.
Glossary 237
Oral medicine: The “American Academy of Oral Paralysis: Impairment of motor function due to
Medicine” defines oral medicine as follows: Oral trauma or lesion of the neuron or muscles e.g.,
Medicine is the specialty of dentistry concerned facial paralysis.
with the oral health care of medically complex Paresis: Partial or incomplete paralysis.
patients and with the diagnosis and non-surgical Pain: Unpleasant sensation created by a noxious
management of medically-related disorders or stimulus, which is mediated along a specific
conditions affecting the oral and maxillofacial nerve pathway to the central nervous system
region. where it is interpreted as such.
Organ: Any part of the body exercising a specific Papule: Raised circumscribed discolored
function e.g., respiration, digestion. elevated area of mucosa or skin, which is less
Orthokeratosis: Keratinization in which nuclei than 1 cm in diameter, e.g., stomatitis nicotina.
are not present. Pathogenesis: The origin and development of a
Osmosis: The net diffusion of water across a disease.
selectively permeable membrane from a region Peduncle: A constricted portion (stalk or stem),
of high water concentration (low solute forming the attachment of a nonsessile tumor.
concentration) to a region that has low water Perinatal: Events that occur at or around the time
concentration (high solute concentration) until of birth.
the concentration on both sides is equal. Periapical abscess: An acute or chronic inflamm-
Osteomyelitis: Inflammation of the medullary ation of the periapical tissues characte-rized by
portion of the bone. a localized accumulation of pus at the apex of a
Palliative: A treatment that provides sympto- tooth. It is generally a sequela of pulp death of
matic relief but not a cure. tooth.
Periapical granuloma: Mass of granulation tissue
Pallor: Paleness. Absence of skin or mucous
surrounded by fibrous capsule, which is attached
membrane.
to the root.
Paresthesia: Abnormal sensation.
Periodontitis: Inflammation of the periodontium
Pandemic: A disease prevalent throughout an (teeth, gingiva, cementum of the root, period-
entire country, continent, or the whole world. ontal ligament) and alveolar bone or alterations
Parakeratinization: Keratinization in which occuring in the periodontium with inflammation.
nuclei are present. Peripheral lesion: Pathology present within the
Passive immunity: Also referred to as acquired soft issue causing enlargement, loss of function
immunity. Resistance resulting from previous and loss of continuity.
exposure to an infectious agent or antigen may Peripheral resistance: Peripheral resistance is the
be active or passive. Passive immunity can be resistance offered by the arterioles to blood flow.
acquired from the transfer of antibodies from Thus, the arterioles are called resistance vessels.
another person or from an animal, either In the body, the maximum peripheral resistance
naturally—as from mother to fetus or to the is offered at the splanchnic region.
newborn via breast milk—or by intentional Petechiae: Capillary hemorrhages producing
inoculation (vaccination). small red or purplish pin head-sized discolora-
Pathogen: Any disease-producing microorga- tions of the mucosa membrane and skin.
nism or material. Plaque: Elevated flat-topped area, usually more
Palsy: Paresis or paralysis. than 5 mm across.
Plasma: The liquid part of the blood and lymph Psychasthenia: Mental disorder characterized by
that contains nutrients, electrolytes (dissolved abnormal reaction to environment.
salts), gases, albumin, clotting factors, wastes, Pulpitis: Inflammation of the pulpal tissue of a
and hormones. tooth.
Plasma cell: Terminally differentiated B lympho- Purpura (bruise): A discoloration of mucous
cyte which actively secretes large amounts of membrane caused by diffuse extravasation of
antibody. blood.
Polyp: Mass of a tissue that bulges outwards or
Pustule: Vesicle containing pus rather than clear
upwards from the normal mucosa or skin, which
fluid.
is either pedunculated or sessile.
Polydipsia: Abnormally increased thirst. Putrefaction (decomposition): The breakdown
of organic matter usually by bacterial action,
Polyuria: The passage of an abnormally
resulting in the formation of other substances of
increased volume of urine. It may result from
less complex constitution and malodorous
increased intake of fluids, inadequate renal
products (e.g., ammonia and hydrogen sulfide
function, uncontrolled diabetes mellitus or
(“rotten egg smell”).
diabetes insipidus, and ascites.
Polyphagia: Abnormally excessive eating. Pyrexia: Elevation of body temperature.
Popping: Distinctly audible sound on opening. qid: Four times a day dosing instructions.
Precancerous condition: Generalized state Radiotherapy (actinotherapy, irradiation,
associated with a significantly increased risk for radiation therapy, X-ray therapy,): The speciality
cancer. of medicine which relates to the use of X-rays to
Precancerous lesion: Morphologically altered kill cancer cells and shrink tumors. Radiation
tissue, in which cancer is more likely to occur therapy injures or destroys cells in the area being
than in its apparently normal counterpart. treated (the “target tissue”) by damaging their
Prevalence: A measure of the proportion of genetic material, making it impossible for these
people in a population affected with a particular cells to continue to grow and divide. Although
disease at a given time. radiation damages both cancer cells and normal
Prodrome: A symptom that indicates the onset cells, most normal cells can recover from the
of a disease. effects of radiation and function properly. The
Prophylaxis: Treatment to prevent the onset of goal of radiation therapy is to damage as many
a particular disease (“primary” prophylaxis), or cancer cells as possible, while limiting harm to
the recurrence of symptoms in an existing nearby healthy tissue.
infection that has been brought under control Reciprocal click: Noise made on opening and
(“secondary” prophylaxis, maintenance closing from centric occlusion position that is
therapy). reproducible on every opening and closing. Can
Proto-oncogene: A gene that has a high rate of be eliminated with anterior repositioning of jaw.
transforming into oncogene. Red lesion: Abnormal area of oral mucosa that
Provisional diagnosis: Diagnosis which is not appears red is of a different texture than the
final or fully worked out or agreed upon. adjacent normal mucosa, e.g., erythroplakia.
Pruritis: Itching. Referred pain: Pain felt at an area that is inner-
Psychosis: Personality disorder characterized by vated by a nerve, which does not mediate the
hallucinations/delusions. primary pain.
Glossary 239
Regurgitation: Backflow of blood through a Seroconversion: The development of antibodies

defective heart valve. to a particular antigen.
Reproducible closing click: Noise with every Sessile: Having a broad base of attachment in
closing, no noise when opening. comparison to pedunculated.
Reproducible laterotrusive click only: Noise Sepsis: The presence of harmful microorganisms
with every full laterotrusive movement, no noise or associated toxins in the blood.
on opening. Shock: A sudden physical or mental disturbance
Reproducible opening click: Noise with every e.g., anaphylactic shock, anesthetic shock,
opening, no noise when closing. cardiogenic shock, electric shock, hemorrhagic
Rheumatoid factor: IgM, IgG, IgA autoanti- shock, hypovolemic shock, irreversible shock,
bodies to IgG, particularly the Fc region. septic shock.
Rhizotomy: Destruction of sensory root and Side effects: The actions or effects of a drug (or
ganglion. vaccine) other than those desired.
RNA: Ribonucleic acid is the genetic material in Signs: Objective evidence of a disease, e.g.,
certain microorganisms and is involved in redness, ulcer, swelling, tenderness to palpation,
transcription and translation (protein synthesis). tenderness to percussion, bad breath, molar
Saliva: The clear, slightly acid mucoserous crossbite.
secretion formed in the exocrine glands namely
Sinusitis: Inflammation of the nasal cavity and
partotid glands (serous fluid), sublingual glands
sinuses.
(mucous fluid), submandibular glands (serous
Sinus: Blind tract, which connects a cavity, from
and mucous fluid), and smaller intraoral salivary
either the bone or soft tissue, to the epithelial
glands.
surface, which is formed by granulation tissue
Sarcoma: Malignant tumor arising from
and may or may not be lined by epithelium.
connective tissue cells.
SOAP: Acronym often seen in medical and
Scale: Dry, horny, plate like excrescence; usually
dental case histories, describes a routine app-
the result of imperfect cornification (keratiniza-
roach to any disease and stands for: Subjective
tion) or surface accumulation of desquamated
symptoms, Objective signs, Assessment of
epithelial cells.
clinical findings, and Plan i.e., treatment plan.
Scar: The end product of wound healing.
Spasm: A sudden involuntary contraction of a
Sepsis: The presence of harmful micro-
muscle or muscle group.
organisms or associated toxins in the blood.
Sphygmo: (Greek for “sphygmos”, pulse) Relating
Sequestrum: A piece of small necrotic bone that
to pulse.
has become separated from vital bone. These
small fragments of necrotic bone may be lysed Sphygmomanometer: Instrument used to
completely, whereas larger ones are isolated by measure blood pressure or a pressure gauge for
a bead of granulation tissue encased in a sheath measuring blood pressure.
of new bone (involucrum). Spot diagnosis: Diagnosis made quickly on the
Serum: The clear, thin, and sticky fluid portion spot.
of the blood that remains after coagulation Stenosis: Stenosis is defined as pathological
(clotting). Serum contains no blood cells, platelets narrowing of the cardiac valve orifice e.g.,
or fibrinogen. narrowing of the aortic valve orifice.
Stethoscope: An instrument originally designed hair follicles. The cystic cavity is usually lined
by Laennec for aid in hearing the respiratory and by a greasy mass of sebaceous material in which
cardiac sounds in the chest; now modified in there is matted hair. There is often a nodule in
various ways and used in auscultation of any the wall, called “umbo”, which contains a variety
vascular or other sounds in the body anywhere. of structures such as bone, teeth, thyroid tissue,
Stereo: Designating sound transmission from brain etc.
two sources through two channels. Teletherapy (external beam therapy): Tele-
Stereotactic surgery: A precise method of therapy is a method for delivering a beam of
destroying deep-seated brain structures, located high-energy X-rays to the location of the patient’s
by the use of three-dimensional coordinates. tumor. The beam is generated outside the patient
Subclinical infection: An infection, or phase of (usually by a linear accelerator and is targeted at
infection, without readily apparent symptoms or the tumor site. These X-rays can destroy the
signs of disease. cancer cells and careful treatment planning
allows the surrounding normal tissues to be
Suppurative: Producing pus or associated with
spared. No radioactive sources are placed inside
the formation of pus.
the patient’s body.
Swelling: It is an increase in size of a tissue
Therapy: Treatment of a disease e.g., antibiotic
caused by the exudation of fluid from the
therapy, corticosteroid therapy, periodontal
capillary vessels into the tissue spaces e.g.,
therapy, radiation therapy, root canal therapy,
cellulitis.
speech therapy.
Syncope: Temporary loss of consciousness or
Thrombocytopenia: Abnormal hematological
fainting due to decreased blood supply to the
condition in which the platelet count is reduced.
brain.
Thrombolus: An embolus composed of
Syndrome: Group of signs and symptoms that
aggregated platelets.
occur together and characterize a disease.
Thrombus: A blood clot in a vessel or in one of
Symptoms: Subjective evidence of a disease or
the chambers of the heart that remains at its place
sensation experienced by the patient indicative
of origin.
of a disease, e.g., pain, sensitivity to hot or cold,
altered taste, inability to open the mouth. tid: Thrice a day dosing instructions.
Systemic: Concerning or affecting the body as a Tissue: An aggregation of similarly specialized
whole. cells, which are united to perform particular
Subluxation: Incomplete dislocation of a joint function e.g., connective tissue (binding and
e.g., TMJ subluxation. supportive tissue of the body).
Teratogenicity: Teratogenicity refers to capacity Translocation: Attachment of a fragment of one
of a drug to cause fetal abnormalities when chromosome to another chromosome. The short
administered to the pregnant mother. arm of the chromosome is designated as p and
the long arm q.
Teratomata: Tumor like malformation, which is
not native to the site. The common sites are the Trauma: External violence producing bodily
ovary and testis e.g., testicular teratomata, injury or degeneration.
ovarian teratomata (they are usually cystic, and Trigger point: Trigger points are tender areas in
the wall is lined by stratified squamous firm bands of skeletal muscles, tendons, or
epithelium and contains sebaceous glands and ligaments.
Glossary 241
Trigger zones: Junction between the two nerve venoconstriction and venodilation are generally
endings where the nerve impulse is normally not used to refer to constriction and dilation of
transmitted (no synapse) is known as ephapse. capacitance vessels (veins).
However, when there is ephaptic transmission Venules: The smallest of the venous blood
(short-circuit) between nociceptive afferents and vessels.
non-nociceptive afferents it results in a trigger Vertical transmission: A term used to describe
zone. the transmission of a disease from parent or
Trismus: Spasms of the muscles of mastication parents to offspring.
resulting in the inability to open the mouth e.g., Vesicle: Elevated fluid-filled blister measuring
pericoronitis. less than a 0.5 cm in diameter.
Tumor suppressor gene: Tumor suppressor Viral load (VL): The amount of HIV RNA in a
genes are normal genes that activate genes that blood sample, reported as number of HIV RNA
promote DNA repair, activate genes that arrest copies per ml of blood plasma. The VL provides
cell division, and activate genes that promote information about the number of cells infected
apoptosis. with HIV and is an important indicator of HIV
Tzanck cell: A degenerated epithelial cell caused progression and how well the treatment is
by acantholysis, which is usually found in working. The VL can be measured by different
pemphigus. techniques, including branched chain DNA
Ulcer: Total loss of epithelium with exposure of (bDNA) and reverse transcriptase-polymerase
underlying connective tissue, e.g., traumatic chain reaction (RT-PCR) assays. VL tests are
ulcer or aphthous ulcer. usually done when an individual is diagnosed
Upper motor neuron: The neuron located in the with HIV infection and at regular intervals after
cerebral cortex and which whose axon projects diagnosis.
caudally to contact the lower motor neuron in Viremia: The presence of virus in the
the brain stem. bloodstream.
Vaccine: A substance that contains antigenic Viricide: Any substance that can destroy or
components from an infectious micro-organism. inactivate a virus.
By stimulating an immune response it protects Virion: A virus particle existing freely outside a
against subsequent infection by that organism. host cell. A mature virus.
There can be preventive vaccines (e.g., measles Virulence: The power of a microorganism to
or mumps) as well as therapeutic (treatment) produce disease.
vaccines. Vitamins: Group of unrelated organic substances
Vasoconstriction: Narrowing of blood vessels. that occurs in small amounts in food and is
Vasodilatation: Dilatation of blood vessels. required in normal metabolic activities and lack
Vegetations: A clot composed blood platelets, of which in the diet causes deficiency diseases.
fibrin, and bacteria adherent to the heart valve. The vitamins may be water soluble or fat soluble.
Veins: Veins are known as capacitance vessels von Recklinghausen’s disease (neurofibro-
because they can store large amounts of blood matosis, neuromatosis, molluscum fibrosum):
especially the splanchnic veins. Therefore, the Disease characterized by development of small
sympathetic nerves richly supply the splanchnic discrete, pigmented skin lesions (café-au-lait
veins. Thus, when there is venoconstriction; spots) that develop in infancy or early childhood,
blood is pumped to important organs. The terms followed by development of multiple
subcutaneous neurofibromas that many slowly Wheezing: A whistling sound made during
increase in size and number over many years. breathing that is caused by a foreign body
Neurofibromas may develop on nerve trunks (mucus) in the bronchi or trachea.
anywhere. White lesion: Abnormal area of oral mucosa that
appears white and is of a different texture than
von Recklinghausen’s disease of bone
the adjacent normal mucosa.
(hyperparathyroidism, generalized osteitis
Window period: The window period is the time
fibrosa cystica, brown tumor): Disease
between initial infection with HIV and the
characterized by an increase in the secretion of
development of enough antibodies to be detected
paratharmone causing elevated serum calcium,
through testing.
and decreased serum phosphorus. It may be
Working diagnosis (provisional diagnosis or
primary, secondary or tertiary.
tentative diagnosis): Diagnosis made when the
Wheal: It is a special form of circumscribed clinical presentation corresponds to a particular
papule produced by edema of epidermis and disease, so that preliminary treatment may
dermis. proceed.
Index
A classification 197 etiology 215
Abrasion 223 clinical examination 199 treatment 219
Acanthosis 223 clinical symptoms 198 Biopsy 10, 226
ACE inhibitors 209 diagnosis 199 contraindications 14
Acquired immunodeficiency drugs for treatment 200 indication 14
syndrome 100, 136 bronchodilators 201 principles 14
causative organism 137 inhaled corticosteroids artifacts in oral biopsies 16
classification of HIV 138 (beclomethasone) 200 modifications 15
course of HIV infection 141 muscarinic receptor precautions to be taken 17
acute phase 141 antagonists 201 types 10
chronic phase 141 systemic corticosteroids 201 aspiration 13
crisis phase 141 pathogenesis 194 brush 11
oral manifestations 142 risk factor 197 excisional 10
HIV genome 138 treatment 200 incisional 10
life cycle of HIV 139 Asthma and dental care 194 laser 13
structure of HIV 137 Atherosclerosis 178, 206 wedge 10
transmission of HIV 138 Atrioventricular bundle 171 Blood pressure 172
Acupuncture 223 Atrioventricular node 171 regulation of normal blood
Acute abdominal pain 161 Atypical facial pain 28 pressure 173
Acute endocarditis 189 Auriculotemporal nerve 35 neural regulation 173
Acute myocardial infarction 181 Avulsion 21 renal regulation 173
Adenopathy 223 Blood pressure 226
Aguesia 217, 224 B BMS protocol 30
AIDS wasting syndrome 224 β2-agonists 201 Bronchi and bronchioles 194
Alcohol 63 Ballon compression rhizotomy 24 Bronchodilators 201, 226
Allodynia 224 Basal cell hyperplasia 71 Bundle of His 171
Alopecia 224 Basic cardiology 168 Burning mouth syndrome 29
Altered wound healing 205 blood supply to the heart 170
Anemia 160, 224 conducting system of the heart C
Anesthesia 37 170 Cancer cachexia syndrome 97
Anesthetic nerve block 38 flow of blood through the heart Candida associated lesions 102
Angina pectoris 180, 181 170 Capsule 33
Angiogenesis 224 heart structure Carcinogenic agents 57
Angular cheilitis 102 external 168 Carcinogens 84
Anticoagulant therapy 184 internal 169 Carcinoma 70, 226
Antioxidants 225 innervation to the heart 171 Cartilaginous joints 31
Antiretroviral drugs 150 parasympathetic 172 CD4+T-lymphocyte 142
Antiretroviral therapy 149 sympathetic 171 Cell crowding 71
Aphthous ulcers 146 venous drainage of the heart Cerebrovascular accident 192
Apoptosis 225 170 Chest radiograph 199
Areca nut 62, 74 Bell’s palsy 210, 213 Chilies 74
Arthrogenous pain 38 clinical features 215 Chromosomes 80, 227
Articular disc 34 clinical presentation 215 Chronic desquamative gingivitis
Articular eminence 32 diagnosis 219 108
Articular fossa 32 differential diagnosis 218 Cigarette smoke 58
Asthma 161, 196 electrodiagnostic testing 217 Clicking 39
Clicking sounds 43 Emergency treatment record 9 Hemorrhage 160

Clinical examination 4 Endocardium 169, 186 Herpes simplex infection 144
Coarse crepitus 43 Epiphora 217 Herpes simplex virus 113
Condyle 32 Epithelial-connective tissue Herpes virus infections 111
Confidentiality 9 interface 109 clinical manifestations
Consultations 8 Erythrocyte sedimentation rate 229 primary HSV infection 114
Coronary artery vasospasm 180 Erythroplakia 72, 229 complications 122
Coronary heart thrombosis 180 clinical appearance 73 diagnosis 117
Corticosteroids 128, 129, 200 clinical features 72 differential diagnosis 117, 122
Counseling 52 differential diagnosis 73
Crepitations 40 management 118, 122
etiology 73
Crepitus 227 Herpes viruses 112
histopathology 73
Cryotherapy 227 Herpetiform aphthous ulcers 132
rate of malignant
Cyclosporine 129 Homogenous leukoplakia 67
transformation 73
Hyalinization 232
treatment 73
D Hypercalcemia 232
Exophytic cancer 89
Dapsone 129 Hyperchromatic nuclei 71
Dementia 228 F Hyperesthesia 37
Demographic data 2 Facial nerve 210 Hyperglycemia 205
Dental care 117 Female sex hormones 158 Hyperpigmentation 232
Dental caries 96 Fibrous connective tissue 32 Hypertension 161, 175
Dental history 2 Fibrous joints 31 complications 177
Desmosomes 104 dental considerations 178
Final diagnosis 8
Diabetes mellitus 100, 202 essential 175
Financial information 2
complications 205 mechanism 176
Financial record 9
diagnostic tests 207 secondary 177
Fine crepitus 43
treatment 208
Fine needle aspiration biopsy 13, Hypoesthesia 37
Diabetic microangiopathy 205
92 Hypoglycemic shock 206
Diabetic nephropathy 206
Follow-up notes 8
Diabetic neuropathy 206
Fructosamine test 207 I
Diabetic retinopathy 206
Diastolic pressure 173 Increased nucleocytoplasmic ratio
Differential diagnosis 8 G 71
Disc displacement 39, 51 Gamma knife Increased susceptibility to
Disturbed epithelial maturation radiosurgery 25 infection 205
71 team 26 Infection 179
Disturbed nuclear polarity 70 Genetic engineering 230 Infective endocarditis 188
DNA/RNA PCR 148 Gestational diabetes Insulin pump 208
Drill biopsy 11 mellitus 161, 203 Internal derangement 50
Drop-shaped rete pegs 70 Giant cell 230 Intraoral herpes 115
Drugs record 9 Glucose metabolism 203 Intraoral muscles 46
Dysacusis 217 Glumerulosclerosis 206 Intraoral punch biopsy 10
Dysesthesia 37 Glycosylated hemoglobin assay Investigations 8
Dysphasia 192 207 Ischemic heart disease 178, 180
Dysrhythmias 192, 193 Greenspan lesion 145
Griseofulvin 129 J
E Growth factor receptors 82 Jaundice 161
Ecchymosis 229 Gustatory lacrimation 218 Jaw excursions 44
Electrocardiographic Joint hypermobility 40
abnormalities 182 H Joint palpation 44, 49
ELISA 147 Hamartomata 231 Joint sounds 43, 44
Index 245
K Nulligravida 155 treatment 71

Keratinization 71 Nullipara 155 Oral lichen planus 123
Nutrition 96 clinical features 123
L clinical variants 124
O etiopathogenesis 125
Laboratory record 9
Occlusal therapy 54 histopathology 128
Ligaments 33
Oncogenes 82 pigmentation 125
Linear eythematous gingivitis 143
Oncogenic viruses 86 treatment 128
Local soft tissue thickenings 40
Oral cancer 80 Oral lichenoid lesions 130
Loose intra-articular bodies 40
clinical appearance 89 Oral submucous fibrosis 74
Loss of taste 96
diagnosis 90 clinical grading 76
Lung function tests 199
diagnostic aids 90 clinical presentation 75
Lungs 195
etiology 84 etiology 74
functional rehabilitation 97 histopathology 77
M pathogenesis 74
genetics 80
Macrotrauma 50
histopathological features 93 treatment modalities 77
Masseter 45
sequelae of radiotherapy 95 Oral warts 146
Masseteric nerve 35
treatment 94 Osteoradionecrosis 96
Master cell 142
complications of
Median rhomboid glossitis 102
radiotherapy 94 P
Medical history 3 dental treatment before Pain 18
Metabolic ketoacidosis 206 radiotherapy 95 Paraneoplastic pemphigus 108
Metastasis 87 Oral candidosis 96, 99, 144 Paresthesia 37
Methylxanthines 202 classification 101 Parturient 155
Microsurgical rhizotomy 25 acute atrophic 101 Patient consent 1
Microtrauma 50 acute pseudomembranous Patient record 2
Microvascular compression 20 101 Peak flow meter 199
Microvascular decompression chronic atrophic candidosis Pemphigus vulgaris 104
surgery 22 101 clinical features 105
Motor neuron 210 chronic hyperplastic 102 clinical presentation 106
lesion 213 chronic mucocutaneous 102 diagnosis 106
Mucositis 95 defense mechanisms 100 pathogenesis 105
Mucous membrane pemphigoid microbiology 99 treatment 107
108 predisposing factors 99
Percutaneous glycerol rhizotomy
Mullan set 24 Oral CDx computer 12
24
Multigravida 155 Oral glucose tolerance test 207
Muscle and joint palpation 49 Percutaneous radiofrequency
Oral hairy leukoplakia 145
Muscular incoordination 40 rhizotomy 25
Oral leukoplakia 65
Mutations 81 Pericardium 168, 186
clinical features 67
Mutipara 155 differential diagnosis 70 Peripheral nerve block 21
Myocardial infarction 206 epidemiology 66 Pharmacological therapy 54
Myocardium 169, 186 etiology 66 Physical therapy 52
Myofascial trigger point 38 alcohol 67 Placental hormones 159
Myogenous pain 38 chronic friction 67 Pleomorphic cells, nuclei, and
microorganisms 67 anisocytosis 71
N tobacco smoking 67 Pleura and pleural cavity 196
Nectrotizing ulcerative ultraviolet radiation 67 Postcentral gyrus 19
periodontitis 143 histopathology 70 Posterior deep temporal nerve 35
Nerve entrapment 39 investigations 70 Posterior disc attachment 46
Nicotine 56 LSCP classification and staging Precancerous lesion 65
replacement therapy 62 68 Pregnancy gingivitis 163
Pregnancy tumor 162 S Tobacco and oral health 59

Pregnant dental patient 155 Sectioning 21 Tobacco habits 58
anatomical and physiological Shingles 119, 120 Tobacco smoking 59
changes 156 Trachea 194
Signal transducers 83
complications of pregnancy
Sinoatrial node 171 Treatment plan 8
160
Smoking cessation 60 Trigeminal leminiscus 19
drug considerations 165
dental management 166 guidelines 61 Trigeminal nerve 18
FDA pregnancy risk categories Speckled leukoplakia 68 Trigeminal neuralgia 19
164 Spirometry 199
Trigeminal nucleus 18
fetal development Spot diagnosis 7
Trismus 96
first trimester 155 Stroke 192
Structure of HIV Tumor suppressor genes 83, 84
second trimester 155
Subacute endocarditis 189 Type of joint 31
third trimester 156
oral manifestations 162 Supine hypotension 162 Tzanck test (mucosal smear) 117
Preleukoplakia 67 Sydenham’s chorea 187
Primigravida 155 Synkinesis 217 U
Primipara 155 Synovial fluid 34 Ulcerative lesion 89
Prinzmetal angina 181 Synovial joints 31 Unstable angina pectoris 181
Progesterone metabolism 159 Synovial lining 34
Prominent nucleoli 71 Systolic pressure 173 V
Prosthetic heart valves 188 Valvular heart diseases 185
Provisional diagnosis 7 T Varicella-zoster virus 119
Puerpera 155 Vasoconstriction 175
Temporalis 45
R Temporomadibular joint 31, 46 Verruciform leukoplakia 68
innervation 35 Verrucous carcinoma 89
Radiation 85
structures involved 32 Vertical range of movement 42
Rapid HIV screening tests 148
Temporomandibular disorder 41 Volatile aldehydes 57
Recordkeeping 1
Recurrent aphthous ulcers 131 Temporomandibular joint pain Volatile N-nitrosamines 58
Recurrent herpes labialis 115 36, 37 Vomiting 150
Reduced cellular cohesion 71 description of pain 37
Referrals 8 diagnosis 36 W
Referred pain 38 history of pain 36 Western blot 148
Reproducible reciprocal click 43 Temporomandibular joint sounds Window period 148
Retinoids 129 39 Working diagnosis 7
Rheumatic fever 185 Tendon of temporalis 46
Rheumatic pancarditis 186 Tentative diagnosis 7 X
Rhizotomies 23 Tobacco 56 Xerostomia 96, 100

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Essentials

Gautam Srivastava MDS

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD.

Essentials of Oral Medicine

First Edition: 2008

My parents, who taught me that the only

Swarnalatha J Wesley MDS

1. Dental Recordkeeping .................................................................................................. 1

3. Orofacial Pain .............................................................................................................. 18

4. Temporomandibular Joint Dysfunction .................................................................. 31

5. Tobacco, Areca Nut and Alcohol .............................................................................. 56

6. Oral Precancer ............................................................................................................. 65

7. Oral Cancer .................................................................................................................. 80

8. Oral Candidosis ........................................................................................................... 99

9. Vesiculobullous and Ulcerative Lesions ............................................................... 104

10. HIV/AIDS in Dental Care ........................................................................................ 136

11. Pregnancy and Dental Care ..................................................................................... 155

12. Systemic Diseases and Dental Care ...................................................................... 168

Glossary ........................................................................................................................ 223

Index ............................................................................................................................. 243

4. Date of last dental visit carcinogenic agent in alcoholic beverages is

roma, fibroma, hemangioma, plunging

g. Muscle and joint palpation

g. Palate (hard and soft)

d. Overbite Spot Diagnosis

Differential Diagnosis Treatment Plan

Definitive (Final diagnosis) Notes of referrals to specialists or other health care

Emergency Treatment Record 6. Directions for use

Definition Incisional biopsy is the partial removal of the

Table 2.3: Classification of Oral CDx specimens

Table 2.4: Surgical applications of dental lasers

10 ml syringe, 22-gauge needle, frosted glass 4. Vascular lesions such as haemangioma

specific inflammatory changes and 4. Mucoceles should be excised completely

Trigeminal Nerve—Sensory Component

Fig. 3.3: Touch pathway

Fig. 3.2: Trigeminal nucleus

synapse in the principal sensory nucleus,

Fig. 3.7: Trigger zones

Fig. 3.5: Trigeminal leminiscus

Fig. 3.6: Cerebrum

Fig. 3.8A: No vascular compression

Fig. 3.9: Progression of trigeminal neuralgia

The various drugs used to treat trigeminal

from the trigeminal nerve root. It is preferred

Microvascular Decompression Surgery

Fig. 3.13: Insertion of Teflon implants

Types of Rhizotomies Balloon Compression Rhizotomy

Percutaneous Glycerol Rhizotomy

Fig. 3.16: Ballon compression rhizotomy.

Components in Mullan Set (Fig. 3.17)

Fig. 3.17: Mullan compression set Fig. 3.18: Radiofrequency rhizotomy

Percutaneous Radiofrequency Rhizotomy Patients experience minimal pain and in most

Fig. 3.19: Gamma knife unit

The Gamma Knife Team wearing stereotactic frame, MRI is taken to

Fig. 3.21: Production of gamma rays

Fig. 3.20: Helmet

approximately 30 curies each, arrayed in a

5. Safe An alternative theory states that AFP is a disease

1. Transcutaneous electric nerve stimulation 1. Mild

Systemic Factors BMS Protocol