ORAL MEDICINE

Diseases are classified according to:

 etiology
 morphological changes
 localization
Refers to the cause of the disease. Two groups: 1) Endogenous – hereditary diseases, genetic
malformations, 2) Exogenous – trauma, medication, infections, nutrition, stress, & 3) Local and
systemic etiology
 efflorescence
 lips, tongue, palate, buccal mucosa, floor of the mouth, gingiva
Classifications are not complete in them but used to be able to observe, classify and identify treatment
disease.
Clinical diagnosis of disease based on the morphologic changes of the oral mucosa but without knowing
the etiology of the disease it cannot be treatment disease.

LIPS
CHEILITIS EXFOLIATIVA
Etiology: - clinic and meteorological conditions
Bad habits – biting, wetting lips
Profession – glass blowers, musicians, factory workers; – cement, textiles, construction workers; -
smokers; - very dry air in home; - lack of vitamin A
The clinical features: mostly occurs on the lower lip
 Acute form: of corneous epithelium thickened, peeling as a quilt- exfoliation, erosion(=chronic),
7-10 days. Subjective: decreased mobility, tightness, dryness, -changes could take months/years
of varying intensity.
 Chronic: edema, erosions, fissures, sores, crusts, susceptibility to infections (candida bacteria)
Therapy: The causal (etiological factor removed) in different ointments (Borogal, Vaseline). Local
corticosteroids in chronic form.

ACTINIC CHEILITIS
Premalignant keratosis of the lip. Occurs mainly in adults. Most prevalent in men.
Etiology: long term exposure to the sunlight; hot, dry regions; outdoor workers (hikers, sailors); fair-
skinned people
Clinical features: lower lip
 Acute: signs of inflammation: edema, redness, tenderness, desquamation, vertical fissuring
 Chronic: epithelial atrophy, or keratosis; the epithelium becomes palpably thickness with small
grey-white patches plaques, erosions, crusts; early sign of malignant alteration in over 10% of
the cases
Diagnosis: is made by: history, clinical features, biopsy
 Possible malignant alterations: ulceration or eriosion occur; persistent peeling and crust; red and
white patches in the region of the borders of vermilion and oral mucosa; generalized atrophy of
vermillion with white focal areas.
Therapy: protection from the sun rays, sunscream with high SPF (over 25), 5-fluoroural 2 x a day for 14
days.
CHEILITIS ANGULARIS
Etiology: Mechanical factor, dental interventions, the loss of vertical dimensions (loss of posterior
teeth & bad prosthesis); fungi, staphylococcus; lack of vitamin B2, folate, iron; diabetes mellitus;
hypersalivation – constant wetting of the lips; hyposalivation – candida
Clinical features: affect corners of the mouth – symmetrically, most commonly presents as triangular
areas of erythema and edema at the both commissures, extend onto the skin, in severe cases & fissures
& sores – crust (hemorrhagic). Subjective: burning & sticking
Treatment: causal

CHEILITIS GLANDURALIS
Rarely. Chronic inflammatory of the mucosa glands in the lower lip. More common in men.
Etiology: idiopathic (unknown)
Clinical features: edema, dotted red duct channel openings; squeeze – serous exudate.
 erosions
 crust
 abscess formation

CHEILITIS APOSTEMATOSA
Bacterial infection. = Complication from the previous (cheilitis gladuralis). At least pressure from the labial
gland is drained purulent exudate. Crusts.
Treatment: antibiotics – antibiogram

CHEILITIS GRANULOMATOSA
Mischer cheilitis. It belongs to the deep cheilitis. Chronic enlargement of the lips caused by
granulomatous inflammation of unknown reason.
Clinical features: granulomatous changes only in the lips (one or both). A painless, diffuse enlargement
of the lips. The sudden emergence and exacerbation with remissions ultimately resulting in permanent lip
enlargement.
Therapy: corticosteroids per os; intralesion application of corticosteroids, surgery (means plastic surgery
for the lips)

SYNDROMA MELKERSSON-ROSENTHA
Younger people. Chrohn’s disease – oral manifestations.
Clinical features: enlargement of lip/s, lingua plicata – thickened, enlarged, paresis or paralysis of
n.facialis
= FACIAL ASSYMETRY
Treatment: corticosteroids …

SYNDROMA ASCHER
Heritage, rheumatic disease. Lips swelling, painlessedema of the eyelids, thyroid gland enlarged.

TONGUE
 FISSURED TONGUE
Congenital condition. The dorsum is devided by deep (3-4mm) irregular fissures about 1 cm in length.
Tongue is normally papillated. This appearance is of no significance. The number and the depth of the
fissure increases with age.
  GEOGRAPHIC TONGUE
Benign migratory glossitis. Etiology – unknown. Has genetic background
Clinical features: irregular demarcated areas of desquamation on the dorsum. Red areas-depapillated.
Red areas are surrounded by a yellow border. Red areas change in shape, increase in size and spread-
and resemble a map (geographic). May cause soreness on food (tomatoes). Often found in patients who
have fissured tongue. The diagnosis is clinical . The condition is not serious and there is no effective
treatment. Is a common condition
 FOLLIATE PAPILITIS
Etiology: mechanical irritation denture, an upper respiratory infection
Clinical features: on the posterolateral margins of the tongue
Papillae- swell, erosion, elongated
Located at a site of high predilection for lingual cancer
 FURRED TONGUE
Common problem in adults. Etiology: in edentulous patients, people eating a soft, non-abrasive diet
with poor oral hygiene, febrile diseases, dehydrated
Clinical features: the dorsum-particularly-posterior thirds- coated with white debris
Treatment- brush the tongue to remove the coating-this is best done in the evenings, maintain good oral
hygiene
 SUPERFICIAL BROWN STAINING
Brown discoloration of the tongue and teeth. May be caused- cigarette and smoking
drugs(iron salts), some food and beverages (cofee,tea), mouth wash chlorhexidine
Discoloration is easily removed and is of little consequences.
 BLACK HAIRY TONGUE
Etiology - Antimicrobial therapy-with broad spectrum-tetreacyclines, proliferation of chromogenic bacteria,
smoking, drugs (iron sats), poor oral hygiene
Clinical features: it is unique in appearance, an area of the dorsum (posterior thirds) develops long
filiform papilae which becomes stained brownish-black
In some patients, excessively long(1 cm) filiform papillae may cause nausea
Should be differentiated from the "Black Tongue" -papillae are not elongated
Treatment: discontinue smoking and any drugs or mouthwashes,brushing the tongue with a toothbrush ,
elongated papillae removed by a curettage
 GLOSSITIS IN DEFECIENCY STATES
Deficiency of > iron, folic acid, vitamin B12 are the cause
Disease of the small intestine(coeliac disease) may lead to malapsorption of folic acid and iron, ileal
disease (Cronhs disease) may lead to vitamin B12 malapsorption.
Clinical features there may be:
 Linear or patchy red lesion (especially in vitamin B12 deficiency)
 Depapillation with erythem(dsepappilation begins at the tip and margins of the dorsum, but later
involves the whole dorsum.
 Pallor (iron deficiency)
Treatment- is replacement therapy after the underlying cause of the deficiency has been established and
rectified.
 GLOSSITIS DUECTO CANDIDOSIS
Etiology: opportunistic infection with candida species, particularly C. albicans may result from
predisposing factors such as: broad-spectrum antibiotics, topical corticosteroids, xerostomia, immune
defects
Clinical features main findings: diffuse erythema and soreness of the tongue but there may also be
patches of thrush. DG. is clinical
SWAB from the lesions
TREATMENT-should first be directed to the predisposing factors
Patients should stop smoking and be given antifungals
 GLOSSITIS RHOMBICA MEDIANA
Was considered to be a development lesion. Current evidence suggests- it is in fact a candidal lesion
usually the patient is a tobacco smoker
Clinical features: A depapillated rhomboidal asymptomatic area in the center line of the dorsum of tongue
anterior to the circumvallate papillae. The lesion may be flat or nodular, red or red and white.
Dg. is made on clinical grounds alone.
TREATMENT- the patient should stop smoking, antifungals
 TONGUE SWELLING
Localized lump may be of various causes: congenital-lingual thyroid(midline lumps in the posterior
tongue), inflammatory-infection,abcess, traumatic-oedema, heamangioma, foreign body, cysts,
neoplasmic-fibrous lump, papilloma, carcinoma, Kaposis Sarcoma.
Generalized lingual swelling may be due to: Down's Syndrome, angioma, inflammatory edema,
angioedema, acromegaly, amyloidosis
 AMYLOIDOSIS
A rare condition characterized by deposistion in tissues of an eosinphilic hyaline material, amyloid, which
has fibrillar structure
Aetiology: Amyloid deposits-not all the same
in PRIMARY amyloid-they consist of immunoglobulin light chains
in SECONDARY and other forms of amyloid, AA proteins are found.
Clinical features: oral amyloidosis-almost exclusively seen in primary amyloidosis.
Manifestation include macroglasia, in up to 50% of patients, and oral petechiae or blood-filled bullae
Dg-biopsy is required
Oral amyloid deposits may be detected histollogicaly even in the absence of clinically apparent lesions.
Management is difficult and requires specialists care.
Surgical reduction of the tongue is inadvised because the tissue is friable often bleeds excessively and
the swelling quickly recurs.

ULCERS
APHTHOUS STOMATITIS
APHTHA SOLITARIA
Most common disease. It begins on childhood – about puberty and disappears, reappearing later.
Affecting up to 25% of the population, both sexes.
Etiology: is unclear.
A genetic predisposition – positive, family history in 1/3 of patients. //Changes in cellular immunity,
crossreactions with streptococcus, sangrius… // Viruses – HSV, HZV, CMV //Stress, trauma //
Deficiencies: iron, folic acid, vitamin B12 // Allergies (coffee, chocolate, nuts…) // smoking cessation //
Menstruation // GIDs – gastritis, ulcerative colitis, celiac disease, chrohn’s disease
Clinical features: Are ovoid or round. Recur. Have a yellowish floor. Have a prominent red inflammatory
halo. There are 3 main clinical types of R.A.S (recurrent aphthous stomatitis; based on the size and
evolution of the lesion):
 minor aphthae (Mikulicz aphthae)
 major aphthae
 herpetiform ulceration
MINOR APHTHAE – less than 1cm in diameter (4mm). Last 7-10 days without treatment. Heals without
scarring. On the non-keratinized mobiled mucosa.
Prodromal stage – sense tingling burning sensation at the site where they appear. The stage of
preulcer – red macula in place of subjective symptoms.
Ulcerating stage – in the centre of the macula defect – expanding ulcer – circular or oval, yellowish floor.
Pain – necrosis extend to the papillary epithelial layer, exposed nerve endings. The stage of healing
depends on the site and location of ulcer.
MAJOR APHTHAE – greater than 1 cm in diameter, last 4-6 weeks without treatment, scar formed during
healing stage. Palatal arches, tongue, buccal and labial mucosa. Ulcers = asymmetric, unilateral,
depressed bottom. Painful, lymphadenopathy.
HERPETIFORM ULCERS – 1-2cm in diameter, multiple, coalesce to leave large, round ulcers. Usually in
the ventral surface of the tongue, lips. Ulcers clinically resemble those of herpetic stomatitis BUT NO
GENERAL SYMPTOMS, no gingivitis, vesicles.

Diagnosis – according to history, clinical features during duration.

Therapy: Ulcers can be controlled but rarely cured. Remedied the cause. 0.2% chlorhexidine solution.
Topical corticosteroids. The solution of tetracycline in adults. 0.2% hyaluronic acid gel.

BEHCET’S SYNDROME
 Easter Asia, Mediterranean, UK. Men 20-30 years of age.
Etiology: unknown.
Immunogenetic basic with a specific association of HLA, BS and HLA-BS1 // HSV – immune complexes //
increased effect of cytokines – interleukin – 6 // hyperactivity PMNL
Clinical features: Oral manifestatios – 90% of ulcers buccal mucosa, lips… Genital changes =
ulcerations of the skin or mucous membranes. Changes in the eyes = photophobia, conjunctivitis, uveitis,
keratitis, iritis, vascular occlusion, optic nerve atrophy --- blindness.
Skin – subcutaneous nodules – ulcerated – crusts
Arthritis of large joints
Vascular thrombosis of large veins (thrombophlebitis)
CNS lesions – meningencephalitis, cerebral infraction, psychosis, cranial nerve palsies, spinal cord
lesions
Diagnosis – Recurrent oral ulceration is the key diagnosis for Behcet’s syndrome and required the
presence of two or more of the following changes:
 recurrent genital ulceration
 eye lesions
 skin lesions
 positive test - dermal hypersensitivity in intracutaneous needle - pustules occur within 24-48h
There are no diagnostic lab tests.
Therapy – same as oral ulcers

CANDIDOSIS
Definition:
 Oral candidosis and oral candidiasis are synonymous.
 Oral candidosis is the most common oral fungal infection in man and it is caused by different
Candida species, usually C.albicans
 Candida is a yeast, which is an obligate organism in humans and a normal constituent of the
digestive and vaginal tracts.
  Candida species are opportunistic pathogens, which may cause disease mostly when there are
changes in oral ecology or when the host defences have been compromised.
 Candida species reside in the oral cavities of a majority of healthy individuals as commensal
organisms, with a colonization prevalence ranging between 30% to 40%.
 The dorsum of the tongue is the primary oral reservoir, which ma, at least partially, explain why
the dorsum of the tongue is a major location of different forms of oral candidosis.
 As the term ‘’candidosis’’ implies, the cause of the disease, is the yeast Candida. Candida
species may cause an ‘’opportunistic’’ infection, under certain predisposing host factors.
 Local and systemic host factors often co-exist and act in a synergistic fashion.
 Virulent yeast-related factors play a role in the development of disease too.
Local host factors:
 Loss of integrity of the oral mucosa.
 Thin or ulcerated epithelium, resulting from an ill-fitting denture, or after anticancer chemotherapy
or head and neck radiotherapy, allows for Candida to adhere on the epithelial cells, penetrate the
mucosa and cause infection.
 Heavy smoking, non-specific leucoplakia and other oral mucosal diseases make oral mucosa
prone to the development of candida infections.
 Xerostomia results in decresed flushing action and in reduced antifungal components of saliva,
thus enhancing the development of candidosis.
 Local corticosteroids, via local immunosuppression, also promote oral candidosis.
Systemic host factors
 Immunodeficiency and immunosuppression are important host factors, especially in view of the
increasing numbers of patients with acquired immunodeficiency syndrome/AIDS and of
individuals who receive corticosteroid or immunosuppressive or cytotoxic treatment (organ and
bone marrow transplant recipients, patients with malignant disease, patients with autoimmune
disorders).
 Broad spectrum antibiotics may enhance the development of candidosis mainly by locally
distributing oral ecology.
 Dietary factors such as poor nutrition, iron and vitamin deficiencies locally after the integrity of the
oral mucosa, promoting the development of candidosis.
 Endocrine disorders, such as diabetes mellitus, haematologic diseases, malignant diseases, age
(neonatal, elderly) also enhance candidosis.
Clinical presentation
 Oralcandidosis may present with a variety of clinical patterns or forms. We can consider: acute
forms (erythematous, pseudomembranous), chronic forms (erythematous, pseudomembranous,
hyperplastic), candida-associated lesions (angular cheilitis, denture-related stomatitis, median
rhomboid glossitis), and oral manifestations of systemic mucocutaneous candidosis.
 Some patients may exhibit more than one clinical form of candidosis and in more than one oral
site, thus presenting with multifocal candidosis. Oral candidosis is, in most cases, endogenous
and most often remain superficial and localized in the oral mucosa.

PSEUDOMEMBRANOUS CANDIDOSIS (THRUSH)

 Appears as semi-adherent, whitish or yellowish, soft, drop-like or confluent membranes or
plaques. These pseudomembranes can be wiped off, and reveal a red underlying mucosa.
 Any mucosal surface may be affected.
 Patient may complain of a burning sensation, xerostomia, dysgeusia or anorexia (loss of
appetite).
  Pseudomembranous candidosis is rarely painful.
ERYTHEMATOUS CANDIDOSIS (ATROPHIC)
 Erythematous candidosis (atrophic) is the most common type. Before the era of AIDS, it was
commonly seen after the use of antibiotics. This acute painful lesion is characterized by a diffuse
loss of the filiform papillae of the dorsum of the tongue, which appears red.
 Erythematous candidosis in HIV disease appears as asymptomatic red areas or patches usually
located on the dorsum of the tongue and the hard palate.

ANGULAR CHEILITIS
 Angular cheilitis (perleche) of candida aetiology presents as red fissures radiating from the
commissures of the mouth, sometimes covered by dry, crusting membranes. The scaling and
fissuring may extend on the vermillion border, thus, presenting similar to exfoliative cheilitis.
Angular cheilitis in general, is bilateral, and may develop alone or with other forms of candidosis.

*Angular cheilitis and erythematous candidosis on the tongue of a 69 year-old male. Patient wore
dentures. Red fissures radiate from both comissures, while a red patch can be seen on the dorsum of the
tongue.

CHRONIC ATROPHIC CANDIDOSIS

Denture stomatitis
 The area involved is usually the palate covered by partial or complete upper dentures.
 The mucosa is bright red
 The explanation for this lesion are thought to be trauma from a poorly fitting denture, loss of
vertical dimension, failure to leave the denture out at night.

CHRONIC HYPERPLASTIC CANIDOSIS

 Chronic hyperplastic candidosis is a rare form of candidosis presenting as white plaque, hard and
rough to the touch, often without symptoms and usually occur on the buccal mucosa.
 This lesion should heal after antifungal treatment.
 Oral hyperplastic candidosis may also be seen in association with immunologic or endocrine
abnormalities.

CHRONIC MUCOCUTANEOUS CANDIDOSIS

Chronic mucocutaneous candidosis is a term given to a group of heterogenous disorders characterized
by persistent superficial candida infection of the mouth, skin, and nail beds, sometimes producing
granulomatous masses over the face and scalp.
The principal clinical features include chronic oral candidosis, chronic cutaneous candidosis, and chronic
vulvovaginal candidosis.
 Oral candidosis has been noted in more than 90% of all CMC patients.
 The tongue can become enlarged, fissured, and may have hyperplastic nodules on the lateral
borders. Painful angular cheilitis is frequent.
The CMC is associated with a variety of primary immunodeficiency such as severe combined
immunodeficiency syndrome (SCID, congenital thymic aplasia), hyperimmunoglobulin E syndrome,
myeloperoxidase deficiency, and endocrine disorders, especially Addison’s disease and
hypoparathyroidism.

Diagnosis – A presumptive diagnosis can be made on the bases of the different clinical forms of
candidosis. Thus, a good knowledge of the clinical forms of the infection is the first important step. The
definitive diagnosis of candidosis is established by the clinical signs, in conjunction with positive direct
microscopic findings or cultures of swabs taken from the mucosal tissues and the undersurface of the
denture are extremely valuable in confirming that a fungal infection is present.
Treatment – The management of patients with oral candidosis involves the identification and elimination
of predisposing factors and the use of antifungal medications. If the predisposing factor can not be
eliminated or treated, candidosis is likely to recur. At present the aim of antifungal treatment is the healing
of the clinical infection. The time required to achieve healing of the clinical infection is usually one to two
weeks.
 Several antifungal agents are available for topical or systemic use, depending on the form and
the extent of the infection, the Candida species isolated and, most importantly, the condition of
the host and the underlying pathology.
 Nystatin (formulated as suspension) was the first effective antifungal drug, for topical use. It is not
absorbed across the gastrointestinal tract.
 Amphotericin B (as suspension and lozenge), clotrimazole (as troche), and miconazole (as gel)
are also useful for tropical treatment. Miconazole oral gel is best for the treatment of angular
cheilitis.
 Ketoconazole (as tablets) due to its potential liver toxicity, is not introduced as initial therapy.
 Fluconazole and itraconazole are triazole agents, formulated, as capsules and suspension, and
for both topical and systemic use.

DEEP MYCOSIS

HISTOPLASMOSIS by the fungus histoplasma capsulatum

 Infection results from inhaling dust contaminated with droppings from infected birds.
 In endemic areas such as the Mississippi and Ohio River, serologic evidence of previous
infection may be found inup to 75% to 80% of the population.
 Primary infection is mild, manifesting as self-limiting pulmonary disease that heals leaving
fibrosis.
 Oral involvement is secondary to pulmonary involvement and occurs in disseminated phase.
 Oral lesion appear as a papule, a nodule, an ulcer or a vegetation.
 The cervical lymph nodes are enlarged and firm.
Diagnosis – Is made by culture of infected tissues or exudates. Biopsy.
Treatment – Is successfully managed with use of IV amphotericin B for 10-12 weeks.
Side effects – Abnormal renal function, cardiac arrhythmias, bone marrow suppression.
BLASTOMYCOSIS by Blastomyces dermatitidis
 Is found as a normal inhabitant of soil and therefor this infection is found in agricultural workers.
 Infection begins by inhalation causing a primary pulmonary infection with symptoms such as
malaise, low-grade fever, mild cough.
 If the infection goes untreated – symptoms will worsen to include shortness of breath, weight loss.
 The most common appearance of oral lesions is a nonspecific, painless verrucous ulcer with
indurated borders.
Diagnosis – Is made on the basis of biopsy and on culturing the organisms from tissue.
Treatment – IV amphotericin B for 8-10 weeks causes resolution of the disease.

MUCORMYCOSIS by sacrophytic fungus that normally occurs in soil.

The fungus is non-pathogenic for healthy individuals and can be cultured from the human nose, throat
and oral cavity. Infection occurs in individuals with decreased host resistance such as those with poorly
controlled diabetes or hematogenic malignancies or those undergoing cancer chemotherapy or
immunosuppressive drug therapy. There are:
 Pulmonary
 Gastrointestinal
 Rhinocerebral form
RHINOMAXILLARY FORM begins with the inhalation of the fungus, invades arteries and causes
thrombosis.
 May spread from the oral and nasal region to the brain causing death.
The most common oral sign is ULCER of the palate, which results from necrosis due to invasion of a
palatal vessel. Ulcer is large and deep.
Early diagnosis is essential. Negative culture do not rule out mucormycosis (difficult to culture form
infected tissue). Biopsy must be taken.
Treatment – Surgical debridement of the infected area and systemic amphotericin B for 1-3 months.

MULTIPLE PERSISTENT ULCERS are mainly caused by: skin diseases such as lichen planus,
pemphigoid or pemphigus, gastrointestinal disease, blood disease, immune defect or drugs.

DIFFERENT DIAGNOSIS OF ORAL ULCERATION

The most important feature of ulceration is whether the ulcer is single, multiple or persistent. Multiple
non-persistent ulcers are most commonly caused by viral infection s or aphthae, when the ulcers heal
spontaneously, usually within a week to a month. If this is not the case or if the ulcers clinically do not
appear to be aphthae, an alternative diagnosis should be considered. A single ulcer that persists may be
caused by neoplasia such as carcinoma, or by chronic trauma (ulcus decubitalae), or a chronic infection
such as syphilis, tuberculosis.

ALLERGIC REACTION
 Allergy as an adverse reactions that results from a patients being immunologically hypersensitive
to an exogenous agent – allergen.
 Hypersensitivity reactions were defined into 4 groups.
 Hypersensitivity 1 type – immediate and mediated by IgE antibodies.
 Type 4 reactions – delayed hypersensitivity reactions and mediated by sensitized T-lymphocytes.
CONTACT CHEILITIS
 An inflammatory reaction provoked by sensitizing actions of chemicals: lipstick, bactericidal
agents, dentifrices (contain pyrophosphate compounds), epimine (containing materials used for
temporary crown and bridges), other dental materials, nail varnish, essencial oils-eugenol,
peppermint, cinnamon, clove and spearmint in food and other materials, wooden and nickel
mouthpieces of musical instruments…
Clinical features – Persistent irritation and scaling or a more acute reaction with edema and vesiculation.
Diagnosis and management – Is clinical. Patch test should be carried of the substance concerned.
Specialist referral.
Treatment – Substance must be traced and avoided. Topical corticosteroids – give symptomatic relief.

ENANTHEMA FIXUM
 The fixed drug eruption – characterised by a localized area of erythema, edema and vesiculation
in a specific area of the mucosa-palate, dorsal tongue whenever a specific allergen is
administrated.
 Salicilate, aspirin, antibiotics, fenobarbiton, sulfonamids, hloramfenikol,
*BACTRIM - sulfametoxazol + trimethoprim

ALLERGIC ANGIOEDEMA
Etiology: food: nuts; drugs: antibiotics; other allergens
Clinical features – Facial edema: cause pronounced labial and periorbital swelling. Edema involves the
tongue and neck: fatal respiratory obstruction.
 Acute allergic edema – can develop alone or may be associated with anaphylactic reactions
(and/or urticaria)
 Angioedema is characterized by the transient nature of the swelling and the lack of scaling
Diagnosis – Is clinically and form the history of atopic disease and exposure to allergen and allergy
testing (prick test).
Management – In severe cases: (real threat to the airway) = intramuscular adrenalin (epinephrine),
systemic corticosteroids, systemic antihistamines. In mild cases: oral antihistamines.

HEREDITARY ANGIOEDEMA
Hereditary angioneurotic edema (HANE) caused by a deficiency of an inhibitor of the enzyme C1
esterase – leads to continued complement activation after trauma and activation of kinin-like substances
– cause a sudden increase in capillary permeability.
Clinical features – Trauma of dental treatment is a potential trigger. HANE typically produces acute onset
of edema affecting the lips, tongue, mouth, face an neck region.
Edema may be persist for many hours and even up to 4 days and involvement of the airway is a constant
threat.
Diagnosis – Family history; Clinical features with history of edema after trauma; Blood tests – low C4,
normal C3 levels, reduced C1 esterase level.
 In 85% of cases C1 esterase levels are reduced (type 1 HANE)
 In 15% the enzyme is present but dysfunctional (type 2 HANE)
Management – Inhibitor replacemet, fresh plasma, plasminogen inhibitors

BACTERIAL INFECTIONS
  ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG)
Caused by spirochaetes and fusiform bacteria-may be present in small number in the healthy gingival
flora.
Predisposing factors
 poor oral hygiene
 smoking
 psychological stress
 chronic anxiety
 malnutrition
Clinical features
 crater-shaped ulcers from initially at the tips of the interdental papillae .
 ulcers-sharply defined by erythema and oedema their surfaces is covered by a greyish or
yelloyish slough
 removal of the slough causes free bleeding
 Lesions mainly spread along the gingival margins
 deep spread can cause rapid destruction of both soft tissues and bone producing triangular
spaces between the teeth.
 pain tenderness profuse salivation metalic taste teeth are sensitive to pressure
 ulceration may spread to adjacent oral mucosa-buccal, tongue, palate.
 oral tissue necrosis is rare in immunocompetent individuals but is a common competent of
infectious disaese in immunocompromised patients
Treatment - oral hygiene is essential, chlorhexidine mouthwash, metronidazole 200mg by mouth taken
after food 3 a day for 3 days

 CARCINOMA ORIS (NOMA)

Oro-facial noma is adisease of early childhood and extreme poverty which develops very rapidly with
serious associated diseases, such as protein deficiencies, infectious diseases, and immune diseases
(HIV).
NOMA starts with an ulcero-necrotizing gingivitis and extend onto the oral mucosa and skin with
gangerenous necrosis.
The gangerenous process starts as a painful small reddish-pirple spot or indurated papule which
ulcerates. the ulcer spreads to involve the labiogingival fold, adjacent mucosa and underlying bone.
Treatment: metronidazole, penicillin, improved nutrition

 TUBERCULOSIS
Clinical features include single chronic painful oral ulcer associated with pulmonary infection.
The ulcer is irregularl with undermined borders and covered by a grey slough. Ulceration commonly
affects the tongue but other areas of the oral mucosa may be involved, particularly towards the posterior
parts of the mouth

 SYPHILIS
Systemic, sexually transmitted infection with Treponemea pallidum
Clinical features:
primary syphilis - incubation period of 9-90 days is followed by regional lymphadenitis and a small
papule, which develops into a large painless, ulcer (chancre) with raised indurate edges, glazed surface
and then heals spontaneously in 1-2 months. Ulcer is seen on the upper lip or usually on the tongue.
secondary syphilis - develops 1-4 months after infection - oral mucous patches, split papules or ulcers are
highly infectious. A rash consists of asymptomatic pinkish (coppery) macules, symetrically distributed and
starting on the trunk.
Condylomata lata and generalized lymph node enlargement can also be present.
SYPHILIS GUMMA-begins as swelling with a yellowish centre which undergoes necrosis, leaving a
painless idolent ulcer. Ulcer is rounded with soft, punched out edges. the floor is depressed and pale in
appearance. It can heal with severe scarring which may distort the soft palate or tongue, or perforate the
hard palate or destroy the uvula.
Dg - serological confirmation of the infection is essential. VDRL(veneral disease reference laboratory)test,
Fluorescent treponemal antibody absorption test , FTA-abs test, Treponemal ELISA assay
Treatment-HIGH DOSES penicillin; 1-up to 1 month; 2,3 up to 12 weeks

 ACTINOMYCOSIS
Is a chronic supparative infection caused by ACTINOMYCES israeliii
Common in the normal mouth
Injuries-dental extractions, fractures of the jaw preceede infection.
Common in men between 30-60 years of age.
Clinical features - swelling near the angle of the jaw is red or purplish, firm and slightly tender.
The skin breaks down as discharged sinus form. Healing leads to scarring and in the absence of
treatment, a large fibrotic mass can form, covered by scarred and pigmented skin on which several
sinuses open.
Treatment: penicillin should be continued for 6 weeks

VIRAL INFECTION
Herpesvirus-DNA viruses charcteerized by latency and can be reactivated during immunospression.
the herpes group of viruses includes:
 Herpes simplex virus type 1, 1(HSV-1.-2)
 Herpes varicella-zosteervirus(VZV)
 Epstein-Barr virus(EBV)
 Cytomegalovirus(CMV)
 Human herpes virus type-6,-7,-8

Herpes simplex infections

HERPETIC STOMATITIS(gingivostomatitis)-primary infection-HSV type 1

 typically a childhood infection, seen between the ages of 2 and 4 years
 incubation period of 4-7 days
 intraepithelial vesicles which may be widespread
 the oral vesicles break down to leave oral erosion that are initially pit point but which fuse to
produce irregular painful erosions
 prominent gingival edema erythema
 a tongue is often coated the patient will have a history of generalized prodomal symptoms that
precede oral lesion by 1-2 days
 these symptoms include fever, headache, nausea and vomiting cervical lymph node enlargement
RECURRENT HERPETIC INFECTIONS
HSV-1- remains latent in the trigeminal gangilion
Factors can reactivate the virus: fever, sunlight, trauma, immunosuppression ® and produce HERPES
LABIALIS, INTRAORAL HERPES

RECURRENT HERPES LABIALIS -cold sores, fever blisters

The lesion- preceded by a prodormal period of burning. This is accompanied by edema at the site of the
lesion, followed by formation of a cluster of small vesicles.
Each vesicle is from 1-3 mm in diameter with the size of the cluster ranging from 1-2 cm.
The vesicles rupture producing areas on which form crust.

RECURRENT INTRAORAL-HERPES
Similar in appearance to HERPES LABIALIS, but vesicles break rapidly to form ulcers.
The lesions are typically a cluster of small vesicles or ulcers, 1-2 mm in diameter, clustered on a small
portion of the palate, alveolar ridge, buccal mucosa. Dg. is largely clinical
Assay of serum atibody gives little help
Symptomatic treatment: a soft food and adequate fluid intake are important, antipyretics/analgesics-
paracetamol-releive pain, fever
Local antiseptics-0.2% aqueous chlorhexidine mouthwash

VARICELLA-ZOSTER INFECTIONS
Varicella(chickenpox)- is airborne infection-caused by VZV
Incubation period of 2-3 weeks, primary clinical infection may be present with chickenpox
Development of itchy maculopopualr lesions on the bach chest and face.
In some cases small areas of oral ulceration affecting the palate may precede the onset of the typical skin
rash.
Typical rash goes through macular, papular vasicualr and pustularstages before cruising.

HERPES ZOSTER(SHINGLES)
Occurs as a result of reactivation of the VZV in adult patients
VZV remains latent in the dorsal root ganglia, including trigeminal ganglion
Reactivation by immunosuppression
Zoster is not a transmissible condition, but non immune persons may contract varicells after close contact
with patients with Zoster
Mainly seen: in elderly patients, immunocompromised patients
Clinical features affects the thoracic region, but 30% is in the trigeminal region.
Pain- unilatertal, severe, toothache-like for several days prior to the onset of more characteristic
cutaneous lesions. Rash-unilateral and in the distributionof the sensory nerve involved.
Rash is like that of chickenpox it goes through macular, papular, vascular and pustular stages before
cruising and healing sometimes with scars
Mouth ulcers- if maxillary or mandibular divisions of the trigeminal nerve are involved
If the maxillary nerve is involved rash develops over the unilateral palate and vestibule
If the mandibular nerve is involved rash and pain develop over the lower unilateral face and lip ulcers and
pain are experienced on the tongue and buccal mucosa and mandibular teeth
Diagnosis and management. Dg. is obvious clinically
If the patient is seen before the rash appears a misdiagnosis of toothache may be made
Acyckovir-orally-800 mg 5× daily at an early stage, Analgesics
Symptomatic treatment for oral ulcers

INFECTIOUS MONONUCLEOSIS
Cause by Epstein Barr virus (EBV) transmitted in saliva during kissing
Occurs in adolescents and young adults
Clinical features: The incubation period of 30-50 days is followed by: fever, anorexia, sore throat with a
whitish exudate, pharyngeal edema may threaten the airway, generalized lymph node enlargement
Oral features may include: palatal petechiae-at the junction of the hard and soft palate
These are pathognomonic. Areas of pseudomembranous lesions or ulceration of the mucosa
Complications: rashes affecting the extensor surfaces of the lims in patients taking ampicillin, hairy
leukoplakia, Burkitts lymphoma, nasopharyngeal carcinoma
Diagnosis and Management: Diagnosis is made from:
Clinical features-should be confirmed serologically
Blood picture-mononucleosis-large numbers of atypical mononuclear cells in blood
Positive paul-bunnel test heterophilic antibodies
Antibody to EBV viral capsid antigen(VCA)
Management – No specific treatment is available
Symptomatic treatment(see herpes simplex)

CMV is contracted from infected saliva, urine or other body fluids after an incubation period of 20-40 days
Can be transmitted by saliva, blood and transplacentally
Hand, Foot and mouth disease
Caused by Coxackie virus A 16 but A5,A7,A9,A10 and B9
Clinical feature: the incubation period is up to a week

SKIN VESICLES-small painful surrounded by inflammatory narrow sea-on the dorsum and lateral aspect
of fingers and toes.
May affect more proximal parts of the limbs
Oral ulcers-affect the tongue or buccal mucosa; are shallow, painful, very small and surrounded by
inflammatory narow area sesembling herpetic stomatitis but WITHOUT GINGIVITIS.
Diagnosis is clinical serology is confirmatory
Treatment-no specific treatment available
Skin vesicled heal spontaneously in about a week
Mouth lesions can be treated symptomatically (see herpes simplex)

HERPANGINA
Caused by Coxsackie viruses A1 to A6, A8, A12, A16 or A22, B1 to B5
Has an incubation period of 2-6 days
Clinical features presents with: Fever, headache, anorexia, vomiting
Oral lesions consisted of multiple vesicles on the soft palate and posterior mouth
The vesicles rupture to leave round painful shallow ulcers surrounded by inflammatory narrow area
resembling herpetic stomatitis but WITHOUT GINGIVITIS
Diagnosis is clinical and serology is confirmatory
Symptomatic treatment for oral ulcers

HUMAN IMMUNODEFICENY VIRUS (HIV) INFECTION

Etiology: infection with retrovirus (RNA viruses) termed HUMAN IMMUNODEFICENY VIRUS (HIV)
damage CD4 cells-T-helper lymphocytes.
Most infections are sexually transmitted by heterosexual homosexual sex. Transmitted in blood and blood
products. Transmitted by infected mothers to their children (verically)
Clinical features: HIV infection may be asymptomatic initially, even for months or years
May cause an initial glandular fever like illness
As the CD4 cell count falls the patients develop opportunistic infections(from commensal organisms)
Oral features onon of which is specific for HIV infection
Oral lesions may include:
 candidosis
 hairy leukoplakia
 kaposis sarcoma
 gingival periodontal disease
 ulcers
 other orofacial conditions
CANDIDOSIS
pseudomemranous-seen in 60% of patients often as an early manifestation it is the most common oral
feature of HIV-related diseases. Other types of oral candidosis- erythematous candidosis-presents as
pink or red macular lesions typically on the palate and dorsum of the tongue
Linear gingival erythema- as a 2-3 mm red band like lesion of marginal gingiva
HAIRY LEUKOPLAKIA
Is another common lesion. Is a predictor of bad prognosis and possible development of lumphoma in HIV
disease. Leukoplakia may be corrugated (or hairy) and affects the lateral margins of the tongue
Caused by Epstein-Barr virus
KAPOSIS SARCOMA
About 50% of patients with HIV-associated Kaposis sarcoma may have oral lesions.
Presents initially as asymptomatic red blue or purple macules on the palate and gingiva. Progresses to
papules, nodules, ulcers and may become painful. Caused by HHV-8-DNA virus
GINGIVAL AND PERIODONTAL DISEASE
Ulcerative gingivitis and destructive periodontitis
ULCERS-different type of ulcers
 non-specific aphthous-type ulcers
 ulcers caused by herpes viruses(herpes simplex infection)
 ulcers caused by bacteria or fungi
 ulcers due to malignant neoplasm
OTHER OROFACIAL CONDITIONS
 cervical lymph node enlargement
 parotitis
 Non-Hodgkins lymphomas
 Viral infections including human papilloma virus infections
Diagnosi is sometimes clear. Patients has obvious lesions such as hairy leukoplakia cansisosis and
Kaposis sarcoma
If more than one lesion is present or if the patient is at high risk ( as intravenous drug user)
Serological confirmation is always required
TREATMENT: highly active antiretroviral therapy (HAART) has improved the quality and length of survival
for many

TRAUMATIC ORAL LESIONS

CHEMICAL BURNS
 Various chemicals or drugs
 Aspirin put in the buccal sulcus to try to relieve toothache
  Use of Mouthwashes
 Accidental ingestion of corrosive fluids.
Clinical features: Burns manifest as a white lesion with sloughing mucosa. Those caused by aspirin are
localized to buccal sulcus and adjacent buccal mucosa often along side a carious tooth.

Diagnosis and Management: Dg. is clinical. Lesions are managed by stopping exposure to the chemical
Lesion is self-healing.

ELECTROGALVANICALLY INDUCED ORAL WHITE LESIONS

Electrogalvanic curettes generated by dissimilar metallic restorations and prostheses in the oral cavity
may be an etiologic factor in oral white lesions. An electrogalvanic lesion is defined as one in close
contact with a metallic restoration and where different metals are present in the mouth.
Additional evidences are signs of corrosion of metallic restoration and where equipment is available
measurement of an electric potential difference greater than 50 millivolts between two dissimilar metallic
restoration the mouth that are considered to be related to the lesion.
Disappearance of the lesion should follow replacement of the restoration adjacent to the lesion with
nonmetallic substitute.
Malignant transformation was described in one third of the lesions.
Long term follow up is recommended even for lesions that regress clinically with elimination of the
electrogalvanic stimulus.

DENTURE RELATED STOMATITIS

Denture related stomatitis indicates as inflammatory process of the mucosa that bears a complete or
partial removable denture
"stomatitis prothetica"
"denture stomatitis"
Denture stomatitis is a common condition. it can affect 30-50% of persons who wear complete dentures.
No racial or sex predilection exists. This disorder is more frequent among elderly people as they are more
likely to wear removable dentures.
Clinical presentation:
Denture stomatitis lesions may show different clinical patterns and are more frequently found in the upper
jaw especially on the palate.
The absence of denture stomatitis in the lower jaw is probably due to the washing action of saliva.
Despite the fact that denture stomatitis is frequently asymptomatic patients may complain of halitosis
slight bleeding and swelling in the involved area, or a burning sensation.
Different classifications have been proposed but the reference classification for denture stomatitis is the
one suggested by NEWTON in 1962, based exclusively on clinical criteria:
 Newton's type 1 : pin-point hyperemic lesions ( localized simple inflammation(
 Newton's type 2 : diffuse erythema confined to the mucosa contacting the denture ( generalized
simple inflammation)
 Newton's type 3: granular surface ( inflammatory papillary hyperplasia)
Related disorders:
Denture stomatitis can occasionally be associated with different lesions of fungal origin such as angular
cheilitits, median rhomboid glossitis and candidal leukoplakia.
The etiology is best considered multifactorial but denture wearing especially when worn during the night
represents then major causative factor.

Among the etiological factors that should be considered are:

  Prosthetic factors
No denture stomatitis can exist without a prosthesis.
Ill-fitting traumatic badly-maintained dentures have been considered as the most frequent causes of
denture stomatitis.
Prosthetic traumatism is favored by denture functional deficiencies like:
 occlusal alterations
 vertical dimension alterations
 retention alterations
 unstable prosthesis
The type of material employed for its construction ( Newton's type 3 is 5-fold more frequent with acrylic
dentures than with metallic ones)
 Infection factors
Denture can produce a number of ecological changes that facilitate the accumulation of bacteria and
yeasts. Certain bacterial species like Staphylococcus species, Streptococcus species, Neisseria species,
Fusobacterium species. or Bacteroids species has been identified in patients with denture stomatitis,
although no direct relationship between bacteria and the etiology of denture stomatitis could be proved.
Candida species particularly candida albicans, have been identified in most patients.
Patients with denture stomatitis show higher intraoral concentration of fungi than individuals without this
disorder and the lesions objectively improve after antifungal drug administration.However the role of this
organism as the sole etiological factor remains unclear.

Diagnosis
The clinical presentation of erythema and edema on the palatal mucosa covered by the denture base (nut
not beyond) is a diagnostic finding. A smear of the palate, Swab cultures can demonstrate the presence
of Candida species.

Treatment
Good oral hygiene is mandatory. The mouth must be kept as clean as possible and a rinse after meals
should be performed. Local factors which promote growth of yeasts such as smoking or wearing the
dentures throughout the night, must be discouraged. Dentures should be removed for as long as possible
and definitely overnight. Dentures should be brushed in warm, soapy water and soaked overnight in an
antiseptic solution such as bleach ( 10 drops of household bleach in a denture cup), chlorehexidine ( not
when the denture has metal components), or in any solution suitable for sterilizing baby's feeding bottles.
Denture fitting and occlusal balance should be checked to avoid trauma.
A new prosthesis should be made, if necessary. Dentures must be adequately polished and glazed as
pores increase denture contamination by oral microorganisms.
Newtons type 1 and 2 denture stomatitis have been successfully treated with a low energy lasers to
reduce inflammation of the supporting mucosa.
Inflammatory papillary hyperplasia usually needs to be surgically removed ( by scalpel, cyrosurgery,
electrosurgery or with a laser beam) before the denture is placed, although mild cases may respond to
antifungal treatment.
Antifungal medications are recommended when yeasts have been isolated, or when lesions do not
resolve with hygiene instructions.
First choice treatment is the topical application of nystatin or miconazole.
Resistance to nystatin is rare the drug is administered as an oral suspension with an unpleasant taste.
Miconazole is available as gel but it tastes better.
Systemic antifungal drugs (i.e. fluconazole, itraconazole, ketoconazole) are almost exclusively reserved
for patients with systemic factors that condition the development and persistence of candidiosis such as
immunosuppression or diabetes.

Prevention
It is mandatory to include denture stomatitis prevention in oral health care programs.
A preventive program should include:
 A routine basis inspection of the oral cavity for screening for this disorder, even when the lesions
are asymptomatic.
 Perform good oral hygiene.
 Appropriate denture-wearing habits, instructing the patient to take his/her denture out of the
mouth for 6-8 hours each day.
 Patients with partial dentures should undergo periodic professional plaque control.

MUCOSITIS
Mucositis is an inflammatory-like process of the oral mucosa due to radiation in head-neck region or
chemotherapy. It is characterized by atrophy of squamous epithelial tissue vascular damage and an
inflammatory infiltrate concentrated at the basement region. Epithelia atrophy is followed by ulceration.
During a course of curative radiation about 80% of the patients will develop different grades of mucositis.
The early radiation reaction causes local discomfort as well as difficulties in drinking, eating, swallowing
and speech. In chemotherapy the incidence and severity of mucositis is influenced by type of anti-
neoplastic drugs and related to tumor type.

Clinical presentation
The first clinical signs of radiation-induced mucositis occur at the end of the first week of a conventional
seven-week radiation protocol ( daily dose of 1.8 to 2.0 Gy, five times a week). A white discoloration of
the oral mucosa, which is an expression of hyperkeratinization of the epithelium, followed by erythema, is
initially seen. In other cases a white discoloration may be observed in combination with areas of erythema
or erythema may appear first. The above clinical signs represent the GRADE 1 mucositis and are mostly
asymptomatic. Towards the end of the second or around the third week of radiotherapy small foci of
ulceration can be observed corresponding to the GRADE 2 mucositis. Patient complains of mild pain and
can take soft diet. Severe GRADE 3 mucositis presents as ulcers covered by pseudomembranes
affecting large areas of the oral mucosa. Pseudomembranes are very painful to rub off, while the patient
complains of severe pain and dysphagia (difficulty in oral intake) and can take liquids only.
GRADE 4 mucositis represents even more severe ukceration covering almost akk mucosal surfaces.
Patients complains of severe pain can take liquids only or may necessitate nasogastric tube or parenteral
support.
Mucositis is most severe in the soft plate followed by the mucosa of the hypopharynx floor of the mouth
check base of the tongue lips and dorsum of the tongue. Patients with compromised oral mucous
membranes secondary to alcoholism and/or excessive smoking exhibit the most sever mucosal lesions.
Mucositis generally persists throughout radiotherapy and develops at its maximum grade at the end of the
irradiation period.
One to three weeks or more depending on the severity are needed for mucositis to heal after the
completion of therapy. Erythematous ulcerates and xerosmotic (dry) oral mucous serves as site for the
development of secondary infection.
About one out of three patients are anticipated to develop pseudomembranous candidosis during
radiotherapy. The local inflammatory reaction caused by candidosis adds to the radiation induced
unflammatory process. Chemotherapy-induced mucositis initially seen between 3 and 7 days after
infusion of the antineoplastic drugs. Presents as atrophy, followed by ulcerations within few days.
The maximum grade of mucositis is observed usually after 11 days, and could last for several days to
weeks. Secondary local infection will delay healing. The most common infection in the oral cavity during
or shortly after radiotherapy and chemotherapy is candidosis. Many patients become colonized intra-
orally with Candida albicans during cancer therapy. The prevalence of positive Candida cultures
increased from 43% at baseline to 62% at completion of cancer therapy and to 75% during the follow up
period.
Some believe that the oral mucositis is aggravated by fungal infections.

Diagnosis
The diagnosis of grade 1 mucositis is based on the presence of asymptomatic mucosal erythema
evaluated on clinical grounds and need no treatment. It has to be differentiated from erythematous
candidiosis a common infection during head and neck radiotherapy and antineoplastic chemotherapy,
which needs antifungal treatment.
GRADE 2 mucositis with small foci of ulcers is also diagnosed upon the clinical presentation.
While it has to be differentiated from an early intraoral herpetic infection or from a superimposed
candidosis.
The most distressing grade 3 and 4 mucositis is diagnosed upon its clinical presentation of superficial
ulcerations covered by pseudomembranes that are very painful rubbed off.
These pseudomembranes ulcerations are to be differentiated from pseudomembranes candidosis
consisting of whitish easy to rub off, pseudomembranes.
The laboratory isolation of yeasts from Swab, taken from the lesions may be helpful but is not critical for
the diagnosis.
Severe mucositis is important to be differentiated from the often clinically identical, herpes simplex virus-1
reactivation. Herpetic infection if not diagnosed and treated promptly, may further aggravate mucositis
and delay healing thus compromising antineoplastic protocol
Early initiation of ulcerative mucositis or herpes labialis may assist in suspecting a herpetic infection.

Treatment
No drugs can prevent mucositis
Ice cooling can minimize chemotherapy induced mucositis.
Relief of pain and discomfort ( anesthetics, analgesics)
Treatment of concomitant secondary mucosal infections (bacteria, fungi and viruses): antiseptics, topical
anti-fungals, antiviral treatment.

PIGMENTS
= physiologic melanotic lesions

 RACIAL PIGMENTATION
*Pigmentation of the gingiva does NOT involve the marginal gingiva!
Not directly related to the color of the skin.

 EPHELIDES
Are brown small macules (5mm). Appear on the sun-exposed areas of the perioral skin and on the lips.
Darker during light exposure. The vermillion border of the lower lip is most commonly involved.
Histologically shows increased melanin pigmentation in the basal cell layer without an increase in the
number of melanocytes.

 PIGMENTED NEVI
Asymptomatic brown or bluish macules less than 1cm across.
Intramucosal – occur on the gingiva, labial mucosa.
Blue nevi – occu on the hard palate.
Clinical significance – lies in their clinical similarities to oral melanoma and their predilection for hard
palate.
Excision biopsy is recommended to exclude the malignancy
® Appear also in the soft palate!

 CHEMICALLY INDUCED MELANOSIS

 Smoking-associated melanosis
The smoker’s melanosis is related to a component of tobacco, predilection for the male sex, related with
female hormones. Smoker’s melanosis is a specific entity characterized by pigmentation of the oral
mucosa, predominantly on the anterior attached gingiva of the mandible and interdental papillae. Buccal
mucosa, palate, tongue.
 Drug-induced melanosis
Tetracycline causes pigmentation of bones and teeth. The single most common is minocycline induced
pigmentation. Usually seen as brown melanin deposits on hard palate, gingiva, tongue. After
discontinuing minocycline, the pigmentation of the bone in most patients is irreversible.
Few drugs, such as antimalarials and tranquilizers = bluish-black discoloration
Chemotherapeutic agents (busulfan), oral contraceptives + phenothiazine could produce a
hyperpigmentation (buccal + gingival mucosa)
Drug-induced oral mucosal pigmentation resolves within weeks to months when the drug is withdrawn
(permanent sometimes)
 AMALGAM TATTOO
Localized, oral pigmentation that usually involves the gums or alveolar mucosa – close to the teeth
restored. Less frequently in buccal mucosa and floor of the mouth. Due to erosions of the mucosa during
restorative procedures or tooth extraction. Asymptomatic lesion, under 0.5cm in size. Tattoos can be
solitary or multiple, grayish-brown to bluish-black macula.
 HEAVY METAL-INDUCED PIGMENTTION
Rare, accidental or occupational expose to heavy metals. Bismuth – once used as a treatment for syphilis
produces diffuse oral pigmentation as well as a thin black line involving the marginal gingiva.
Lead poisoning can result in diffuse pigmentation and a blue-lead line (Burtonian line) along the
interproximal and free gingival margins.
These lines (bismuth, lead) seem to be result of the reaction of the heavy metals with hydrogen sulphide
in the inflammatory areas of the gingiva. Patients with good oral hygiene can significantly decrease the
incidence of pigmentation.
Oral features of mercury poisoning include diffuse greyish discoloration of the alveolar gingiva. The level
of mercury released from dental amalgam has not been reported to have adverse systemic effects.
Arguria – (silver pigmentation) produce a permanent diffuse bluish-gray pigmentation with a shiny metallic
luster, most frequently in the hard palate. The deposition of silver can be observed as a dark black
discoloration after the application of silver nitrate to oral ulcerations.
Þ Systemic toxicity with heavy metals was observed with greater frequency in the past when they were
employed as medicinal, still occur and may be easily overlooked.
  DISEASE-ASSOCIATED MELANOSIS
 PEUTZ-JEGHERS SYNDROME
Includes intestinal polyposis and melanotic spots on the face, mouth and less commonly found in hands
and feet. It is an inherited dominant disease. Are multiple ephelides – like spots on the lips + oral mucosa,
around the nose + eyes.
Pigmented macules, often confluent + varying in size and shades of brown
® lips and buccal mucosa
Any or all oral sites may be involved.
 ADDISONS DISEASE
Disease is due to bilateral destruction of the adrenal cortices/tuberculosis, histoplasmosis or autoimmune
destruction of adrenal parenchyma.
Clinically – there is hypotension, weakness, nausea + vomiting, abdominal pain, diarrhoea + weight loss.
A diffuse pigmentation of the skin (skin of the face and hands) and mucous membranes is one of the
early symptoms of disease. An examination of oral cavity ® diffuse pigmentation of gingiva, lateral
margins buccal mucosa. Diagnosis: ACTH injection test is a screening test. Treatment: corticosteroids,
skin pigmentation returns to normal after the treatment.

 ORAL MELANOACANTHOMA
Benign, mixed proliferation of keratinocytes and melanocytes. Related to a local trauma.
Clinically ® elevated and well-circumscribed , solitary, asymptomatic plaque. Location: buccal, palatal,
gingival mucosa, lips.
Histologic exam: benign tumor with acanthosis, hyperpigmentation, presence of normal melanocytes.
Generally regress after removal of traumatic irritants or following performance of a biopsy. Persistent
lesions may respond to topical corticosteroids. Histologic continuation is required

 ORAL MELANOMA
Is a proliferation of melanocytes arises on a skin and more rarely on oral mucosa. Malignant. Develops in
the 40-70y. On hard palate + maxilla gingiva. Clinical presentation: macular pigmentation, asymptomatic,
dark brown or black macula ® progressively increases in size. Melanomas can infrequently appear as
rapidly enlarging nodules ® result in ulceration, bleeding, pain and loosing of teeth.
Symptoms are asymmetry, irregular margins + mixture of colours.
Classification:
 Radial growth phase
 Exhibiting a vertical growth
 Amelanotic
Treatment: Primarily by radical surgery. Immunochemotherapy. Usual screening of the oral cavity should
be performed regularly. Be excised.

ORAL WHITE LESIONS

Appear white because they are composed of thickened keratin, which assumes a white appearance when
wet.

DEFINABLE WHITE LESIONS

 LINEA ALBA (buccal mucosa)
Presents on a whitish-grey horizontal line on buccal mucosa (parallel to the adjacent occlusal plane of
teeth. Bilateral and represents a hyperkeratonic response. No treatment.
  LEUKOEDEMA
Observed normal, buccal mucosa. Affected areas shows a greyish-white line. Diagnosis established by
gently stretching + affect tissue. No treatment.

 FORDYCE SPOTS
Can occur in any age + any sex (more males). Are yellowish soft granules, the oral mucosa caused by
ectopic sebaceous glands. Seen in buccal mucosa, retromolar region + lips (upper). Can be seen as
creamy yellow dots along the border between the vermillion + the oral mucosa of the upper lip. Benign
and no treatment indicated.

 WHITE SPONGE NEVUS

Rare, benign autosomal dominant condition affecting the nonkeratinized stratified epithelia of the mucosa,
nose, esophagus, genitals and anus. Present bilaterally as thicker, diffuse, corrugated. During early age.
No treatment indicated.

 CHRONIC CHEEK, TONGUE, LIP BITING

Presents self-inflicted trauma in which patient habitually bites or chews their cheek, tongue, lip. Buccal
mucosa frequently present. Psychologic stress can be a factor. Females are more commonly affected.
Lesions present as greyish-white, frayed or shaggy patches intermixed with areas of erosion or
ulceration. Treatment not necessary. Extreme cases – professional counselling.

 FRICTIONAL KERATOSIS
Chronic irritation by sharp edges of tooth, dentures… Friction of mastication in the partially dentate on
edentulous ridge. Characteristic by hyperkeratosis of mucosa, limited to the areas being traumatized. In
early stage ® patch are pale + translucent but later become dense + white. Diagnosis is clinical. It is
benign lesion. Treatment: should be eliminated the traumatic lesion (return normal after 2-3 weeks).
Biopsy for reveal white lesion.

 TOBACCO-INDUCED LESIONS
Smokers palate
Occur hard palate of pipe. Male older than 45y. 1. kind of lesion: greyish-white appear with small
umbilicated swelling with red centre (2.) ® represent . Easily diagnosed, not considered as premalignant
lesion. Treatment: stop smoking, no biopsy, no treatment.

 REVERSE SMOKERS KERATOSIS

Habit of reverse smoking. In reverse smoking, the lit end is held inside the mouth. Exhibit palatal changes
include leucoplakia, mucosal thickening, fissuring, pigmentation, nodularity, erythema, and ulceration.
Oral squamous cell carcinoma may develop with chronic lesions.

 SMOKERS TOBACCO
Moist stuff in most common form. Stuff is tucked between the gingiva and the lip or cheek. 2 nd form is
chewing tobacco placed in the cheek. Usually contains one or both 2 basic ingredients.
Paan is placed between the teeth and the buccal mucosa and gently chewed or sucked over a period of
several hours. Lime has been shown to release reactive oxygen species from extracted areca nuts.
Snuff’s dippers patch characteristic keratotic white lesion exhibits a corrugated or wrinkled appearance
under the area of tobacco placement. The severity of the lesions depends on a variety of factors. Lesions
resolve within 2 to 6 weeks.

 SUBLINGUAL KERATOSIS
Etiology is unknown. Soft, white plaque in the sublingual region with a wrinkled surface. On floor of the
tongue. Diagnosis: According to clinical + biopsy

 ORAL SUBMUCOUS FIBROSIS (1966)

As precancerous chronic disease that may affect the entire oral cavity ad that sometimes extends to the
pharynx. Have been implicated in the development of OSF. Associated with tobacco use + vitamin
deficiency. It is extremely rare in white population. Also the condition affects more females 45-54y. OSF is
always associated with subepithelial inflammatory reaction followed by fibroelastic changes of the lamina
propria, associated by epithelial atrophy. Process leads to stiffness of oral mucosa ® result in trismus –
protrusion of tongue !!Diagnosis: palpate fibrous bands; tough, leathery texture of the mucosa; blanching
of the mucosa.

 PAPILLOMA
Human papilloma virus. Cauliflower-like lesion with white colours. Treatment – should be excised and
examined histologically. Buccal mucosa, dorsal surface of tongue present mostly.

 VERRUCAE
It is caused by HPV, usually being transmitted from skin warts (verruca vulgaris). The prevalence is
higher in patients with sexually transmitted diseases or those who are immunocompromised. There are
warty or smooth-surfaced papules. Treatment – removed by excision biopsy, laser or cryosurgery.

 CONDYLOMA ACUMINATA
(Genital warts) – Usually seen on the tongue or fauces in sexually active persons. It is caused by HPV. A
higher prevalence is seen in patients with sexually transmitted diseases or those who are
immunocompromised. Condyloma acuminate are found on the tongue or palate as warty or smooth-
surfaced papules. Treatment – Is by excision biopsy, laser or cryosurgery.

LEUKOPLAKIA
Definition
Leukoplakia is the most common premalignant or potentially malignant lesion of the oral mucosa.
Leukoplakia is predominantally white lesion of the oral mucosa that cannot be clinicopathologically
characterized as any other definable lesion.
The term leukoplakia is a clinical descriptor only and should not be used once histological information is
available .

Epidemiology
The incidence and the prevalence of leukoplakia vary in different parts of the world. In general reported
prevalence ranges from 0.2 to 5% with remarkable regional differences - India(0.2 to 4.9%) Sweden
(3.6%) Germany (1.6% )Holland (1.4%).
Leukoplakia is seen most frequently in middle aged and older men. Gender distribution is also variable.
Men are more affected in some countries while this is not the case in western countries.

Clinical presentation
Leukoplakia can be either solitary or multiple. Leukoplakia may appear on any site of the oral cavity the
most common sites being : buccal mucosa alveolar mucosa floor of the mouth tongue lips and palate
Classically two clinical types of leukoplakia are recognized homogenous and non homogenous which can
co exist. Homogenous leukoplakia is defined as a predominantly white lesion of uniform flat and thin
appearance that may exhibit shallow cracks and that has a smooth wrinkled or corrugated surface with a
consistent texture throughout. This type is usually asymptomatic. Non homogenous lekuplakia has been
defined as a predominant white or white and red lesion ( eritroleukoplakia )that may be either irregularly
flat nodular (speckled leukoplakia ) or exophytic (exophytic or verrucous leukoplakia ). These types of
leukoplakia are often associated with mild complaints of localised pain or discomfort.
Proliferative verrucous leukoplakia is an aggressive type of leukoplakia that almost invariably develops
into malignancy. This type is characterized by widespread and multifocal appearance often in patients
without known risk factors.
In general non homogenous leukoplakia has a higher malignant transformation risk but oral carcinoma
may develop from any leukoplakia
The etiology of leukoplakia is still unclear although tobacco seems to be the major inductor factor its
association cannot be determined in all cases. A variety of smokeless tobacco habits have been reported
as leukoplakia inductors eg snuff chewing these lesions have shown to have a low malignant
transformation risk. A higher malignant transformation rate has been reported in candida infected
leukoplakias. However there is no agreement whether candida infection is the cause of leukoplakia or is
an infection superimposed in a preexisting lesion.
The possible implication of human papillamovirus hpv and other virus has been studied high risk hpv 16
and 18 have been associated with oral cancer. Other factors such as alcohol inadequate intake vitamin
deficiencies example vitamin a and c.
Areca nut betel different mouthwashes chronic traumatic irritation poor oral hygiene poor socioeconomic
status galvanism and even genetic factors have considered and studied in leukoplakia

Diagnosis
Leukoplakia has clinical and histopathological approaches.
Provisional clinical diagnosis: clinical evidence from a single visit using inspection and palpation as the
only diagnostic means. Definitive clinical diagnosis clinical evidence obtained by lack of changes after
eliminating suspected etiologic factors during a follow-up period of 2-4 weeks(in some cases the time may
be longer). Histopathologically proven diagnosis definitive clinical diagnosis complemented by biopsy in
which histopathologically no other definable lesion id observed.

Prognosis and complication

The malignant transformation rate of oral leukoplakia varies from 0 to 33% overall 3 to 8% of leukoplakias
develop malignant transformation in an average follow up period of five years. Any leukoplakia could
transform into carcinoma even those which did not show epithelial dysplasia initially ( or in which
dysplasia happened to be absent from biopsy taken). The main problem is that the malignant
trasnsformation cannot be raliably predicted yet. Some data could help identifyinmg the possible risk.
Leukoplakias show a high trasnformation risk when they:
 Affect women
 Persist for long periods
 Appear in non smokers
  Are located on the floor of the mouth or tongue
 Are seen in patients with a previous head and neck carcinoma
 Are non homogenous
 Are infected by candida
 Show epithelial dysplasia

Of all these factors the presence of epithelial dysplasia still seems to be the most indicator of malignant
potential. Regular checkups of these patients is essential probably every 3,6 and then 12 months both in
treated and untreated patients.

Prevention
There is no known therapy to prevent development of oral leukoplakia and there is no known therapy to
prevent oral squamous cell carcinoma developing from oral leukoplakia.
It has been demonstrated that a healthy life style and the abstinence of tobacco are the best way to
prevent both. Fresh fruits and vegetables may have a protective effect in the primary prevention of oral
cancer and precancer. Early diagnosis and treatment of leukoplakia can reduce high rates of oral cancer
morbidity and mortality in many countries.
Screening programs for oral cancer and precancer may be indicated in individuals at risk such as
predetermined age 40-70 years gender males in some countries) risk habits.
(tobacco alcohol users)and in certain geographic areas with a high incidence of oral cancer.

ORAL LICHEN PLANUS

Definition: Oral lichen planus is a common chronic inflammatory mucocutaneous disorder that tipically
affects the skin and/or mouth; can also affect other non-oral mucosal surfaces such as the genitals, anus
and pharynx, and rarely the conjuctiva and oesophagus.
Epidemiology: Lichen planus affects 1-2% of examined populations. It most typically arises in the middle
to late aged females, although can arise in childhood and adults. It has a worldwide distribution. There
appear to be no notable increased risks associated with particular ethnic groups.
Clinical presentation: Oral lichen planus has a bilateral distribution that typically affects the buccal
mucosa, dorsum and ventral surfaces of the tongue and/or gingiva. Other mucosal surfaces can be
affected but palatal involvement is particularly rare. The variable clinical presentations of oral lichen
planus comprise white patches, erosions, ulcers and, very rarely, blisters.
The classification of the clinical presentation of lichen planus can be split into the following:
Reticular oral lichen planus – this is the most common presentation, manifesting as a network of white
striations. These lesions are often painless, although patients may complain of a slight roughness or
dryness to the affected mucosal surfaces.
Plaque-like oral lichen planus – this manifests as areas of homogenous whiteness. This typically arises
on the buccal mucosa or dorsum of tongue and may be more prevalent amongst those who are smokers.
Papular oral lichen planus – this manifests as small white raised areas approximately 1-2 mm in diameter.
These again typically arise on the buccal mucosa and dorsum of tongue, although may also present on
other mucosal surfaces.
Erosive oral lichen planus – this is sometimes termed atrophic oral lichen planus. In this form there are
areas of redness within the aforementioned white patches. Patients with this type of disease often
complain of oral soreness.
Ulcerative lichen planus – there are frank ulcers within the areas of whiteness. Patients complain of
continued soreness, this being particularly severe with spicy or acidic foods.
Bullous lichen planus – this rare presentation manifests as small vesicles or blisters (bullae) within the
white patches.
Patients with disease involving the gingiva may have areas of white patches or striae superimposed upon
redness of the gums. The latter is often termed desquamative gingivitis and can be extremely painful.
Likewise the oral features may precede, accompany or follow lichen planus affecting other sites:
Skin: rash characterized by shiny flat-topped purple polygonal and pruritic papules varying from pin point
size to larger than a centimetre. They are often crossed by fine white lines (Wickham striae). As the lichen
planus papules clear they are often replaced by areas of brown discoloration, especially in dark skinned
people. LP may affect any area, but is most seen on the: front (flexor surface) of the wrists, lower back,
ankles.
Aetiopathogenesis:
It is believed that oral lichen planus represents a cell-mediated immunological reaction within the affected
tissues. The precise trigger for this is not known. The precise cause of oral lichen planus remains unclear
in most cases.
Diagnosis: The diagnosis of oral lichen planus is initially based upon the clinical presentation of bilateral
white patches with or without erosions, ulcers or blisters, typically affecting the buccal mucosa, dorsum of
the tongue and gingiva. Biopsy with subsequent histopathological examination of affected tissue is
essential to exclude other disease that may mimic oral lichen planus – such as lupus erythematosus. In
addition, it is advantageous to undertake a biopsy to identify possible areas of cellular atypia (dysplasia)
within the involved tissue.
Treatment: Patients with white patches are generally asymptomatic, although they may complain of mild
oral roughness, soreness or dryness of the oral mucosa. This generally does not require treatment.
Individuals with erosive, ulcerative or bullous disease generally tend to have oral discomfort, particularly
with spicy or acidic foods, and thus require treatment.
The management of painful oral lichen planus usually comprise:
-Relief of painful symptoms – this can be achieved with regular use of 2% lidocaine gel to painful areas;
-Treatment of definitive disease – topical corticosteroids are the mainstay of treatment of oral lichen
planus. A wide range of agents are suggested to be effective. These include: Triamcinolone acetonide
(0,1%), Betamethasone mouthrinse (500 mg dissolved in 10-15ml of water) used as a mouthrinse up to 3
times daily, Clobetasol ointment (0,05%) applied to painful areas 3-4 times daily, Fluticasone spray (50
mcg per puff) – sprayed on affected areas up to 3-4 times daily.
Prognosis and complications: Oral lichen planus persists for many years, resolving rarely. The principle
aim of treatment is to heal areas of painful erosion, ulceration or blistering. Long-standing oral lichen
planus rarely gives rise to any notable complications. However, there is some concern that lichen planus
of the mouth may have some malignant potential. This possible association with oral squamous cell
carcinoma remains controversial. It is presently suggested that 1-3% of patients with long-standing oral
lichen planus may develop squamous cell carcinoma of the mouth.
Isolated areas of increasing whiteness, redness, speckling (areas of redness and whiteness) or solitary
ulceration unlikely to reflect local trauma require further specialist. Investigation (usually by
histopathological investigation of lesional tissue.) All patients with oral lichen planus should be advised of
the controversy regarding the malignant potential of oral lichen planus, and provided with appropriate
preventative advice – particularly the avoidance od tobacco and alcohol and betel, and empirically a diet
rich in vitamins A,C and E and the maintenance of good oral hygiene.
Prevention: At the present time, as the cause of lichen planus is unknown, there is no specific
preventative programme for this disorder.
 ERYTHEMA MULTIFORME

Definition
ERYTHEMA MULTIFORME (EM) is an acute inflammation disorder usually self limiting and often
recurrent.
Epidemiology
young adults males from 20 to 40 years of age and most commonly affected although children over 3
years and teenagers represent 20% if cases. It is seen worldwide
Although many factors may be involved in the EM often the basic cause of the disease is unkown. In
contrast to skin EM, which is mostly caused by :
 Systemic drugs (barbiturates, sulfonamides, non steroidal antinflammatory drugs and antibiotics)
 infective agent-herpes simplex virus (HSV) infection
 immune conditions BCG or hepatitis B
 immunization sarcoidosis graft versus host disease inflammatory bowel diseases
 food additives or chemicals benzoates, nitrobenzene perfumes
The etiologic agents remain unclear in many oral EM cases.

Clinical presentation
EM often preceded by systemic symptoms such as malaise fever headache. The classic skin lesion of EM
consists of concentration erythematous rings separated by skin of near normal appearance the tissue in
the centre of the target may be erythematous.
These lesions disappear in about 1-4 weeks leaving a transiently hyperchronic skin. Extremities
especially extensor surfaces as palm and soles are typically involved usually with a symmetric distribution
whereas face neck and trunk are less commonly involved. Early oral EM presents erythematous spots
which progress to blisters that quickly break resulting in erosion and/or ulcers. Lesions are irregular but
well demercated sometimes associated with pseudomemranous or crusting. Any area of the mouth may
be involved especially the lips and the anterior part of the oral cavity ( tongue and buccal mucosa).
Gingival involvement can also be seen.
Symptoms range from mild discomfort to severe pain that can leave patients unable to open the mouth to
speak or to eat.
The reported incidence of oral lesions in EM varies considerably ranging from 25 to 70% but several
authors have reported exclusive intraoral lesions in EM patients.
Oral lesions include:
 Lips: cracked, bleeding, crusting and swollen
 Ulcers: diffuse and widespread
 Oral lesions progress through macules to blisters and ulceration typically most pronounced in the
anterior parts of the mouth
 EYE involvement-cause lacrimation and photophobia
 Genital lesions are painful and may result in urinary retention

Forms of EM:
Minor form
Affects only one side
May affect the mouth alone or skin or other mucosa
Major EM ( Stevens-Johnson syndrome)
Almost invariably involves the oral mucosa
Causes widespread lesions also affecting the eyes pharynx larynx esophagus skin and genitals.
With a prodorme in about 30% of cases may begin within 1-3 weeks of starting a new drug lasts 1-2
weeks before the onset of the mucocutaneous manifestations and presents with flu-like symptoms, sore
throat, headache, fever, arthralgias. May present also with bullous and other rashes, prneumonia,
arthritis, nephritis, myocarditis.

Diagnosis
Since there are no specific markers for EM, the diagnosis based mainly on the clinical features and
history. All the patients referred to a stomatological clinic should also have a dermatological examination (
including genitalia) in order to evaluate the presence of lesions involving the skin and/or other mucosal
sites. The role of precipitating agents such as herpes infection and drugs should be established.
Herpes involvement can be established by evaluating the following criteria recurrent EM, history of
recurrent Herpes recent clinical herpes ( preceding EM by 3 weeks) and demonstration of a recent HSV
infection. Drug involvement is possible if there is a chronological relationship between drug use and
eruption.
Major form-may need hospital care should be treated with systemic corticosteroids.
Minor form-Oral hygiene should be improved with 0.2% aqueous chlorhexidine mouthwash and treatment
with topical corticosteroids

Prognosis and complication

In case of severe SJS the mortality rate ranges from 10% to 30%. in cases of oral EM, EM minor and
moderate SJS, appropriate therapy generally gives a complete resolution within 10-15 days.

Prevention
There are no means to reliably prevent EM episodes nor recurrences. some authors suggest the
prophylactic use of an antiviral agent such as aciclovir in patients with oral recurrent EM.
However there are insufficient data to support this. it is important to remember that drug use can cause a
wide range of EM manifestations. For this reason at the first episode of EM it is imperative to look for any
drug that could be responsible, in order to avoid future administration- since the severity of the
manifestations often increases in further episodes and in case of severe SJS this could be lethal.

LUMPS AND SWELLINGS

LOCALIZED
PREGNANCY GINGIVITIS AND EPULIS
Etiology: is an exacerbation of chronic gingivitis by pregnancy
Poor oral hygiene + increased progesteron level – changes in gingiva
Pregnancy gingivitis is characterized by:
-soft, reddish enlargements of the gingival papilla
-mainly labial location of swelling
-gingival bleeding on eating or tooth-brushing
Pregnancy epulis – pregnancy tumor, granuloma gravidarum
-localized gingival lump
-appears about the second month of pregnancy and reach a peak at the eight month
Conservative treatment is indicated, unless an epulis interferes with occlusion or extremely usightly, when
may be excised. In any event, oral hygiene instruction is indicated.

FIBROUS EPULIS
-is induced by chronic irritation
Clinical features:
-variable inflammatory changes account for the different clinical presentation
-red, shiny and soft lump
-pale, stippled and firm
-commonly, lesions are round, painless, pedunculated arising from the marginal or papillary gingiva,
adjacent to sites of irritation (sharp edge of the carious cavity, calculus)
Rarely involve the attached gingiva and rarely exceed 2 cm in diameter.
Dg is clinical – needs to be removed and examined histologically

„LEAF FIBROMA“ is fibrous overgrowth, forms under a denture but may be difficult to see unil lifted away
from its bed.

PYOGENIC GRANULOMA (PG)

-is a common reactive neoformation of the oral cavity, which is composed of granulation tissue and
develops in response to local irritation or trauma
-used term does not adequately describe the lesion's characteristics. The term „pyogenic“ implies pus
production; however, no pus-producing microorganisms are associated with PG
-PG is a relatively common oral lesion, possibly affecting 1% of general population with predilection for
the female sex
-PG is not ant infectious but a reactive lesion, due to local irritating factors. Therefore, PG is included in
the large group of inflammatory hyperplasias
-The traumatic agents responsible for gingival PG are gingival and periodontal irritants, including plaque
accumulation, supra- or infra-gingival calculus, overhanging margins of crowns and fillings, implantation
or foreign material etc.
-The predominant location for PGs is the gingiva, the labial maxillary gingiva being the most frequently
affected site
-Any other oral location may be affected, including the lips, buccal mucosa, and tongue
-PGs present clinically as exophytic, widely based or pedunculated lesions. The surface is smooth or
rough and deep red in colour and the consistency is softer than the rest of the mucosa
-Ulceration is a frequent finding, sometimes covered by a fibrinous pseudomembrane (a whitish
appearance). This white necrotic material may resemble pus.
-Depending on the duration and degree of fibrosis, the lesion may be firmer and paler.
-The size of PG is usually between 1-3cm, although much larger lesions are not uncommon
-Surgical excision of PGs is the treatment of choice
-Elimination of the responsible chronic irritating factor is always importance

GIANT CELL EPULIS

-usually found in the gingival margin between teeth anterior to the permanent molars
-Its development may be related to the resorption of deciduous teeth
-The swelling is rounded, soft and purplish
-Can be a manifestation of hyperparathyroidism – specialist referral is thus indicated
-Biopsy is required to establish the diagnosis
-Treatment is surgical

WEGENER'S GRANULOMATOSIS
-is a rare, potentially lethal disseminating granulomatous condition and is seen mainly in adults
-unknown cause
-initially affects the respiratory tract, and is followed by widespread arteritis of small vessels and renal
damage
-may produce painless, progressive gingival enlargement that may have fairly characteristic „strawberry-
like“ appearance
-DG: Reqiures biopsy and pulmonary and renal investigations. Specialist care is needed.

GENERALIZED

HEREDITARY GINGIVAL FIBROMATOSIS

-is an uncommon condition trasmitted by an autosomal dominant gene
-presents as generalized gingival enlargement
-the changes involve the papillae and later the attached gingiva
-may cover the teeth
-the gingiva is usually of normal colour but firm in consistency, and the surface is initially smooth and
becomes stippled
-DG is clinical. Surgery is indicated.

LEUKEMIA
-gingival enlargement – the presence od leukemic inflitrate- gingiva become packed and swollen with
leukemic cells
-most commonly in monocyte leukemia
-gingiva is purplish and may become nectrotic and ulcerate
-leukemic inflitrates also involve the palates, alveolar bone
-the lesions regress after chemotherapy

DRUG-INDUCED GINGIVAL OVERGROWTH

-occurs as a side effect of some systemic medications
-is aggravated by poor oral hygiene
The pharmacological agents mainly associated with gingival overgrowth are:

-PHENYTOIN
-CYCLOSPORIN
-NIFEDIPINE

PHENYTOIN (anti-epileptic drug)

-often produces variable amount of gingival enlargement,which affects the interdental papillae first, and
later involve the marginal and attached gingiva
-buccal and lingual gingivae are involved
-early lesions may be soft and red and later gingiva is firm,pale

CYCLOSPORIN –is an immunosuppressive drug, used to suppress the cell-mediated response after
organ transplants; may produce gingival hyperplasia or the interdental gingiva

NIFEDIPINE (an antihypertensive drug) and other calcium-channel blockers

-gingival enlargements are characterized by a nodular lobulated spongy aspect and secondary
inflammatory that may induce oedema, ulcerations and bleeding on brushing
-gingiva is red, puffy and tend to bleed
SCURVY- deficiency of vitamin C
- Lesions include: diffusely swollen, boggy and purplish gingiva with purpura and haemorrhage

SARCOIDOSIS
-chronic disease of unknown cause, in which granulomas form in the lungs, lymph nodes, salivary glands
and the mouth
-oral lesions – painless swellings
-the most frequently affected sites are gingiva, lips, palate and buccal mucosa
-gingival enlargement affecs the attached gingiva

PLASMA CELL GINGIVITIS

-is a rare benign condition of the gingiva characterized by dense infiltrate of normal plasma cells into
subepithelial gingival connective tissue
-the cause is still not fully understood
-has been associated with chewing gums, use of mint-candy toothpaste ingredients, chilli pepper,
environmental & food flavoring allergens
-clinically, the patient presented with severe inflammation of the gingival tissues, from the free gingival
margin to the mucogingival junction

PEMPHIGOID

is the term given to a group of uncommon sub-epithelial immunologically mediated vesiculobullous

disorders (SEIMD) which can affect stratified squamous epithelium characterized by damage to one of
the protein constituents of the basement membrane zone (BMZ) anchoring filaments components.

A number of other sub-epithelial vesicullobullous disorders may produce similar clinical features(table1)

table 1: uncommon sub-epithelial vesiculobullous disorders:

 pemphigoid variants
 acquired epidermolysis bullosa (EBA)
 toxic epidermal necrolysis(TEN)
 Erythema multiforme
 Dermatitis herpetiforms
 linear IgA disease
 chronic bullous dermatosis of childhood

the main types of pemphigoid that involve the mouth are:

 mucous membrane pemphigoid(MMP) in which mucosal lesions predominate but skin lesions are
rare
  oral mucosal pemphigoid patients with oral lesions only without a progressive ocular scarring
process and without serologic reactivity to bullous pemphigoid (BP) antigens
 bullous pemphigoid (BP) which affects mainly the skin
 ocular pemphigoid which is sometimes termed cicatricial pemphigoid (CP) since it may cause
serous conjunctival scarring.

Mucous membrane/oral pemphigoid

mucous membrane pemphigoid (benign mucous membrane pemphigoid) is an uncommon chronic

disease twice as common in females and usually presenting in the fifth to sixth decades.

Mucous membrane pemphigoids is an autoimmune type of disorder with a genetic predisposition.

The precipitating event is unclear in most cases but rare cases are drug induced(eg by furosemide or
penicillamine).

it is characterized immunologically by deposition of IgG and C3 antibosies directed against the epithelial
basement memrane zone(BMZ)

There are also circulating antibodies in BMZ components and desmosomes of the lamina ........?

the antibodies damage the BMZ and histollogically there is a sub-basilar split.

Clincal features

The oral lesions affect especially the gingivae and palate and include bullae or vesicles which are tense
may be blood filled and remain intact for several days

persistent irregular ulcers appear after the blisters rupture anf if on the gingivae can produce
desquamative gingivitis -the most common oral finding.

This is characterized by erythematous ulcerated tender gingiva in a patchy rather than continuous
distribution.

The majority of the people with MMP have only oral lesions but general involvement can cause great
morbidity and untreated ocular involvement can lead to blindness . Nasal laryngeal and skin blisters are
rare.

Diagnosis

the oral lesions of the pemphigoid may be confused clinically with pemphigus or occasionally erosive
lichen planus erythema multiforme or the subepithelial blistering conditions shown in table1

biopsy of prelesional tissue with histological and immunstaining examination can therefore be essential to
the diagnosis

Management

spontaneous remission is rare and thus treatment is indicated. Specialist advice is usually needed.

An opthalmology consultation can be needed .

The majority of cases respond well to topical corticosteroids. Non-steroidal immunosupresive agents may
be needed if the response is inadequate.

severe pemphigoid may need to be treated with systemic corticosteroids.

PEMPHIGUS

pemphigus is a group of rare potentially life-threatening chronic disease characterized by epithelial

blistering affecting cutaneous and/or mucosal surfaces.

There are several varients with different autoantibody profiles and clinical manifestations but the main
type is pemhigus vulgaris this includes an uncommon variant pemhigus vegetans.

pemphigus vulgaris is seen mainly in middle aged and elderly females of Mediterranean Arabs,
Ashkenazi jewish or south Asian descent.

Pemphigus vulgaris is an autoimmune disorder in which there is fairly srong genetic background.

Rare cases have been trigered by medications ( especially captopril, penicillamine, rifampine and
diclofenac) or other factors.

The autoantibodies are directed against stratified squamous epithelium desmosomes .

Damage to the Desmosomes leads to loss of cell-cell contact (acantholysis), and thus INTRA-
EPITHELIAL vesiculation.

Clinical features

pemphigus vulgaris typically runs to chronic course, causing blisters, erosions on the mucosa and blisters
and scabs on the skin.

oral lesions are common(95%) may be an early manifestation (50%).

Blisters rapidly breakdown to leave erosions seen mainly on the palate (soft palate and posterior hard
palate),buccal mucosa,lips and gingiva white lesions usually comprise severe desquamative or erosive
gingivitis, flaps of peeling tissue with red erosions or deep ulcerative craters are seen, mainly on the
attached gingiva)

The NIKOLSKY sign(the spreading of a blister by pressure) is positive.

Diagnosis

to differentiate pemphigus from other vesiculobullous diseases, a careful history and physical examination
are important, but biopsy of prelesional tissue, with histological and immunostaining examination are
crucial.

serum should be collected for antibody titres.

Management
Before the introduction of corticosteroids, pemphigus vulgaris typically was fatal, mainly from dehydration
or secondary systemic infections.

Current treatment, by systemic immunosupression, has significantly reduced the mortality to about 10%.

Specialist care is mandatory.