Oral Diseases

Introduction:

Module content guide.

Outline

Prior Knowledge (For student to revise) Anatomy and histology of the oral mucosa.Defense mechanisms of the Oral Cavity.Microbiology of the oral cavity and of

infectious diseases. Oral Ulcerative Lesions.. Oral Pigmentations Oral White Lesions

Revision: The Normal Oral Mucosa Transition zone between skin and gastro intestinal mucosa. 3 main types:

Masticatory mucosa. (attached gingiva, Hard palate, dorsum of tongue

Lining Mucosa. (floor of the mouth, ventral surface of the tongue, buccal mucosa)

Lingual Mucosa.( filiform, fungiform and circumvalate papillae-taste buds)

Differ from skin in the following ways: Papillary dermis and reticular dermis are indistinguishable. Have a greater vascularity Lack hair follicles

SDL: Draw the structure of skin and the oral mucosa. List the differences between skin and oral Mucosa)

Revision: The Normal Oral Mucosa Epithelium:

Stratified squamous epitheliumKeratinised (Masticatory) or non

keratinised (lining)Contains: Melanocytes, Merkel cells,

Langerhans cells tissue macrophages) and Lymphocytes.

(SDL: What is the function of each of these different types of cells)

Revision: The Normal Oral Mucosa Masticatory Mucosa.

Adapted to resist forces of mastication Keratinised Lines attached gingivae, palate and dorsum of the

tongue Fused to mucoperiosteum by dense collagenous

band Has a dense collagenous corium which in in certain

areas contains fat and minor salivary glands.

SDL: Describe the appearance of normal healthy gingivae)

Revision: The Normal Oral Mucosa Lining Mucosa

Covers parts of the mouth not subject to masticatory forces. Floor of the mouth, buccal mucosa, alveolar mucosa, soft palate, and ventral surface of the tongue.

Non Keratinised epithelium with short wide or absence of rete processes.

Corium is less dense and bound to underlying muscle or alveolar bone

Contains varying amounts of fat, minor salivary glands and sebaceous gland (Fordyce spots) on labial and buccal mucosa.

Revision: The Normal Oral Mucosa Lingual Mucosa;

Specialised epithelium containing taste buds.• Filiform papillae: anterior dorsum of the tongue.

Keratinised• Fungiform papillae: lateral aspects of the tongue.

Les keratinised.• Circumvalate papillae: junction between anterior

2/3rds and posterior 1/3rd of the tongue.SDL: What taste sensations are localised to the

anterior, lateral and posterior portions of the tongue? How is taste perceived by the central nervous system?

Revision: The Normal Oral Mucosa

The color of the normal oral mucosa is determined by:Epithelial thicknessDegree of KeratinisationEpithelial thicknessVascularity of the mucosaMelanin pigmentation.

Revision: The Normal Oral Mucosa

Keratoses: Conditions characterized by thickening of the epithelium and degree of Keratinisation.

Colorations: Coloration of the oral mucosa due:

• Intravascular or extravascular lesions• Pigmentations (deposition of pigment

within the epithelium. Epithelial tumors: neoplasms arising

from epithelium of the oral mucosa.

Oral ulcerative lesions:

Acute

Chronic

Recurrent

Recurrent Apthous Ulceration. Recurrent Apthous Ulcers RAS:

Aetiology: • Common. Affect 40%+ of the population. • Commonest in the first to decades of life. • May have a familial tendency• associated with food allergies e.g. cinnamon,

benzoic acid, chocolate, tomatoes, egg plant); haematological disorders; psychological stress.

• More common in professionals. Clinical Features:

• May start as a small mucosal swelling that ruptures

• Painful ulcer with a fibrinous base.• Last 10 days or more.

RAS

Classification- Minor <1.0cm, comprise 85% of all ulcers

• usually anterior portion of oral cavity, ulcerative episode 7 to 10 days, no scarring

Major > 1.0 cm deeper, more painful, posterior aspect of oral cavity, 6 weeks or longer in immunocompromised

Herpetiform- multiple pinhead-sized, pain greater than size of lesion

Treatment- symptomatic, topical steroids, for larger lesions intralesional steroids. Severe- short term systemic steroids.

RAS- Pathogenesis

No sign of vesicle or blistering formation

Lesions over non-keratinizing mucosal surfaces (labial, buccal, ventral, and lateral tongue, floor of mouth, soft palate, tonsillar pillars)

Acute ulcerative

Viral Infections Herpes simplex- 600,000 new cases annually,

prodrome followed by small vesicles that ulcerate, primary infection involves the gingiva, and can involve the entire oral cavity

Recurrent herpes simplex- prodrome present,• herpes labialis, limited to keratinized epithelium and

can involve the gingiva and hard palate

• Varicella zoster virus- distribution of trigeminal nerve

• Coxsackie- prodrome, vesicular, pharynx, tonsils, soft palate

Herpetic Stomatitis

Aetiology: HSV type I and II: Cold sores or generalised

gingivostomatitis. Associated with H/o fever, exposure to

sunlight or cold, trauma Pathogenesis:

Viral infection, Focal intracellular edema, ballooning degeneration of epidermal cells followed by acantholysis with formation of intraepithelial vesicle which then erupts.

Primary Herpetic Gingivostomatitis

Recurrent herpes simplex

Herpetic Stomatitis

Clinical Features Primary: acute fever and toxaemia. Multiple

ulcerations on lips, gingivae, and buccal mucosa. Ulcers may coalesce (come together) forming a large ulcer.

Secondary: usually associated with fever, stress, trauma or exposure to cold.

Management: Symptomatic management with bland (sodium bicarbonate mouth rinses)

Acute ulcerative lesions: Bacterial Bacterial:

Acute necrotizing ulcerative gingivostomatitis• Poor oral hygiene, Punched-out ulcer at interdentally

papillae, seen in young adults with poor nutrition, heavy smoking

Streptococcal gingivostomatitis• B hemolytic strep, bright red gingivae

Oral tuberculosis• Rare. Associated with lesions in the lung and HIV aids• Deep punched out ulcer with indurated erythematous edges

or chronic asymptomatic fissures.• Commonest on the tongue and gingivae or extraction sockets

Syphilis

Acute ulcerative

Syphilis Congenital syphilis- Hutchinson’s incisors, “moon’s molars” Primary-painless, indurated, ulcerated, usually involving the lips,

tongue: Chancre Secondary- mucous patches, split papules Tertiary- Gummas, can involves palate, tongue

Fungal Oral Candidiasis Histoplasmosis- disseminated form, oropharyngeal lesions may

present as• ulcerative, nodular, or vegetative. • Biopsy will provide the diagnosis

Acute ulcerative: Autoimmune

Acute ulcerative: Autoimmune Erythema Multiforme

Acute ulcerative: Autoimmune Erythema multiforme

Mucocutaneous hypersensitivity reactionEtiology- infectious (strong association

with HHV-1, viral, mycoplasma), drugs (antiseizure medications, sulfonamides)

Clinically- target lesions develop over the skin with erythematous periphery and central area that can develop bullae, vesicles.

Acute ulcerative: Autoimmune Erythema Multiforme

Clinically- Oral mucosa and lips demonstrate aphthous

like ulcers and occasionally vesicles or bullae may be present. Gingiva rarely involved; common sites include labial mucosa, palate, tongue, and buccal mucosa

Mucosal ulcers are irregular in size and shape, tender and covered with fibrinous exudate

Sialorrhea, pain, odynophagia, dysathria Severe EM are associated with involvement of

other mucosal sites- eyes, genitalia, and less common esophagus and lungs

Acute ulcerative: Autoimmune Erythema Multiforme

HistopathologyIntense lymphocytic infiltration in a

perivascular distribution and edema from submucosa into the lamina propria, epithelium lack antibodies, blood vessels contain fibrin, C3, IgM

Treatment- with oral involvement only can treat symptomatically/short course of corticosteroids

Acute ulcerative: Autoimmune Acute ulcerative

Lupus erythematosus- chronic discoid and systemic lupus

erythematosus (SLE) formsDiscoid type- lip, intraoral lesions, most common site is buccal

mucosa; central depressed, red atrophic area surrounded by slightly, raised keratotic border

SLE form- common site posterior hard palate, superficial ulcerations that vary in size without keratinization of the oral mucosa

Immunofluorescence shows staining of the basement membrane with immunoglobulin, and complement

Acute ulcerative: Autoimmune Acute Ulcerative

Reiter’s Syndrome- mainly young men 20 to 30. Classis triad of conjunctivitis, arthritis, and urethritis. Oral lesions range from erythema to papules to ulcerations involving the buccal mucosa, gingiva, and lips. Lesions on the tongue resemble geographic tongue

Behcet’s Syndrome- recurrent oral and genital ulcers, arthritis, and inflammatory disease of eyes and GI tract.

Acute ulcerative: Drug Induced

Drug reactions

Barbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, and dilantin

Chronic Ulcerative

Autoimmune chronic ulcerative lesions Pemphigus vulgaris- 0.1 to 0.5

patients/100,000; 70% present with upper aerodigestive lesions

Desmoglein 3 is the Pemphigus antigen

IgG, IgA Deposition of antibodies in the

intracellular spaces produces direct damage to the desmosomes

Autoimmune chronic ulcerative lesions Clinical presentation- ulceration and pain

with collapse of vesicles Lesions extend from gingival margin to

alveolar margin Oropharyngeal lesions favor lateral aspects

of soft palate to lateral pharyngeal wall Lesions heal quickly without scarring Treatment- immunosuppression with

steroids supplemented with azathioprine5% mortality with immunosuppression

Autoimmune chronic ulcerative lesions

Mucous Membrane (Cicatricial) PemphigoidAuto antibodies directed at molecular

components of the basement membrane

Most common Head and Neck sites-oral, followed by ocular, nasal, and nasopharynx sites

Autoimmune chronic ulcerative lesions

Diagnosis is with immunofluorescence showing linear immune deposits along the basement membrane

Site directed therapy. Oral cavity- topical vs. systemic steroids.

Chronic Ulcerative

Traumatic (Eosinophilic) Granuloma- self-limiting, relatively long duration, deep

mucosal injury, origin unknown Clinical presentation- 5th to 7th decade, painful

rapid onset, 1 to 2 cm in diameter with crater center and firm periphery that is white in appearance

Pathology- deep ulceration extending into skeletal muscle, intense, diffuse inflammatory infiltrate of histiocytes, endothelial cells, and eosinophils

Treatment- observation, topical or intralesional corticosteroids, excision if clinical presentation in question

Pigmented Lesions

Clinical approach and classification

Causes Melanin Blood Foreign material

Rarely painful Solitary or multiple May be neoplastic :.

Biopsy in case of suspicion of malignancy

Patterns of pigmentation. Single or localized area of pigmentation.

• Amalgam tatoo, hemagioma, melanocytic nevus, melanotic macule,malignant melanoma, kaposi’s sarcoma

Multiple or diffuse areas of pigmentation.• Hereditary hemorrhagic telangiectasia, sturge-

weber syndrome, physiologic pigmentation, addisons disease, betel nut/an chewing, peutz-jeghers syndrome, thrombocytopenia, black hairy tongue, drug-induced pigmentation, smoker associated melanosis.

•

Amalgam tatoo.

Etiology Iatrogenic Traumatic implantation

of amalgam particles into soft tissue

Clinical features In gingivae, palate,

buccal mucosa and tongue

Slate gray/black macule that does not changein appearance with time.

Diagnosis If in doubt, biopsy Histology shows

black particulate staining of collagen fibres

Management No Rx required.

HemangiomaBenign angioma consisting of a mass of blood vessels; some appear as birthmarks from word web diction.

Etiology vascular malformation.

Clinical Features Commonest on

tongue, lips and buccal mucosa

Well circumscribed flat or raised lesion with blue discoloration.

Diagnosis Blanching when pressure

applied using a glass slide (diascopy) >cavernous hemangioma

Management Non symptomatic>no Rx Symptomatic> surgical excision,

cryotherapy, sclerosing, embolization

Hemangioma

Etiology vascular

malformation.

Clinical Features Commonest on

tongue, lips and buccal mucosa

Well circumscribed flat or raised lesion with blue discoloration.

Diagnosis Blanching when

pressure applied using a glass slide (diascopy)>cavernous hemangioma

Management Non symptomatic>no

Rx Symptomatic>

surgical excision, cryotherapy, sclerosing, embolization

Sturge-weber syndrome:

Etiology Congenital

encephalotrigeminal angiomatosis> angiomatous defect associated with the distribution of the trigeminal nerve.

Clinical Features Port wine stain appearance

of face from birth +/- unilateral limited to distribution of trigeminal nerve.

Ipsilateral leptomeningeal vascular anomaly

ircumscribed flat or raised lesion with blue discoloration.

Diagnosis Blanching when

prassure applied ising a glass slide (diascopy)>cavernous hemangioma

Management Non symptomatic>no

Rx Symptomatic>

surgical excistion, cryotherapy, sclerosing, embolization

Red(Erythematous lesions)

Clinical approach and classification. Causes:

Trauma, infection, immune-related disease, neoplasia.

Painful/painless with or without ulceration.

Some may be premalignant

Usually widespread.

Patterns Painful and Ulcerate:

• Post radiation mucositis, contact hypersensitivity reaction, erosive lichen planus.

Painful with no ulceration• Acute erythematous

candidosis, geographic tongue, median rhomboid glossitis, angular cheilitis, pernicious anemia, folate deficiency

Painless with no ulceration• Erythroplakia, chronic

erythematous candidosis Painless and ulcerate.

• Squamous cell carcinoma, infectious mononucleosis

Contact hypersensitivity reactions

Etiology Sensitivity to a variety of

foreign materials Cell mediated immune

reaction Clinical features.

Diffuse lesion or localized to area of contact

Erythematous patches that may show vesicular to granular red pathches.

Diagnosis History and

exmination =/- biopsy Cutaneous patch

testing is helpful r/o candidal infection.

Management. Eliminate primary

cause Topical corticosteroid

therapy

Candidiasis

Candidiasis: Etiology

Opportunistic infection, Candida albicans Risk factors:

Local- topical steroids, antibiotic therapy xerostomia, heavy smoking, denture appliances. Systemic- Poorly controlled diabetes

mellitus, immunosuppression

Candidiasis: Clinical Manifestations

Symptoms: burning, dysgeusia, sensitivity, generalized discomfort

Angular cheilitis, co-infection with staphylococcus spp may be present

Acutely- atrophic red patches or white curd-like surface colonies

Pseudomembranous (thrush), erythematous, atrophic, hyperplastic

Chronic- denture related form confined to area of appliance

Angular cheilitis

Etiology Colonization of the

angles of the mouth by Candida spp +/- staphylococci and streptococci.

Clinical features. Erythema with yellow

encrusting at corners of the mouth.

Diagnosis Smear or swab of corners of

the mouth, palate and fitting surface of denture (if present) or oral rinse.

Swab of the anterior nares for staphylococci in the nose.

Management. Eradicate Candida reservoir in

the mouth (topical miconazole 6 hourly) or staphylococci in the nose (Topical fusidic acid/mupirocin 6 hourly)

Investigate for DM, hematinic deficiency if cheilitis persists following local Rx.

Acute erythematous candidosis Etiology:

Systemic antibiotic therapy,

inhaled steroid therapy

Immunosuppression Clinical features

Red areas especially midline of the tongue.

Painful Associated underlying

HIV infection

Diagnosis Smear, swab or imprint

culture. Management

If on antibiotics consider stopping

If using steroid inhaler advise to rinse and gargle with water after use.

Systemic antifungal e.g. Fluconazole 50mg daily X 7 days in medically compromised patent

Do RCT for HIV

Chronic erythematous candidosis Etiology

Denture wearers Clinical features

Erythematous palatal mucosa with margins corresponding to fitting surface of denture.

Occasional papillary hyperplasia.

Diagnosis Smear, swab or imprint of

the denture fitting surface and mucosal surface.

Denture surface usually heavily colonized.

Management Adequate denture

hygiene>daily mechanical cleaning and overnight soak in dilute hypochlorite (acrylic base denture) or chlorhexidine (Metal base dentures).

Topical antifungals applied to the denture fitting surface 6 hourly sped up healing process.

Candidiasis: Diagnosis and Management

Confirmation with KOH smear, tissue PAS or silver stains

Treatment- topical or systemic, polyenes, azoles

Geographic tongue.(Beign migratory glossitis, erythema migrans)

Etiology. Unknown Frequently seen in

patients with psoriasis Clinical features:

Irregular depapillatd erythematous areas surrounded by pale well demarcated margins on the dorsal and lateral surfaces of the tongue.

Lesions regress and reappear in different areas.

Discomfort on hot and spicy foods

Diagnosis Clinical appearance and

history

Management Reassurance Exclude nutritional

deficiency :. CBC, Vit B12, folate, Zinc

Dispersible zinc sulphate: 125mg dissolved in water used as a mouth wash or 2-3 mins 8 hourly for 3 months.

Median rhomboid glossitis

Etiology ? Persistent tuberculum

impar Recent evidence shows

lesions to contain Candida albicans and resolve with antifungal therapy.

Clinical features Smooth well demarcated

area of erythema at junction of anterior 2/3rd and posterior 1/3rd of the tongue.

Kissing lesion may be found on the palate.

Diagnosis Clinical

appearance Imprint culture.

Management Systemic

antifungals e.g. fluconazole and itraconazole.

Iron Deficiency anaemia

Etiology Commonest anemia Due to decreased

• Fe intake• starvation/malnutrition• Malabsorption• Chronic bleeding• Increase Fe demand.

Clinical Features. Females>male Lethargy, fatigue, palor,

shortness of breath, koilonychia

Smooth reddened painful oral mucosa

Diagnosis Clinical findings Hypochromic normocytic

blood film with reduced hematocrit.

decreased serum ferritin with increased transferrin.

Management. Determine and correct

underlying cause of iron deficiency

Iron supplements to replenish stores once etiology identified.

Pernicious anemia

Etiology Vit B12 deficiency: >autoimmune destruction

of gastric parietal cells. Dietary deficiency. (Vegans)

Clinical features Clinical signs of anemia Neurological Manifestations with peripheral

neuropathies Erythematous depapillated painful tongue

with angular cheilitis.

Diagnosis Peripheral blood film Megaloblasitic anemia, raised MCV, Schilling test. Serum antibodies to gastric parietal cells and

intrinsic factor in saliva. Management

Parenteral injections of B12 on a weekly basis the at 1-3 monthly intervals for life.

Folate Deficiency.

Etiology C.f pernicious anemia without the neurological

symptoms. Malnutrition, overcooked foods, alcoholism, small

bowel disease, pregnancy, phenytoin, methotrexate therapy.

Clinical features Symptoms of anemia As for pernicious anemia with angular cheilitis and

RAS but without neurological symptoms.

Diagnosis Megaloblastic macrocytic blood film Decreased serum and red cell folate Increased urinary excretion of

formiminoglutamic acid (FIGlu) after histidine administration.

Management. Determine and correct cause of deficiency Oral folate 5mg daily will correct

megaloblastic anemia but not neurological degeneration of B12 deficiency.

Erythroplakia

Etiology Red plaque or patch that cannot be rubbed off and cannot

be characterized clinically as any specific condition. Associated with tobacco, alcohol, invasive candida

infection, hematinic deficiency and chronic trauma. 5-10% malignant transformation rate

Clinical Features Middle aged to older population All sites especially floor of the mouth May have white patches >speckled leukoplakia

DiagnosisBiopsy>determine degree of dysplasia

within lesion.

ManagementNo dysplasia>No Rx. Observe

periodically every 6 monthsMild and severe dysplasia> manage

as for leukoplakia

Post-radiotherapy mucositis

Etiology: Effect of Ionizing radiation in therapeutic doses or as

a result of accidental exposure. Clinical features.

Multiple painful red patches and areas of ulceration. Non keratinized surfaces particularly susceptible Begins 1-2/52 after start of therapy and persists for

several weeks after termination of therapy.

.

Diagnosis Clinical history and examination Bx is contraindicated.

Management Sodium bicarbonate rinses 0.2%chlorhexidine mouth rinse Topical anesthetics. Avoid alcohol containing mouthwashes.

Squamous cell carcinoma

See notes on ulcerations, and white patches.

Infectious mononucleosis

Etiology EBV infection

Clinical Features. Childhood and early

adolescence. Lymph node

enlargement Fever and pharyngitis. Purpura or petechea in

the palate and oral ulceration

Occasional features similar to ANUG occur

Diagnosis Serologic IgM antibody

to EBV capsid antigen + Positive Paul-Bunnel test

Management No specific Rx. Hospitalization and

supportive therapy for severe cases with hepatic and splenic involvement.

Avoid ampicillin and its derivatives >cause maculo papular rash.

White Lesions

Frictional Keratosis.

Etiology: Chronic irritation f the oral

mucosa c.f. callous formation.

Trauma from eating o chewing.

Clinical features: Any site especially lips and

buccal mucosa at the occlusal line or on an edentulous ridge.

Homogenous white surface with corrugated appearance.

Diagnosis. History and clinical

appearance. Biopsy to confirm Dx

and r/o neoplasia or an inflammatory lesion.

Mucosal biopsy: hyperkeratosis without dysplasia.

Management. Remove cause. Night guard to

prevent lip and cheek biting.

Nicotinic Stomatitis.

Etiology: Tobacco related keratosis

associated with pipe, cigar or cigarette smoking.

reaction to heat and chemical substance in tobacco smoke.

Clinical features Hard palate most affected. White pathh with areas

erythema and puctate red spots representing inflammed salivary ducts orifices.

Diagnosis. H/o tobacco use and

clinical appearance Mucosal biopsy: not

indicated as low risk of malinat tranformation.

Management. Encourage to

discontinue habit. Observe or similar

lesions in areas at high risk of developing oral cancer

Dyskeratosis Congenita (White sponge nevus)

Etiology: Inherited syndrome with

premature ageing and predisposition to malignancy.

X-linked autosomal disorder Gene encodes abnormal

protein called dyskerin which is abnormal

Clinical features Become evident in 1st 10 years

of life. Reticulated skin

hyperpigmentation of the upper chest, dysplastic nail changes

Mucosal erosions and leukoplakia> 30% of lesions progress to OSCC in 10-30 years.

Rapidly progressive periodontal disease, thrombocytopenia and aplastic anemia.

Diagnosis. Clinical presentation and

history Mucosal biopsy: non specific

findings: hyperkeratosis with epithelial atrophy and dysplasia.

Management. Symptomatic. Observation of oral mucosa

and biopsy for suspicious lesions to detect malignant transformation.

Medical management of systemic manifestations.

Oral lichen planus

Oral lichen planus

0.2%- 2% population affected Usually asymptomatic, reticular from,

white striaform symmetric lesions in the buccal mucosa

T-cell lymphocytic reaction to antigenic components in the surface epithelial layer

Other variants: plaque, atrophic/erythematous, erosive

Oral lichen planus

Small risk of squamous cell carcinoma, more likely seen in the atrophic or erosive types

Studies show that dysplasia with lichenoid features have significant degree of alleic loss. Recommendation is to remove these lesions/follow patient closely

Leukoedema

Leukoedema

Diffuse, filmy grayish surface with white streaks, wrinkles, or milky alteration

Symmetric, usually involving the buccal mucosa, lesser extent labial mucosa

Normal variation; present in the majority of black adults, and half of black children

At rest, opaque appearance. When stretched dissipates

Oral Leukoplakia

Oral Leukoplakia

Oral Leukoplakia

Clinically defined white patch or plaque that has been excluded from other disease entities

Presence of dysplasia, carcinoma in situ, and invasive carcinoma from all sites 17-25% (Bouqot and Gorlin 1986)

Etiology- associated with tobacco (smoking, smokeless tobacco), areca nut/betel preparations

Oral Leukoplakia

May be macular, slightly elevated, ulcerative, erosive, speckled, nodular, or verrucous

Clinical shift in appearance from homogenous to heterogenous, speckled, or nodular, a rebiopsy is mandatory

Correlation between increasing levels of dysplasia and increases in regional heterogeneity or speckled quality

Oral Hairy Leukoplakia

Oral hairy leukoplakia

Asymptomatic, seen with systemic immunosuppression

EBV Lateral tongue bilaterally; subtle white

keratotic vertical streaks to thick corrugated ridges

Diagnosis by microscopy and in situ hybridization

Management includes establishing diagnosis and treating immunosuppression

Proliferative Verrucous Leukoplakia

Proliferative Verrucous Leukoplakia

Uncommon variant of leukoplakia Multifocal, occurring more in women,

and in those without the usual risk factors

Evolution from a thin, flat white patch to leathery, then papillary to verrucous

Development of squamous cell CA in over 70% of cases

Site of Leukoplakia

Risk of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites

Epithelial Dysplasia

Treatment

Trial of cessation of offending agent, follow-up

Guided by microscopic characterization Benign, minimally dysplastic- periodic

observation or elective excision Complete excision can be performed with

scalpel excision, laser ablation, electrocautery, or cryoablation

Chemoprevention

Conclusions

Must rule out dysplasia, squamous cell carcinoma with leukoplakia

Duration of lesion, as well as location help to narrow your differential diagnosis

Biopsy of persistent lesions can help guide management

References

Cohen, Lawrence. Ulcerative Lesions of the Oral Cavity. International Journal of

Dermatology Sept 1980, 362-373. Sciubba, James. Oral Mucosal Lesions.

Cummings Otolaryngology Head and Neck Surgery. Philadelphia, 2005, 1448- 91.

Odell,Morgan. Biopsy Pathology of The Oral Tissues, Chapman & Hall Medical 1998. 1-90.

Cotran, Kumar, Robbins. Robbins Pathologic basis of disease, 4th edition. Pgs 817-818.