A, Narendra

Case study Mucosal lesions Ulcerative lesions Conclusions

33 yo male admitted for throat pain, fever. Patient developed a vesiculopapular rash, fever as high as 103F, and thick coating on tongue, and penile ulcers following one week history of fevers and sore throat.

Physical exam- Crusted lesions over face and neck,3 mm tender lesion on upper lip, tongue-tender, thick white coating with 2 erythematous areas on tip, numerous white lesions across uvula, hard and soft palate, Neck- No lymphadenopathy

ESR- 44

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

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

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

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

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

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

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

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

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

Opportunistic infection, Candida albicans Pseudomembranous (thrush),

erythematous, atrophic, hyperplastic Risk factors: Local- topical steroids,

xerostomia, heavy smoking, denture appliances. Systemic- Poorly controlled diabetes mellitus, immunosuppression

Symptoms: burning, dysgeusia, sensitivity, generalized discomfort

Angular cheilitis, coinfection with staph may be present

Acutely- atrophic red patches or white curd-like surface colonies Chronic- denture related form confined to area of appliance

Confirmation with KOH smear, tissue PAS or silver stains

Treatment- topical or systemic, polyene,azoles

Acute Chronic Recurrent

BacterialAcute necrotizing ulcerative gingivostomatitis

Poor oral hygiene, Punched-out ulcer atinterdental papillae, seen in young adults with poor nutrition, heavy smokingStreptococcal gingivostomatitis

B hemolytic strep, bright red gingivaeOral tuberculosisGonococcal stomatitis

SyphilisCongenital syphilis- Hutchinson’s incisors, “moon’s molars”Primary-painless, indurated, ulcerated, usually involving the lips, tongueSecondary- mucous patches, split papulesTertiary- Gummas, can involve palate, tongue

Fungal Oral CandidiasisHistoplasmosis- disseminated form, oropharyngeal lesions may present as ulcerative, nodular, or vegetative. Biopsy will provide the diagnosis

Viral InfectionsHerpes simplex- 600,000 new cases annually, prodrome followed by small vesicles that ulcerate, primary infection involves the gingiva, and can involve the entire oral cavityRecurrent herpes simplex- prodrome present,

herpes labialis, limited to keratinized epithelium and can involve the gingiva and hard palateVaricella zoster virus- distribution of trigeminal nerveCoxsackie- prodrome, vesicular, pharynx,tonsils, soft palate

Erythema multiformeMucocutaneous hypersensitivity reaction

Etiology- 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.

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 mucosaMucosal ulcers are irregular in size and shape, tender and covered with fibrinous exudateSialorrhea, pain, odynophagia, dysathriaSevere EM are associated with involvement of other mucosal sites- eyes, genitalia, and less common esophagus and lungs

Histopathology- Intense 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

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 borderSLE form- common site posterior hard palate, superficial ulcerations that vary in size without keratinization of the oral mucosaImmunofluorescence shows staining of the basement membrane with immunoglobulin, and complement

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, athritis, and inflammatory disease of eyes and GI tract.

Drug reactionsBarbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, and dilantin

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

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

Mucous Membrane (Cicatricial) PemphigoidAutoantibodies directed at molecular components of the basement membraneMost common Head and Neck sites-

oral, followed by ocular, nasal, and nasopharynx sitesOcular scarring- symblepharon, corneal opacification, entropion

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

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

Traumatic (Eosinophilic) Granuloma-self-limiting, relatively long duration, deep mucosal injury, origin unknownClinical presentation- 5th to 7th decade, painful rapid onset, 1 to 2 cm in diameter with crater center and firm periphery that is white in appearancePathology- deep ulceration extending into skeletal muscle, intense, diffuse inflammatory infiltrate of histiocytes, endothelial cells, and eosinophilsTreatment- observation, topical or intralesional corticosteroids,excision if clinical presentation in question

Recurrent aphthous stomatitis (RAS) Frequency range of 20-40% of population, most common non-traumatic form of oral

ulcerationData indicates a greater prevalence among those in professional groups, higher socioeconomic status, and non-smokers

Seen in a variety of conditionsCrohn’s disease, Behcet’s syndrome, gluten-sensitive enteropathy, food hypersensitivity (nuts, spices, chocolate)Certain medications- NSAIDS, B-blockers, K+channel blockersSweet’s syndrome- acute febrile neutrophilic dermatosisPFAPA- Periodic fever, aphthous ulcers, pharyngitis,

and adenitisFamilial variety

Pathogenesis- No sign of vesicle or blistering formationLesions over non-keratinizing mucosal surfaces (labial, buccal, ventral, and lateral tongue, floor of mouth, soft palate, tonsillar pillars)

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.

Prodrome Rash present, major aphthous ulcers,

genital findings No eye findings No prior history

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

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.