Download - Benign Mucosal Lesions of the Oral Cavity1
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A, Narendra
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Case study Mucosal lesions Ulcerative lesions Conclusions
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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
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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
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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
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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
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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
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Risk of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites
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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
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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
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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
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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
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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
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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
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Confirmation with KOH smear, tissue PAS or silver stains
Treatment- topical or systemic, polyene,azoles
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Acute Chronic Recurrent
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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
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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
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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
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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.
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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
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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
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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
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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.
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Drug reactionsBarbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, and dilantin
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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
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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
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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
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Diagnosis is with immunofluorescence showing linear immune deposits along the basement membrane
Site directed therapy. Oral cavity- topical vs. systemic steroids.
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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
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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
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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
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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)
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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.
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Prodrome Rash present, major aphthous ulcers,
genital findings No eye findings No prior history
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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
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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.