03 02-06 benign mucosal-lesions_of_the_oral_cavity1

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  • No reported cases of dysplastic alteration or transformation to carcinoma. Important is to separate this condition from leukoplakia.
  • Multiple biopsies may be required. Also include all suspicious areas such as erythematous, granular, ulcerated, or indurated areas. Chemoprevention is an active area of research for mild dysplasia (retinoids, antioxidants, COX-2 inhibitors)
  • 03 02-06 benign mucosal-lesions_of_the_oral_cavity1

    1. 1. Benign Mucosal Lesions of the Oral Cavity Grand Rounds 3/2/2006
    2. 2. Outline  Case study  Mucosal lesions  Ulcerative lesions  Conclusions
    3. 3. Case Study  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
    4. 4. Leukoedema
    5. 5. 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
    6. 6. Oral Leukoplakia
    7. 7. Oral Leukoplakia
    8. 8. 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
    9. 9. 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
    10. 10. Proliferative Verrucous Leukoplakia
    11. 11. 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
    12. 12. Site of Leukoplakia  Risk of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites
    13. 13. Epithelial Dysplasia
    14. 14. 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
    15. 15. Oral Hairy Leukoplakia
    16. 16. 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
    17. 17. Oral lichen planus
    18. 18. 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
    19. 19. 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
    20. 20. Candidiasis
    21. 21. Candidiasis  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
    22. 22. Candidiasis  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
    23. 23. Candidiasis  Confirmation with KOH smear, tissue PAS or silver stains  Treatment- topical or systemic, polyene,azoles
    24. 24. Oral ulcerative lesions  Acute  Chronic  Recurrent
    25. 25. Acute ulcerative  Bacterial Acute necrotizing ulcerative gingivostomatitis Poor oral hygiene, Punched-out ulcer at interdental papillae, seen in young adults with poor nutrition, heavy smoking Streptococcal gingivostomatitis B hemolytic strep, bright red gingivae Oral tuberculosis Gonococcal stomatitis
    26. 26. Syphilis
    27. 27. Acute ulcerative  Syphilis Congenital syphilis- Hutchinson’s incisors, “moon’s molars” Primary-painless, indurated, ulcerated, usually involving the lips, tongue Secondary- mucous patches, split papules Tertiary- Gummas, can involve palate, tongue  Fungal Oral Candidiasis Histoplasmosis- disseminated form, oropharyngeal lesions may present as ulcerative, nodular, or vegetative. Biopsy will provide the diagnosis
    28. 28. Primary Herpetic Gingivostomatitis
    29. 29. 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
    30. 30. Recurrent herpes simplex
    31. 31. Erythema Multiforme
    32. 32. Acute ulcerative  Erythema multiforme Mucocutaneous 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.
    33. 33. 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
    34. 34. Erythema Multiforme  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
    35. 35. Acute ulcerative  Lupus erythematosus- chronic discoid and systemic lupus erythematosus (SLE) forms Discoid 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
    36. 36. 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, athritis, and inflammatory disease of eyes and GI tract.
    37. 37. Acute ulcerative  Drug reactions Barbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, and dilantin
    38. 38. Chronic Ulcerative
    39. 39. Chronic ulcerative  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
    40. 40. Pemphigus vulgaris  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 azathioprine 5% mortality with immunosuppression
    41. 41. Chronic Ulcerative  Mucous Membrane (Cicatricial) Pemphigoid Autoantibodies directed at molecular components of the basement membrane Most common Head and Neck sites- oral, followed by ocular, nasal, and nasopharynx sites Ocular scarring- symblepharon, corneal opacification, entropion
    42. 42. Mucous Membrane Pemphigoid  Diagnosis is with immunofluorescence showing linear immune deposits along the basement membrane  Site directed therapy. Oral cavity- topical vs. systemic steroids.
    43. 43. 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
    44. 44. Major aphthous ulcer
    45. 45. Recurrent ulcerative  Recurrent aphthous stomatitis (RAS) Frequency range of 20-40% of population, most common non-traumatic form of oral ulceration Data indicates a greater prevalence among those in professional groups, higher socioeconomic status, and non-smokers
    46. 46. RAS  Seen in a variety of conditions Crohn’s disease, Behcet’s syndrome, gluten-sensitive enteropathy, food hypersensitivity (nuts, spices, chocolate) Certain medications- NSAIDS, B-blockers, K+channel blockers Sweet’s syndrome- acute febrile neutrophilic dermatosis PFAPA- Periodic fever, aphthous ulcers, pharyngitis, and adenitis Familial variety
    47. 47. PAS  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)
    48. 48. 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.
    49. 49. Case Study  Prodrome  Rash present, major aphthous ulcers, genital findings  No eye findings  No prior history
    50. 50. 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
    51. 51. 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.

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