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Boards' Fodder boards’ fodder Oral Disease, Part 1 by Helena Pasieka, MD CLINICAL PATHOLOGY TREATMENT ASSOCIATIONS DEVELOPMENTAL CONDITIONS Fordyce Granules 1-2mm yellowish papules on buccal “Free” sebaceous glands. None indicated. mucosa and vermillion. Asymptomatic. Geographic Well-defined red patches on lateral & Psoriasiform mucositis. If symptoms, potent topical Tongue dorsal tongue with a serpiginous white steroids. border. Fissured Tongue Multiple grooves on dorsum of tongue. Numerous grooves on dorsum of None indicated. Melkerson-Rosenthal (“Scrotal tongue”) Asymptomatic. tongue. & Down syndrome. Occasionally in Cowden, pachyo- nychia congenita & acromegaly (in set- ting of macroglossia). Hairy Tongue Hair-like elongation of lengthening of Pronounced accumulation of para- Identification & cessation of cause Smoking, poor papillae on dorsum of tongue, espe- keratosis at tips of otherwise normal and if symptoms, scraping or hygiene, oxidizing cially in central area. filiform papillae. brushing tongue. mouthwashes, and hot beverages. Median Rhomboid Well-demarcated, diamond-shaped Loss of filiform papillae. Consistently Anticandidal treatment, such as Glossitis eroded area in midline of posterior dor- associated with candidiasis. clotrimazole troches or PO fluco- sal tongue. nazole. PERIODONTAL AND GINGIVAL DISEASE Necrotizing Necrosis and/or ulceration of the inter- Non-specific, as disease etiology is Debridement of necrotic areas, Ulcerative dental papillae “punched-out papillae”. bacteria from normal oral flora. oral hygiene instruction, and con- Gingivitis Painful and hemorrhagic. trol of pain. Desquamative Diffuse painful gingival erythema. Depends on the vesiculoerosive dis- Treatment directed at underlying Erosive lichen pla- Gingivitis Epithelium readily mechanically sloughs ease it represents. Biopsy for H&E + dx. Meticulous dental prophylaxis nus, cicatricial pem- leaving behind a smooth appearance. DIF should be performed. & hygiene can decrease severity phigoid, pemphigus of lesions. vulgaris, lichenoid mucositis, linear IgA bullous dermatitis, SLE, EBA, or chronic ulcerative stomatitis Intraoral Dental Soft, non-tender, erythematous papule Necrosis surrounding a non-vital tooth. Elimination of the focus of infec- Sinus Tract on alveolar process +/- diffuse, tender tion (extraction). swelling of facial soft tissues. PHYSICAL & CHEMICAL INJURIES Fibroma Firm, smooth, nodule in the mouth; Unencapsulated mass of hyperplastic Excision is curative. usually the same color as surround- fibrous connective tissue with minimal ing tissue. Most commonly on buccal inflammation. Overlying epithelium mucosa. may show atrophy or hyperkeratosis from friction/biting. Chemical Burn Initially, erythema. In time, a wrinkled Coagulative necrosis, extending from Should self resolve after preven- white membrane representing superfi- surface either partially or fully into the tion of exposure to the offending cial necrosis appears. epithelium. agent. Morsicatio Bilateral shaggy white or shredded Marked hyperparakeratosis of the sur- Benign condition, requires no Buccarum lesions of the anterior buccal mucosa face epithelium with ragged morphol- treatment. that approximate the occlusal plane. ogy +/- spongiosis in the superficial portion of the epithelium. Colonization by bacteria can also be seen. Traumatic Ulcer Mild erythema surrounding a central Normal histology with mixed inflam- As traumatic ulcers clinically ulcer covered by a yellow fibrinopurulent mation. mimic oral SCCs, biopsy is indi- membrane. Can have a white border of cated if the ulcer does not resolve hyperkeratosis adjacent to the ulcer. Most within 2 weeks. commonly on the tongue, lips and buccal mucosa. Drug-Related Gingival enlargement of the interdental Redundant tissue of normal com- Discontinuation of the offending Gingival papillae of the anterior teeth. Edentulous position or an increased amount of drug or substitution with another Hyperplasia areas usually spared, but can involve collagen with a normal density of drug of the same class may areas under poorly maintained den- fibroblasts. Often with a plasmocytic result in cessation/regression. tures. infiltrate. Extirpation of the excess gingival tissue is the treatment of choice. ALLERGIC AND CONTACT DISEASE Contact Stomatitis Variable; cinnamon and dental amalgam Lichenoid mucositis, epithelium may Discontinuation of the offending most common. Cinnamon causes shag- show hyperkeratosis, basilar crowding product. Polishing or replacing Helena Pasieka, MD, is gy, white hyperkeratotic areas on the lat- and atypia, atrophy of the spinous the dental work with inoffensive eral tongue & buccal mucosa. Amalgam layer, lymphocytic exocytosis +/- material. a second year resident causes superficial erosions w/radiating ulceration. in the department of white striae localized to the buccal dermatology at Johns mucosa adjacent to a restoration. Recurrent Painful, <5 mm diameter, round or oval Non-specific. Early lesions show spon- Mostly supportive. Potent topical Hopkins University. Aphthous creamy-colored “cookie-cutter” ulcers giosis, usually show prominent fibrin- steroids may shorten duration of Stomatitis with an intense erythematous halo. ous neutrophilic membrane. ulcer. Complex aphthosis may require therapy with oral colchi- cine, dapsone or thalidomide. irinections D Residency p. 4 • Summer 2012 boards’ fodder Oral Disease, Part 1 (continued) by Helena Pasieka, MD CLINICAL PATHOLOGY TREATMENT ASSOCIATIONS Do you have an ALLERGIC AND CONTACT DISEASE (continued) interesting Boards’ Behçet’s Disease Aphthae usually multiple, <6 mm diam- Perivascular lymphocytic and mono- Topical anesthetics, NSAIDs for Fodder? We’re eter, lasting approximately 1-3 weeks. cytic cellular infiltration +/- fibrin symptoms of arthritis and inflam- expanding our Ocular involvement is the clue. deposition in the vessel wall and sur- matory skin lesions. Colchicine, rounding tissue necrosis. dapsone or thalidomide for Boards’ Fodder mucocutaneous lesions. Ocular archives and you involvement is organ-threatening and requires systemic steroids can be a part of +/- immunosuppresives. it. Contact Dean Eosinophilic Rapidly enlarging, firm nodule(s) Ulcer w/dense infiltrate of eosinophils Most resolve spontaneously Monti, managing Ulcer of the Oral that develop a central ulceration with and pleomorphic mononuclear cells within a few months, no treatment editor, special Mucosa elevated borders and indurated base. extending deep into the submucosal necessary. Becomes 1-2cm in size. +/- pain. tissue and underlying striated muscle. publications, at Typically covered with a fibrinous exu- Large atypical cells are CD30+ T lym- [email protected]. date. Usually tongue, but the buccal, phocytes. Base of ulcer is composed labial, alveolar and palatal mucosa can of poorly formed granulation tissue +/- also be affected. increased capillaries with prominent endothelial cells. Orofacial Initially intermittent, then persistent non- Non-necrotizing granulomatous inflam- Intralesional corticosteroids, Often with undiag- Watch for Granulomatosis tender swelling of the lip and/or face. mation. sometimes repeatedly. Dapsone, nosed GI disease. Oral Disease, Part 2 clofazimine, hydroxychloroquine, Referral to GI for thalidomide,TNF inhibitors, or scopes to rule out in the next systemic corticosteroids have also enteric involvement. Boards’ Fodder. been used. Wegener’s Pathognomonic friable ‘strawberry Skin biopsy can demonstrate leuko- Systemic corticosteroids and Granulomatosis gums’. Necrotizing granulomatous vas- cytoclastic vasculitis and/or granulo- cyclophosphamide. culitis of the upper and lower respiratory matous inflammation. Such classic tract. Destructive ulcerated lesions of features are infrequently observed in the oral and nasal cavity. oral biopsy specimens. Need more Boards’ EPITHELIAL PATHOLOGY Fodder? Visit Oral Leukoplakia Sharply demarcated, homogeneous or Simple hyperkeratosis seen most fre- Cessation of smoking. Biopsy the Directions in speckled white plaque, often on floor of quently. +/- epithelial dysplasia (mild mandatory, as considered pre- Residency archive mouth, lateral & ventral surfaces of the to severe). Carcinoma in situ or even malignant. If no or mild dysplasia tongue, and the soft palate. invasive SCC possible. evident, site of the lesion dictates listed under treatment. Low-risk sites (buccal “Publications” at mucosa, labial mucosa, hard www.aad.org. palate) warrant periodic clinical follow-up. Moderate or severely dysplastic lesions require com- plete removal. Oral Erythroplakia Flat or slightly elevated, velvety, sharply Advanced epithelial dysplasia w/90% Prompt surgical removal and circumscribed plaque. The lesions are of lesions demonstrating carcinoma in careful follow-up. Cessation of often asymptomatic. situ or invasive carcinoma at the time smoking. of biopsy. Nicotine Posterior hard palate & anterior soft Hyperkeratosis and parakeratosis, Cessation of smoking typically Stomatitis palate w/grayish-white mucosa. acanthosis, and mild chronic sialo- results in complete resolution Sometimes, umbilicated papules w/red dochitis. within 1-2 weeks. central puncta are found, representing inflamed palatal mucous salivary gland orifices. Actinic Keratosis/ Loss of normal dermatoglyphics, atro- Thickening of epithelium and hyper- Cryosurgery, topical agents such Cheilitis phy, and blurring of vermilion border. keratosis. Different degrees of epi- as 5-FU or imiquimod, and Blu-U. The development of hyperkeratotic scal- thelial dysplasia possible
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