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A 36-year-old woman developed progressive dyskeratotic leukoplakia of the palate, lips, attached gingiva, and labial surfaces of the genitalia. On microscopic examination, clusters of dyskeratotic cells were found throughout the epithelium, except in the basal cell layer. The clinical and histologic differential diagnosis included candidiasis, oral hairy leukoplakia, lichen planus, condyloma acuminatum, Darier's disease, hereditary benign intraepithelial dyskeratosis, and white sponge nevus. Her clinical and histologic findings do not permit classification into any of these well-recognized entities.

Excerpt Various oral lesions have been associated with human immunodeficiency virus (HIV) infection. Oral candidiasis is the most commonly recognized infectious process involving the oral cavity, a...

To define the role of Epstein-Barr virus (EBV) in the pathogenesis of oral hairy leukoplakia, 13 human immunodeficiency virus—seropositive men with clinical and histologic evidence of oral hairy leukoplakia were enrolled in an open-label trial of orally administered acyclovir therapy (3.2 g/d for 20 days). Of six patients who received therapy, five exhibited clinical regression. Once therapy was discontinued, recurrences occurred in all responders. Among seven patients who refused therapy, no spontaneous remissions occurred. Before therapy, EBV replication within the leukoplakia was demonstrated by immunofluorescence tissue staining or electron microscopy in five patients who were studied. Human papillomavirus was not detected by immunocytochemistry or electron microscopy from tissue specimens of six patients. After therapy, biopsy specimens from two patients with complete responses revealed a normalization of histologic abnormalities and an inability to detect EBV in previously involved mucosa by immunofluorescence or in situ DNA hybridization assays. It was concluded that EBV replication within the epithelial cells of the tongue is necessary for the development of oral hairy leukoplakia. (JAMA1988;259:384-388)