A 47-year-old man comes to the office due to a white patch on the inside of his lower lip. It is painless and does not bleed. The patient has used smokeless tobacco for the past 20 years. He drinks on average 5 beers a week. On physical examination, a 3.5-cm flat, white patch is seen on the inside of the lower lip, reflecting onto the gingival surface of the lower teeth. There is no cervical adenopathy. Biopsy of the mucosal lesion is shown in the image below:
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Which of the following is most likely to occur if this patient's condition is left untreated?
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This patient with a history of tobacco and alcohol use has persistent leukoplakia (white mucosal lesion) on the buccal and gingival mucosa. Biopsy shows full-thickness dysplasia characterized by abnormal cytology (eg, squamous cells with pleomorphic and hyperchromatic nuclei, dyskeratosis) and architecture (eg, loss of normal squamous maturation). These findings are consistent with squamous cell carcinoma in situ.
Most cancers of the head and neck arise from squamous epithelial cells that undergo stepwise, premalignant changes that progress to carcinoma (ie, hyperplasia → dysplasia → carcinoma in situ → invasive carcinoma). Premalignant lesions may initially manifest in the oral cavity as hyperplastic or dysplastic, white (leukoplakia) or red (erythroplakia) patches. The likelihood of progression to invasive cancer (which has a propensity to spread first to the cervical lymph nodes) depends on the degree of dysplasia, with severe dysplasia having a high likelihood of developing into invasive carcinoma. For this reason, oral leukoplakic lesions with severe dysplasia are typically surgically removed.
(Choice A) Patients with systemic lupus erythematosus can have painless oral plaques or ulcerations. Histopathology typically shows hyperkeratosis and degeneration of the basal epithelial cells with perivascular inflammation, not dysplasia.
(Choice B) Lichen planus can present with lesions in the oral mucous membranes; pruritic, purple/pink, polygonal papules and plaques often develop on the flexural surfaces of the wrists and ankles. Histology usually shows a band of lymphocytic inflammation, degeneration of the basal epithelium with apoptotic cells (ie, Civatte or colloid bodies), saw-toothed rete ridges, hyperkeratosis, and hypergranulosis. Dysplasia would not be seen.
(Choice D) Oral hairy leukoplakia has a distinct, corrugated appearance and is caused by Epstein-Barr virus (EBV). It occurs almost exclusively in patients with significant immunosuppression (eg, HIV) and often resolves with antiretroviral treatment; it is not premalignant. Pathology usually shows hyperparakeratosis and hyperplastic epithelium with viral cytopathic effect (not dysplasia).
(Choice E) Leukoplakia that shows benign hyperkeratosis and epithelial hyperplasia or even mild dysplasia may regress, especially if risk factors are modified (eg, cessation of tobacco and alcohol use). When severe or full-thickness dysplasia is present (as in this case), it is unlikely to spontaneously regress.
Educational objective:
Oral leukoplakia is a potentially premalignant lesion; the risk for progression to invasive carcinoma is related to the degree of dysplasia.