Painful Oral Lesions: What to Look For, How to Treat, Part 1

Risk factors for oral cancer include tobacco use and alcohol intake (especially in conjunction with tobacco use). Many benign conditions may be confused with squamous cell carcinoma, the most common type of intraoral neoplasm. Any red and/or white lesion that has surface corrugation, stippling, or induration is considered dysplastic or neoplastic until proved otherwise. Even without these clinical signs, white plaques of any size that persist for several months may represent dysplasia. These lesions should be assessed by biopsy. Risk factors for lichen planus include stress, exposure to certain foods and medications, and systemic illness. Erosive lichen planus may cause significant pain and oral dysfunction. Malignant oral lesions--particularly in their early stages--can resemble benign conditions. In this 2-part series, I will offer practical advice on how to identify symptomatic lesions. Here I focus on oral cancer and lichen planus. In a future article, I will discuss viral infections, candidiasis, benign mucous membrane pemphigoid, and erythema multiforme. ORAL CANCER Oral squamous cell carcinoma accounts for about 3% of all cancers in the United States. Risk increases with age, although recent years have seen a trend toward increasing prevalence in younger men. Oral squamous cell carcinoma affects more men than women, and risk varies according to country and race. In the United States, the incidence is about 12.3% in blacks, 10% in whites, 5.7% in Hispanics, and 6% in Asians. Mortality is about 4.8% in blacks, 2.5% in whites, 2.3% in Asians, and 1.3% in Hispanics.1 The overall 5-year survival rate is about 50%. This relatively low rate is largely attributable to delayed diagnosis of an initially innocuous-appearing, asymptomatic lesion in a location difficult for the patient and clinician to observe readily.1 Risk factors for oral malignancy. These include heavy cigarette smoking and the use of smokeless tobacco; alcohol intake (especially when coupled with tobacco use); low serum levels of b-carotene; radiation therapy; iron deficiency; infection with oncogenic viruses, including human papillomavirus (HPV) and herpes simplex virus (HSV); immunosuppression; and the activity of proto-oncogenes, tumor suppressor genes, and gatekeeper molecules in association with alcohol and tobacco use.2 The mechanisms and interactions involved in malignant transformation are complex, but the result of the combination of environmental factors and genetics is defective carcinogen metabolism and cellular DNA repair capabilities, which lead to tumor growth. Figure 1