RESUMO
Oral cancer is a process that involves different etiological factors and mechanisms in the light of current view of viral cocarcinogenesis. Evidence from histology and DNA hybridization studies suggests that HPV is engaged in oral carcinogenesis. The Pathology Laboratory of the Dentistry School, National University of Córdoba, admits approximately 20% of all patients with cancerous lesions in this city. In the January 1992-December 1997 lapse, we examined 1950 biopsies with oral lesions, 4.77% (93/1950) of which were malignant neoplasms, 79.57% (74/93) were oral carcinomas. Thirty-three oral carcinomas (44.6%; 33/74) were selected at random and included in this study, 33 cells smears of normal oral mucosa of controls individuals were included. They were analyzed by conventional light microscopy and an in situ hybridization technique for the detection of HPV. Data were analyzed with chi square test. The prevalence of HPV among the 33 cancer samples studied was 27.27%, 9/33 tested positive for HPV in low stringent conditions. Only one was positive in high stringent condition for HPV16, a verrugous carcinoma. No HPV-DNA was detected in cells smears of controls. Among the HPV positive, 3/9 (33.33%) were squamous carcinomas and 5/9 (55.56%) were verrugous carcinomas. Only one was a melanoma. Verrugous carcinoma was the carcinoma most associated with the HPV infection (x2 = 20.5; 95% level of confidence). This would indicate a major role of HPV in the pathogenesis of verrucous carcinomas. The viral prevalence found in cancerous lesions reinforces the concept of heterogenic natures of oral cancer. HPV is a circumstance that increase the probability of malignancy, and when reducing, diminish the frequency of cancer.