Excessive consumption of tobacco and alcohol are the most important etiological factors in the development of oral cavity carcinoma, however 15 - 20% of patients develop carcinoma without being exposed to these factors. It is clear from this that there are other factors that influence the development of OSCC, and one of them is human papillomavirus infection. HPV is thought to be responsible for a very small proportion of oral cavity carcinoma, although prevalence data vary considerably from study to study. High-risk genotypes are associated with the development of oral cavity carcinoma, with HPV 16 being the most frequently isolated, followed by HPV 18. The oncogenic potential of high-risk HPV types is attributed to their ability to insert specific fragments of their DNA, the E6 and E7 genes, into the genome of infected cells, followed by the expression of viral proteins of the same name. These proteins are key drivers of carcinogenesis because they inactivate the two most important tumor suppressor proteins, p53 and pRb. Risky sexual behavior, including orogenital sex, has been found to be the most likely mode of transmission of HPV between the genitals and the oral cavity. The current gold standard for detection of oncogenic HPV infection in oral cavity carcinoma is E6/E7 mRNA in situ hybridization. The impact of HPV infection on the prognosis of patients with oral cavity carcinoma is still not entirely clear, but according to many studies, HPV status does not affect the overall survival of patients with OSCC. Additional research is needed to further clarify the impact of HPV infection on the development and prognosis of oral cavity carcinoma.