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HPV can also infect cutaneous epithelial cells and oral mucosal epithelial cells. Cutaneous HPV infection is ubiquitous and associated with increased risk for nonmelanoma skin cancer, while oral HPV infection is responsible for 20% of HNSCC. Although oral HPV infection is rare in the general population compared to genital HPV infection, the incidence of HPV-positive HNSCC has increased significantly over the last two decades, with HPV 16 being the most prevalent type (Table 2). Detection of HPV 16 infection in oral exfoliated cells increases the odds of oropharyngeal cancer more than 14 fold, and HPV-positive HNSCCs have better prognosis compared to HPV-negative HNSCCs. Limited natural history studies on oral HPV infection suggest that the most significant risk factor for oral HPV infection is oral sexual behavior, and oral HPV can be transmitted from oral-genital, oral-digital contact. Recent studies including ours also suggest the presence of novel HPV types in oral cavity, predominantly beta and gamma HPV types, though their role in oral carcinogenesis is unclear.
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