Abstract

To evaluate the etiologic role of human papillomavirus (HPV) in oral carcinogenesis, DNA samples were purified from 103 oral squamous cell carcinoma (OSCC) and 30 normal oral mucosal (NOM) specimens. A nested polymerase chain reaction, DNA sequencing, and gene-chip HPV typing were used to identify multiple HPV types in our samples. We found that the positive rates of all HPV types and of high-risk HPV types were significantly higher in OSCC samples (49.5% and 41.7%, respectively) than in NOM samples (6/30 [20%; P < .01] and 5/30 [17%; P < .05], respectively) and significantly higher in non–oral habits (OH)-associated OSCC samples (31/51 [61%] and 28/51 [55%], respectively) than in OH-associated OSCC samples (20/52 [38%; P < .05] and 15/52 [29%; P < .001], respectively). High-risk HPV types and all HPV types had odds ratios of 3.97 (P = .0097) and 3.92 (P = .006), respectively. Our results suggest that HPVs, particularly high-risk HPVs, might be associated with the development of OSCCs, especially the non–OH-associated OSCCs.