"High risk" HPV types are frequently detected in potentially malignant andmalignant oral lesions, but not in normal oral mucosa

Studies on the involvement of the human papillomavirus (HPV) in initiation and progression of oral neoplasia have generated conflicting results. The o bserved discrepancy is attributable mainly to the varying sensitivity of th e applied methodologies and to epidemiologic factors of the examined patien t groups. To evaluate the role of HPV in oral carcinogenesis, we analyzed 5 3 potentially neoplastic and neoplastic oral lesions consisting of 29 cases of hyperplasia, 5 cases of dysplasia, and 19 cases of squamous cell carcin omas, as well as 16 oral specimens derived from healthy individuals. A high ly sensitive nested polymerase chain reaction (PCR) assay was used, along w ith type-specific PCR, restriction fragment length polymorphism analysis, d ot blotting, and nonisotopic in situ hybridization. Nested PCR revealed the presence of HPV DNA in 48 of the 53 (91%) pathologic samples analyzed, whe reas none (0%) of the normal specimens was found to be infected. Positivity for HPV was independent of histology and the smoking habits of the analyze d group of patients. At least one "high risk" type, such as HPV 16, 18, and 33, was detected by type-specific PCR in 47 (98%) infected specimens, wher eas only 1 (2%) squamous cell carcinoma was solely infected by a "low risk" type (HPV 6). HPV 16 was the prevailing viral type, being present in 71% o f infected cases. Single HPV 16 and HPV 18 infections were confirmed by res triction fragment length polymorphism. HPV 58 was detected by dot blotting in three hyperplastic lesions. HPV positivity and genotyping were further c onfirmed, and the physical status of this virus was evaluated by nonisotopi c in situ hybridization. Diffuse and punctate signals, indicative of the ep isomal and integrative pattern of HPV infection, were observed for low- and high-risk types, respectively. Our findings are suggestive of an early inv olvement of high-risk HPV types in oral carcinogenesis.