Detection of human papillomavirus (HPV) structural antigens and DNA types in inverted papillomas and squamous cell carcinomas of the nasal cavities and paranasal sinuses

To assess the suggested etiological role of human papillomavirus (HPV), biopsies from 14 patients operated on for an inverted papilloma (11 cases) and squamous cell carcinoma (3 cases) of the nasal cavity and paranasal sinuses were analysed for light microscopical evidence of HPV, by indirect immunoperoxidase (IP-PAP) to demonstrate HPV structural proteins, and using in situ DNA-hybridization to disclose the DNA of HPV types 6, 11 and 16. The majority of the inverted papillomas contained areas of metaplastic squamous cells, including koilocytes as well as dysplastic changes consistent with intra-epithelial neoplasia as described in uterine cervix. In 3 patients, frankly invasive squamous cell carcinomas were found, originating from dysplastic squamous epithelium. Of the 14 lesions, 7 (50%) expressed HPV antigens, usually confined to only a few cells close to the surface of the epithelium. None of the malignant lesions expressed HPV antigens. In situ DNA-hybridization disclosed HPV 11 DNA alone in 5 lesions, but none of the lesions contained HPV 6 DNA. HPV 16 DNA was found in 2 lesions as a single HPV type, and in 3 other lesions concomitant with HPV 11. All three carcinomas contained HPV 16 DNA. The HPV DNA distribution proved to be different from that found in the genital tract HPV lesions; HPV DNA was less abundant in the nasal papillomas, and it was also found in the basal and suprabasal cells. Although further studies are needed to exclude the possibility of HPV being innocent bystanders, the present results suggest that the 'high risk' HPV type 16 might be involved in nasal squamous cell carcinomas arising from pre-existing inverted papillomas. The applicability of the in situ DNA hybridization technique is emphasized, making possible the analysis of extensive retrospective series necessary to elucidate the role of HPV in nasal squamous cell carcinogenesis.