RESUMEN
Sinonasal papillomas are rare, usually benign tumors arising from the Schneiderian membrane. Human papillomaviruses (HPV) can infect differentiating skin and mucosal cells and can induce uncontrolled growth patterns. Their effect on development of sinonasal papillomas has been discussed controversially in recent years. A monocentric, retrospective study was conducted to investigate histopathologic features of sinonasal papillomas and to establish an assay for HPV detection and genotyping in papillomas. Schneiderian papillomas are divided into three groups according to histopathologic features: the largest group are inverted papillomas, followed by fungiform (exophytic) and oncocytic papillomas. HPV screening was performed with high sensitivity by PCR employing My09/11 and 125 consensus primers. Adding a third primer pair (GP5+/GP6+) d increase sensitivity. Reverse hybridization microarrays achieved HPV genotyping better than pyrosequencing in our setting. HPV infection rates were higher in papillomas (46.7%) than infection rates reported for healthy mucosa (up to 13%). P16(INK4a) was not a reliable surrogate marker for HPV infection in sinonasal papillomas. Data from our study endorses the hypothesis that HPV infection promotes formation of sinonasal papillomas. However, apart from HPV genotypes that are frequently found in e.g. anogenital lesions (such as 6, 11, or 16), tissue samples of sinonasal papillomas also displayed infection with "rare" HPV types (such as 58, 42, 83, or 91).
Asunto(s)
Neoplasias Nasales/virología , Papiloma/virología , Infecciones por Papillomavirus/genética , Neoplasias de los Senos Paranasales/virología , Genotipo , Humanos , Neoplasias Nasales/patología , Papiloma/patología , Papillomaviridae/genética , Neoplasias de los Senos Paranasales/patología , Estudios RetrospectivosRESUMEN
PURPOSE AND METHODS: A retrospective study was conducted to identify and assess potential clinical and molecularbiological risk factors for development and recurrence of sinonasal papillomas (i.e. inverted (IP), fungiform (FP), and oncocytic papillomas (OCP)). Investigated risk factors included age, gender, tumor size and localization, tobacco smoking, regular alcohol consumption, essential hypertension, anticoagulant medication, allergies, surgical approach, and HPV infection. Risk factors were evaluated by regression analysis. RESULTS: Apart from age and incomplete tumor resection, the recurrence of Schneiderian papillomas is independent of conventional risk factors. Patients in this study displayed higher HPV infections rates in IP (38.8%) and in FP (100%) than in healthy mucosa, which is reported 0-5.8% in Germany and central Europe. The proportion of HPV-positive IP decreased with advanced tumor stages: 100% HPV positivity of T1 IP (2/2), 40.9% of T2 IP (9/22), and 35.7% of T3 IP (20/56). Most commonly detected HPV types were HPV 6, 11, and 16; however, patients in this study also displayed HPV types that have rarely or not at all been described in sinonasal papillomas before, such as HPV 58, 42, 83, and 91. Recurrent sinonasal papillomas displayed higher rates of HPV infections than non-recurrent tumors. CONCLUSIONS: Young age at initial diagnosis and incomplete tumor resection are risk factors for recurrence of sinonasal papillomas. Our data suggest that HPV infection supports development and/or perpetuation of sinonasal papillomas. Additionally, sinonasal papillomas seem to display a unique subset of HPV genotypes, including genotypes that have not often been described before.