Significance of human papillomavirus in sinonasal papillomas

Abstract

Recent investigations have suggested human papillomavirus (HPV) to be involved in the development of sinonasal papillomas (SNP). Forty-three patients operated for SNP were studied to determine the prevalence of HPV-DNA sequences in these tumours and to evaluate their value as a prognostic parameter. The original sections of all cases were reviewed and reclassified according to the WHO. Paraffin blocks available from 37 patients were subjected to in situ hybridization (ISH) and polymerase chain reaction (PCR). Histology revealed 34 cases of inverted papilloma (IP) (79 per cent), five cases of exophytic papilloma (EP) (12 per cent) and four cases of columnar cell papilloma (CCP) (nine per cent). Recurrences developed in seven of 41 patients (17 per cent), and malignancy occurred in four of 43 patients (nine per cent). HPV was detected in four of 37 specimens (11 per cent) both by ISH and PCR. In particular, HPV-11 was found in three lesions (two EP, one IP) (eight per cent), and HPV-6b was detected in one lesion (one EP) (three per cent). Our findings suggest a possible role for HPV in the pathogenesis of exophytic papillomas. As no correlation was found to malignancy and recurrence of disease, screening for HPV seems not to be useful as a prognostic parameter.

In Inverted Papillomas HPV more likely represents incidental colonization than an etiological factor

“…Nineteen of 20 HPV-positive IPs in our study showed HPV-11, and one showed HPV-6. These data were compared with the results of 22 published studies in which PCR was used for HPV detection [15,22,23,[26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44]. As summarized in Table 2, a total of 720 IPs have been analyzed in previous studies, and HPV DNA was detected in 203 (28.1%).…”

The Role of the Human Papillomavirus in the Pathogenesis of Schneiderian Inverted Papillomas: An Analytic Overview of the Evidence

“…Multiple infections were separated into constituent types; thus, type-specific detection represents types found alone or with other HPV types. Consensus PCR primers MY09/11, PGMY09/11, GP5+/6+, and SPF10 were considered to amplify the 18 HPV types most commonly associated with cervical and head and neck cancers (6,11,16,18,31,33,35,39,45,51,52,56,58,59,66,68,70,73,82, and 83) as well as additional high-and low-risk types. It is important to note that an HPV type was only considered tested for if it was, a) amplified by the primers and subsequently genotyped in analyses using PCR-based methods, or b) probed for using sequences specific to those types in the DNAbased (SB) and RNA-based (ISH) analyses.…”

“…Low-risk/highrisk coinfections are rare and found in three studies [2,9,29]. Several studies also specifically tested for HPV 31/33/ 35 [12, 16, 20-22, 24, 28, 31] as well as HPV 42-45, 51, 52, 56, 58 [1,22,24,31] with negative results. Ogura [1] found HPV 57 in 1 of 3 cases and Wu [8] detected 57b in 9 of 15 IP studied; however this could not be confirmed by others [30].…”

Update on Inverted Epithelial Lesions of the Sinonasal and Nasopharyngeal Regions

“…Hicks W Jr et al [12] and Schwerer MJ et al [28] evaluated the expression patterns of cytokeratins in nasal polyps and IP, The columnar differentiation cytokeratins (ex: CK 7,8,18,19,20) were positive in both NPs and IPs but the squamous differentiation cytokeratins (ex: CK 10,10/13, 1/ 2/10/11) were positive in IP but not in NP. For both group of cases the immature cell type CKs were positive at the basal layer.…”

“…HPV is evaluated both for IP and nasal polyps but not for REAH [9,13,19]. Kraft et al [19] identified HPV11 in only 1(3%) out of 29 IP cases, while HPV 6b, 16 and 18 were negative by in situ hybridization. Hoffman M et al [13] detected HPV DNA type 6 and 11 in 3 of 26 cases, while 20 nasal polyps were negative.…”