Inverted papilloma (IP), often referred to as Schneiderian Papilloma, is a locally destructive benign tumour of the sino- nasal mucosa with a tendency for malignant transformation and a high propensity for recurrence. It arises from the transitional epithelium, the Schneiderian membrane. In a Swedish population-based study it was shown to have significantly increased over the last decades. Sinonasal SCC ( squamous cell carcinoma) has been shown to be more common among patients with IP than in the general population.The etiology is unknown. Proposed etiological factors are environmental pollutants, organic solvents, smoking and chronic rhino –sinusitis.The possibility of a viral etiology has been put forward where Human Papilloma Virus (HPV) has been the most discussed Studies on HPV and IP have shown very diverging results.The aim of this study is to analyse the presence of HPV in IP in Stockholm and to investigate if there is any correlation between presence of HPV and recurrence, dysplasia or malignant transformation in IP.
From the Swedish Cancer Registry we identified all patients diagnosed with IP in Sweden 1960-2010. From the patients in our data set diagnosed from 2001 and onwards, diagnosed in the county of Stockholm, we retrieved paraffin embedded blocks with their IP from Biobank Stockholm. After histological re-evaluation of the original diagnosis by a qualified pathologist, and loss of samples due to technical problems, 99 cases out of 126 were included in the study. By analyzing the medical reports we retrieved information about recurrence, dyspasia in the specimens and malignant transformation.The study was approved by the Ethical Committee at the Karolinska Institute, Stockholm, Sweden.The parsfin embedded tumors were cut in 2x15µ sections and DNA was extracted.Detection of HPV was done by PCR using the Magpix(Luminex). The results were confirmed with insitu hybridization.
In all, 13 of the 99 specimens of IP were found to be HPV-positive. 8 were positive for HPV 11, 4 for HPV 6, and 1 for HPV 45.Among the patients with HPV, 4/13 were seen to recur and 4/13 showed dysplasia. This is to be compared with 33/86 and 8/86 respectively in patients with HPV-negative IP. None of the 13 patients with HPV-positive IP developped SCC while two of the HPV-negative did.
13% of the IP were HPV positive but only one with a high oncogenicrisk HPV. The HPV-positive IP's were found to have a higher rate of dysplasia compared to the non HPV-positive ( 30% vs 9%) but no difference was found in their recurrencerate. Patients with HPV-positive IP did not have a higher rate of malignant transformation.