Table of Contents
ISRN Pathology
Volume 2013 (2013), Article ID 807095, 7 pages
http://dx.doi.org/10.1155/2013/807095
Research Article

Role of HPV-16 in Pathogenesis of Oral Epithelial Dysplasia and Oral Squamous Cell Carcinoma and Correlation of p16INK4A Expression in HPV-16 Positive Cases: An Immunohistochemical Study

1Department of Oral Pathology and Microbiology, SMBT Dental College and Hospital, Sangamner 422605, India
2Department of Oral Pathology and Microbiology, Vasantdada Patil Dental College and Hospital, Sangli 416416, India
3Department of Oral Pathology and Microbiology, Vananchal Dental College and Hospital, Garhwa, India

Received 15 January 2013; Accepted 14 February 2013

Academic Editors: M. Mokni, A. Sonzogni, and A. Stringer

Copyright © 2013 Gaurav Pralhad Agrawal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The objective of current study is to evaluate the role of HPV-16 in the pathogenesis of oral epithelial dysplasias (OED) and oral squamous cell carcinoma (OSCC) by immunohistochemistry (IHC) and to know whether HPV-16 participates in disruption of the regulation of p16 INK4A suppressor protein in OED and OSCC by IHC. Histopathologically diagnosed 20 cases of OED and 20 cases of OSCC were selected from amongst the patients attending the OPD of Vasantdada Patil Dental College and Hospital, Sangli. Biopsy tissue section were then tested for HPV-16 by IHC. HPV-16 positive tissue sections were then again tested by p16 by IHC. Overall 22.5% of cases in our study were found to be positive for HPV 16 which includes 10% of cases of OED and 35% cases of OSCC. Amongst the HPV 16 positive cases, more than 60% of cells were positive for p16INK4A IHC in OED (50%) and OSCC (85.71%). Thus, HPV 16 participates in disruption of the regulation of p16INK4A suppressor protein and can be used as surrogate biomarker for detection of HPV infection in OED and OSCC.