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
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. 1. Introduction Cancer is a disease of cells that escape the control mechanisms of orderly cell growth and acquire the ability to proliferate, invade normal tissues and metastasize [1]. Head and neck cancer is the sixth most common cancer worldwide, with an estimated annual burden of 563,826 incident cases (including 274,850 oral cavity cancers, 159,363 laryngeal, and 52,100 oropharyngeal cancers) [2, 3]. In India oral cancer constitute around 9.8% of total cancer cases & ranks first among the all cancer cases in males & third most common among females. Age standardized incidence rate varies between 7 and 17/1000,000 person-years. The incidence rate is higher than the rate of 3 to 4/1000,000/year found in western countries [4–6]. India has one of the world’s highest incidences of head and neck cancers which were primarily caused by tobacco habits and alcohol consumption [5]. The association between high risk human papillomavirus [HR HPV] and risk of oral cancer development dates to back 1983, when HPV16 was detected in oral squamous cell tumors. Since then HPV DNA has repeatedly been found in a variable proportion of head and neck cancers [6–9]. HPV is a ~7.9？kb, nonenveloped, double-stranded, circular DNA virus that has been implicated in a variety of anogenital & aerodigestive diseases, ranging from common warts to laryngeal papilloma to cervical cancer. The first isolation of this virus particle was performed in 1933 in rabbit papillomatosis [10]. The oral cavity is covered by an epithelium that has
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