1Assistant Professor, Department of Oral Pathology, Government Dental College & Hospital, Jaipur
2Professor, Department of Oral Pathology, Government Dental College & Hospital, Jaipur
3Reader, Department of Oral Pathology, Royal Dental College, Challissery, Palakkad
*Corresponding author: Shikha Shrivastava, Assistant Professor, D-42, Mahesh Marg, Malviya Nagar, Jaipur (Raj.) E- mail- shikhashrivastava29@gmail.com, Mob: +91 7597510584
Online published on 9 September, 2013.
The incidence of head and neck squamous cell carcinoma has been gradually increasing over the last three decades. Recent data have now attributed a viral aetiology to a subset of head and neck cancers. Human papilloma virus-16 genotype is present in many oral and oropharyngeal squamous cell carcinoma. Several studies indicate that oral HPV infection is likely to be sexually acquired. The HPV-associated cytopositive oral and oropharyngeal carcinoma is thought to be initiated and maintained by high-risk HPV E6/E7 oncoprotein-induced dysregulation of cell cycle control mechanisms, leading to genomic instability. Loss of cell cycle and apoptosis control, therefore, constitutes an early and central event in HPV-mediated carcinogenesis. It has an essential aetiologic role in the development of oropharyngeal squamous cell carcinoma in a subset of subjects who are typically younger, are more engaged with high-risk sexual behaviour and were found to have higher human papilloma virus -16 serum antibody titer.
Human Papilloma Virus, Oral Carcinogenesis, Squamous Cell Carcinoma
