Oral Submucous Fibrosis: Review on Etiopathogenesis
Sunita N Dyavanagoudar*
Department of Oral Pathology, Sri Hassanamba Dental College and Hospital, Vidyanagar, Hassan, Karnataka, India
- *Corresponding Author:
- Dr. Sunita N Dyavanagoudar
Basav Nivas, Jayanagar, Dharwad
E-mail : [email protected]
Received Date: November 16, 2009; Accepted December 16, 2009; Published Date: December 21, 2009
Citation: Dyavanagoudar SN (2009) Oral Submucous Fibrosis: Review on Etiopathogenesis. J Cancer Sci Ther 1: 072-077. doi:10.4172/1948-5956.1000011
Copyright: © 2009 Dyavanagoudar SN. This is an open-access article distributed under the terms of the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Summary data from recent epidemiological studies provide overwhelming evidence that areca nut is the main aetiological factor for OSF. Commercially freeze dried products such as pan masala, Guthka and mawa have high concentrates of areca nut per chew and appear to cause OSF more rapidly than by self prepared conventional betel quid that contain smaller amounts of areca nut. It is logical to hypothesize that the increased collagen synthesis or reduced collagen degradation as possible mechanisms in the development of the disease. These chemicals appear to interfere with the molecular processes of deposition and/or degradation of extracellular matrix molecules such as collagen. In vitro studies on human fibroblasts using areca extracts or chemically purified arecoline support the theory of fibroblastic proliferation and increased collagen formation that is also demonstrable histologically in human OSF tissues. The copper content of areca nut is high and the possible role of copper as a mediator of fibrosis is supported by the demonstration of up regulation of lysyl oxidase in OSF biopsies. It has been postulated that areca nut may also induce the development of the disease by increased levels of cytokines in the lamina propria. Current evidence implicates collagen-related genes in the susceptibility and pathogenesis of OSF. The individual mechanisms operating at various stages of the disease– initial, intermediate and advanced–need further study in order to propose appropriate therapeutic interventions.