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,
Karnataka, India,
Tel : 91-9742366645,
E-mail : drsunitad@yahoo.com |
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| Received October 28, 2009; Accepted November 30, 2009; Published
November 30, 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. |
| Abstract |
| 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. |
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