Journal ArticleDOI
Stimulation of human buccal mucosa fibroblasts in vitro by betel-nut alkaloids
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TLDR
Fibroblasts are responsive to the major metabolite of arecoline and hydrolysis of the ester group may be necessary for this action, which may contribute to the accumulation of collagen in OSF.About:
This article is published in Archives of Oral Biology.The article was published on 1986-01-01. It has received 187 citations till now. The article focuses on the topics: Arecoline & Arecaidine.read more
Citations
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Journal ArticleDOI
Oral submucous fibrosis: review on aetiology and pathogenesis.
Wanninayake Mudiyanselage Tilakaratne,M.F. Klinikowski,Takashi Saku,Tim J Peters,Saman Warnakulasuriya +4 more
TL;DR: Current evidence implicates collagen-related genes in the susceptibility and pathogenesis of OSF and the individual mechanisms operating at various stages of the disease-initial, intermediate and advanced need further study in order to propose appropriate therapeutic interventions.
Journal ArticleDOI
Alert for an epidemic of oral cancer due to use of the betel quid substitutes gutkha and pan masala: a review of agents and causative mechanisms
TL;DR: Evidence that strongly supports causative mechanisms for genotoxicity and carcinogenicity of these substitute products, including gutkha and pan masala, are strongly implicated in the recent increase in the incidence of oral submucous fibrosis is reviewed.
Journal ArticleDOI
Role of areca nut in betel quid-associated chemical carcinogenesis: current awareness and future perspectives
TL;DR: It would appear that AN toxicity is not completely due to its polyphenol, tannin and alkaloid content, and further studies are needed to delineate the metabolism of AN ingredient and their roles in the multi-step chemical carcinogenesis, to enhance the success of the future chemoprevention of oral cancer and oral submucous fibrosis.
Journal ArticleDOI
Molecular pathogenesis of oral submucous fibrosis--a collagen metabolic disorder.
P. Rajalalitha,S. Vali +1 more
TL;DR: The objectives of this review are to highlight the molecular events involved in the overproduction of insoluble collagen and decreased degradation of collagen occurring via exposure to BQ and stimulation of the TGF-beta pathway, and elucidate the cell signaling that is involved inThe etiopathogenesis of the disease process.
Journal ArticleDOI
The oral health consequences of chewing areca nut.
TL;DR: There is new information linking oral cancer to pan chewing without tobacco, suggesting a strong cancer risk associated with this habit and public health measures to quit areca use are recommended to control disabling conditions such as submucous fibrosis and oral cancer among Asian populations.
References
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Journal Article
Lymphocyte-Mediated Activation of Fibroblast Proliferation and Collagen Production
TL;DR: The fibroplasia consisting of increased numbers of fibroblasts and of increased collagen deposition associated with chronic inflammatory diseases may be the direct consequence of a specific antigenic challenge.
Journal ArticleDOI
Lymphokine stimulation of collagen accumulation.
R L Johnson,M Ziff +1 more
TL;DR: Fibroblast-stimulating activity may be implicated in the abnormal fibrosis seen in association with chronic inflammation in a variety of disease states, and may have special relevance to progressive systemic sclerosis.
Journal Article
The aetiology of oral submucous fibrosis: the stimulation of collagen synthesis by extracts of areca nut.
J P Canniff,W Harvey +1 more
TL;DR: Preparations from varieties of A. catechu nuts have been tested for their ability to stimulate collagen synthesis in microwell cultures of human fibroblasts, using a pulse of 3H-proline and subsequent analysis of the cultures for radioactive collagen.
Journal ArticleDOI
Betel nut constituents as inhibitors of gamma-aminobutyric acid uptake.
TL;DR: It is found that arecaidine and guvacine are competitive inhibitors of GABA uptake in rat brain slices and it is proposed that some of the psychic effects of betel nut consumption may be the result of inhibition of GABA absorption.