Areca nut in pathogenesis of oral submucous fibrosis: revisited

Angadi, Punnya V.; Rao, Sanjay S.

doi:10.1007/s10006-010-0219-8

Cited by 115 publications

(163 citation statements)

References 84 publications

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“…It has been demonstrated that arecoline, a major areca nut alkaloid, was found to stimulate human buccal mucosal fibroblasts (BMFs) proliferation and collagen synthesis in vitro [34]. Thus, the increased collagen synthesis or reduced collagen degradation may be a possible mechanism in the development of the disease [1].…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Interventions in Oral Submucous Fibrosis: An Experimental and Clinical Study

Singh

Mohammad

Pant³

et al. 2014

J. Maxillofac. Oral Surg.

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Introduction Oral submucous fibrosis (OSF) is a chronic debilitating disease and premalignant condition of the oral cavity and is a serious public health issue in India and many parts of the world. The treatment is still elusive and empirical because of poorly understood etiopathogenesis, which is believed to be multifactorial including areca nut chewing, ingestion of chillies, genetic and immunologic processes, nutritional deficiencies, and many others. The present investigations was focused to understand the possible therapeutic interventions of anti-OSF agents in arecoline induced experimental in vitro model of OSF and clinical application of these anti-OSF agents in the restoration of various grade of the disease. Materials and Methods The 127 subjects were selected from patients who visited the OPD of Department of Oral and Maxillofacial Surgery, Faculty of Dental Sciences, K.G. Medical University, Lucknow. Further the subjects were divided in two groups on the basis of clinical examination. Group-1 subjects showed presence of fibrosis bands in the labial and/or buccal mucosa, loss of elasticity, difficulty to open the mouth and had a habit chewing arecanut in some form. Group-2 subjects had no habit of chewing areca-nut, were apparently healthy with no mucosal disorder. The samples were collected and were immediately transported to Indian Institute of Toxicology Research, Lucknow, for isolation and cultivation of primary cultures of mucosal fibroblast cells. Then isolation and cultivation of oral mucosal fibroblast, identification of non-cytotoxic doses of arecoline, real time PCR, immunocytochemistry, cytokine determination in culture cells, western blot analyses, functional activity of collagenase, lysyl oxidase enzyme activity, collagen beads assay, cyclooxygenase (COX-2) expression analysis was done. Results and Conclusions This study, shows that the reduction of phagocytic cells was strongly related to the arecoline levels in fibroblast culture when we exposed arecoline to normal oral mucosal cells (NOMC) and cells from OSF patient. An enhancement of phagocytic cells was observed following the pre exposure of cells to 1 lM dexamethasone, a glucocorticoids, In this study, histologic evidence is presented which supports the finding that COX-2 expression is upregulated in OSF specimens compared to normal oral submucosal cells. Strong immunostaining for COX-2 was detected in arecoline exposed NOMC and cells from OSF patient. Areca nut extract up-regulates prostaglandin production, cyclooxygenase-2 mRNA and protein expression of human oral keratinocytes. The number of phagocytic cells and phagocytic activity in cultured human oral fibroblasts from OSF site was lower than the fibroblasts from the normal regions of the same person.

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Section: Introductionmentioning

confidence: 99%

Therapeutic Interventions in Oral Submucous Fibrosis: An Experimental and Clinical Study

Singh

Mohammad

Pant³

et al. 2014

J. Maxillofac. Oral Surg.

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“…Persistent hepatic inflammation is a hallmark of habitual BQ chewing (Sarma et al, 1992;Lin et al, 2008;Angadi and Rao, 2011) and/or chronic HBV/HCV infection (Bouchard and Navas-Martin, 2011;El-Serag, 2012). Hepatic fibrosis, or cirrhosis, is a common end-stage condition of many chronic liver diseases (Bouchard and Navas-Martin, 2011;Luedde and Schwabe, 2011;El-Serag, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Hepatic fibrosis, or cirrhosis, is a common end-stage condition of many chronic liver diseases (Bouchard and Navas-Martin, 2011;Luedde and Schwabe, 2011;El-Serag, 2012). During fibrosis progression, hepatocellular damage and inflammation trigger complex cellular events that result in collagen deposition (Angadi and Rao, 2011;Bouchard and Navas-Martin, 2011;Luedde and Schwabe, 2011;ElSerag, 2012;Kong et al, 2012). Serial liver biopsies are the current gold standard to evaluate the progression of fibrosis.…”

Section: Introductionmentioning

confidence: 99%

“…This increases the possibility of severe toxic effects of betel quid at sites other than the oral cavity (Gupta and Warnakulasuriya, 2002). Habitual BQ chewing independently contributes to the risk of oral submucous fibrosis (IARC, 2004;Angadi and Rao, 2011). It is a precancerous lesion of oral squamous cell carcinoma (IARC, 2004;Angadi and Rao, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Habitual BQ chewing independently contributes to the risk of oral submucous fibrosis (IARC, 2004;Angadi and Rao, 2011). It is a precancerous lesion of oral squamous cell carcinoma (IARC, 2004;Angadi and Rao, 2011). On the other hand, animals feeding BQ in the long term developed both chronic hepatocyte necroinflammation (Sarma et al, 1992) and liver cancer (Bhide et al, 1979;Nishikawa et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Impact of Chronic Hepatitis B and Hepatitis C on Adverse Hepatic Fibrosis in Hepatocellular Carcinoma Related to Betel Quid Chewing

Jeng

Tsai²,

Tsai³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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The pathogenesis of hepatocellular carcinoma (HCC) related to habitual betel quid (BQ) chewing is unclear. Risk of HCCis increased with adverse hepatic fibrosis. This study aimed to assess the impact of chronic viral hepatitis on adverse hepatic fibrosis in HCC related to BQ chewing. This hospital-based case-control study enrolled 200 pairs of age-and gender-matched patients with HCC and unrelated healthy controls. Serologic hepatitis B surface antigen (HBsAg), antibodies to hepatitis C virus (anti-HCV), α-fetoprotein (AFP), and surrogate markers for significant hepatic fibrosis were measured. Information on substance-use habits was obtained with a questionnaire. By analysis of surrogate markers for hepatic fibrosis, the prevalence of significant hepatic fibrosis in patients chewing BQ was between 45.8% and 91.7%, whereas that for patients without BQ chewing was between 18.4% and 57.9%. The difference was significant (P <0.05 for each surrogate marker). Multivariate analysis indicated that cirrhosis with Child-Pugh C (odds ratio (OR) = 3.28; 95% confidence interval (CI), 1.29-8.37), thrombocytopenia (OR = 3.92, 95% CI, 1.77-8.68), AFP >400 mg/L (OR = 2.21, 95% CI, 1.05-4.66) and male gender (OR = 4.06, 95% CI, 1.29-12.77) were independent factors associated with habitual BQ chewing. In conclusion, adverse hepatic fibrosis and severe liver damage play important roles in the pathogenesis of BQrelated HCC, which could be aggravated by chronic hepatitis B and hepatitis C. BQ-cessation programs and prevention of chronic HBV/HCV infection are needed to prevent HCC related to BQ chewing.

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Interventions for managing oral submucous fibrosis

Jones,

Veale,

et al. 2024

Cochrane Database of Systematic Reviews

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Areca nut in pathogenesis of oral submucous fibrosis: revisited

Cited by 115 publications

References 84 publications

Therapeutic Interventions in Oral Submucous Fibrosis: An Experimental and Clinical Study

Therapeutic Interventions in Oral Submucous Fibrosis: An Experimental and Clinical Study

Impact of Chronic Hepatitis B and Hepatitis C on Adverse Hepatic Fibrosis in Hepatocellular Carcinoma Related to Betel Quid Chewing

Interventions for managing oral submucous fibrosis

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