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Quid Chewing (quid + chewing)
Kinds of Quid Chewing Selected AbstractsBetel quid not containing tobacco and oral cancer: A report on a case,control study in Papua New Guinea and a meta-analysis of current evidenceINTERNATIONAL JOURNAL OF CANCER, Issue 6 2007Steven J. Thomas Abstract Smoking and betel quid chewing are associated with increased risk of oral cancer but few studies have reported on associations in populations where betel quid does not contain tobacco. We conducted a case,control study in Papua New Guinea and a systematic review. Our case,control study recruited 143 cases with oral cancer and 477 controls. We collected information on smoking and betel quid chewing. Current smoking was associated with an increased risk of oral cancer with an adjusted odds ratio (OR) for daily smokers of 2.63 (95% confidence intervals (95% CI) 1.32, 5.22) and amongst heaviest smokers of 4.63 (95% CI 2.07, 10.36) compared to never-smokers. Betel chewing was associated with increased risk of oral cancer with an adjusted OR for current chewers of 2.03 (95% CI 1.01, 4.09) and in the heaviest chewers of 2.47 (95% CI 1.13, 5.40) compared to nonchewers. The OR in those who both smoked tobacco and chewed betel quid was 4.85 (95% 1.10, 22.25), relative to those who neither smoked nor chewed. The systematic review identified 10 previous studies that examined risk of oral cancer associated with betel quid chewing that controlled for smoking in populations where betel quid did not contain tobacco. In studies that reported results for non-smokers the combined OR was 2.14 (95% CI 1.06, 4.32) in betel quid chewers and in studies that adjusted for smoking the combined OR was 3.50 (95% CI 2.16, 5.65) in betel quid chewers. Preventive efforts should discourage betel quid chewing as well as smoking. © 2006 Wiley-Liss, Inc. [source] Relationship between betel quid additives and established periodontitis among Bangladeshi subjectsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2008Rahena Akhter Abstract Aim: To determine the relationship between betel quid chewing additives and established periodontitis in Bangladeshi subjects. Material and Methods: A total of 864 subjects participated in this study. Among them, 140 pairs of sex- and age-matched case subjects and control subjects were selected. A case was defined as a person who had at least two sites with a clinical attachment level (CAL)6 mm and at least one site with probing depth (PD)5 mm. Subjects who did not fulfill these criteria were considered as controls. Information on sociodemographic variables, psychological stress, dental health behaviour, smoking and betel quid chewing habits was obtained. Results: Multiple logistic regression analysis showed that current betel quid chewers had greater probabilities of having established periodontal disease than did non-chewers (odds ratio=3.97, p<0.05). Mean PD, mean CAL, mean percentage of bleeding on probing and number of missing teeth were significantly higher in chewers of betel quid with tobacco and masala than in chewers of betel quid without such additives adjusting for age, sex, smoking habit, body mass index, dental visit pattern, stress and plaque index. Higher frequency and longer duration of betel quid chewing showed a significant relation to an increase in periodontal parameters. Conclusion: The results indicate that betel quid additives might significantly enhance periodontitis in the population studied. [source] Effect of betel chewing, tobacco smoking and alcohol consumption on oral submucous fibrosis: a case,control study in Sri LankaJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 4 2006A. Ariyawardana Background:, Oral submucous fibrosis (OSMF) is a chronic, insidious, disabling potentially malignant condition of the oral mucosa seen predominantly in south and Southeast Asia. No reports are hitherto available on the aetiological factors of OSMF based on Sri Lankan patients. Methods:, A total of 74 patients with OSMF and 74 controls who consecutively attended the Oral Medicine clinic at the Dental Hospital (Teaching) Faculty of Dental Sciences, University of Peradeniya, Sri Lanka were included in the study. Binary logistic regression analyses were performed to model the influence of betel chewing, smoking and alcohol use and to determine the effects of different combinations of chewing habits on OSMF. Results:, Betel chewing was the only significantly associated factor in the aetiology of OSMF (OR = 171.83, 95% CI: 36.35,812.25). There were no interaction effects of chewing, smoking and alcohol consumption in the causation of OSMF. Conclusion:, The present study has shown a strong association of betel quid chewing (including tobacco as an ingredient) with the causation of OSMF. [source] Synergistic effects of nicotine on arecoline-induced cytotoxicity in human buccal mucosal fibroblastsJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 8 2001Yu-Chao Chang Abstract: Areca quid chewing has been linked to oral submucous fibrosis and oral cancer. Arecoline, a major areca nut alkaloid, is considered to be the most important etiologic factor in the areca nut. In order to elucidate the pathobiological effects of arecoline, cytotoxicity assays, cellular glutathione S-transferase (GST) activity and lipid peroxidation assay were employed to investigate cultured human buccal mucosal fibroblasts. To date, there is a large proportion of areca quid chewers who are also smokers. Furthermore, nicotine, the major product of cigarette smoking, was added to test how it modulated the cytotoxicity of arecoline. At a concentration higher than 50 ,g/ml, arecoline was shown to be cytotoxic to human buccal fibroblasts in a dose-dependent manner by the alamar blue dye colorimetric assay (P<0.05). In addition, arecoline significantly decreased GST activity in a dose-dependent manner (P<0.05). At concentrations of 100 ,g/ml and 400 ,g/ml, arecoline reduced GST activity about 21% and 46%, respectively, during a 24 h incubation period. However, arecoline at any test dose did not increase lipid peroxidation in the present human buccal fibroblast test system. The addition of extracellular nicotine acted synergistically on the arecoline-induced cytotoxicity. Arecoline at a concentration of 50 ,g/ml caused about 30% of cell death over the 24 h incubation period. However, 2.5 mM nicotine enhanced the cytotoxic response and caused about 50% of cell death on 50 ,g/ml arecoline-induced cytotoxicity. Taken together, arecoline may render human buccal mucosal fibroblasts more vulnerable to other reactive agents in cigarettes via GST reduction. The compounds of tobacco products may act synergistically in the pathogenesis of oral mucosal lesions in areca quid chewers. The data presented here may partly explain why patients who combined the habits of areca quid chewing and cigarette smoking are at greater risk of contracting oral cancer. [source] Head and neck cancer in the betel quid chewing area: recent advances in molecular carcinogenesisCANCER SCIENCE, Issue 8 2008Yin-Ju Chen Head and neck cancer (HNC) is one of the 10 most frequent cancers worldwide, with an estimated over 500 000 new cases being diagnosed annually. The overall 5-year survival rate in patients with HNC is one of the lowest among common malignant neoplasms and has not significantly changed during the last two decades. Oral cavity squamous cell carcinoma (OSCC) shares part of HNC and has been reported to be increasing in the betel quid chewing area in recent years. During 2006, OSCC has become the sixth most common type of cancer in Taiwan, and it is also the fourth most common type of cancer among men. It follows that this type of cancer wreaks a high social and personal cost. Environmental carcinogens such as betel quid chewing, tobacco smoking and alcohol drinking have been identified as major risk factors for head and neck cancer. There is growing interest in understanding the relationship between genetic susceptibility and the prevalent environmental carcinogens for HNC prevention. Within this review, we discuss the molecular and cellular aspects of HNC carcinogenesis in Taiwan, an endemic betel quid chewing area. Knowledge of molecular carcinogenesis of HNC may provide critical clues for diagnosis, prognosis, individualization of therapy and molecular therapeutics. (Cancer Sci 2008; 99: 1507,1514) [source] | ||||||||||