Mohammed Junaid1, M B Aswath Narayanan2, D Jayanthi2, S G Ramesh Kumar2, A Leena Selvamary2. 1. Department of Public Health Dentistry, Meenakshi Ammal Dental College and Hospital, Chennai, 600095, India. mohammedjnd@gmail.com. 2. Department of Public Health Dentistry, Tamilnadu Government Dental College and Hospital, Chennai, 600 003, India.
Abstract
OBJECTIVE: To determine the association between maternal tobacco use or exposure, presence of variant transforming growth factor alpha (TGFA) gene, and the occurrence of oral clefts. METHODS: The present case control study was carried out for 5 months in three tertiary government hospitals in Chennai city with a sample of 100 children (50 children with non syndromic cleft and 50 control) aged 0-24 months. The details of maternal risk factors during the period of gestation were recorded from case and control parents through a pre-validated questionnaire, following which blood samples from 92 children (46 case and 46 controls) based on consent were obtained and evaluated for TGFA gene polymorphism. RESULTS: A significant number of case mothers (48%) were exposed to secondhand smoke during the period of gestation than their control counterparts (24%) (P = 0.01) with an odds ratio of 2.46 (95% CI = 0.99-6.08). Electrophoresis of the restriction fragment length polymorphism (RFLP) product revealed the presence of the homozygous C1C1 allele in all the tested 92 samples with no homozygous C2C2 allele or heterozygous C1C2 allele. CONCLUSION: The present study has highlighted the role of passive smoking in the causation of non syndromic oral clefts in a developing country like India; however, the involvement of TGFA in causing the same disease in an ethnically Dravidian Indian population is uncertain. CLINICAL SIGNIFICANCE: The study has brought into forth the role of passive smoking in the development of oral clefts thereby warranting an effective public health policy to tackle the same.
OBJECTIVE: To determine the association between maternal tobacco use or exposure, presence of variant transforming growth factor alpha (TGFA) gene, and the occurrence of oral clefts. METHODS: The present case control study was carried out for 5 months in three tertiary government hospitals in Chennai city with a sample of 100 children (50 children with non syndromic cleft and 50 control) aged 0-24 months. The details of maternal risk factors during the period of gestation were recorded from case and control parents through a pre-validated questionnaire, following which blood samples from 92 children (46 case and 46 controls) based on consent were obtained and evaluated for TGFA gene polymorphism. RESULTS: A significant number of case mothers (48%) were exposed to secondhand smoke during the period of gestation than their control counterparts (24%) (P = 0.01) with an odds ratio of 2.46 (95% CI = 0.99-6.08). Electrophoresis of the restriction fragment length polymorphism (RFLP) product revealed the presence of the homozygous C1C1 allele in all the tested 92 samples with no homozygous C2C2 allele or heterozygous C1C2 allele. CONCLUSION: The present study has highlighted the role of passive smoking in the causation of non syndromic oral clefts in a developing country like India; however, the involvement of TGFA in causing the same disease in an ethnically Dravidian Indian population is uncertain. CLINICAL SIGNIFICANCE: The study has brought into forth the role of passive smoking in the development of oral clefts thereby warranting an effective public health policy to tackle the same.
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