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Enamel Formation Genes Are Associated with High Caries Experience in Turkish ChildrenPatir A.a · Seymen F.a · Yildirim M.a · Deeley K.b · Cooper M.E.b · Marazita M.L.b, d, e · Vieira A.R.b, c, d
aDepartment of Pedodontics, Istanbul University, Istanbul, Turkey; bDepartment of Oral Biology and Center for Craniofacial and Dental Genetics and cDepartment of Pediatric Dentistry, School of Dental Medicine, dDepartment of Human Genetics, Graduate School of Public Health, and eDepartment of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, Pa., USA Corresponding Author
Alexandre R. Vieira
614 Salk Hall, Department of Oral Biology, School of Dental Medicine
University of Pittsburgh, 3501 Terrace Street
Pittsburgh, PA 15261 (USA)
Tel. +1 412 383 8972, Fax +1 412 624 3080, E-Mail firstname.lastname@example.org
There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes and their interaction with Streptococcus mutans levels may contribute to caries. For the present study, we used DNA samples collected from 173 unrelated children from Istanbul: 91 children with 4 or more affected tooth surfaces and 82 caries-free children. Six single-nucleotide polymorphism markers were genotyped in selected candidate genes (ameloblastin, amelogenin, enamelin, tuftelin 1 and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Regression analysis was used for the evaluation of individual gene effects, environmental effects and gene-environment interactions. Overrepresentation of the C allele of the amelogenin marker was seen in cases with dmft scores higher than 8 (p = 0.01) when compared to controls. Also, overrepresentation of the T allele of the ameloblastin marker was seen in cases with dmfs scores higher than 10 (p = 0.05) when compared to controls. In addition, the CT genotype of the tuftelin rs3790506 marker was overrepresented in cases with dmft scores higher than 5 (p = 0.05) and dmfs scores higher than 6 (p = 0.05) compared to controls. The best-fitting model showed that dmfs is increased when the following factors are present: (1) females and both the anterior and posterior teeth are affected simultaneously, (2) when the T allele of the tuftelin rs3790506 is involved, and (3) the C allele of the amelogenin rs17878486 is involved. Our study provides support that genes involved in enamel formation modify caries susceptibility in humans.
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