Gene-environment Interactions in the Etiology of Dental Caries

Dental caries is a multifactorial disease that can be conceptualized as an interaction between genetic and environmental risk factors. The aim of this study is to examine the effects of AMELX, CA6, DEFB1, and TAS2R38 gene polymorphism and gene-environment interactions on caries etiology and susceptibility in adults. Genomic DNA was extracted from the buccal mucosa, and adults aged 20 to 60 y were placed into 1 of 2 groups: low caries risk (DMFT ≤ 5; n = 77) and high caries risk (DMFT ≥ 14; n = 77). The frequency of AMELX (+522), CA6 (T55M), DEFB1 (G-20A), and TAS2R38 (A49P) single-nucleotide polymorphisms was genotyped with the polymerase chain reaction–restriction fragment length polymorphism method. Environmental risk factors examined in the study included plaque amount, toothbrushing frequency, dietary intake between meals, saliva secretion rate, saliva buffer capacity, mutans streptococci counts, and lactobacilli counts. There was no difference between the caries risk groups in relation to AMELX (+522) polymorphism (χ2 test, P > 0.05). The distribution of CA6 genotype and allele frequencies in the low caries risk group did not differ from the high caries risk group (χ2 test, P > 0.05). Polymorphism of DEFB1 (G-20A) was positively associated, and TAS2R38 (A49P) negatively associated, with caries risk (χ2 test, P = 0.000). There were significant differences between caries susceptibility and each environmental risk factor, except for the saliva secretion rate (Mann-Whitney U test, P = 0.000). Based on stepwise multiple linear regression analyses, dental plaque amount, lactobacilli count, age, and saliva buffer capacity, as well as DEFB1 (G-20A), TAS2R38 (A49P), and CA6 (T55M) gene polymorphism, explained a total of 87.8% of the variations in DMFT scores. It can be concluded that variation in CA6 (T55M), DEFB1 (G-20A), and TAS2R38 (A49P) may be associated with caries experience in Turkish adults with a high level of dental plaque, lactobacilli count, and age and when saliva buffer capacity is low.

[1]  M. Marazita,et al.  Caries: Review of Human Genetics Research , 2014, Caries Research.

[2]  Poul Erik Petersen,et al.  Oral Health Surveys -Basic Methods , 2013 .

[3]  H. Inoue,et al.  A case study on the association of variation of bitter-taste receptor gene TAS2R38 with the height, weight and energy intake in Japanese female college students. , 2013, Journal of nutritional science and vitaminology.

[4]  P. Renuka,et al.  Review On "Influence Of Host Genes On Dental Caries" , 2013 .

[5]  M. Ateş,et al.  Efficiency of caries risk assessment in young adults using Cariogram , 2012, European journal of dentistry.

[6]  J. Granjeiro,et al.  Genetic variation in MMP20 contributes to higher caries experience. , 2012, Journal of dentistry.

[7]  L. Greco,et al.  Taste Perception and Food Choices , 2012, Journal of pediatric gastroenterology and nutrition.

[8]  K. Safranow,et al.  MBL2, MASP2, AMELX, and ENAM gene polymorphisms and dental caries in Polish children. , 2012, Oral diseases.

[9]  S. Akyüz,et al.  The investigation of genetic polymorphisms in the carbonic anhydrase VI gene exon 2 and salivary parameters in type 2 diabetic patients and healthy adults , 2011, Molecular Biology Reports.

[10]  S. Kang,et al.  Association between AMELX polymorphisms and dental caries in Koreans. , 2011, Oral diseases.

[11]  R. Werneck,et al.  A critical review: an overview of genetic influence on dental caries. , 2010, Oral diseases.

[12]  M. Marazita,et al.  Taste Genes Associated with Dental Caries , 2010, Journal of dental research.

[13]  J. T. Wright Defining the Contribution of Genetics in the Etiology of Dental Caries , 2010, Journal of dental research.

[14]  A. Vieira,et al.  The Antimicrobial Peptide DEFB1 Is Associated with Caries , 2010, Journal of dental research.

[15]  L. S. Mofatto,et al.  Association of polymorphisms in the carbonic anhydrase 6 gene with salivary buffer capacity, dental plaque pH, and caries index in children aged 7–9 years , 2010, The Pharmacogenomics Journal.

[16]  A. El-Sohemy,et al.  TAS2R38 Genotypes and Phenylthiocarbamide Bitter Taste Perception in a Population of Young Adults , 2010, Lifestyle Genomics.

[17]  M. Marazita,et al.  Enamel Formation Genes Are Associated with High Caries Experience in Turkish Children , 2008, Caries Research.

[18]  Y. Imamura,et al.  Analysis of mutations in the amelogenin and the enamelin genes in severe caries in Japanese pediatric patients , 2008 .

[19]  A. Bagherian,et al.  Comparison of allele frequency for HLA-DR and HLA-DQ between patients with ECC and caries-free children. , 2008, Journal of the Indian Society of Pedodontics and Preventive Dentistry.

[20]  W. L. Owen,et al.  Acidic Proline-rich Protein Db and Caries in Young Children , 2007, Journal of dental research.

[21]  M. Marazita,et al.  Possible Association of Amelogenin to High Caries Experience in a Guatemalan-Mayan Population , 2007, Caries Research.

[22]  N. Anthonisen,et al.  Contribution of alpha- and beta-defensins to lung function decline and infection in smokers: an association study , 2006, Respiratory research.

[23]  M. Marazita,et al.  Tuftelin, Mutans Streptococci, and Dental Caries Susceptibility , 2005, Journal of dental research.

[24]  D. Reed,et al.  Genetic and Environmental Determinants of Bitter Perception and Sweet Preferences , 2005, Pediatrics.

[25]  A. Banerjee Dental Caries. The Disease and its Clinical Management , 2004, British Dental Journal.

[26]  D. Zero Dental caries process. , 1999, Dental clinics of North America.

[27]  Jones Js,et al.  Life in the 21st century - a vision for all. , 1998 .

[28]  W R Grigsby,et al.  The dental caries process. , 1974, Virginia dental journal.

[29]  W H Bowen,et al.  Dental caries. , 1972, Archives of disease in childhood.

[30]  P. Armitage Oral Health Surveys: Basic Methods , 1972 .