Abstract
There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity.
Highlights
Caries continues to be a great burden to individuals, children, families, and society
We investigated genetic markers in genes involved in enamel formation that were previously studied [2,3,4] to provide independent replication of the original results, which suggested that variation in amelogenin, tuftelin, and enamelin contribute to higher caries experience in humans
It is likely that the phenotype definition we used is not sensitive enough to precisely detect these effects
Summary
Caries continues to be a great burden to individuals, children, families, and society. Genes responsible for enamel formation have been proposed as potentially involved in caries susceptibility, and positive associations between genetic variation in amelogenin, tuftelin, and enamelin and higher caries experience have been reported [2,3,4]. These results are promising because one can propose that variation in the enamel surface could predispose individuals to development of carious lesions. We investigated genetic markers in genes involved in enamel formation that were previously studied [2,3,4] to provide independent replication of the original results, which suggested that variation in amelogenin, tuftelin, and enamelin contribute to higher caries experience in humans. We tested if enamel microhardness varies depending on genetic variation and cariogenic challenge to unveil a possible mechanism for higher caries susceptibility related to enamel structure
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