Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

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. © 2012 Shimizu et al

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

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

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

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

Correlations of enamel microhardness values in the several experimental points.

<p>Statistically significant correlations are presented in bold font.</p

Single marker association results for enamel microhardness.

<p>p-values <0.05 are presented in bold font.</p>*<p>Samples from buccal and lingual surfafes were analyzed together.</p><p>Artificial Caries/Baseline; The ratio of change for microhardness after creation of artificial caries.</p><p>Fluoride/Artificial Caries; The ratio of change for microhardness after fluoride treatment.</p><p>pH-cycling/Fluoride; The ratio of change for microhardness after pH-cycling treatment.</p

Association results for caries experience in Filipinos and in the replication sample sets.

<p>P-values <0.05 are presented in bold font.</p

Family-based association test results for caries experience in Filipino familes.

<p>Statistically significant p-values (p<0.05) are presented in bold font.</p

Previously reported associations between enamel formation genes and caries susceptibility.

*<p>In the presence of <i>Streptococcus mutans</i>.</p>#<p>Only is less severely affected cases.</p

Demographics and caries experience of the replication study populations.

a<p>Decayed, Missing due to caries, Filled Teeth.</p>b<p>Standard deviation.</p>c<p>High and low caries experience was defined based on criteria 1 on <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045022#pone-0045022-t001" target="_blank">Table 1</a>.</p

Definitions of caries experience based on age and DMFT (Decayed, Missing due to caries, Filled Teeth) scores used in the Filipino families.

a<p>DMFT cut-offs were modified from the World Health Organization (World Health Organization, 2003),</p>b<p>Standard deviation.</p