Genetic approaches have shown that several genes could modify caries susceptibility; AmelogeninX (AMELX) has been repeatedly designated. Here, we hypothesized that AMELX mutations resulting in discrete changes of enamel microstructure may be found in children with a severe caries phenotype. In parallel, possible AMELX mutations that could explain resistance to caries may be found in caries-free patients. In this study, coding exons of AMELX and exon-intron boundaries were sequenced in 399 individuals with extensive caries (250) or caries-free (149) individuals from nine French hospital groups. No mutation responsible for a direct change of amelogenin function was identified. Seven single-nucleotide polymorphisms (SNPs) were found, 3 presenting a high allele frequency, and 1 being detected for the first time. Three SNPs were located in coding regions, 2 of them being non-synonymous. Both evolutionary and statistical analyses showed that none of these SNPs was associated with caries susceptibility, suggesting that AMELX is not a gene candidate in our studied population.

In the literature, the enamelin gene ENAM has been repeatedly designated as a possible candidate for caries susceptibility. Here, we checked whether ENAM variants could increase caries susceptibility. To this aim, we sequenced coding exons and exon-intron boundaries of ENAM in 250 children with a severe caries phenotype and in 149 caries-free patients from 9 French hospital groups. In total, 23 single-nucleotide polymorphisms (SNPs) were found, but none appeared to be responsible for a direct change of ENAM function. Six SNPs had a high minor allele frequency (MAF) and 6 others were identified for the first time. Statistical and evolutionary analyses showed that none of these SNPs was associated with caries susceptibility or caries protection when studied separately and challenged with environmental factors. However, haplotype interaction analysis showed that the presence, in a same variant, of 2 exonic SNPs (rs7671281 and rs3796704; MAF 0.12 and 0.10, respectively), both changing an amino acid in the protein region encoded by exon 10 (p.I648T and p.R763Q, respectively), increased caries susceptibility 2.66-fold independent of the environmental risk factors. These findings support ENAM as a gene candidate for caries susceptibility in the studied population.

The primary objective of this study was to evaluate the effects of sealants in preventing pit and fissure caries in primary molars. The secondary objective was to assess the sealant retention during a 2‐yr study period. A 2‐yr split‐mouth randomized clinical trial including 90 3–7‐yr‐old children was conducted in the paediatric dental department of Montpellier hospital. The dentition of each included patient was divided into an experimental side and a control side, with annual follow‐up visits. Caries increments, measured as the number of new occlusal cavitated lesions, were not different between the sealed (mean 0.23) and the control primary molars (mean 0.29). A multiple mixed‐effects logistic regression showed that male gender, moderate/high caries risk, and a higher oral hygiene index score, had a statistically significant effect resulting in higher caries increments in the primary molars, than did female gender, low caries risk, and lower oral hygiene index scores. Sealing showed no statistically significant influence on the development of new caries lesions. After 2 yr, the percentages of partially or totally lost sealants were 22.7% and 32.0%, respectively. In this sample of children, the caries increment was not significantly different between the sealed and the unsealed molars. At the end of this 2‐yr study, more than half of the sealants were totally or partially lost, which could explain the low sealant effectiveness.

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