Association Between Genetic Polymorphisms in Metaloproteinases of the Matrix and Delayed Tooth Emergence: A Cross-sectional Study

Abstract

Background and Aims: Animal models have been demonstrating that MMPs have an important function in the tooth eruption process. The aim of this study was to evaluate the association between genetic polymorphisms in MMP8 and MMP13 and delayed tooth eruption of permanent teeth. Materials and Methods: This cross-sectional study selected 216 children, 9- to 12-year-old, from public schools at Manaus, Amazonas, Brazil. During oral clinical examination, each permanent tooth emerged in the oral cavity was evaluated. Children were considered with delayed tooth eruption when at least one permanent tooth was delayed and were classified in 2 groups: children “with delayed tooth emergency” and “without delayed tooth emergency.” Saliva samples were collected from DNA extraction. The genetic polymorphisms rs17099443 and rs3765620 in MMP8, and rs478927 and rs2252070 in MMP13 were genotyped. Statistical Analysis: PLINK V1.07 ( http://pngu.mgh.harvard.edu/purcell/plink/ ) and GraphPad Prism 5.0 (San Diego, CA, USA) were used. The c2 or Fisher exact test was used to calculate genotypes and alleles distributions. To compare the mean number of delayed teeth according to genotypes, the Kruskal-Wallis test with multiple comparison Dunn test was used. The established alpha for all comparisons was .05. Results: The polymorphism rs17099443 in MMP8 was associated with delayed tooth eruption in the genotype distribution ( P = .05). In the allele distribution, the C allele was underrepresented in children with delayed tooth eruption ( P = .01; OR = 0.61, 95% confidence interval, 0.41–0.9). Conclusion: The genetic polymorphism rs17099443 in MMP8 is associated with delayed tooth eruption.

Single Nucleotide Polymorphisms in COX2 Is Associated with Persistent Primary Tooth and Delayed Permanent Tooth Eruption

“…The authors identified that a total of 51 different variations of the PTH1R (parathyroid hormone 1 receptor) gene were associated with the primary failure of eruption [ 12 ]. More recently, some studies have also raised the suggestion that the mild forms of tooth eruption alterations, such as delayed tooth eruption with or without PPT, also have a genetic background involved in its etiology [ 4 , 13 , 14 , 15 ]. Variations (SNPs) in genes such as the receptor activator of NF-κB ligand (RANKL) [ 13 ] and Matrix metalloproteases 8 (MMP8) [ 14 ] could be involved in this common condition.…”

“…More recently, some studies have also raised the suggestion that the mild forms of tooth eruption alterations, such as delayed tooth eruption with or without PPT, also have a genetic background involved in its etiology [ 4 , 13 , 14 , 15 ]. Variations (SNPs) in genes such as the receptor activator of NF-κB ligand (RANKL) [ 13 ] and Matrix metalloproteases 8 (MMP8) [ 14 ] could be involved in this common condition. Since all cases of tooth agenesis (excluding third molars agenesis) were excluded from our study, it is worth mentioning that all PPT cases also present with the delayed permanent tooth eruption of its successor.…”