ABSTRACT
Objective: Bruxism is a condition defined as a masticatory muscle activity with an unexplored genetic background. The aim of this study was to evaluate the association between genetic polymorphisms in ACTN3 and bruxism. Study design: A total of 151 biological-unrelated children, aged 7-12 years were included in a case control ratio of 1:1.5. The data collection was performed during interview and clinical examination. Saliva samples were collected from all children and 3 genetic polymorphisms in the ACTN3 (rs678397, rs1671064 and rs1815739) were selected for genotyping using real time PCR. Pearson chisquare calculation was used to assess Hardy-Weinberg equilibrium and to evaluate the association between genotypes and alleles frequencies for each genetic polymorphism in the co-dominant and recessive models. An alpha of 5% was used. Results: The genetic polymorphisms rs678397, rs1671064 and rs1815739 were associated with bruxism in the co-dominate model and in the recessive model (p<0.05). Allele distribution was also associated with bruxism for the polymorphisms rs678397 and rs1671064 (p<0.05). Conclusion: The genetic polymorphisms rs678397, rs1671064 and rs1815739 in ACTN3 are associated with bruxism and can contribute to the etiology of this condition in children.
Subject(s)
Actinin/genetics , Bruxism , Genotype , Child , Gene Frequency , Humans , Polymorphism, GeneticABSTRACT
Purpose: Recent studies have suggested that disruptions in the RANKL/RANK/OPG system might be involved in enamel conditions. The aim of this study was to test whether genetic polymorphisms in RANK, RANKL and OPG are associated with dental caries, developmental defects of enamel (DDE) and enamel microhardness. Study design: Saliva samples were collected from two subsets for the purpose of genomic DNA extraction. In the first subset, composed of 248 children, dental caries and DDE were evaluated during their clinical examination. In the second subset, composed of 72 children, enamel samples from the buccal surface of primary teeth were used for enamel microhardness analysis. Genetic polymorphisms in RANK, RANKL and OPG were genotyped by real-time polymerase chain reactions in all samples from both populations. The chi-square test was used for dental caries and DDE analysis while, one-way ANOVA with Tukey's post-test was used for microhardness analysis. Hardy-Weinberg equilibrium was also calculated. The established alpha was 5%. Results: Caries experience analysis demonstrated a statistically-significant difference for OPG allele distribution in primary dentition (p=0.033). The studied polymorphisms in RANK, RANKL and OPG were not associated with DDE or enamel microhardness (p>0.05). Conclusion: The genetic polymorphism rs2073618 in OPG is associated with dental caries experience in primary dentition.
