RESUMO
Bruxism is a masticatory muscle activity characterized by grinding of the teeth and clenching of the jaw that causes tooth wear and breakage, temporomandibular joint disorders, muscle pain, and headache. Bruxism occurs in both adults and children. Clinical characteristics and habits were evaluated in an adult sample. Moreover, we used DNA samples from 349 adults and 151 children to determine the presence of association with specific genes. Genomic DNA was obtained from saliva. The markers rs2241145 and rs243832 (metalloproteinase 2 (MMP2)), rs13925 and rs2236416 (metalloproteinase 9 (MMP9)), and rs6269 (cathecol-o-methyltransferase (COMT)) were genotyped. Data were submitted to statistical analysis with a significance level of 0.05. In adults, in univariate logistic regression, presence of caries, attrition, and use of alcohol were increased in bruxism individuals (p < 0.05). In addition, in adults, there was an association between bruxism and MMP9 (rs13925, p = 0.0001) and bruxism and COMT (rs6269, p = 0.003). In children, a borderline association was observed for MMP9 (rs2236416, p = 0.08). When we performed multivariate logistic regression analyses in adults, the same clinical characteristics remained associated with bruxism, and orthodontic treatment was also associated, besides rs13925, in the AG genotype (p = 0.015, ORa: 3.40 (1.27-9.07)). For the first time, we provide statistical evidence that these genes are associate with bruxism.
RESUMO
OBJECTIVES: The aim was to review the literature regarding genetic contributions to temporomandibular joint disorder (TMD) after our 2008 publication. SETTING AND SAMPLE POPULATION: Literature review. MATERIAL AND METHODS: PubMed and MEDLINE were used to obtain literature in any language regarding genes and TMD, using the keywords "temporomandibular joint disorder" and "temporomandibular joint dysfunction" for studies published from 2009 to 2017. RESULTS: In our search, 274 studies were found. We excluded 76 studies from animal models, 22 studies that were in vitro and 120 reports that were not cohort or case-control studies. Of the 274 results, 56 articles were selected for this review. Genes that are suggested to contribute to TMD included the ones related to disc and bone alterations as well as pain sensation. CONCLUSION: Currently, no evidence of associated genetic variants, which can determine the development of TMD in individuals, could be translated to novel clinical management and public health strategies for patients suffering from TMD.
