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Objective : To evaluate the association of bruxism phenotypes with single nucleotide polymorphisms in FKBP5, DRD2, ANKK1 , and COMT . Methods : Clinical oral examination was performed to diagnose bruxism phenotypes in 150 children. DNA was collected from saliva. Logistic univariate regression, Chi-square, and Fisher's exact tests were performed ( p < 0.05). Results : Bruxism was associated with DRD2 ( p = 0.02). Tooth grinding while awake was associated with ANKK1 ( p < 0.001), and tooth grinding while asleep was associated with DRD2 in the additive ( p = 0.030) and dominant ( p = 0.008) model. Tooth clenching while awake was associated with ANKK1 in the additive ( p = 0.005) and dominant ( p = 0.008) models, whereas tooth clenching while asleep was associated with ANKK1 ( p < 0.001) and with COMT in the additive ( p = 0.001) and dominant ( p = 0.003) models. Discussion : Polymorphisms in DRD2, ANKK1 , and COMT are associated with bruxism phenotypes.

Objectives: This research aimed to evaluate the frequency of single nucleotide polymorphisms (SNPs) in dopaminergic pathway genes (DRD1, DRD2, DRD3, DRD4, DRD5, and MAOB) in patients undergoing bruxism treatment and controls., Subjects and Methods: Patients submitted to bruxism treatment were classified in awake bruxism (61 patients), sleep bruxism (26 patients), and awake-sleep bruxism (43 patients). Control group included 59 patients. Association between circadian manifestations of bruxism and SNPs was investigated using Fisher's exact test, chi-squared test, and calculating the odds ratios and their respective 95% confidence intervals., Results: The G allele of DRD2 rs1800497 SNP was associated with a significant risk reduction of awake-sleep bruxism (p = 0.041), while the C allele of DRD3 rs6280 SNP was associated with increased risk of sleep bruxism (p = 0.02), and the C allele of DRD5 rs6283 SNP was associated with decreased risk of awake bruxism (p = 0.01)., Conclusions: To our knowledge, this is the first report exploring the contribution of genetic variants in dopaminergic pathways to bruxism development, considering all circadian manifestations. Our findings indicate a possible genetic influence in the etiology of awake, sleep, and awake-sleep bruxism. Therefore, further research is needed to increase the current understanding of bruxism physiopathology.

Bruxism (BRX) is a condition of great interest for researchers and clinicians in dental and medical areas. BRX has two circadian manifestations; it can occur during sleep (sleep bruxism, SB) or during wakefulness (awake bruxism, WB). However, it can be suffered together. Recent investigations suggest that central nervous system neurotransmitters and their genes could be involved in the genesis of BRX. Serotonin is responsible for the circadian rhythm, maintaining arousal, regulating stress response, muscle tone and breathing. Thus, serotonin could be associated with BRX pathogenesis. The aim of this work was to evaluate the frequency of genetic polymorphisms in the genes HTR1A (rs6295), HTR2A (rs1923884, rs4941573, rs6313, rs2770304), HTR2C (rs17260565) and SLC6A4 (rs63749047) in subjects undergoing BRX treatment. Patients included were classified according to their diagnosis in awake bruxism (61 patients), sleep bruxism (26 patients) and both (43 patients). The control group included 59 healthy patients with no signs of BRX. Data showed significant differences in allelic frequencies for the HTR2A rs2770304 polymorphism, where the C allele was associated with increased risk of SB (odds ratio = 2·13, 95% confidence interval: 1·08-4·21, P = 0·03). Our results suggest that polymorphisms in serotonergic pathways are involved in sleep bruxism. Further research is needed to clarify and increase the current understanding of BRX physiopathology., (© 2016 John Wiley & Sons Ltd.)