ABSTRACT
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.
Subject(s)
Bruxism , Polymorphism, Single Nucleotide , Receptors, Dopamine D2/genetics , Bruxism/genetics , Catechol O-Methyltransferase , Genotype , Humans , Phenotype , Protein Serine-Threonine KinasesABSTRACT
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.
Subject(s)
Bruxism/genetics , Polymorphism, Single Nucleotide , Receptors, Dopamine D2/genetics , Receptors, Dopamine D3/genetics , Receptors, Dopamine D5/genetics , Adult , Alleles , Female , Genotype , Humans , Male , Polymerase Chain Reaction , Sleep Bruxism/geneticsABSTRACT
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.
Subject(s)
Bruxism/genetics , Bruxism/physiopathology , Circadian Rhythm/genetics , Genetic Predisposition to Disease , Polymorphism, Single Nucleotide , Serotonin/metabolism , Adult , Bruxism/diagnosis , Case-Control Studies , Chile , Female , Gene Frequency , Humans , Male , Masseter Muscle/physiopathology , Receptors, Serotonin/genetics , Receptors, Serotonin/metabolism , Serotonin Plasma Membrane Transport Proteins/genetics , Serotonin Plasma Membrane Transport Proteins/metabolism , Sleep , WakefulnessABSTRACT
Bruxismo se define como un trastorno del movimiento mandibular que se caracteriza por apretamiento o rechinamiento dentario. Se estima que la prevalencia de éste puede variar desde un 8 por ciento a un 20 por ciento de la población adulta. Quienes padecen esta parafunción relatan manifestación en otras personas del grupo familiar. Existen teorías que buscan explicar la etiología del bruxismo, basados principalmente en estudios clínicos y encuestas a pacientes. Estas proponen que los principales factores etiológicos de Bruxismo serían estrés y alteraciones en ciertos neurotransmisores o sus vías (Dopamina, Ácido Gamma-Aminobutírico y Serotonina). La posibilidad de que alteraciones genéticas del ADN influyan en la aparición de bruxismo no ha sido considerada. Dado que no existe en la literatura consultada estudios genético-moleculares y/o funcionales que confirmen las teorías basadas en estudios clínicos, parece necesario iniciar investigaciones en esta área que lleven a una mejor comprensión de esta parafunción, con el ánimo final de aportar en el desarrollo de más y mejores terapias para el tratamiento del bruxismo...
Bruxism has been defined as a sleep-related movement disorder characterized by tooth grinding or clenching. Between 8 percent to 20 percent of adult population is affected by this parafunction. Relatives of these patients have reported to be affected by bruxism as well. There are theories that want to explain bruxism ethiology based on factors as stress and alteration in neurotransmitters (Dopamine, GABA and Serotonin). Possible epigenetic alterations in DNA influencing bruxism appearance have not been considered. It is therefore necessary to perform genetic, epigenetic and molecular research to confirm theories related to bruxism ethiology, with the aim to improve knowledge in this field as well as to contribute in the development of new and better therapies in bruxism treatment...