Polymorphisms in COMTrs4818 were significantly associated with myofascial pain (OR<sub>c</sub> = 2.15; CI 95%: 1.08-4.29; P = 0.02) and were borderline for painful TMD (OR<sub>c</sub> = 1.85; CI 95%: 0.97-3.51; P = 0.06) and disc displacement (OR<sub>c</sub> = 2.42; CI 95%: 1.00-5.87; P = 0.05).
The purpose of this study was to evaluate the associations of variability in pulp sensitivity with sex, psychosocial variables, the gene that encodes for the enzyme catechol-O-methyltransferase (COMT), and chronic painful conditions (temporomandibular disorders [TMDs]).
Functional pain syndromes, such as fibromyalgia and temporomandibular disorder, are associated with enhanced catecholamine tone and decreased levels of catechol-O-methyltransferase (COMT; an enzyme that metabolizes catecholamines).
Furthermore, a significant (P = 0.04) interaction of COMT diplotype and time-varying stress showed that a postbaseline increase of 1.0 standard deviation in PSS more than doubled risk of TMD incidence in subjects with low-activity COMT diplotypes (hazard ratio = 2.35; 95% confidence limits: 1.66, 3.32), an effect not found in subjects with high-activity COMT diplotypes (hazard ratio = 1.42; 95% confidence limits: 0.96, 2.09).
Results show that the COMTrs4680 (rs4680;s4680;rs1200746244" genes_norm="1312;4524">val(158)met) polymorphism is most strongly associated with outcome measures, such that individuals with the minor A allele (met) exhibit reduced COMT activity, increased TMD risk, and increased musculoskeletal pain.
Results show that the COMT rs4680 (val(158)met) polymorphism is most strongly associated with outcome measures, such that individuals with the minor A allele (met) exhibit reduced COMT activity, increased TMD risk, and increased musculoskeletal pain.
Our data extend the number of SNPs present in the promoter region that could play a regulatory role in COMT gene and suggest that the genetic polymorphisms rs 165656 and rs 4646310 exert a role in TMD susceptibility.
Cross-sectional data from the population-based Study of Health in Pomerania (SHIP) in Germany were used to estimate additive interactions between depressive symptoms and 22 single-nucleotide polymorphisms (SNPs) of the COMT gene and the neighbouring thioredoxin reductase 2 (TXNRD2) gene on TMD pain.
Forty Caucasian female participants meeting the Research Diagnostic Criteria for TMD were genotyped for COMT polymorphisms and completed a randomized, double-blind, placebo-controlled, two-period crossover pilot study.
Recently, our group demonstrated that three common haplotypes of the human COMT gene, divergent in two synonymous and one nonsynonymous position, are associated with experimental pain sensitivity and onset of temporomandibular joint disorder.
Enhancement of chondrocyte autophagy is an early response in the degenerative cartilage of the temporomandibular joint to biomechanical dental stimulation.
Enhancement of chondrocyte autophagy is an early response in the degenerative cartilage of the temporomandibular joint to biomechanical dental stimulation.
Enhancement of chondrocyte autophagy is an early response in the degenerative cartilage of the temporomandibular joint to biomechanical dental stimulation.
Enhancement of chondrocyte autophagy is an early response in the degenerative cartilage of the temporomandibular joint to biomechanical dental stimulation.
136 participants with at least one of four orofacial pain diagnoses (temporomandibular disorders [TMD, n = 41], acute dental pain [ADP, n = 41], trigeminal neuralgia [TN, n = 19], persistent dentoalveolar pain disorder [PDAP, n = 14]) and a group of pain-free controls (n = 21) completed the modified S-LANSS, a previously adapted version of the original questionnaire devised to detected patients suffering from intraoral pain with neuropathic characteristics.
TMD sign using the Research Diagnostic Criteria for Temporomandibular Disorders and TMD pain intensity using a visual analog scale (VAS) in the morning and daytime were evaluated at baseline (pre-exercise) and at 2-weeks, 1-month, and 3-months after OA insertion.