Format

Send to

Choose Destination
Int J Oral Maxillofac Surg. 2019 Jul 5. pii: S0901-5027(19)31224-X. doi: 10.1016/j.ijom.2019.06.027. [Epub ahead of print]

Evaluation of genetic risk related to catechol-O-methyltransferase (COMT) and β2-adrenergic receptor (ADRB2) activity in different diagnostic subgroups of temporomandibular disorder in Brazilian patients.

Author information

1
School of Medicine of Petropolis, Petropolis, Rio de Janeiro, Brazil. Electronic address: ricardotesch@fmpfase.edu.br.
2
Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
3
School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
4
National Institute of Metrology, Quality and Technology, Rio de Janeiro, Brazil.
5
Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

The aim of this study was to evaluate the possible association between polymorphisms in the catechol-O-methyltransferase (COMT) and β2-adrenergic receptor (ADRB2) genes and muscular temporomandibular disorders (TMD). This was a case-control study. Individuals were evaluated using the Research Diagnostic Criteria for Temporomandibular Disorders and were divided into three groups: unaffected (no TMD) (n=154); exclusively muscular TMD (n=49); exclusively articular TMD (n=49). Genomic DNA was obtained from saliva samples, and single nucleotide polymorphisms in the COMT (rs165774, rs6269, rs9332377) and ADRB2 (rs2053044, rs1042713, rs1042714) genes were investigated. The TT genotype for the COMT rs9332377 gene was highly associated with the presence of muscular TMD (P= 0.03). With respect to the ADRB2 gene, the non-polymorphic AA genotype in the rs1042713 region was more prevalent in the articular TMD group than in the muscular TMD group (P= 0.05). This study supports the hypothesis that alterations in the COMT and ADRB2 genes influence the muscular pathophysiology.

KEYWORDS:

chronic pain; genetic polymorphism; pain; temporomandibular joint dysfunction syndrome

PMID:
31285095
DOI:
10.1016/j.ijom.2019.06.027

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center