Molecular genetics and epigenetics of temporomandibular disorder

Abstract

Temporomandibular joint (TMJ) has an important role in stomatognathic system. Its role during function is facilitated from rotation and translation movement. Any deviation from TMJ normal anatomy and movement could lead into either clicking, crepitus, or pain in preauricular area. These sign and symptoms, which are widely referred as TMJ Temporomandibular joint disorder (TMD), extremely common in world population. Several genes have been identified contribute in susceptibility towards TMD. Genetic polymorphism are a form of gene sequences variance that is found in more than 1% of world population. Epigenetics is an interaction between internal and external environments that leads to a change in chromatin structures that switches the gene expression on and off. There are several factors that posibly affect the genetic polymorphisms in TMD such as; serotonin, cathecolamine, estrogen, folate, human leukocyte antigen (HLA), extracellular matrix, transcription factors, transforming growth factor beta (TGFβ), epithelial growth factor, β-catenin, and discoidin. Epigenetic mechanisms such as DNA methylation, histone modification, and microRNA are found in chondrocyte of TMD patients. In a temporomandibular joint, miRNA-140 controls bone homeostasis especially on the articular remodeling. Genetic molecular and epigenetic study will benefit in diagnosis and treatment of TMD patient. The aim of this paper is author want to inform about molecular genetics and epigenetics of TMD.

Neuroendocrine Influencers and Associated Factors That Shape Jaw Movement and Growth in Temporomandibular Joint Disorder Management: A Systematic Review of Clinical and Radiographic Evidence

“…An interplay between genetic and environmental factors is responsible for facial height and mandibular morphology, reflected on cephalograms by Ar-Pog measurements, which may be responsible for jaw movement and translation. Epigenetic mechanisms such as DNA methylation, histone modification, and microRNA can cause abnormal joint remodelling and TMJ destruction [ 8 ]. A decreased expression of lubricin can distort the hourglass shape of the articular disc in the intermediate zone, [ 5 ] while Col2 and Adamts1 genes may be responsible for mandibular prognathism in Chinese populations, and masticatory muscle load can affect the growth of the mandible and maxilla [ 8 , 16 ].…”

“…Epigenetic mechanisms such as DNA methylation, histone modification, and microRNA can cause abnormal joint remodelling and TMJ destruction [ 8 ]. A decreased expression of lubricin can distort the hourglass shape of the articular disc in the intermediate zone, [ 5 ] while Col2 and Adamts1 genes may be responsible for mandibular prognathism in Chinese populations, and masticatory muscle load can affect the growth of the mandible and maxilla [ 8 , 16 ]. Orthognathic surgery can also alter the mRNA compositions of masseter muscle, suggesting that a history of surgery is an important factor to consider when evaluating jaw movements [ 16 ].…”

“…Important neuroendocrine biomarkers reflecting gene inheritances, such as catecholamine, oestrogen, folate, and HLA, can lead to the diagnosis of degenerative disorders, and genetic polymorphism causing persistent TMJ pain and altered jaw motions [ 8 ]. Genetic alterations also increase proteoglycan secretion, leading to the secretion of matrix-degrading enzymes that degrade type 2 collagen in TMJ, while alterations in cholecalciferol uptake can lead to degenerative disorders, reduce bone thickness, and increase inflammatory mediators [ 8 ].…”

“…Important neuroendocrine biomarkers reflecting gene inheritances, such as catecholamine, oestrogen, folate, and HLA, can lead to the diagnosis of degenerative disorders, and genetic polymorphism causing persistent TMJ pain and altered jaw motions [ 8 ]. Genetic alterations also increase proteoglycan secretion, leading to the secretion of matrix-degrading enzymes that degrade type 2 collagen in TMJ, while alterations in cholecalciferol uptake can lead to degenerative disorders, reduce bone thickness, and increase inflammatory mediators [ 8 ]. Excess bone remodelling and degradation of cartilage in TMJ result from transforming growth factor (TGF) increase, and osteophyte formation on TMJ can occur due to the overproduction of epithelial growth factor (EGF), often caused by the absence of inhibitor genes.…”

“…The site and rate of growth are determined by genetics, endocrine influence, and are interdependent on daily jaw motion routines such as mastication and swallowing [ 6 , 7 ]. TMJ movement and occlusion in humans is therefore, unsurprisingly, very specific to endogenous and exogenous neuroendocrine phenotypes [ 8 ].…”