Involvement of the MAPK pathway in the pressure-induced synovial metaplasia procedure for the temporomandibular joint

Abstract

ABSTRACT. Abnormal pressure is an important factor that contributes to bone adaptation in the temporomandibular joint (TMJ). We determined the effect of the mitogen-activated protein kinases (MAPK) pathway on the pressure-induced synovial metaplasia procedure for the TMJ, both in vitro and in vivo. Synovial fibroblasts (SFs) were exacted from rat TMJs and exposed to different hydrostatic pressures. The protein extracts were analyzed to determine the activation of ERK1/2, JNK, and p38. Surgical anterior disc displacement (ADD) was also performed on Japanese rabbits, and the proteins of TMJ were isolated to analyze pressure-induced MAPK activation after 1, 2, 4, and 8 weeks. The results showed that the activation of ERK1/2 and JNK in SFs significantly changed with increasing hydrostatic pressure, whereas p38 activation did not change. Moreover, p38 was activated in animals 1 week after surgical ADD. The levels of p38 gradually increased after 2 and 4 weeks, and then slightly decreased but remained higher than in the control 8 weeks after surgical ADD. Nevertheless, JNK was rarely activated after the ADD treatment. Our findings suggest the involvement of MAPK activation in the pressure-induced synovial metaplasia procedure with pressure loading in TMJ.

Polyphenols as Potential Agents in the Management of Temporomandibular Disorders

“…It is associated with inflammation through the regulation of several mechanisms, including the activation of cytokine production, modulation of naive T-cell differentiation into T helper-1 or T helper-2 cells, and the suppression of glucocorticoid receptor [31]. Moreover, Mitogen-Activated Protein kinases (MAPKs), serine-threonine kinases, also mediate intracellular signaling involved in the regulation of inflammation associated with gene expression, cell survival, proliferation, inducible nitric oxide synthase (iNOS) cytokine expression, and collagenase production in synoviocytes, chondrocytes, and synovial fibroblasts, suggesting the involvement in the development of synovial injury by regulating the expression of IL-1β in synovial membranes [32][33][34].…”