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Mediators of Inflammation
Volume 2016, Article ID 7694921, 7 pages
Research Article

Effect of Toll-Like Receptor 4 on Synovial Injury of Temporomandibular Joint in Rats Caused by Occlusal Interference

1Key Laboratory of Oral Biomedicine of Shandong Province, Stomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, China
2Jinan Stomatological Hospital, Number 101, Jing Liu Lu, Shandong Province, Jinan 250001, China
3Ningbo Medical Treatment Center Lihuili Hospital, Ningbo, Zhejiang 315000, China

Received 25 February 2016; Revised 9 May 2016; Accepted 25 May 2016

Academic Editor: Eda Holl

Copyright © 2016 Jingjing Kong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Synovitis is an important disease that causes intractable pain in TMJ. Some investigations suggested that the increasing expression of IL-1β secreted by synovial lining cells plays an important role in synovial inflammation and cartilage destruction in TMJ. In our previous research, the results demonstrated that TLR4 is involved in the expression of IL-1β in SFs from TMJ with lipopolysaccharide stimulation. However, the inflammatory response that occurred in synovial membrane is not caused by bacterial infection. In the current study, we investigated whether or not TLR4 participates in the inflammatory responses and the expression of IL-1β in synovial membrane of rats induced by occlusal interference. The results showed that obvious inflammation changes were observed in the synovial membranes and the expression of TLR4 and IL-1β was increased at both mRNA and protein levels in the occlusal interference rats. In addition, the inflammation reactions and the increased expression of IL-1β could be restrained by treatment with TAK-242, a blocker of TLR4 signaling. The results prompted us that the activation of TLR4 may be involved in the inflammatory reactions and increased expression of IL-1β in patients with synovitis and participate in the mechanisms of the initiation and development of synovial injury by regulating the expression of inflammatory mediators like IL-1β in synovial membranes.