TLR4 contributes to the damage of cartilage and subchondral bone in discectomy‐induced TMJOA mice

Abstract

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Cinnamic Aldehyde, the main monomer component of Cinnamon, exhibits anti‐inflammatory property in OA synovial fibroblasts via TLR4/MyD88 pathway

“…Meanwhile, the role of innate immune system in the progression of OA has also received increasing attention. Some studies suggested that the innate immune system is an active participant in synovial inflammation and cartilage catabolism and can initiate a series of molecular mechanisms to repair and reverse the damage 40,41 . Two modules were identified in these co‐targeted genes, and the KEGG pathway enrichment analysis results of these two modules both included the TLR and TNF signalling pathway.…”

“…Some studies suggested that the innate immune system is an active participant in synovial inflammation and cartilage catabolism and can initiate a series of molecular mechanisms to repair and reverse the damage. 40 , 41 Two modules were identified in these co‐targeted genes, and the KEGG pathway enrichment analysis results of these two modules both included the TLR and TNF signalling pathway. Previous research suggested that synovial inflammation can affect the cartilage innate immune system through TLR4/MyD88 signalling pathway, induce cartilage inflammation and degeneration and then aggravate the OA process.…”

Molecular signaling in temporomandibular joint osteoarthritis

“…IL-17, IL-1β and TNF-α expressed by synovial cells induce the RANKL expression in synovial fibroblasts and osteoblasts, promoting osteoclast formation and bone resorption [ 16 ]. Toll-like receptor 4 (TLR4), which mediates the innate immune reaction, aggravates the damage of cartilage and subchondral bone in discectomy-induced TMJ OA through activation of MyD88/NF-κB pathway in mice [ 17 ]. In addition, inflammatory cytokines are also in close correlation with pain in TMJ OA.…”

“…It has been shown that expression of TLR4 and NF-κB was elevated in the synovium in TMJ OA patients and in discectomy-induced TMJ OA in mice. TLR4 was also elevated in the damaged cartilage and subchondral bone through activation of MyD88/NF-κB [ 17 ]. It has been shown that the cartilage degeneration of TMJ OA can be inhibited by blocking the periostin–NF–κB-ADAMTS5 pathway [ 76 ].…”

Animal Models of Temporomandibular Joint Osteoarthritis: Classification and Selection

“…It can cause structural damage and abnormal articular forces to induce OA-like lesions directly by using surgical and mechanical devices. The common surgical methods include discectomy ( Hinton, 1992 ; Lan et al, 2017 ; Liu X. et al, 2020 ; Saito et al, 2021 ), partial discectomy ( Man et al, 2009 ; Xu et al, 2009 ; Lei et al, 2022 ), disc perforation ( Embree et al, 2015 ; Luo et al, 2020 ; Ruscitto et al, 2020 ), anterior disc displacement ( Togni et al, 2018 ; Xu et al, 2018 ; Nguyen et al, 2020 ), injury of the condylar surface ( Ishimaru and Goss, 1992 ; Wang F. et al, 2017 ), and postero-superior displacement of the mandible ( Imai et al, 2001 ; Liu et al, 2006 ) ( Table 3 ). These six methods well mimic advanced symptoms of joint injury in clinical patients, but they are not starting factors in general TMJOA.…”