Aberrant activation of latent transforming growth factor-beta initiates the onset of temporomandibular joint osteoarthritis #MMPMID30210898
Zheng L; Pi C; Zhang J; Fan Y; Cui C; Zhou Y; Sun J; Yuan Q; Xu X; Ye L; Cao X; Zhou X
Bone Res 2018[]; 6 (?): 26 PMID30210898show ga
There is currently no effective medical treatment for temporomandibular joint osteoarthritis (TMJ-OA) due to a limited understanding of its pathogenesis. This study was undertaken to investigate the key role of transforming growth factor-beta (TGF-beta) signalling in the cartilage and subchondral bone of the TMJ using a temporomandibular joint disorder (TMD) rat model, an ageing mouse model and a Camurati-Engelmann disease (CED) mouse model. In the three animal models, the subchondral bone phenotypes in the mandibular condyles were evaluated by microCT, and changes in TMJ condyles were examined by TRAP staining and immunohistochemical analysis of Osterix and p-Smad2/3. Condyle degradation was confirmed by Safranin O staining, the Mankin and OARSI scoring systems and type X collagen (Col X), p-Smad2/3a and Osterix immunohistochemical analyses. We found apparent histological phenotypes of TMJ-OA in the TMD, ageing and CED animal models, with abnormal activation of TGF-beta signalling in the condylar cartilage and subchondral bone. Moreover, inhibition of TGF-beta receptor I attenuated TMJ-OA progression in the TMD models. Therefore, aberrant activation of TGF-beta signalling could be a key player in TMJ-OA development.
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Bone+Res 2018 ; 6 (?): 26
