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-β (TGF-β) 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 µCT, 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-β signalling in the condylar cartilage and subchondral bone. Moreover, inhibition of TGF-β receptor I attenuated TMJ-OA progression in the TMD models. Therefore, aberrant activation of TGF-β signalling could be a key player in TMJ-OA development.

由于对颞下颌关节骨关节炎的发病机理了解有限，因此目前尚无有效的药物治疗方法。进行了这项研究，以探讨颞下颌关节疾病（TMD）大鼠模型，衰老小鼠模型和Camurati-Engelmann模型对转化生长因子-β（TGF-β）信号在TMJ软骨和软骨下骨中的关键作用疾病（CED）小鼠模型。在这三种动物模型中，通过µCT评估下颌con的软骨下骨表型，并通过TRAP染色以及Osterix和p-Smad2 / 3的免疫组织化学分析检查TMJ dy的变化。通过番红O染色，Mankin和OARSI评分系统以及X型胶原蛋白（Col X），p-Smad2 / 3a和Osterix免疫组织化学分析证实了的降解。我们在TMD，衰老和CED动物模型中发现了TMJ-OA的明显组织学表型，在dy突软骨和软骨下骨中TGF-β信号的异常激活。此外，在TMD模型中，对TGF-β受体I的抑制会减弱TMJ-OA的进程。因此，TGF-β信号转导的异常激活可能是TMJ-OA发展的关键因素。