The TGF-I was used to inhibit TGF-β1 signalling to rescue cartilage damage induced by OA.56 Moreover, the TGF-I ameliorated the abnormal role of high levels of active TGF-β1 in bone formation and directly attenuated Smad2/3 phosphorylation.57,58 In our study, injection of the TGF-I significantly decreased the number of p-Smad2/3-positive cells in the condylar cartilage and subchondral bone in the TMD model. Here, SMAD2 is linked to temporomandibular joint disorder.