Temporomandibular joint osteoarthritis (TMJ OA) is an important subtype of temporomandibular disorders (TMD). Articular cartilage destruction is considered a common pathological feature of TMJ OA, which is reported to be mainly induced by chondrocyte apoptosis. Synovial sterile inflammation is an initial factor of TMJ OA-associated articular cartilage destruction. Therefore, determining the mechanism of synovial membrane inflammation-induced articular cartilage destruction in TMJ OA is important for the TMJ OA therapy. In this study, we detected the function of synoviocytes in chondrocyte apoptosis under lipopolysaccharide (LPS)-induced inflammatory conditions and explored the underlying mechanism. We found that synoviocytes in inflammatory conditions facilitated LPS-induced chondrocytes apoptosis by secreting increased Tumor Necrosis Factor α (TNF-α), which was induced by long non-coding RNA plasmacytoma variant translocation 1 (PVT1) upregulation. PVT1 served as a competing endogenous RNA that sponged the microRNA miR-211-3p and prevented the inhibition of TNF-α expression. In conclusion, our in vitro study revealed that PVT1 has a previously unknown role in chondrocyte apoptosis, which may also be a mechanism underlying synoviocyte involvement in TMJ OA.

颞下颌关节骨关节炎（TMJ OA）是颞下颌关节疾病（TMD）的重要亚型。关节软骨破坏被认为是TMJ OA的常见病理特征，据报道主要由软骨细胞凋亡诱导。滑膜无菌性炎症是TMJ OA相关关节软骨破坏的初始因素。因此，确定TMJ OA中滑膜发炎引起的关节软骨破坏的机制对于TMJ OA治疗很重要。在这项研究中，我们检测了滑膜细胞在脂多糖（LPS）诱导的炎症条件下在软骨细胞凋亡中的功能，并探讨了其潜在机制。我们发现在炎性条件下的滑膜细胞通过分泌增加的肿瘤坏死因子α（TNF-α）来促进LPS诱导的软骨细胞凋亡，而肿瘤坏死因子α是由长期的非编码RNA浆细胞瘤变位1（PVT1）上调诱导的。PVT1充当竞争性内源RNA，使microRNA miR-211-3p吸收海绵并阻止TNF-α表达的抑制。总之，我们的体外研究表明，PVT1在软骨细胞凋亡中具有以前未知的作用，这可能也是滑膜细胞参与TMJ OA的潜在机制。