Osteoarthritis (OA) is mainly caused by ageing, strain, trauma, and congenital joint abnormalities, resulting in articular cartilage degeneration. During the pathogenesis of OA, the changes in subchondral bone (SB) are not only secondary manifestations of OA, but also an active part of the disease, and are closely associated with the severity of OA. In different stages of OA, there were microstructural changes in SB. Osteocytes, osteoblasts, and osteoclasts in SB are important in the pathogenesis of OA. The signal transduction mechanism in SB is necessary to maintain the balance of a stable phenotype, extracellular matrix (ECM) synthesis, and bone remodelling between articular cartilage and SB. An imbalance in signal transduction can lead to reduced cartilage quality and SB thickening, which leads to the progression of OA. By understanding changes in SB in OA, researchers are exploring drugs that can regulate these changes, which will help to provide new ideas for the treatment of OA.

中文翻译：

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软骨下骨细胞和信号通路在骨关节炎中的作用。

骨关节炎（OA）主要是由衰老、劳损、创伤和先天性关节异常引起，导致关节软骨退变。在OA发病过程中，软骨下骨（SB）的变化不仅是OA的继发表现，也是疾病的活跃部分，且与OA的严重程度密切相关。在OA的不同阶段，SB的微观结构发生变化。SB 中的骨细胞、成骨细胞和破骨细胞在 OA 的发病机制中很重要。SB 中的信号转导机制对于维持关节软骨和 SB 之间稳定表型、细胞外基质 (ECM) 合成和骨重塑的平衡是必要的。信号转导失衡会导致软骨质量下降和 SB 增厚，从而导致 OA 的进展。通过了解OA中SB的变化，研究人员正在探索能够调节这些变化的药物，这将有助于为OA的治疗提供新思路。