Hu Yan, Chen Xiao, Wang Sicheng, Jing Yingying, Su Jiacan
Department of Orthopedics Trauma, Shanghai Changhai Hospital, Naval Military Medical University, Shanghai, China.
Institute of Translational Medicine, Shanghai University, Shanghai, China.
Bone Res. 2021 Mar 17;9(1):20. doi: 10.1038/s41413-021-00147-z.
Osteoarthritis comprises several joint disorders characterized by articular cartilage degeneration and persistent pain, causing disability and economic burden. The incidence of osteoarthritis is rapidly increasing worldwide due to aging and obesity trends. Basic and clinical research on osteoarthritis has been carried out for decades, but many questions remain unanswered. The exact role of subchondral bone during the initiation and progression osteoarthritis remains unclear. Accumulating evidence shows that subchondral bone lesions, including bone marrow edema and angiogenesis, develop earlier than cartilage degeneration. Clinical interventions targeting subchondral bone have shown therapeutic potential, while others targeting cartilage have yielded disappointing results. Abnormal subchondral bone remodeling, angiogenesis and sensory nerve innervation contribute directly or indirectly to cartilage destruction and pain. This review is about bone-cartilage crosstalk, the subchondral microenvironment and the critical role of both in osteoarthritis progression. It also provides an update on the pathogenesis of and interventions for osteoarthritis and future research targeting subchondral bone.
骨关节炎包括几种以关节软骨退变和持续性疼痛为特征的关节疾病，会导致残疾和经济负担。由于老龄化和肥胖趋势，骨关节炎的发病率在全球范围内正在迅速上升。关于骨关节炎的基础和临床研究已经开展了数十年，但许多问题仍未得到解答。软骨下骨在骨关节炎的起始和进展过程中的确切作用仍不清楚。越来越多的证据表明，包括骨髓水肿和血管生成在内的软骨下骨病变比软骨退变出现得更早。针对软骨下骨的临床干预已显示出治疗潜力，而针对软骨的其他干预则产生了令人失望的结果。异常的软骨下骨重塑、血管生成和感觉神经支配直接或间接导致软骨破坏和疼痛。本综述围绕骨-软骨相互作用、软骨下微环境及其在骨关节炎进展中的关键作用展开。它还提供了骨关节炎发病机制和干预措施的最新情况，以及针对软骨下骨的未来研究方向。
