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.

骨关节炎包括多种以关节软骨退化和持续性疼痛为特征的关节疾病，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世界范围内迅速增加。骨关节炎的基础和临床研究已经开展了几十年，但仍有许多问题没有得到解答。软骨下骨在骨关节炎发生和发展过程中的确切作用仍不清楚。越来越多的证据表明，软骨下骨病变，包括骨髓水肿和血管生成，比软骨退化更早发生。针对软骨下骨的临床干预已显示出治疗潜力，而其他针对软骨的干预却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。这篇综述是关于骨-软骨串扰、软骨下微环境以及两者在骨关节炎进展中的关键作用。它还提供了骨关节炎的发病机制和干预措施的最新信息以及针对软骨下骨的未来研究。