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Bone-cartilage interface crosstalk in osteoarthritis: Potential pathways and future therapeutic strategies

机译：骨关节炎的骨-软骨界面串扰：潜在途径和未来治疗策略

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Currently, osteoarthritis (OA) is considered a disease of the entire joint, which is not simply a process of wear and tear but rather abnormal remodelling and joint failure of an organ. The bone-cartilage interface is therefore a functioning synergistic unit, with a close physical association between subchondral bone and cartilage suggesting the existence of biochemical and molecular crosstalk across the OA interface. The crosstalk at the bone-cartilage interface may be elevated in OA in vivo and in vitro. Increased vascularisation and formation of microcracks associated with abnormal bone remodelling in joints during OA facilitate molecular transport from cartilage to bone and vice versa. Recent reports suggest that several critical signalling pathways and biological factors are key regulators and activate cellular and molecular processes in crosstalk among joint compartments. Therapeutic interventions including angiogenesis inhibitors, agonists/antagonists of molecules and drugs targeting bone remodelling are potential candidates for this interaction. This review summarised the premise for the presence of crosstalk in bone-cartilage interface as well as the current knowledge of the major signalling pathways and molecular interactions that regulate OA progression. A better understanding of crosstalk in bone-cartilage interface may lead to development of more effective strategies for treating OA patients.
机译：当前，骨关节炎（OA）被认为是整个关节的疾病，这不仅仅是简单的磨损过程，而是器官的异常重塑和关节衰竭。因此，骨-软骨界面是功能性的协同单元，软骨下骨与软骨之间的紧密物理联系表明跨OA界面存在生化和分子串扰。在体内和体外OA中，骨-软骨界面处的串扰可能会增加。在OA期间，与关节中异常的骨骼重塑相关的血管化和微裂纹的形成增加，促进了分子从软骨向骨骼的运输，反之亦然。最近的报告表明，几个关键的信号通路和生物学因素是关键的调节器，并激活关节隔间串扰中的细胞和分子过程。包括血管生成抑制剂，分子激动剂/拮抗剂和靶向骨重构的药物在内的治疗干预措施可能是这种相互作用的候选者。这篇综述总结了在骨-软骨界面中存在串扰的前提，以及调节OA进展的主要信号通路和分子相互作用的当前知识。更好地了解骨-软骨界面的串扰可能会导致开发出更有效的策略来治疗OA患者。

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