Centre for Orthopaedic & Trauma Research, The University of Adelaide, Adelaide, South Australia 5000, Australia; Biomedical Orthopaedic Research Group, Centre for Orthopaedic & Trauma Research, The University of Adelaide, Adelaide, South Australia 5000, Australia.
Centre for Orthopaedic & Trauma Research, The University of Adelaide, Adelaide, South Australia 5000, Australia.
Osteoarthritis Cartilage. 2024 May;32(5):493-500. doi: 10.1016/j.joca.2023.10.010. Epub 2023 Dec 30.
Osteoarthritis (OA) is a disease of joints, in which the bone under the articular cartilage undergoes increased remodelling activity. The question is whether a better understanding of the causes and mechanisms of bone remodelling can predict disease-modifying treatments.
This review summarises the current understanding of the aetiology of OA, with an emphasis on events in the subchondral bone (SCB), and the cells and cytokines involved, to seek an answer to this question.
SCB remodelling across OA changes the microstructure of the SCB, which alters the load-bearing properties of the joint and seems to have an important role in the initiation and progression of OA. Bone remodelling is tightly controlled by numerous cytokines, of which Receptor Activator of NFκB ligand (RANKL) and osteoprotegerin are central factors in almost all known bone conditions. In terms of finding therapeutic options for OA, an important question is whether controlling the rate of SCB remodelling would be beneficial. The role of RANKL in the pathogenesis and progression of OA and the effect of its neutralisation remain to be clarified.
This review further makes the case for SCB remodelling as important in OA and for additional study of RANKL in OA, both its pathophysiological role and its potential as an OA disease target.
骨关节炎（OA）是一种关节疾病，其中关节软骨下的骨经历了增强的重塑活动。问题是，对骨重塑的原因和机制的更好理解是否可以预测疾病修饰治疗。
本综述总结了 OA 病因学的当前理解，重点是软骨下骨（SCB）中的事件以及涉及的细胞和细胞因子，以寻求对这个问题的答案。
OA 中 SCB 重塑改变了 SCB 的微观结构，这改变了关节的承载性能，并且似乎在 OA 的起始和进展中具有重要作用。骨重塑受众多细胞因子的紧密控制，其中核因子κB 配体（RANKL）和骨保护素是几乎所有已知骨病的核心因素。就 OA 的治疗选择而言，一个重要的问题是控制 SCB 重塑的速度是否有益。RANKL 在 OA 的发病机制和进展中的作用及其中和作用仍有待阐明。
本综述进一步证明了 SCB 重塑在 OA 中的重要性，以及对 RANKL 在 OA 中的进一步研究，包括其病理生理学作用及其作为 OA 疾病靶点的潜力。
