软骨下骨病变在骨关节炎发病机制中的作用

Roles of Subchondral Bone Lesion in the Pathogenesis of Osteoarthritis

骨–软骨下骨是一个由关节透明软骨、钙化软骨和软骨下骨组成的整体功能单位,其中任何一个组织的变化都会直接或间接影响该复合单位内其他组织的结构及功能。它们之间的生物力学与生物化学分子的相互作用在关节稳态维持和关节退化中起到重要的作用。在骨关节炎中,关节软骨的损伤或缺损,使传递到软骨下骨上的机械负荷明显增加,导致软骨下骨异常骨重塑,同时出现微裂纹,使其正常力学性能被破坏。软骨下骨正常力学性能的破坏反过来又使得关节软骨承受更大的应力,导致软骨的损伤和退行性病变进一步加重。此外,软骨下骨异常骨重塑导致软骨下骨板孔隙增加和血管新生,为骨–软骨单元的生物化学分子的双向交流提供可能,从而促进骨关节炎的发生发展。

Osteochondral junction is a functional unit composed of articular cartilage,calcified cartilage,and subchondral bone.Alteration in any individual component of this composite unit can disrupt joint integrity and function directly or indirectly.Biomechanical and biochemical signals mediate the crosstalk between the tissues and play an essential role in the initiation and progression of OA(osteoarthritis).During the pathogenesis of OA,the damage or defect in articular cartilage results in significantly more mechanical loading onto subchondral bone,leading to abnormal bone remodeling and microcracks,which further impair the normal mechanical properties of cartilage-bone unit.As the OA progresses,articular cartilage is exposed to excessive mechanical loading,which exacerbates the damage and degeneration of cartilage.Conversely,abnormal bone remodeling leads to increased angiogenesis and porosity in subchondral plate,which further triggers biochemical signals to mediate the crosstalk between cartilage and bone,and contributes to the progression of OA.