退行性膝骨关节炎中软骨下骨病变的研究进展

Research progress on subchondral bone lesions in degenerative knee osteoarthritis

软骨下骨在退行性膝骨关节炎(KOA)中发挥的作用愈加受到重视,KOA初期,软骨下骨改建增加,总体骨结构参数降低,出现应力性微骨折,促使局部微循环障碍,不典型骨髓病变(BMLs)显现,骨软骨间微孔为血管侵入关节软骨深层提供了通道,随之带来软骨降解酶类;KOA进展期,维持软骨基质抗压强度的蛋白聚糖丢失,局部应力过载,软骨下骨吸收和骨形成失衡,骨改建降低,骨形成净增加,KOA晚期,出现明显的软骨下骨硬化,局部微循环障碍进一步加重,表现为BMLs范围扩大或信号强度增加,形成软骨下骨囊肿,局部的酸性环境使成骨细胞矿化功能受损,导致骨材料自身强度不足,出现软骨下骨塌陷,其上方附着的关节软骨在此种正反馈调节下持续丢失。任何以保护关节软骨为目的KOA药物或外科治疗靶点,均应有针对性地调整不同阶段软骨下骨中破骨细胞或/和成骨细胞的功能水平及其生存的内环境,而非片面地追求软骨保护。

The role of the subchondral bone in the pathophysiological processes of knee osteoarthritis(KOA)is receiving increasing attention.During the early stages of KOA, micro-fractures due to stress occurr with increased subchondral bone remodeling and decreased subchondral bone structural parameters, promoting the development of local microcirculatory disorders and atypical bone marrow lesions(BMLs). The micro-pores in cartilage provide pathways for blood vessel invasion into the deep layers of articular cartilage and subsequently bring in cartilage-degrading enzymes.With the pathogenesis of KOA, the loss of proteoglycans, which resist pressure to maintain the integrity of articular cartilage, results in stress overloading and then metabolic imbalances, leading to decreased bone resorption and increased bone formation.In the late stages of KOA, significant subchondral bone sclerosis further obstructs local blood microcirculation, which manifests as extended BMLs or increased signal intensity and even subchondral bone cysts.The acidic local environment impairs osteoblast function and erodes bone strength, contributing to subchondral bone collapse.Consequently, there is continued loss of the attached articular cartilage because of the positive feedback.Drug or surgical treatment aimed at cartilage protection should focus on functional modulation of osteoblasts and/or osteoclasts in the subchondral bone and the internal environment at different stages, instead of merely on the protection of articular cartilage.