Research progress on subchondral bone lesions in degenerative knee osteoarthritis

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. Key words: Cartilage; Osteoarthritis; Knee