New therapeutic target for osteoarthritis: modulating immune-metabolic aberrations and micromilieu remodeling in underlying bone

Abstract

Traditionally, osteoarthritis (OA) has been thought of as a degenerative disease mostly caused by mechanical wear and tear. However, recent research suggests that immunometabolic pathways drive the active process of subchondral bone remodeling. According to this study, the immunometabolic axis is a key regulatory network in the subchondral bone microenvironment of osteoarthritis (OA), facilitating metabolic interaction between osteocytes and immune cells like macrophages. Bone homeostasis is destroyed by immune cell infiltration, which also promotes the release of inflammatory mediators and local metabolic reprogramming. These results support the idea that OA is an immunometabolic disease. Intervening in the immunometabolic network of subchondral bone can be accomplished by focusing on immune cell metabolic pathways, particularly those that control the phenotypic transition of M1/M2 macrophages. It is anticipated that this approach will control the immunometabolic dialogue, slow the advancement of osteoarthritis, end the vicious cycle of inflammatory metabolic disorders, and ultimately offer a new approach to treating osteoarthritis.