| Rheumatoid arthritis (RA) is a chronic autoimmune disease, characterized by chronic synovitis and progressive bone erosion. It carries a high risk of disability and joint deformity, and conventional therapies are often ineffective in blocking the process of bone destruction. This review summarizes the core mechanisms of bone destruction in RA, focusing on the synovial tissue destruction, imbalance of the bone immune microenvironment, the regulation of inflammatory cytokine networks, and the role of migrasomes. Immune cells infiltrating the synovial tissue, such as lymphocytes, macrophages, and neutrophils, pathologically secrete pro-inflammatory cytokines like RANKL, TNF-α, IL-6, and IL-17. Under specific environmental stimuli, macrophages, dendritic cells, and B lymphocytes can transform into osteoclasts. The disrupted interaction networks between these immune cells and osteoclasts, as well as between cells and mediators, disturb the skeletal remodeling homeostasis, driving increased osteoclast activity and inhibiting osteoblast function, leading to bone destruction in RA. Moreover, migrasomes, as a novel type of organelle, may play a key role in the migration, fusion, and recycling of osteoclast precursors, providing a new research direction for bone destruction. A deeper understanding of these mechanisms is expected to offer new strategies for targeted intervention of bone destruction in RA. |