Progressive bone destruction in rheumatoid arthritis (RA) represents a core pathological mechanism leading to joint dysfunction. Its pathogenesis involves multiple critical pathways, including abnormal activation of immune and synovial cells, excessive pro-inflammatory cytokine secretion, and disrupted bone remodeling balance. Recent advancements in research techniques and academic exploration have progressively refined our understanding of RA-related bone destruction regulatory mechanisms. Programmed cell death (PCD), long noncoding RNAs (lncRNAs), and the significantly enhanced glycolytic metabolism observed in RA patients all mediate the onset and progression of RA bone destruction by targeting these pathological pathways. These findings collectively reveal a complex regulatory network intertwining cell demise processes, epigenetic regulation, and metabolic reprogramming. This not only deepens our understanding of the pathological mechanisms underlying RA bone destruction but also provides novel theoretical support and potential therapeutic targets for developing multi-targeted intervention strategies against this pathological process.
Lu et al. (2026) studied this question.