Osteoarthritis (OA), long regarded as simply a disease of articular cartilage degeneration, has increasingly been recognized as a complex disorder involving multiple joint tissues, including the synovium. This review explores the emerging evidence that synovial changes seen in OA are not merely secondary to cartilage breakdown but may actively drive OA progression. We detail the physiological role of the synovium in joint homeostasis and highlight pathological remodeling processes, such as synovial hyperplasia, immune cell infiltration, and fibroblast activation, that contribute to joint degeneration. Mechanistic insights implicate fibroblast-like synoviocytes and synovial macrophages in initiating and perpetuating inflammatory and catabolic cascades that alter synovial fluid composition, impair cartilage integrity, and exacerbate disease symptoms. Clinical and preclinical data increasingly link synovitis and synovial damage to structural disease progression and pain, underscoring their prognostic and therapeutic significance. Despite promising targets, effective disease-modifying therapies remain elusive due to the molecular complexity and clinical heterogeneity of the disease and limitations in early diagnostic evaluations. To overcome this, innovative research methods, improved diagnostic tools, and interdisciplinary collaboration will be critical. Collectively, this work advocates for a paradigm shift that the synovium is a central player in OA pathogenesis and a viable target for therapeutic intervention.
Miller et al. (Thu,) studied this question.
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