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<p>Osteoarthritis (OA), the leading global cause of joint-related disability, is increasingly viewed as an immune-mediated disorder rather than mere mechanical wear-and-tear. Yet how resident and infiltrating immune cells, inflammatory mediators and dysregulated signaling networks act in concert to perpetuate synovitis, erode cartilage and remodel subchondral bone remains a central enigma. This review dissects the cellular and molecular choreography underlying OA pathology. We detail how macrophages, dendritic cells (DCs), neutrophils, mast cells (MCs), natural killer cells (NK cells), T cells, and B cells orchestrate destructive immune-bone crosstalk within the joint microenvironment. Key inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), interleukins (e.g., interleukin (IL)-1β, IL-6), and chemokines sustain this inflammatory loop, further perpetuating inflammation and cartilage damage. Dysregulated signaling pathways, such as nuclear factor-kappa B (NF-κB) and Wingless-type (Wnt)/β-catenin, are coordinated with inflammatory mediators, thereby contributing to the pathophysiology of OA. Beyond mechanism, we critically evaluate cutting-edge therapeutic strategies targeting these osteoimmunological and molecular mechanisms, such as immunomodulatory therapy, mesenchymal stem cell (MSC) therapy and small-molecule pathway inhibitors. Preclinical successes underscore the feasibility of targeting immune-signaling axes to halt or reverse OA progression. By elucidating these mechanisms and therapeutic targets, this review aims to advance the development of disease-modifying therapies and improve outcomes for OA patients.</p>

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Pathogenesis and therapeutic strategies of osteoarthritis: roles of immune cells, inflammatory mediators, and pathogenic signaling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月15日

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  • Zhenglin He,
  • Hanming Hao,
  • Baoer Chen,
  • Xuechao Li,
  • Dezhi Mao,
  • Yi Jin,
  • Kai Zhao,
  • Guanyu Chen

摘要

Osteoarthritis (OA), the leading global cause of joint-related disability, is increasingly viewed as an immune-mediated disorder rather than mere mechanical wear-and-tear. Yet how resident and infiltrating immune cells, inflammatory mediators and dysregulated signaling networks act in concert to perpetuate synovitis, erode cartilage and remodel subchondral bone remains a central enigma. This review dissects the cellular and molecular choreography underlying OA pathology. We detail how macrophages, dendritic cells (DCs), neutrophils, mast cells (MCs), natural killer cells (NK cells), T cells, and B cells orchestrate destructive immune-bone crosstalk within the joint microenvironment. Key inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), interleukins (e.g., interleukin (IL)-1β, IL-6), and chemokines sustain this inflammatory loop, further perpetuating inflammation and cartilage damage. Dysregulated signaling pathways, such as nuclear factor-kappa B (NF-κB) and Wingless-type (Wnt)/β-catenin, are coordinated with inflammatory mediators, thereby contributing to the pathophysiology of OA. Beyond mechanism, we critically evaluate cutting-edge therapeutic strategies targeting these osteoimmunological and molecular mechanisms, such as immunomodulatory therapy, mesenchymal stem cell (MSC) therapy and small-molecule pathway inhibitors. Preclinical successes underscore the feasibility of targeting immune-signaling axes to halt or reverse OA progression. By elucidating these mechanisms and therapeutic targets, this review aims to advance the development of disease-modifying therapies and improve outcomes for OA patients.