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Synovium and the Innate Inflammatory Network in Osteoarthritis Progression

  • OSTEOARTHRITIS (MB GOLDRING, SECTION EDITOR)
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Abstract

This review focuses on the recent advancements in the understanding of innate immunity in the pathogenesis of osteoarthritis, particularly with attention to the roles of damage-associated molecular patterns (DAMPs), pattern recognition receptors (PPRs), and complement in synovitis development and cartilage degradation. Endogenous molecular products derived from cellular stress and extracellular matrix disruption can function as DAMPs to induce inflammatory responses and pro-catabolic events in vitro and promote synovitis and cartilage degradation in vivo via PRRs. Some of the DAMPs and PRRs display various capacities in driving synovitis and/or cartilage degradation in different models of animal studies. New findings reveal that the inflammatory complement cascade plays a key in the pathogenesis of OA. Crosstalk between joint tissues such as synovium and cartilage communicated at the cellular level within the innate immune inflammatory network is implicated to play an important role in OA progression. Further studies on how the innate immune inflammatory network impacts the OA disease process at different stages of progression will lead to the development of new therapeutic strategies.

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Acknowledgment

Ru Liu-Bryan’s research is supported by National Institutes of Health grant no. AR1067966.

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Ru Liu-Bryan declares that she has no conflict of interest.

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  1. Veterans Affairs Medical Center and University of California San Diego, 3350 La Jolla Village Drive, 111K, San Diego, CA, 92161, USA

    Ru Liu-Bryan

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Correspondence to Ru Liu-Bryan.

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This article is part of the Topical Collection on Osteoarthritis

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Liu-Bryan, R. Synovium and the Innate Inflammatory Network in Osteoarthritis Progression. Curr Rheumatol Rep 15, 323 (2013). https://doi.org/10.1007/s11926-013-0323-5

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