Innate Immunity and Synovitis: Key Players in Osteoarthritis Progression.

Int J Mol Sci

Laboratory of Immunorheumatology and Tissue Regeneration, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Published: November 2024

AI Article Synopsis

  • Osteoarthritis (OA) is a common joint disease primarily affecting the elderly, characterized by chronic inflammation rather than just wear and tear of cartilage.
  • Synovial inflammation (synovitis) plays a critical role in the disease's progression and the onset of pain, highlighting a shift in understanding OA as an inflammatory condition.
  • The interaction between synovial tissue and innate immune cells contributes significantly to ongoing inflammation, leading to structural and functional joint alterations.

Article Abstract

Osteoarthritis (OA) is a chronic progressive disease of the joint. Although representing the most frequent cause of disability in the elderly, OA remains partly obscure in its pathogenic mechanisms and is still the orphan of resolutive therapies. The concept of what was once considered a "wear and tear" of articular cartilage is now that of an inflammation-related disease that affects over time the whole joint. The attention is increasingly focused on the synovium. Even from the earliest clinical stages, synovial inflammation (or synovitis) is a crucial factor involved in OA progression and a major player in pain onset. The release of inflammatory molecules in the synovium mediates disease progression and worsening of clinical features. The activation of synovial tissue-resident cells recalls innate immunity cells from the bloodstream, creating a proinflammatory milieu that fuels and maintains a damaging condition of low-grade inflammation in the joint. In such a context, cellular and molecular inflammatory behaviors in the synovium could be the of the structural and functional alterations of the whole joint. This paper focuses on and discusses the involvement of innate immunity cells in synovitis and their role in the progression of OA.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11594236PMC
http://dx.doi.org/10.3390/ijms252212082DOI Listing

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