• T A Nees, N Rosshirt, T Reiner, M Schiltenwolf, and B Moradi.
• Klinik für Orthopädie und Unfallchirurgie, Zentrum für Orthopädie, Unfallchirurgie und Paraplegiologie, Universitätsklinikum Heidelberg, Schlierbacher Landstraße 200a, 69118, Heidelberg, Deutschland.
• Schmerz. 2019 Feb 1; 33 (1): 4-12.

AbstractOsteoarthritis (OA) is one of the major causes of chronic pain. Although OA has long been considered a non-inflammatory "wear and tear" disease leading to loss of articular cartilage, recent findings provide convincing evidence that inflammatory mechanisms play a pivotal role in the pathophysiology of OA. In OA mononuclear cells (e. g. T‑cells and macrophages) infiltrate the synovial membrane and the levels of pro-inflammatory cytokines in peripheral blood and synovial fluid samples are elevated. Increased release of inflammatory mediators including interleukin (IL) IL-1β, IL-6, IL-8, IL-15 und tumor necrosis factor alpha (TNF‑α) induces the expression of proteolytic enzymes such as matrix metalloproteinases resulting in cartilage breakdown. Molecular and cellular interactions between the immune and nervous system are also involved in the development of OA-related pain. Inflammatory mediators including IL-6 und TNF‑α lead to peripheral sensitization of joint nociceptors and growth factors (e. g. NGF) trigger the expression of TRPV1 channels in primary afferents. Moreover, neuropeptides reduce the threshold of nociceptors of OA joints. The current review highlights the role of inflammatory mechanisms in OA-induced joint pain considering clinical signs of inflammation and major inflammatory pathways.

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