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Die Rolle der Inflammation bei Arthroseschmerzen

Inflammation and osteoarthritis-related pain

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Zusammenfassung

Die Arthrose ist weltweit eine der häufigsten Ursachen für chronische Schmerzen. Entgegen der ursprünglichen Annahme einer nichtentzündlichen Verschleißerkrankung mit Abnutzung des Gelenkknorpels („wear and tear“) wird immunologisch-inflammatorischen Prozessen inzwischen eine entscheidende Beteiligung an der Pathogenese der Arthrose beigemessen. Im Rahmen der Erkrankung kommt es zu einer chronischen Inflammation des gesamten Gelenks mit Infiltration von mononukleären Zellen (Makrophagen und T‑Zellen) in die Synovialmembran und erhöhten Konzentrationen proinflammatorischer Zyto- und Chemokine in der Synovialflüssigkeit und im Blut. Die vermehrte Freisetzung von Entzündungsmediatoren wie Interleukin (IL) IL-1β, IL-6, IL-8, IL-15 und Tumornekrosefaktor‑α (TNF‑α) induziert die Expression chondrodestruktiver Matrixmetalloproteinasen und damit die enzymatische Gelenkdegeneration. Humorale und zelluläre Mechanismen interagieren zwischen Immun- und Nervensystem auch bei der Entwicklung von Arthroseschmerzen. Entzündungsmediatoren wie IL-6 und TNF‑α führen zur peripheren Sensibilisierung freier Nervenendigungen im Gelenk. Weiterhin können entzündungsassoziierte Wachstumsfaktoren wie nerve growth factor (NGF) die Expression von Schmerzrezeptoren an primären Afferenzen triggern, während inflammatorische Neuropeptide die Erregungsschwelle von Gelenknozizeptoren herabsetzen. Der vorliegende Übersichtsartikel diskutiert den Stellenwert der Inflammation bei arthrosebedingten Gelenkschmerzen unter Berücksichtigung der klinischen Symptomatik und wichtiger inflammatorischer Pathomechanismen.

Abstract

Osteoarthritis (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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  1. Klinik für Orthopädie und Unfallchirurgie, Zentrum für Orthopädie, Unfallchirurgie und Paraplegiologie, Universitätsklinikum Heidelberg, Schlierbacher Landstraße 200a, 69118, Heidelberg, Deutschland

    T. A. Nees, N. Rosshirt, T. Reiner, M. Schiltenwolf &  B. Moradi

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  1. T. A. Nees
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T. A. Nees, N. Rosshirt, T. Reiner, M. Schiltenwolf und B. Moradi geben an, dass kein Interessenkonflikt besteht.

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Nees, T.A., Rosshirt, N., Reiner, T. et al. Die Rolle der Inflammation bei Arthroseschmerzen. Schmerz 33, 4–12 (2019). https://doi.org/10.1007/s00482-018-0346-y

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