Abstract
Rheumatic diseases are characterized by chronic inflammation of synovial joints and are often associated with persistent pain and increased pain sensitivity. The inflammatory process is a complex cascade of events involving several mediators, which can lead to a chronic condition of pain. Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation. Inflammatory pain arises from tissue damage via the sensitization of pain receptors (nociceptors). The main peripheral mechanism underlying nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons, and ligaments), which renders them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). Neuroimmune interaction has been considered to play an essential role in rheumatic disease. Neurogenic inflammation, which influences normal central nervous system signaling, leads to insufficient signaling/bioavailability of various cytokines. These central mechanisms play an important role in the increased pain sensitivity following inflammation and are responsible for the development of secondary hyperalgesia in regions beyond the injured tissue. Reduction of pain in rheumatic disease requires familiarity with various pain mechanisms.
Zusammenfassung
Rheumatische Erkrankungen, die durch chronische Entzündungen der Synovialgelenke gekennzeichnet sind, gehen häufig mit anhaltenden Schmerzen und erhöhter Schmerzempfindlichkeit einher. Der Entzündungsprozess ist eine komplexe Kaskade von Ereignissen, an denen mehrere Mediatoren beteiligt sind, und kann zu einem chronischen Schmerzzustand führen. Eine Entzündung kann die Angiogenese stimulieren, dadurch können wiederum Entzündungsprozesse stimuliert werden. Entzündliche Schmerzen im Rahmen von Gewebeschäden werden durch Sensibilisierung von Schmerzrezeptoren (Nozizeptoren) vermittelt. Der hauptsächliche periphere Mechanismus, der nozizeptiven Schmerzen zugrunde liegt, ist eine Veränderung der Aktivität der Nozizeptoren in den betroffenen anatomischen Strukturen (Gelenke, Sehnen und Bänder), wodurch sie empfindlicher auf normalerweise schmerzhafte Reize (Hyperalgesie) oder normalerweise nicht schmerzhafte Reize (Allodynie) reagieren. Es wird angenommen, dass die Interaktion von Nervensystem und Immunsystem eine wesentliche Rolle bei rheumatischen Erkrankungen spielt. Neurogene Entzündungen, die die normale Signalübertragung des zentralen Nervensystems beeinflussen, führen zu einer veränderten Signalübertragung/Bioverfügbarkeit verschiedener Zytokine. Diese zentralen Mechanismen spielen eine wichtige Rolle bei der Erhöhung der Schmerzempfindlichkeit nach Entzündungen und sind für die Entwicklung einer sekundären Hyperalgesie in Regionen außerhalb des entzündlichen Gewebes verantwortlich. Therapeutisch resultiert daraus für die Schmerzreduzierung bei rheumatischen Erkrankungen, dass die Behandelnden mit verschiedenen Schmerzmechanismen vertraut sein sollten.
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O. Seifert and C. Baerwald declare that they have no competing interests.
For this article no studies with human participants or animals were performed by any of the authors. All studies performed were in accordance with the ethical standards indicated in each case.
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C. Baerwald, Leipzig
H.-I. Huppertz, Bremen
G. Pongratz, Düsseldorf
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Seifert, O., Baerwald, C. Interaction of pain and chronic inflammation. Z Rheumatol 80, 205–213 (2021). https://doi.org/10.1007/s00393-020-00951-8
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DOI: https://doi.org/10.1007/s00393-020-00951-8