Zusammenfassung
□ Hintergrund
Die systemische Osteoporose ist eine häufig und pathogenetisch heterogene Komplikation der rheumatoiden Arthritis. Verschiedene Faktoren wie Erkrankungsaktivität, Glukokortikoidtherapie und Immobilisation sind in den Pathogeneseprozeß der Osteoporose bei rheumatoider Arthritis einbezogen.
□ Einfluß der Entzündung auf den Knochenstoffwechsel
Von immunkompetenten Zellen sezernierte proinflammatorische Zytokine regulieren die Funktion von Osteoblasten und Osteoklasten, können die Knochenformation hemmen und die Knochenresorption steigern. Interleukin-6 und Stickstoffmonoxid (NO) sind wichtige Mediatoren bei der Vermittlung von Effekten proinflammatorischer Zytokine auf Osteoblasten und Osteoklasten. Darüber hinaus kann der Knochenstoffwechsel bei der rheumatoiden Arthritis auch durch von der entzündlichen Aktivität abhängige Veränderungen in der Funktion endogener hormoneller Systeme, wie der Sekretion von Glukokortikoiden und dem Vitamin-D-Metabolismus, moduliert werden. Mit der Immobilisation verbundene Veränderungen des Knochen-Remodellings sind wesentlich für den systemischen Knochenmasseverlust.
□ Schlußfolgerung
Der entzündliche Prozeß bei der rheumatoiden Arthritis kann über verschiedene zytokin- und hormonvermittelte Mechanismen zu periartikulären und systemischem Knochenmineralverlust führen. Ausgehend von pathogenetischen Gesichtspunkten der Osteoporose bei der rheumatoiden Arthritis dürfte in prophylaktischer und therapeutischer Hinsicht dem Einsatz von Bisphosphonaten und aktiven Vitamin-D-Metaboliten eine wesentliche Bedeutung zukommen.
Summary
□ Background
Systemic osteoporosis is a common and pathogenetically heterogenous complication in rheumatoid arthritis. Various factors such as disease activity, dosage and duration of glucocorticoid treatment and immobilization are involved in pathogenesis of osteoporosis in rheumatoid arthritis.
□ Inflammation and Bone Metabolism
Proinflammatory cytokines secreted by immunocompetent cells have a role in the regulation of the activity of osteoblasts and osteoclasts. The effects of these proinflammatory cytokines include the inhibition of bone formation and an increase in bone resorption. Interleukin-6 and nitric oxide induced in osteoblasts by proinflammatory cytokines are likely to be important mediators between these cytokines and the function of osteoblasts and osteoclasts. Furthermore, disease activity dependent changes in the secretion of glucocorticoids and in vitamin D metabolism may be involved in the pathogenesis of osteoporosis in this disease. Alteration of bone remodeling associated with immobilization is an important factor of systemic bone loss in rheumatoid arthritis.
□ Conclusion
The inflammatory process in rheumatoid arthritis may cause periarticular and systemic bone loss by various cytokine and hormone mediated mechanisms. Concluding from these pathogenetic mechanisms, bisphosphonates and active vitamin D metabolites are likely to be effective therapeutic options in osteoporosis associated with rheumatoid arthritis.
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Herrn Professor Dr. Günter Stein zum 60. Geburtstag.
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Oelzner, P., Hein, G. Entzündung und Knochenstoffwechsel bei rheumatoider Arthritis. Med Klin 92, 607–614 (1997). https://doi.org/10.1007/BF03044788
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DOI: https://doi.org/10.1007/BF03044788