Intraarticular Corticosteroids Modulate the Osteoprotegerin/Receptor Activator of Nuclear Factor-κB Ligand System in the Synovial Fluid in Patients with Rheumatoid Arthritis
Purpose: Despite the fact that intraarticular corticosteroids are a longstanding adjuvant treatment for inflammatory arthritis, their mechanisms of action are not completely understood. This study evaluated the osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) levels i...
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Veröffentlicht in: | The journal of the Korean Orthopaedic Association 2008, 43(2), , pp.227-233 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Purpose: Despite the fact that intraarticular corticosteroids are a longstanding adjuvant treatment for inflammatory arthritis, their mechanisms of action are not completely understood. This study evaluated the osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) levels in the serum and synovial fluid before and 2 weeks after injecting intraarticular corticosteroid.
Materials and Methods: Sixty seven patients were identified with joint effusions of the knee and suffering from rheumatoid arthritis. All the patients received an intraarticular injection of 40 mg of triamcinolone acetonide. The sera and synovial fluid were obtained before and 2 weeks after the injections. the erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, serum OPG and RANKL levels and synovial OPG and RANKL levels were measured before and 2 weeks after the injections.
Results: The intraarticular corticosteroids induced a significant decrease in the levels of synovial RANKL. The decrease in the level of synovial RANKL caused a significant increase in the synovial OPG/RANKL ratio. There were no changes in the hematological factors, serum OPG, serum RANKL or synovial OPG observed after the corticosteroid injection.
Conclusion: Treatment with intraarticular corticosteroids modulates the OPG/RANKL system in the synovial fluid toward a bone-protective effect in patients with rheumatoid arthritis. This mechanism might explain part of the mode of action of intraarticular corticosteroids. KCI Citation Count: 1 |
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ISSN: | 1226-2102 2005-8918 |
DOI: | 10.4055/jkoa.2008.43.2.227 |