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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
Published on: March 18, 2019
Osteoclasts are essential for TNF-alpha-mediated joint destruction.
Kurt Redlich1, Silvia Hayer, Romeo Ricci
1Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Vienna, Austria.
The Journal of Clinical Investigation
|November 20, 2002
Summary
Osteoclasts drive bone destruction in rheumatoid arthritis. Inhibiting osteoclasts may treat this inflammatory joint disease, even without affecting inflammation itself.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) involves joint destruction driven by proinflammatory cytokines.
- The precise cellular mechanisms of RA-induced joint destruction remain unclear.
- Osteoclasts are implicated in bone erosion, but their exact role in RA pathogenesis requires further investigation.
Purpose of the Study:
- To determine if osteoclasts are essential for joint destruction in TNF-induced arthritis.
- To investigate the role of osteoclasts in the inflammatory and destructive processes of RA.
Main Methods:
- Transgenic mice expressing human TNF (hTNFtg) were crossed with c-fos-deficient mice lacking osteoclasts.
- The resulting c-fos(-/-)hTNFtg mice were analyzed for arthritis development, inflammation, and joint destruction.
- Histological and molecular analyses assessed synovial inflammation, cartilage damage, and bone erosion.
Main Results:
- TNF-dependent arthritis developed in c-fos(-/-)hTNFtg mice, with similar synovial inflammation and cartilage damage compared to hTNFtg mice.
- Despite severe inflammation, c-fos(-/-)hTNFtg mice were completely protected from bone destruction.
- These findings indicate that osteoclasts mediate TNF-dependent bone erosion in RA.
Conclusions:
- Osteoclast absence prevents bone destruction in TNF-induced arthritis, while inflammation progresses.
- TNF-mediated bone erosion is dependent on osteoclast activity.
- Osteoclast inhibition represents a potential therapeutic strategy for treating bone erosion in rheumatoid arthritis, complementing anti-inflammatory treatments.
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