The molecular mechanism of osteoclastogenesis in rheumatoid arthritis

Description

Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte–macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-κB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte–macrophage colony-stimulating factor and IFN-γ, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.

Resources

Name Format Description Link
21 Visit the original government dataset for complete information, documentation, and data access. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC128939/

Tags

  • bone-resorption
  • rheumatoid-arthritis
  • nih
  • rankl-cytokine
  • osteoclastogenesis

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