Journal of Bone and Mineral Metabolism

, Volume 21, Issue 6, pp 337–343

The mechanism of osteoclast differentiation from macrophages: possible roles of T lymphocytes in osteoclastogenesis

Authors

  • Nobuyuki Udagawa
    • Department of BiochemistryMatsumoto Dental University
Review article

DOI: 10.1007/s00774-003-0439-1

Cite this article as:
Udagawa, N. J Bone Miner Metab (2003) 21: 337. doi:10.1007/s00774-003-0439-1

Abstract

Osteoclasts, which are present only in bone, are multinucleated giant cells with the capacity to resorb mineralized tissues. These osteoclasts are derived from hemopoietic progenitors of the monocyte-macrophage lineage. Osteoblasts are involved in osteoclastogenesis through a mechanism involving cell-to-cell contact with osteoclast progenitors. The recent discovery of osteoclast differentiation factor (ODF)/receptor activator of nuclear factor (NF)-ΚB ligand (RANKL) allowed elucidation of the precise mechanism by which osteoblasts regulate osteoclastic bone resorption. 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 interleukin (IL)-17, granulocyte macrophage-colony stimulating factor (GM-CSF) and interferon (IFN)-Γ, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in osteoclast differentiation are described.

Key words

RANKL IL-17 IL-18 IFN-Γ GM-CSF

Copyright information

© Springer-Verlag Tokyo 2003