[Regulatory mechanism of bone resorption: roles of bone remodeling-regulatory cytokines 'osteokines' in osteoclast differentiation and function].
The recent discovery of receptor activator of NF-kappa B ligand(RANKL)-RANK interaction confirms the well-known hypothesis that osteoblasts play an essential role in osteoclast differentiation. Osteoblasts express RANKL, a tumor necrosis factor alpha (TNF-alpha) family member, as a membrane-associated factor. Osteoclast precursors that express RANK, a receptor for RANKL, recognize RANKL through the cell-cell interaction and differentiate into osteoclasts. Recent Studies have shown that lipopolysaccharide and inflammatory cytokines such as TNF-alpha and interleukin 1 directly regulate osteoclast differentiation and function through a mechanism independent of the RANKL-RANK interaction. Interferon-gamma and beta are also shown to be important negative regulators in osteoclastogenesis. These findings have opened new areas for exploring the regulatory mechanisms osteoclast differentiation and function by immune and inflammatory cells.
Kobayashi
Yasuhiro
Y
Division of Hard Tissue Research, Institute for Oral Science, Matsumoto Dental University.
Takahashi
Naoyuki
N
D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000503:physiopathology; D002352:Carrier Proteins / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology*; D010010:Osteoclasts / Q000502:physiology*; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D015398:Signal Transduction / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology
D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505686:TNFRSF11A protein, human; C505688:TNFSF11 protein, human; D016212:Transforming Growth Factor beta