Mechanisms involved in bone resorption |
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Authors: | Udagawa Nobuyuki |
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Institution: | (1) Department of Biochemistry, Matsumoto Dental University, 1780 Hiro-oka Gobara, Shiojiri, Nagano 399-0781, Japan |
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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 or bone marrow-derived
stromal cells are involved in osteoclastogenesis through a mechanism involving cell-to-cell contact with osteoclast progenitors.
Experiments on the osteopetrotic op/op mouse model have established that a product ofosteo blasts, macrophage colony-stimulating
factor (M-CSF), regulates differentiation of osteoclast progenitors into osteoclasts. Recent discovery of osteoclast differentiation
factor (ODF)/receptor activator of NF-κ Bligand (RANKL) allowed elucidation of the precise mechanism by which osteoblasts
regulate osteoclastic bone resorption. Treatment of osteoblasts with bone-resorbing factors up-regulated expression of RANKL
mRNA. In contrast, TNF α stimulates osteoclast differentiation in the presence of M-CSF through a mechanism independent of
the RANKL system. IL-1 also directly acts on mature osteoclasts as a potentiator of osteoclast activation. In addition, TGF-β
super family members, such as bone morphogenetic proteins(BMPs) strikingly enhanced osteoclast differentiation from their
progenitors and survival of mature osteoclasts induced by RANKL. These results suggest that BMP-mediated signals cross-communicate
with RANKL-mediated ones in inducing osteoclast differentiation and function.
This revised version was published online in July 2006 with corrections to the Cover Date. |
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Keywords: | BMP bone resorption M-CSF osteoblast osteoclast differentiation osteoporosis osteoprotegerin RANKL TGF-β |
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