The Mechanism of Coupling between Bone Resorption and Formation
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- Udagawa Nobuyuki
- Department of Biochemistry and Institute for Oral Science, Matsumoto Dental University
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- Nakamura Midori
- Department of Biochemistry and Institute for Oral Science, Matsumoto Dental University
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- Sato Nobuaki
- Department of Biochemistry and Institute for Oral Science, Matsumoto Dental University
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- Takahashi Naoyuki
- Department of Biochemistry and Institute for Oral Science, Matsumoto Dental University
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Abstract
Deficiency of osteoprotegerin (OPG), a soluble decoy receptor for receptor activator of NF-κB ligand (RANKL), in mice induces osteoporosis caused by enhanced bone resorption but also accelerates bone formation. We examined if bone formation is coupled with bone resorption in OPG-deficient (OPG-/-) mice, using risedronate, an inhibitor of bone resorption. Histomorphometric analysis showed that bone formation-related parameters in OPG-/-mice sharply decreased with the suppression of bone resorption by the daily injection of risedronate for 30 days. OPG-/-mice exhibited high serum alkaline phosphatase activity and osteocalcin concentrations, both of which were decreased to the levels of wild-type mice by risedronate injection. The ectopic bone formation induced by bone morphogenetic protein-2 implantation into OPG-/-mice was not accelerated. These results suggest that bone formation is coupled with bone resorption at local sites in OPG-/-mice. Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin-1 (IL-1) receptor family. Toll-IL-1 receptor domain-containing adapter inducing interferon-β (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Using MyD88-deficient (MyD88-/-) mice and TRIF-deficient (TRIF-/-) mice, we examined the roles of MyD88 and TRIF in osteoclast differentiation and function. LPS and IL-1α stimulated osteoclastogenesis in co-cultures of osteoblasts and hemopoietic cells obtained from TRIF-/-mice but not MyD88-/-mice. Bone histomorphometry showed that MyD88-/-mice exhibited osteopenia with reduced bone resorption and formation. These results suggest that the MyD88-mediated signal is essential for the osteoclastogenesis and function induced by IL-1 and LPS, and that MyD88 is physiologically involved in bone turnover.
Journal
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- Journal of Oral Biosciences
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Journal of Oral Biosciences 48 (3), 185-197, 2006
Japanese Association for Oral Biology
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Details 詳細情報について
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- CRID
- 1390001205212571136
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- NII Article ID
- 130004475621
- 10018041877
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- NII Book ID
- AA11896386
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- ISSN
- 18803865
- 13490079
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed