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, numerous questions remain about its mechanism. Histomorphometric studies of GIO revealed an increase in the number of osteoclasts and bone-resorbing sites as well as a reduction in bone formation ( Bressot et al. 1979 ). However, these changes in bone
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, Immunodiagostic Systems) were analyzed as a marker of bone formation. Primary bone cell cultures Primary murine osteoblasts and osteoclasts were cultured in complete α-MEM medium (MEM alpha medium (Gibco) supplemented with 10% heat-inactivated FBS (Merck
Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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Department of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts, USA
Department of Cell Biology and Neuroscience, Rutgers University, Rutgers, New Jersey, USA
Department of Orthopedics, School of Medicine, Juntendo University, Tokyo, Japan
21st Century Center of Excellence (COE) Program for Frontier Research on Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo, Japan
JSPS Core to Core Program, Japan
Hard Tissue Genome Research Center, Tokyo Medical and Dental University, Tokyo, Japan
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only resorption inhibitors, which so far reduce the fracture risk only by 50%, but also stimulators for bone formation especially in patients who already have lost a significant amount of bone mass ( Rosen & Bilezikian 2001 ). Parathyroid hormone (PTH
UMR‐1132 Inserm, Université Paris Diderot, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
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UMR‐1132 Inserm, Université Paris Diderot, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
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UMR‐1132 Inserm, Université Paris Diderot, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
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UMR‐1132 Inserm, Université Paris Diderot, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
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UMR‐1132 Inserm, Université Paris Diderot, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
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Introduction Bone loss associated with ageing is characterised by decreased bone formation relative to bone resorption, resulting in altered bone microarchitecture, osteoporosis and increased risk of fractures ( Khosla et al . 2011 ). The age
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Institute of Dental Research, The Research Center for Bone and Stem Cells, Department of Medicine, Stomatological College
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occurring in the 1α(OH)ase −/− mice on the normal diet was responsible for the increased bone formation. Moreover, the bone volume of the normocalcemic 1α(OH)ase −/− mice on the rescue diet was less than that observed in the wild-type mice, suggesting that
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( Ross 1996 , Ray et al . 1997 ). Estrogen deficiency is regarded as the main causative factor in PMO. Withdrawal of estrogen or estrogen deficiency stimulates bone resorption by 90%, while increasing bone formation by 45%, as measured using biochemical
Skeletal Biology Laboratory, Center for Healthy Aging Research, Biostatistics, School of Biological and Population Health Sciences
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Skeletal Biology Laboratory, Center for Healthy Aging Research, Biostatistics, School of Biological and Population Health Sciences
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-deficient mice and leptin-receptor-deficient mice and rats have reduced overall bone mass, reduced longitudinal bone growth ( Steppan et al . 2000 , Kishida et al . 2005 ), and decreased bone formation ( Gat-Yablonski & Phillip 2008 ). In addition, impaired
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. 2010 ). In addition to any coupling-mediated actions, we found that sCT treatment also increased the expression of sclerostin ( Gooi et al . 2010 ), an inhibitor of bone formation that is secreted by osteocytes. This stimulation of sclerostin by sCT is
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Department of Endocrinology and Metabolism, Concord Repatriation General Hospital, Sydney, Australia
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. (2010) disrupted the GR specifically in the skeletal primordium cells using a Runx2-Cre promoter (Runx2-Cre; GR flox/flox ). These GR Runx2 mice displayed efficient recombination at all sites of endochondral and intramembranous bone formation
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et al. 2016 ), very few studies have analyzed effects of vitamin A on bone formation in vivo . Kneissel et al. and Lind et al. found that hypervitaminosis A decreased mineralizing surfaces on the periosteal side of cortical bone in the femur and