title: Low-dose risedronate sodium protects bone cells after abrupt oestrogen withdrawal.
abstract: OBJECTIVE
  To investigate the effects of low-dose risedronate sodium on the in vitro cellular profile of osteoblasts, adipocytes, osteocytes and osteoclasts in a rat model of abrupt oestrogen deficiency.
  
  
  METHODS
  Oestrogen deficiency was induced by ovariectomy in 24 female rats.  The rats were treated with low-dose (0.24 μg/kg) or high-dose (2.4 μg/kg) risedronate sodium for 4 days presurgery, continuing every 3 days until 15 days postsurgery. Osteogenic and adipogenic differentiation were determined in cultured bone marrow cells by alkaline phosphatase and Oil  Red O staining, respectively, and by osteogenic and adipogenic gene expression. Osteoclast formation was measured in bone marrow cells stimulated with macrophage colony-stimulating factor and receptor activator of nuclear factor κB ligand, and stained with tartrate-resistant acid phosphatase.  Osteocyte apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling assay and B-cell lymphoma-2 (Bcl-2) immunohistochemistry.
  
  
  RESULTS
  Low-dose risedronate sodium enhanced osteoblast differentiation, suppressed adipocyte differentiation  and osteoclast formation, and reduced osteocyte apoptosis through regulation of Bcl-2 and Bcl-2-associated X protein.
  
  
  CONCLUSIONS
  Low-dose risedronate sodium may have clinical benefit in protecting against bone loss after abrupt oestrogen deficiency.
authors.affiliation: Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
authors.forename: G
authors.initials: G
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Zhu
authors.forename: C
authors.initials: C
authors.lastname: Lei
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.forename: F
authors.initials: F
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Mao
authors.forename: Z
authors.initials: Z
authors.lastname: Yu
authors.forename: M
authors.initials: M
authors.lastname: Liu
authors.forename: X
authors.initials: X
authors.lastname: Zhao
authors.forename: T
authors.initials: T
authors.lastname: Tang
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000502:physiology; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D050071:Bone Density Conservation Agents / Q000008:administration & dosage* / Q000494:pharmacology; D002454:Cell Differentiation; D049109:Cell Proliferation; D002478:Cells, Cultured; D019610:Cytoprotection; D004305:Dose-Response Relationship, Drug; D004967:Estrogens / Q000172:deficiency*; D012968:Etidronic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000187:drug effects; D010006:Osteoblasts / Q000187:drug effects / Q000502:physiology; D010010:Osteoclasts / Q000187:drug effects / Q000502:physiology; D010011:Osteocytes / Q000187:drug effects / Q000502:physiology; D015663:Osteoporosis, Postmenopausal / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D010052:Ovariectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D000068296:Risedronic Acid
chemical_list: D050071:Bone Density Conservation Agents; D004967:Estrogens; D000469:Alkaline Phosphatase; D000068296:Risedronic Acid; D012968:Etidronic Acid