title: Anabolic effects of intermittent PTH on osteoblasts.
abstract: Intermittent parathyroid hormone (iPTH) is the only FDA-approved therapy for bone loss due to conditions such as osteoporosis that increases bone formation by osteoblasts; all other therapies approved for osteoporosis block bone resorption by osteoclasts. The anabolic effects of iPTH are likely due to a combination of multiple mechanisms, including induction of immediate-early genes, increased expression and/or activity of essential osteoblast transcription factors, and downregulation of anti-osteogenic proteins, such as sclerostin. In contrast, continuous administration of PTH induces bone loss primarily due to up-regulation of RANKL expression and inhibition of osteoprotegerin expression.
authors.affiliation: Department of Orthopaedics, Case Western Reserve University and Case Medical Center, Cleveland OH 44106, USA. emg3@po.cwru.edu
authors.forename: Edward M
authors.initials: EM
authors.lastname: Greenfield
mesh_terms: D045930:Anabolic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017781:Genes, Immediate-Early / Q000187:drug effects; D006801:Humans; D010006:Osteoblasts / Q000187:drug effects* / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism; D010012:Osteogenesis / Q000187:drug effects; D010024:Osteoporosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D010281:Parathyroid Hormone / Q000494:pharmacology* / Q000627:therapeutic use; D053245:RANK Ligand / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D045930:Anabolic Agents; D010281:Parathyroid Hormone; D053245:RANK Ligand