title: Impact of treatments for postmenopausal osteoporosis (bisphosphonates, parathyroid hormone, strontium ranelate, and denosumab) on bone quality: a systematic review.
abstract: The objective of this systematic review was to examine the influence of treatments for postmenopausal osteoporosis (parathyroid hormone [PTH], bisphosphonates, strontium ranelate, and denosumab) on bone quality and discuss the clinical implications. Most bone-quality data for PTH is from teriparatide. Teriparatide results in a rapid increase in bone-formation markers, followed by increases in bone-resorption markers, opening an "anabolic window," a period of time when PTH is maximally anabolic. Teriparatide reverses the structural damage seen in osteoporosis and restores the structure of trabecular bone. It has a positive effect on cortical bone, and any early increases in cortical porosity appear to be offset by increases in cortical thickness and diameter. Bisphosphonates are antiresorptive agents which reduce bone turnover, improve trabecular microarchitecture, and mineralization. Concerns have been raised that the prolonged antiresorptive action of bisphosphonates may lead to failure to repair microdamage, resulting in microcracks and atypical fragility. Strontium ranelate is thought to have a mixed mode of action, increasing bone formation and decreasing bone resorption. Strontium ranelate improves cortical thickness, trabecular number, and connectivity, with no change in cortical porosity. Denosumab exerts rapid, marked, and sustained effects on bone resorption, resulting in falls in the markers of bone turnover. Evidence from bone-quality studies suggests that treatment-naive women, aged 60-65 years, with very low BMD T scores may benefit from PTH as primary therapy to improve bone substrate and build bone. Post-PTH treatment with bisphosphonates will maintain improvements in bone quality and reduce the risk of fracture.
authors.affiliation: Southern General Hospital, 1345 Govan Road, Glasgow, G51 4TF, UK. stephen.gallacher@ggc.scot.nhs.uk
authors.forename: S J
authors.initials: SJ
authors.lastname: Gallacher
authors.forename: T
authors.initials: T
authors.lastname: Dixon
mesh_terms: D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D001862:Bone Resorption / Q000378:metabolism; D000069448:Denosumab; D004164:Diphosphonates / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008875:Middle Aged; D009942:Organometallic Compounds / Q000627:therapeutic use*; D015663:Osteoporosis, Postmenopausal / Q000188:drug therapy*; D010281:Parathyroid Hormone / Q000627:therapeutic use*; D053245:RANK Ligand / Q000627:therapeutic use*; D019379:Teriparatide / Q000627:therapeutic use; D013876:Thiophenes / Q000627:therapeutic use*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D009942:Organometallic Compounds; D010281:Parathyroid Hormone; D053245:RANK Ligand; D013876:Thiophenes; C081587:strontium ranelate; D019379:Teriparatide; D000069448:Denosumab