title: Change in lumbar spine BMD and vertebral fracture risk reduction in teriparatide-treated postmenopausal women with osteoporosis.
abstract: Increases in lumbar spine BMD account for 30-41% of the vertebral fracture risk reduction with teriparatide treatment. The remaining fracture risk reduction is caused by improvements in non-BMD determinants of bone strength.
  
  
  BACKGROUND
  Changes in BMD account for a small percentage of the fracture risk reduction seen in patients treated with antiresorptive drugs. The relationship between changes in lumbar spine BMD and vertebral fracture risk reduction with teriparatide treatment has not been assessed.
  
  
  METHODS
  The relationship between spine BMD and the risk of new vertebral fractures after teriparatide treatment was assessed using data from the Fracture Prevention Trial. Postmenopausal women with osteoporosis (n = 1637) were randomized to placebo or teriparatide 20 or 40 microg/day for a median of 19 months. Spine BMD was assessed at baseline and 18 months. Vertebrae whose fracture status changed during the trial were removed from the calculation of BMD. Baseline and endpoint lateral spine radiographs were assessed using a visual semiquantitative technique.
  
  
  RESULTS
  Both the baseline and change in spine BMD were contributors to vertebral fracture risk. The mean spine BMD increase in teriparatide-treated patients was 0.09 g/cm(2) across tertiles of baseline spine BMD. Compared with placebo, teriparatide significantly reduced the risk of new vertebral fracture for all endpoint BMD values. Teriparatide-mediated increases in spine BMD accounted for 30% (in the low baseline spine BMD tertile) to 41% (in the high baseline spine BMD tertile) of the reduction in vertebral fracture risk.
  
  
  CONCLUSIONS
  Increases in BMD account for approximately one third of the vertebral fracture risk reduction seen with teriparatide. The majority of the risk reduction, however, results from improvements in non-BMD determinants of bone strength.
authors.affiliation: Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana, USA. chenpe@lilly.com
authors.forename: Peiqi
authors.initials: P
authors.lastname: Chen
authors.forename: Paul D
authors.initials: PD
authors.lastname: Miller
authors.forename: Pierre D
authors.initials: PD
authors.lastname: Delmas
authors.forename: Derek A
authors.initials: DA
authors.lastname: Misurski
authors.forename: John H
authors.initials: JH
authors.lastname: Krege
mesh_terms: D000368:Aged; D015519:Bone Density; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D008159:Lumbar Vertebrae / Q000473:pathology*; D008875:Middle Aged; D010024:Osteoporosis / Q000150:complications* / Q000188:drug therapy*; D010919:Placebos; D017698:Postmenopause; D012306:Risk; D016103:Spinal Fractures / Q000517:prevention & control*; D019379:Teriparatide / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D050071:Bone Density Conservation Agents; D010919:Placebos; D019379:Teriparatide