title: Abnormalities in cortical bone, trabecular plates, and stiffness in postmenopausal women treated with glucocorticoids.
abstract: BACKGROUND
  The mechanisms by which glucocorticoids (GCs) increase skeletal fragility are not well understood.
  
  
  OBJECTIVE
  The objective of the study was to evaluate the microarchitecture, trabecular morphology, and biomechanical properties of bone in postmenopausal women treated with GCs.
  
  
  METHODS
  This was a case-control study.
  
  
  METHODS
  The study was conducted at a university hospital outpatient facility.
  
  
  METHODS
  Postmenopausal women treated with oral GCs for longer than 3 months (n = 30) and age/race-matched controls (n = 60) participated in the study.
  
  
  METHODS
  Areal bone mineral density aBMD (BMD) by dual-energy x-ray absorptiometry (DXA) was measured. Trabecular and cortical volumetric BMD (vBMD) and microarchitecture by high-resolution peripheral computed tomography of the distal radius and tibia were also measured. Whole-bone stiffness was estimated by finite element analysis. A novel technique, individual trabecula segmentation, was used to evaluate trabecular type (as plate or rod), orientation, and connectivity.
  
  
  RESULTS
  DXA T-scores did not differ significantly at any site. GC subjects had significantly lower total, cortical, and trabecular vBMD and thinner cortices, fewer, thinner, more widely, and irregularly spaced trabeculae. They had fewer trabecular plates, fewer axially aligned trabeculae, and lower trabecular connectivity. Differences ranged from 4% to 65% for these trabecular measures and 5% to 17% for the cortical measures. Whole-bone stiffness was significantly lower (11%-16%) in GC subjects. Markers of bone formation (osteocalcin and amino-terminal propeptide of type I procollagen) and resorption (C-telopeptide) were lower in the GC subjects.
  
  
  CONCLUSIONS
  Despite similar areal BMD by DXA, GC-treated women had abnormal cortical and trabecular vBMD and microarchitecture at both the radius and tibia, including fewer trabecular plates, a less axially aligned trabecular network, lower trabecular connectivity, thinner cortices, and lower whole-bone stiffness. Further research into these abnormalities as mechanisms for fracture in GC-treated women is warranted.
authors.affiliation: Department of Medicine (S.S., K.K.N., A.K., D.J.M., E.M.S.), Columbia University College of Physicians and Surgeons, New York, New York 10032; and Bone Bioengineering Laboratory (B.Z., J.W., X.E.G.), Department of Biomedical Engineering, Columbia University, New York, New York 10027.
authors.forename: Stephanie
authors.initials: S
authors.lastname: Sutter
authors.forename: Kyle K
authors.initials: KK
authors.lastname: Nishiyama
authors.forename: Anna
authors.initials: A
authors.lastname: Kepley
authors.forename: Bin
authors.initials: B
authors.lastname: Zhou
authors.forename: Ji
authors.initials: J
authors.lastname: Wang
authors.forename: Donald J
authors.initials: DJ
authors.lastname: McMahon
authors.forename: X Edward
authors.initials: XE
authors.lastname: Guo
authors.forename: Emily M
authors.initials: EM
authors.lastname: Stein
mesh_terms: D000368:Aged; D015519:Bone Density / Q000187:drug effects*; D001842:Bone and Bones / Q000187:drug effects*; D002118:Calcium / Q000097:blood; D016022:Case-Control Studies; D003404:Creatinine / Q000097:blood; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000097:blood / Q000139:chemically induced*; D017698:Postmenopause / Q000097:blood*; D012709:Serum Albumin
chemical_list: D005938:Glucocorticoids; D012709:Serum Albumin; D003404:Creatinine; D002118:Calcium