title: SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength.
abstract: OBJECTIVE
  The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength.
  
  
  METHODS
  Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) was measured by dual-energy X-ray absorptiometry. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the nondominant distal radius were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT). Bone strength was estimated by HR-pQCT-based micro-finite element analysis.
  
  
  RESULTS
  Adjusted for menopausal status and adjusted calcium level, when compared with controls, SLE/non-GC patients had significantly lower aBMD at femoral neck and total hip, and diminished radial total vBMD, cortical area, vBMD and thickness, respectively, by 8.3%, 8%, 2.7% and 9.2%, as well as significant compromised bone strength (stiffness, failure load and apparent modulus) by 8.3%, 9.1% and 9.5%, respectively. Similar alterations were also found in SLE/GC patients when compared to controls. In the premenopausal subgroup analysis, when compared with controls, total hip aBMD and radial cortical area were significantly lower in SLE/non-GC patients, and cortical area and thickness were significantly deficit in SLE/GC patients. However, no significant difference in any bone variables was present between SLE/GC and SLE/non-GC patients in the entire cohort or in the premenopausal subgroup.
  
  
  CONCLUSIONS
  SLE disease per se contributes to the deterioration in bone density, cortical microstructure and bone strength. This might help to explain the considerably higher fracture risk seen in SLE patients.
authors.affiliation: 1Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Hong Kong; Department of Imaging and Interventional Radiology, The Chinese University of Hong Kong, Hong Kong; Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong; Jockey Club Centre of Osteoporosis Care and Control; The Chinese University of Hong Kong, Hong Kong; and Department of Medicine & Geriatrics, Tai Po Hospital, Hong Kong.
authors.forename: X L
authors.initials: XL
authors.lastname: Tang
authors.forename: J F
authors.initials: JF
authors.lastname: Griffith
authors.forename: L
authors.initials: L
authors.lastname: Qin
authors.forename: V W
authors.initials: VW
authors.lastname: Hung
authors.forename: A W
authors.initials: AW
authors.lastname: Kwok
authors.forename: T Y
authors.initials: TY
authors.lastname: Zhu
authors.forename: E W
authors.initials: EW
authors.lastname: Kun
authors.forename: P C
authors.initials: PC
authors.lastname: Leung
authors.forename: E K
authors.initials: EK
authors.lastname: Li
authors.forename: L-S
authors.initials: LS
authors.lastname: Tam
mesh_terms: D000328:Adult; D015519:Bone Density; D001842:Bone and Bones / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D014057:Tomography, X-Ray Computed
chemical_list: D005938:Glucocorticoids
keywords: HR-pQCT; Systemic lupus erythematosus; bone microstructure; bone mineral density; bone strength; glucocorticoid; inflammation