FRI0325 Sle disease per se, rather than glucocorticoid treatment, contributes more to deterioration in bone density, microstructure and strength
Authors: X. L. Tang, J. F. Griffith, S.-K. Au, L. Qin, V. W. Hung, A. W. Kwok, E. K. Li, L.-S. Tam
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The disparity between fracture prevalence and areal bone mineral density (aBMD) measured by dual-energy x-ray absorptiometry (DXA) has become a well-recognized feature in senile osteoporosis, glucorticoid (GC) use and systemic lupus erythematosus (SLE). Bone microstructure, a key component for bone strength, was measured by invasive histomorphometry of biopsy specimens. The recent development of high-resolution peripheral quantitative computed tomography (HR-pQCT) has allowed this information to be obtained non-invasively through acquisition of detailed 3D image datasets of the distal radius and tibia. In addition, in vivo HR-pQCT-based micro-finite element analysis (μFEA) allows accurate prediction of bone strength. Using HR-pQCT our group had demonstrated that low cortical volumetric BMD can reliably discriminate SLE patients on long-term GC with and without vertebral fracture; and SLE patients had deteriorated cortical bone density and microarchitecture and compromised bone strength compared with age-matched controls. Since all these studies involved SLE patients on long-term GC therapy, the effect of SLE disease per se on bone quality could not be ascertained. <h3>Objectives</h3> The aim of this study is therefore to compare BMD, bone microstructure and bone strength in SLE patients with and without treatment with GC and healthy controls. <h3>Methods</h3> Thirty age-and sex-matched SLE patients on long-term GC (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) of the femoral neck, total hip, lumbar spine and non-dominant distal radius were measured by DXA. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the non-dominant distal radius were assessed by HR-pQCT. Bone strength was estimated by μFEA. <h3>Results</h3> The mean age of the whole cohort was 46 years old and the mean disease duration for patients was over 10 years. Compared with healthy controls, aBMD at femoral neck and total hip were significantly lower, and using HR-pQCT, radial average vBMD, cortical area, vBMD and thickness were significantly reduced by 8.3%, 8%, 2.7% and 9.2% respectively in SLE/non-GC patients. Bone strength (i.e. stiffness, failure load and apparent modulus) in SLE/non-GC patients was inferior to that of controls by 8.3%, 9.1% and 9.5% respectively. Similar alterations were found in SLE/GC patients when compared to controls. However, no significant difference in any bone density, microstructure or strength variables was present between SLE/GC and SLE/non-GC patients. <h3>Conclusions</h3> SLE disease per se seems to contribute more to the deterioration in bone density, microstructure and strength seen in SLE patients than treatment with GC. HR-pQCT can provide an insightful analysis of the bone changes occurring in SLE, show the specific peripheral component of bone affected and improves our understanding of the mechanisms behind SLE-related bone loss, which at least partly contributes to the higher fracture risk in SLE patients. <b>Disclosure of Interest</b>: None Declared