Background Ankylosing spondylitis (AS) is associated with high risk of osteoporosis and fractures. Fracture risk is predicted by bone mineral density (BMD), bone microarchitecture and strength.BMD is measured by DXA. However, BMD of the spine as assessed by DXA may be measured as falsely normal because of the presence of syndesmophytes in patients with AS. Thus lumbar spine is an unreliable site for DXA in patients with AS. Moreover DXA cannot differentiate between trabecular and cortical bone. Not much data exist on how AS affects bone microarchitecture and strength.
Objectives This study aimed to assess bone microarchitecture and strength in patients with AS since these are known to be important predictors of fracture risk.
Methods AS was defined by Modified New York criteria. Age and sex matched healthy controls were also included in the sub group analysis. DXA was done to assess BMD. Volumetric BMD (vBMD) and microarchitecture were measured using high-resolution peripheral quantitative CT (HRpQCT). Bone strength was determined using finite element analysis (FEA).
Results There were 44 cases (25 men, 82% Caucasian). The mean (±SD) age and duration of disease were 44±2 and 19±13 years respectively. The mean BASDAI was 6.3± 1.8. At the time of the study, two patients were using bisphosphonates and corticosteroids. Serum ESR and CRP were 22±23 mm, and 13±16 respectively. On regression analysis, age, disease duration, gender and mSASSS were significant predicotrs of bone microarchitecture.In the sub-group analysis, though cases (n=24) and controls (n=38) had similar BMD (measured by DXA) at lumbar spine and total hip, cases had lower femoral neck BMD (707±110 vs. 943±196 in controls, p≤0.0001, percentage difference=25%). Patients with AS had significantly lower cortical volumetric BMD (819±51 vs. 858±60 in controls, p=. 010) and total volumetric BMD (282±55 vs. 331±54, p=. 001) at the radius. Similarly, the total volumetric BMD at tibia was lower in cases (276±48 vs. 303 ± 48 in controls, p=.033). There was a trend towards lower trabecular vBMD at the radius as well as trabecular and cortical volumetric BMD at the tibia in cases (151±46 vs. 170±41, p=. 104, 150±39 vs. 168±39, p=. 087 and 831±78 vs. 858±42, p=. 077 respectively). BV/TV also tended to be lower in cases. Cases had significantly thinner cortices than controls at the radius. Cortical porosity was not different between cases and controls. Trabecular parameters such as trabecular number, separation and thickness were relatively preserved. Bone stiffness (1.168± 0.279 vs. 1.380±0.302, p=0.008) and stress at the radius (22.5±7.0 vs. 27.5±7.9, p=0.008) as measured by FEA, were significantly lower in cases than controls.
Conclusions This is the first study to have documented abnormalities of bone structure and strength in patients with AS. Patients with AS have lower volumetric BMD at the trabecular and cortical regions of radius and tibia. Trabecular microarchitecture was preserved but cortical thickness was less in cases than controls. Bone stiffness and stress at the radius as measured by FEA, were significantly lower in cases than controls. These abnormalities might partly contribute to the high fracture risk in patients with AS.
Disclosure of Interest N. Nigil Haroon Grant/research support: Salary support from AMGEN, A. Cheung Grant/research support: AMGEN, PFIZER, E. Szabo: None declared, J. Raboud: None declared, A. Anton: None declared, R. Josse: None declared, R. Inman Grant/research support: AMGEN
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