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. 2011 Feb;19(2):180-5.
doi: 10.1016/j.joca.2010.11.002. Epub 2010 Nov 16.

In vivo structural analysis of subchondral trabecular bone in osteoarthritis of the hip using multi-detector row CT

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Free article

In vivo structural analysis of subchondral trabecular bone in osteoarthritis of the hip using multi-detector row CT

K Chiba et al. Osteoarthritis Cartilage. 2011 Feb.
Free article

Abstract

Objective: With developments in clinical computed tomography (CT), in vivo analysis of patients' bone microstructure has become increasingly possible. We analyzed the subchondral trabecular bone of hip osteoarthritis (OA) patients using multi-detector row CT (MDCT) to closely examine the structural changes that occur as OA progresses.

Design: 47 female hip joints were studied: 20 with OA secondary to hip dysplasia (11 advanced OA, nine early-moderate OA), seven with hip dysplasia without OA, and 20 normal. The images' maximal spatial resolution was 280 × 280 × 500 μm. Regions of interest (ROIs) were the subchondral trabecular bones of the acetabulum and femoral head. Measurement parameters were bone volume fraction (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular separation (Tb.Sp), structure model index (SMI), trabecular bone pattern factor (TBPf), Euler's number, and degree of anisotropy (DA). Relationships between joint space volume and these parameters were analyzed.

Results: With decreasing joint space, Tb.Th and BV/TV increased, and Tb.Sp, Tb.N, SMI, TBPf, and DA decreased significantly. The microstructures were significantly different between the early to advanced OA groups and the normal and dysplasia groups; there was no significant difference between the normal and dysplasia groups.

Conclusions: Changes of subchondral trabecular bone structure in OA could be evaluated using MDCT, despite imperfect spatial resolution and limited accuracy. Trabecular bone thickening and associated structural changes may be closely related to OA. Changes were observed in early to advanced OA, but not in dysplasia. This method may help to further elucidate OA pathogenesis, determine the therapeutic strategy, and evaluate therapy.

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