Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


The Clinical Benefit of Joint Distraction in Treatment of Advanced Ankle OA May Be Partly Explained by Subchondral Bone Changes.

Intema1,  F., Thomas2,  T. P., Anderson2,  D. D., Elkins2,  J., Mastbergen1,  S. C., Lafeber1,  F. P. J. G., Brown2,  T. D.

Rheumatology & Clinical Immunology, University Medical Center Utrecht, The Netherlands
The University of Iowa, Iowa City, IA
The University of Utah, Salt Lake City, UT

Background:

In osteoarthritis (OA), it has long been understood that cartilage degeneration is accompanied by sclerosis of subchondral bone. The subsequent stiffening of the bone decreases its capacity to absorb mechanical impact energy, which might play a role in the development and/or progression of cartilage degeneration. Joint distraction as a treatment for advanced ankle OA has been shown to provide pain relief and improve clinical function, with some evidence accruing that cartilage repair is involved. However, the underlying mechanism(s) remain unclear. This study evaluated whether long-term changes in subchondral bone density are associated with extended joint distraction.

Methods:

Twenty-six patients with advanced post-traumatic ankle OA were treated with joint distraction for three months using an Ilizarov frame. Follow-up was two years, and clinical outcome was assessed using the ankle OA scale (AOS).

Dual-contrast CT scans were obtained at baseline (before treatment), and at one- and two-year follow-ups after treatment, to analyse joint space width and bone density. The tibia and talus bones were manually segmented at each time point, and the bone segmentations from the two follow-up CT scans were registered to the baseline scans for each patient. The resulting spatial transformations were then used to bring all CT datasets for a given patient into a common spatial reference frame, using purpose-written MATLAB code. Changes in bone density (Hounsfield Units (HU), relative to baseline) were calculated at a number of discrete locations beneath the tibial and talar weight-bearing regions. The measurement grid covered a subchondral patch of nominally 650 mm2, with ~4000 point measurements per surface (~0.17mm2/point). Bone density calculations were performed at 1 mm intervals beneath the bone surface, along the surface normals and extending subchondrally up to 8 mm (total of roughly 30,000 sampled point locations for each bone).

Results:

Joint distraction resulted in a statistically significant long-term decrease in pain (mean value decreased from 60 to 35, on a scale of 100; p<0.01) and function (mean decreased from 67 to 36; p<0.01) at two years post-treatment. These clinical changes were accompanied by changes in bone density. The initial subchondral bone density was 569±14 HU for the tibia, and 490±19 HU for the talus. The average decrease in density was 133±17 HU (p<0.01) for the tibia and 95±17 HU (p<0.01) for the talus, one year after treatment. These density changes persisted two years after treatment (124±16 HU; p<0.01, and 88±18 HU; p<0.01, for tibia and talus, respectively), and they were not significantly different from the bone density one year after treatment (p=0.11).

Conclusion:

Treatment of advanced post-traumatic ankle OA with three months of joint distraction produced decreases in subchondral bone density that persisted for at least two years of follow-up. This could lead to a more physiologically normal distribution of mechanical stresses by the less dense bone, encouraging cartilage repair activity. As such, these prolonged bone changes may in part explain the clinical benefits of joint distraction.

To cite this abstract, please use the following information:
Intema, F., Thomas, T. P., Anderson, D. D., Elkins, J., Mastbergen, S. C., Lafeber, F. P. J. G., et al; The Clinical Benefit of Joint Distraction in Treatment of Advanced Ankle OA May Be Partly Explained by Subchondral Bone Changes. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :176
DOI: 10.1002/art.27945

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