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Effect of Intraarticular Hyaluronan Injection on Vertical Ground Reaction Force and Progression of Osteoarthritis After Anterior Cruciate Ligament Transection
GERALD N. SMITH Jr, STEPHEN L. MYERS, KENNETH D. BRANDT, ELIZABETH A. MICKLER, and MARJORIE E. ALBRECHT
ABSTRACT. Methods. OA was induced in 30 adult dogs of mixed breed by ACLT. The dogs were divided into 3 groups and given 5 weekly IA injections into the unstable knee during Weeks 1–5 and 13–17. The prophylactic treatment group received HA in the first series and saline during the second series. The therapeutic group received saline in the first series and HA in the second series. The control group received saline during both injection series. The progression of joint damage of OA was evaluated by arthroscopy 12 weeks after ACLT and by gross examination 32 weeks after ACLT. Histologic and biochemical changes of OA were evaluated. Loading of the unstable limb during gait was determined by force-plate analysis before surgery, after each series of injections, and the week before euthanasia. Results. Arthroscopic examination 12 weeks after ACLT revealed OA changes in the cruciate-deficient knees. Chondropathy scores ranged from 0 to 8 (possible range 0–65). The mean chondropathy score was 2.5 ± 1.3 (mean ± SD) for the controls, 2.5 ± 2.5 for the therapeutic group, and 2.1 ± 1.3 for the prophylactic group. At the termination of the experiment 32 weeks after ACLT, the gross chondropathy scores were 14.0 ± 5.2 for controls, 17.6 ± 6.8 for the therapeutic group, and 13.3 ± 5.0 for the prophylactic group. There were no significant differences among the means of the gross scores, the histologic scores, or biochemical composition of articular cartilage. The peak vertical ground reaction force (VGRF) generated by the unstable limb was reduced by ~60% after ACLT, and slowly increased to ~75% of the baseline value over the 32 weeks after ACLT. HA injection had no effect on the VGRF or on the pathologic changes of OA. Conclusion. Intraarticular HA injection did not alter the progression of OA in the cruciate-deficient canine knee or alter the loading of the unstable limb. (J Rheumatol 2005;32:325-34) Key Indexing Terms:
OSTEOARTHRITIS
From the Rheumatology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA. Supported in part by NIH grants AR45383 (Dr. Smith) and AR20582 (Dr. Brandt) from the National Institute of Arthritis and Musculoskeletal Diseases. G.N. Smith Jr, PhD, Associate Professor; S.L. Myers, MD, Professor; K.D. Brandt, MD, Professor; E.A. Mickler, MS, Research Associate; M.E. Albrecht, BS, Research Associate. Address reprint requests to Dr. G.N. Smith, Rheumatology Division, 1110 West Michigan, LO 545, Indianapolis, IN 46202-5100. E-mail: gnsmith@iupui.edu Submitted September 5, 2003; revision accepted August 30, 2004. |