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Biochemical Markers of Bone and Cartilage Remodeling in Prediction of Longterm Progression of Knee Osteoarthritis
OLIVIER BRUYERE, JULIEN H. COLLETTE, OLIVIER ETHGEN, LUCIO C. ROVATI, GIAMPAOLO GIACOVELLI, YVES E. HENROTIN, LAURENCE SEIDEL, and JEAN-YVES L. REGINSTER
ABSTRACT.
Methods. Mean and minimal joint space width (JSW) of the femorotibial joint were measured from standardized radiographs taken at baseline and at the end of a 3-year longitudinal study of patients with knee OA. Pain, stiffness, and physical function subscales of the Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index were assessed at the same time points. Biochemical markers [serum keratan sulfate (KS), serum hyaluronic acid (HA), urine pyridinoline (PYD) and deoxypyridinoline (DPD), serum osteocalcin (OC), cartilage oligomeric matrix protein (COMP)] were assessed at baseline and after 1 year. Results. At baseline, no significant correlations were observed between values of biochemical markers and JSW or any of the WOMAC scores. Baseline markers were not correlated with 3-year percentage changes observed in mean or minimal JSW and WOMAC scores. Changes observed after 1 year in OC and HA were significantly correlated with 3-year progression in mean JSW (r = –0.24, p = 0.04 and r = 0.27, p = 0.02, respectively) and in minimal JSW (r = –0.31, p = 0.01 and r = 0.24, p = 0.04, respectively). In patients from the lowest quartile of 1-year changes in HA (< –21.22 ng/ml), mean JSW decreased after 3 years by 0.76 (1.23) mm compared to an increase of 0.11 (0.83) mm in patients in the highest quartile (> +14.34 ng/ml) (p = 0.03). Conclusion. The 3-year radiological progression of knee OA could be predicted by a 1-year increase in OC or a 1-year decrease in HA levels. (J Rheumatol 2003;30:1043-50) Key Indexing Terms:
OSTEOARTHRITIS From the WHO Collaborating Center for Public Health Aspect of Osteoarticular Disorders (CCPHAOD), Liege; the Department of Public Health and Epidemiology, the Bone and Cartilage Research Unit, and the Biostatistics Department, University of Liege, Liege, Belgium; the Department of Clinical Pharmacology, Rotta Research Laboratorium, Monza, Italy; and Georgetown University Medical Center, Washington, DC, USA. O. Bruyere, MSc, CCPHAOD, Department of Public Health and Epidemiology, Bone and Cartilage Research Unit, University of Liege; J.H. Collette, PhD, Bone and Cartilage Research Unit, University of Liege; O. Ethgen, MSc, CCPHAOD, Department of Public Health and Epidemiology, University of Liege; L.C. Rovati, MD; G. Giacovelli, PhD, Rotta Research Laboratorium; Y.E. Henrotin, PhD, Bone and Cartilage Research Unit, University of Liege; L. Seidel, MSc, Biostatistics Department, University of Liege; and J-Y.L. Reginster, MD PhD, CCPHAOD, Department of Public Health and Epidemiology, Bone and Cartilage Research Unit, University of Liege, Georgetown University Medical Center. Address reprint requests to Prof. J-Y. Reginster, Bone and Cartilage Metabolism Unit, Quai G. Kurth 45, 4000 Liege, Belgium. E-mail : jyreginster@ulg.ac.be Submitted January 25, 2002; revision accepted November 15, 2002. |