PROCOLLAGEN-II C-PROPEPTIDE IN JOINT FLUID - CHANGES IN CONCENTRATIONWITH AGE, TIME AFTER KNEE INJURY, AND OSTEOARTHRITIS

Citation
Ls. Lohmander et al., PROCOLLAGEN-II C-PROPEPTIDE IN JOINT FLUID - CHANGES IN CONCENTRATIONWITH AGE, TIME AFTER KNEE INJURY, AND OSTEOARTHRITIS, Journal of rheumatology, 23(10), 1996, pp. 1765-1769
Citations number
34
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
0315162X
Volume
23
Issue
10
Year of publication
1996
Pages
1765 - 1769
Database
ISI
SICI code
0315-162X(1996)23:10<1765:PCIJF->2.0.ZU;2-3
Abstract
Objective. To determine in a cross sectional study the concentrations in joint fluid of the C-propeptide of collagen II (pCol II-C) in patie nts with knee injury and developing osteoarthritis (OA). Methods. Syno vial fluid (SF) samples were collected from knees of healthy volunteer s, from patients with injury to the knee causing lesions of the anteri or cruciate ligament and/or menisci, and from patients with posttrauma tic or primary OA. Concentrations of pCol II-C were determined by enzy me immunoassay with a polyclonal antiserum against the bovine propepti de. Results. The median concentration of pCol II-C in joint fluid in t he reference group was 1.3 ng/ml (range 0.1-5.7 ng/ml). Median concent rations of pCol II-C in joint fluid were increased 2-4-fold in all 3 s tudy groups over that in the reference group. Very high concentrations of propeptide were noted in samples from patients younger than about 18 years. Propeptide concentrations were increased after knee injury, with a suggested peak at about 1-4 years evident for patients with cru ciate ligament injury. pCol II-C levels were increased at all stages o f OA development, except in the most advanced phases. Conclusion. The increased levels of pCol II-C in SF may reflect an increased rate of s ynthesis of collagen II in the joint cartilage of patients with knee i njury and developing OA. The increase reaches a maximum well before ra diographic changes indicative of OA are apparent, and occurs during a disease phase characterized by signs of increased degradation of colla gen II, aggrecan, and other matrix components. Further studies of mark ers of matrix metabolism of cartilage, bone, and other joint tissues i n human and animal models of OA may aid in the identification of proce ss markers, individuals at risk, and new therapeutic targets.