Hindawi Publishing Corporation Mediators of Inlammation Volume 2013, Article ID 183653, 6 pages http://dx.doi.org/10.1155/2013/183653 Clinical Study Serum Matrix Metalloproteinase-3 in Comparison with Acute Phase Proteins as a Marker of Disease Activity and Radiographic Damage in Early Rheumatoid Arthritis Mahmood M. T. M. Ally, 1 Bridget Hodkinson, 2 Pieter W. A. Meyer, 3 Eustasius Musenge, 4 Mohammed Tikly, 2 and Ronald Anderson 3 1 Department of Internal Medicine, Faculty of Health Sciences, University of Pretoria, Private Bag X663, Pretoria 0001, South Africa 2 Division of Rheumatology, Department of Medicine, Chris Hani Baragwanath Hospital, University of the Witwatersrand, Johannesburg, South Africa 3 Medical Research Council Unit for Inlammation and Immunity, Department of Immunology, Faculty of Health Sciences, University of Pretoria and Tshwane Academic Division of the National Health Laboratory Service, Pretoria, South Africa 4 Biostatistics and Epidemiology Division, School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Correspondence should be addressed to Mahmood M. T. M. Ally; tar@up.ac.za Received 10 December 2012; Accepted 26 February 2013 Academic Editor: Antonio Macci` o Copyright © 2013 Mahmood M. T. M. Ally et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Matrix metalloproteinase-3 (MMP-3) is involved in the immunopathogenesis of rheumatoid arthritis (RA), but little is known about its relationship to genetic susceptibility and biomarkers of disease activity, especially acute phase reactants in early RA. MMP-3 was measured by ELISA in serum samples of 128 disease-modifying, drug-na¨ ıve patients and analysed in relation to shared epitope genotype, a range of circulating chemokines/cytokines, acute phase reactants, autoantibodies, cartilage oligomeric protein (COMP), and the simpliied disease activity index (SDAI). MMP-3 was elevated >1.86 ng/ml in 56.25% of patients ( < 0.0001), correlated with several biomarkers, notably IL-8, IL-6, IFN , VEGF and COMP ( values = 0.22–0.33,  < 0.014–0.0001) and with CRP and SAA levels ( = 0.40 and 0.41, resp.,  < 0.0000) and SDAI ( = 0.29,  < 0.0001), but not with erosions or nodulosis. However, the correlations of CRP and SAA with SDAI were stronger (respective values of 0.63 and 0.54,  < 0.001 for both). COMP correlated with smoking, RF, and MMP-3. MMP-3 is signiicantly associated with disease activity, inlammatory mediators and cartilage breakdown, making it a potential biomarker of disease severity, but seemingly less useful than CRP and SAA as a biomarker of disease activity in early RA. 1. Introduction Rheumatoid arthritis (RA) is characterised by a progres- sive, erosive polyarthritis,resulting in immune-mediated joint destruction and eventual disability.Components of the immunoinlammatory response include acute phase proteins, auto-reactive T cells, B cells, and their respective inlam- matory mediators. he consequence is a self-perpetuating chronic inlammatory response involving a complex interplay between iniltrating inlammatory cells and the structural cells of the synovial joint [1, 2]. Matrix metalloproteinase-3 (MMP-3) is produced pre- dominantly by chondrocytes and synovial ibroblasts and is found in high concentrations in the synovial luid, with elevated levels also found in the serum of RA patients [3]. MMP-3 production is upregulated by the proinlammatory cytokines IL-1, TNF, IFN , and IL-17A, as well as by serum amyloid A (SAA), an acute phase reactant, with counter-regulatory inhibition from IL-4 and IL-13 [4–10]. Cytokine/SAA-driven production of MMP-3 in the rheuma- toid joint appears to be a key mediator of cartilage destruc- tion, while bone resorption is facilitated by MMP-3-mediated