Obesity Contribution in Synthesis and Degradation of Cartilage Marker Through Inflammation Pathway in Osteoarthritis Patient: Analysis of Adiponectin, Leptin, Ykl-40 and Cartilage Oligomeric Matrix Proteinase (Comp) Synovial Fluid

Abstract

Background: To determine the role of obesity in osteoarthritis (OA) through inflammation pathway byanalyzing articular cartilage synthesis and degradation markers in synovial fluid.Methods: We performed observational study with cross sectional approach. Obesity was determinedbased on WC. OA genu diagnosed based on American College of Rheumatology (ACR) 1986 criteria. Weexamined leptin as inflammation marker, adiponectin as anti-inflammation marker, YKL-40 as cartilagesynthesis marker and COMP as cartilage degradation marker in synovial joint using ELISA.Results: From 70 OA genu patients, 61 subjects with central obesity and 9 subjects with non-central obesity.In OA patient with central obesity group, WC does not correlate directly with COMP and YKL-40, butthrough level of adiponectin and leptin. WC correlates with adiponectin and leptin level, and then adiponectinlevel correlate with YKL-40 level, and leptin level correlate with COMP level, the greater the WC, the loweradiponectin level and the higher leptin level. The lower the adiponectin level, the lower the YKL-40 leveland the higher the leptin level, the higher the COMP level. Whereas in OA patient with non-central obesitygroup, WC is directly correlated with COMP level (not through adiponectin or leptin); the greater WC, thehigher COMP level. WC does not correlate directly with YKL-40, but through adiponectin due to increasingage, not because of changes in WC. In non-central obesity, the older a person is, the lower adiponectin level;and the lower adiponectin level, the lower YKL-40 level.Conclusions: Obesity contributed in central obese OA, group on destruction of articular cartilage wasdirectly correlated with WC without involving inflammation pathway.