Adiponectin in patients with knee osteoarthritis

Abstract

Background Investigations suggest that adipokines may play an important role in pathogenesis and cartilage damage in osteoarthritis (OA). Whether adiponectin (ADN) has proinflammatory or anti-inflammatory actions in OA remain controversial. Aim The aim of this study was to measure the serum level of ADN in patients with knee osteoarthritis (KOA) and to evaluate the relationship between its level and clinical and radiological picture of OA. Patients and methods The study included 56 patients with primary symptomatic KOA and 30 matched controls. Parameters of obesity and serum ADN, leptin (LEP), and matrix metalloproteinase (MMP)-3 were measured in all participants. Clinical features of KOA severity and activity were evaluated in the patients. Extent of knee joint damage due to OA was evaluated by means of plain radiograph and MRI. The volume of the infrapatellar fat pad was measured using MRI. Results KOA patients had high serum ADN, LEP, and MMP-3 compared with controls and they were higher in female KOA patients than in male KOA patients. Serum ADN, LEP, and MMP-3 were significantly correlated with parameters of obesity and with each other. The serum ADN level was significantly correlated with tenderness, visual analogue scale pain, OA activity, OA severity, and also with Western Ontario and McMaster Universities Osteoarthritis Index score. Serum LEP level was significantly correlated with OA severity. Serum level of MMP-3 was significantly correlated with the tenderness score. Higher ADN serum levels were associated with increased Kellgren–Lawrence grade, increased Noyes MRI grade, increased OA severity MRI grade, and increased meniscal degeneration MRI grade. Serum levels of ADN, LEP, and MMP-3 were significantly correlated with the Hoffa fat pad volume. Conclusion ADN serum level was associated with radiological evidence of OA severity and was correlated with serum LEP and MMP-3 levels. These findings strongly suggest that ADN is involved in the pathogenesis of joint inflammation and cartilage destruction in OA and may be a target for disease-modifying drug development.