Osteoarthritis as part of metabolic syndrome?

Czech version

Authors: Karel Pavelka
Authors‘ workplace: Revmatologický ústav, Praha
Published in: Vnitř Lék 2017; 63(10): 707-711
Category: Reviews

Overview

Osteoarthritis (OA) is the most frequent joint disease, whereas etiopathogenesis of OA is not entirely clarified. It is a heterogeneous disorder and genetic as well as biomechanical, endocrine and inflammatory effects may be involved in its origin. The author examines the problems concerning relationships between the metabolic syndrome and OA, and states that the prevalence of metabolic syndrome in patients with OA is higher than in those without OA (59 % vs 23 %). It remains problematic that one of the main components of metabolic syndrome is obesity which in itself is a risk factor for arthrosis development in the weight-bearing joints, not for OA in the hands. After adjustment for BMI the relationships between the metabolic syndrome and OA are less expressed. Over the last decade evidence has been gained about adipose tissue being the source of numerous cytokines and adipokines which may cause inflammation of low-activity synovial tissue, sometimes also called “meta-inflammation.” The most data was gathered on leptin, resistin, adiponectin and visfatin. Mostly there were serum levels of these adiponectins assessed and the results were sometimes inconsistent. Two studies have been published this year presenting a histological and immunohistochemical evaluation of the fat stored in 2 tissues right in the joints of patients with metabolic syndrome and OA, and the fat on an experimental OA model, concluding that the secretion activity of the potentially pro-inflammatory adipokines through adipocytes may differ in the synovial membrane, infrapatellar fat body and in abdominal fat. It is evident that the components of metabolic syndrome and OA can share a common pathological process which is an “adipose tissue associated inflammation.” The changed secretion profile of pro-inflammatory adipokines is present in obese individuals, an older population and postmenopausal women, the populations at high risk for both metabolic syndrome and OA. Significant mechanical loads may stimulate OA of the knee joints in obese patients, however not of the hands, and further differences between arthrosis of the knee joints and the hands. The adipose tissue induced inflammation is the common pathological mechanism for both metabolic syndrome and OA and it may account for some of the variations.

Key words:
adiponectins – metabolic syndrome – osteoarthritis

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