Pavelka Karel
Vnitr Lek. 2017 Fall;63(10):707-711.
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.
骨关节炎(OA)是最常见的关节疾病,然而其发病机制尚未完全阐明。它是一种异质性疾病,遗传因素以及生物力学、内分泌和炎症效应可能都参与其发病过程。作者研究了代谢综合征与OA之间关系的相关问题,并指出OA患者中代谢综合征的患病率高于无OA者(59%对23%)。代谢综合征的主要组成部分之一是肥胖,而肥胖本身是负重关节发生关节病的危险因素,而非手部OA的危险因素,这一点仍然存在问题。在调整体重指数(BMI)后,代谢综合征与OA之间的关系表现得较弱。在过去十年中,有证据表明脂肪组织是多种细胞因子和脂肪因子的来源,这些因子可能导致低活性滑膜组织发生炎症,有时也称为“元炎症”。关于瘦素、抵抗素、脂联素和内脂素的研究数据最多。大多数研究评估的是这些脂联素的血清水平,结果有时并不一致。今年发表了两项研究,对代谢综合征和OA患者关节内两个组织中储存的脂肪以及实验性OA模型中的脂肪进行了组织学和免疫组化评估,得出结论:潜在促炎脂肪因子通过脂肪细胞的分泌活性在滑膜、髌下脂肪体和腹部脂肪中可能存在差异。显然,代谢综合征和OA的组成部分可能共享一个共同的病理过程,即“脂肪组织相关炎症”。促炎脂肪因子分泌谱的改变存在于肥胖个体、老年人群和绝经后女性中,这些人群是代谢综合征和OA的高危人群。显著的机械负荷可能会刺激肥胖患者膝关节发生OA,但不会刺激手部,这进一步显示了膝关节和手部关节病之间的差异。脂肪组织诱导的炎症是代谢综合征和OA的共同病理机制,它可能解释了一些差异。关键词:脂联素;代谢综合征;骨关节炎