骨关节炎是一种代谢性(即体质性)疾病,因为它也涉及非负重关节

 Osteoathritis is a metabolic disease, as it also involves non-weight bearing joints

 

 

 

文摘

骨关节炎是一种与年龄有关的退行性疾病,是西方世界的主要障碍。有趣的是,迄今为止,除了对症治疗和关节置换手术之外,还没有可用的早期诊断生物标志物,也没有任何有效的治疗方法。

 

OA长期以来一直与肥胖有关,主要是由于关节的机械过载。然而,最近的研究指出,骨关节炎(OA)是一种代谢 性(即体质性)疾病,因为它也涉及非负重关节

 

 

 

事实上,脂质代谢的改变可能是潜在的原因。首先,脂肪因子已被证明是OA发病机制的关键调控因子。第二,流行病学研究表明血清胆固醇是OA发展的危险因素。第三,在骨组织变化发生之前,在OA的早期观察到关节脂质沉积。第四,蛋白质组分析显示OA与脂类代谢之间有重要的联系。最后,最近的基因表达研究揭示了胆固醇流入和流出的解除管制以及脂质代谢相关基因的表达。有趣的是,脂质和脂质代谢被认为与另一种与年龄有关的退化性疾病动脉粥样硬化(ATH)的发展和进展有关。

 

 

因此,尽管人们很容易推测骨关节炎软骨细胞已经转化为泡沫细胞,但还没有得到证实。然而,这可能是一个连接ATHOA的有趣理论,这可能为利用ATH以前的知识对OA进行新的治疗干预开辟新的途径。

 

 

 

 

Lipid metabolism and osteoarthritis: Lessons from atherosclerosis

 

Abstract

Osteoarthritis (OA) is an age-related degenerative disease comprising the main reason of handicap in the Western world. Interestingly, to date, there are neither available biomarkers for early diagnosis of the disease nor any effective therapy other than symptomatic treatment and joint replacement surgery. OA has long been associated with obesity, mainly due to mechanical overload exerted on the joints. Recent studies however, point to the direction that OA is a metabolic disease, as it also involves non-weight bearing joints. In fact, altered lipid metabolism may be the underlying cause. First, adipokines have been shown to be key regulators of OA pathogenesis. Second, epidemiological studies have shown serum cholesterol to be a risk factor for OA development. Third, lipid deposition in the joint is observed at the early stages of OA before the occurrence of histological changes. Fourth, proteomic analyses have shown an important connection between OA and lipid metabolism. Finally, recent gene expression studies reveal a deregulation of cholesterol influx and efflux and in the expression of lipid metabolism-related genes. Interestingly, lipids and lipid metabolism are known to be implicated in the development and progression of another age-related degenerative disease, atherosclerosis (ATH). Thus, although it is tempting to speculate that the osteoarthritic chondrocyte has been transformed to foam cell, it has not been proven yet. However, this may be an intriguing theory linking ATH and OA, which may open new avenues to novel therapeutic interventions for OA taking advantage of previous knowledge from ATH.

 

https://www.researchgate.net/publication/49642773_Lipid_metabolism_and_osteoarthritis_Lessons_from_atherosclerosis