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。

 

https://s.click.taobao.com/xJt8MNw

 

 

 

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

 

 

骨关节炎发病机制的新方面:成纤维样软骨细胞在疾病晚期的作用

据认为,到2020年,预期寿命的普遍增加将使骨关节炎成为致残的第四大原因。尽管尚未完全阐明特发性骨关节炎的发病机理,但疾病过程的主要特征是两者之间相互作用的改变。软骨细胞及其周围的细胞外基质。在这些紊乱的过程中,关节软骨的病理改变的细胞外基质中通常存在三种类型的软骨细胞:不断发生变性的健康软骨细胞,不断降解的退化细胞以及最终似乎没有的成纤维样软骨细胞。受此过程的影响,因此数量不断增加。这些成纤维细胞样的软骨细胞即使在骨关节炎的晚期也参与组织再生,但仅在它们形成纤维软骨或疤痕组织的情况下参与,因为我们已经证明,它们主要合成I型胶原而不是II型胶原。 ,典型用于健康软骨。然而,我们进一步能够证明,成纤维细胞样软骨细胞还产生越来越多的蛋白聚糖decorin和biglycan,它们在生理上参与II型胶原以及perlecan的形成。如果可以对这些多功能的成纤维细胞样软骨细胞进行修饰以合成通常用于软骨的II型胶原蛋白,从而有助于逆转骨关节炎晚期所引起的关节软骨损伤,则它们可能是理想的治疗起点。

New aspects of the pathogenesis of osteoarthritis: the role of fibroblast-like chondrocytes in late stages of the disease - PubMed
https://pubmed.ncbi.nlm.nih.gov/15578449/