骨关节炎(OA)是一种影响人类和动物的衰弱疾病。在早期阶段,OA的特征在于细胞外基质(ECM)的损伤以及软骨细胞的凋亡和消耗。OA进展的特征是透明软骨丧失,软骨和骨赘形成,关节囊增厚和后期功能丧失。由于软骨的再生潜力非常有限,骨关节炎的变化是不可逆的,预防OA,调节现有的骨关节炎关节炎症,减少关节疼痛和支持关节功能是唯一的选择。OA和疼痛的进展可能需要通过关节置换或关节固定术作为终末期手术进行手术干预。在人类医学中,脂肪因子在OA发生和发展中的作用越来越受到关注.目前,已知的脂肪因子包括瘦素,脂联素,visfatin,抵抗素,前颗粒蛋白,chemerin,脂质运载蛋白-2,vaspin,omentin-1和nesfatin。已经证明脂肪因子通过调节合成代谢和分解代谢平衡在关节稳态中起关键作用,自噬,细胞凋亡和炎症反应。在小动物身上,就狗和猫而言,自然发生的OA已被清楚地证明是一个临床问题。和人类一样,OA的病因是多因素的,尚未完全阐明。人类,狗和猫共有许多关节相关的退行性疾病导致OA。在这次审查中,关节稳态,OA,讨论了脂肪因子和导致自然发生的OA的小动物中最常见的关节疾病及其与脂肪因子的关系。这篇综述的目的是强调小动物患者中OA和脂肪因子研究的转化潜力。
Osteoartritis (OA) is a debilitating disease affecting both humans and animals. In the early stages, OA is characterized by damage to the extracellular matrix (ECM) and apoptosis and depletion of chondrocytes. OA progression is characterized by hyaline cartilage loss, chondrophyte and osteophyte formation, thickening of the joint capsule and function loss in the later stages. As the regenerative potential of cartilage is very limited and osteoarthritic changes are irreversible, prevention of OA, modulation of existing osteoarthritic joint inflammation, reducing joint pain and supporting joint function are the only options. Progression of OA and pain may necessitate surgical intervention with joint replacement or arthrodesis as end-stage procedures. In human medicine, the role of adipokines in the development and progression of OA has received increasing interest. At present, the known adipokines include leptin, adiponectin, visfatin, resistin, progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin. Adipokines have been demonstrated to play a pivotal role in joint homeostasis by modulating anabolic and catabolic balance, autophagy, apoptosis and inflammatory responses. In small animals, in terms of dogs and cats, naturally occurring OA has been clearly demonstrated as a clinical problem. Similar to humans, the etiology of OA is multifactorial and has not been fully elucidated. Humans, dogs and cats share many joint related degenerative diseases leading to OA. In this review, joint homeostasis, OA, adipokines and the most common joint diseases in small animals leading to naturally occurring OA and their relation with adipokines are discussed. The purpose of this review is highlighting the translational potential of OA and adipokines research in small animal patients.