Department of Clinical Sciences, University of Pennsylvania School of Veterinary Medicine, New Bolton Center, Kennett Square, PA, USA.
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Osteoarthritis Cartilage. 2020 Oct;28(10):1303-1315. doi: 10.1016/j.joca.2020.05.009. Epub 2020 Jun 3.
Lubricin is increasingly being evaluated as an outcome measure in studies investigating post-traumatic and naturally occurring osteoarthritis. However, there are discrepancies in results, making it unclear as to whether lubricin is increased, decreased or unchanged in osteoarthritis. The purpose of this study was to review all papers that measured lubricin in joint injury or osteoarthritis in order to draw conclusions about lubricin regulation in joint disease.
A systematic search of the Pubmed, Web of Knowledge, and EBSCOhost databases for papers was performed. Inclusion criteria were in vivo studies that measured lubricin in humans or animals with joint injury, that investigated lubricin supplementation in osteoarthritic joints, or that described the phenotype of a lubricin knock-out model. A methodological assessment was performed.
Sixty-two studies were included, of which thirty-eight measured endogenous lubricin in joint injury or osteoarthritis. Nineteen papers found an increase or no change in lubricin and nineteen reported a decrease. Papers that reported a decrease in lubricin were cited four times more often than those that reported an increase. Fifteen papers described lubricin supplementation, and all reported a beneficial effect. Eleven papers described lubricin knock-out models.
The human literature reveals similar distributions of papers reporting increased lubricin as compared to decreased lubricin in osteoarthritis. The animal literature is dominated by reports of decreased lubricin in the rat anterior cruciate ligament transection model, whereas studies in large animal models report increased lubricin. Intra-articular lubricin supplementation may be beneficial regardless of whether lubricin increases or decreases in OA.
黏蛋白作为一种评估创伤后和自发性骨关节炎的生物标志物，其在研究中的应用日益广泛。然而，不同研究的结果存在差异，使得黏蛋白在骨关节炎中是增加、减少还是不变尚不清楚。本研究旨在回顾所有测量关节损伤或骨关节炎中黏蛋白的文献，以总结关节疾病中黏蛋白的调控机制。
通过 Pubmed、Web of Knowledge 和 EBSCOhost 数据库对相关文献进行系统性检索。纳入标准为：测量黏蛋白的体内研究，包括人类或动物的关节损伤、骨关节炎关节内黏蛋白补充、黏蛋白敲除模型表型描述。对纳入文献进行方法学评估。
共纳入 62 项研究，其中 38 项研究测量了关节损伤或骨关节炎患者的内源性黏蛋白。19 项研究发现黏蛋白增加或不变，19 项研究报道黏蛋白减少。报道黏蛋白减少的文献被引用的次数是报道黏蛋白增加的文献的 4 倍。15 篇文献描述了黏蛋白补充，所有文献均报道了有益的效果。11 篇文献描述了黏蛋白敲除模型。
人类文献中报道黏蛋白增加和减少的比例相似，而动物文献主要报道大鼠前交叉韧带切断模型中黏蛋白减少，而大动物模型研究则报道黏蛋白增加。关节内黏蛋白补充可能有益，无论 OA 中黏蛋白增加还是减少。
