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关节内骨折后促炎细胞因子水平升高-系统评价。

Elevation of Pro-Inflammatory Cytokine Levels Following Intra-Articular Fractures-A Systematic Review.

机构信息

Department of Orthopedics and Traumatology, Odense University Hospital, 5000 Odense, Denmark.

Department of Clinical Research, University of Southern Denmark, 5000 Odense, Denmark.

出版信息

Cells. 2021 Apr 14;10(4):902. doi: 10.3390/cells10040902.

DOI:10.3390/cells10040902
PMID:33919965
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8070895/
Abstract

Intra-articular fractures are a major cause of post-traumatic osteoarthritis (PTOA). Despite adequate surgical treatment, the long-term risk for PTOA is high. Previous studies reported that joint injuries initiate an inflammatory cascade characterized by an elevation of synovial pro-inflammatory cytokines, which can lead to cartilage degradation and PTOA development. This review summarizes the literature on the post-injury regulation of pro-inflammatory cytokines and the markers of cartilage destruction in patients suffering from intra-articular fractures. We searched Medline, Embase, and Cochrane databases (1960-February 2020) and included studies that were performed on human participants, and we included control groups. Two investigators assessed the quality of the included studies using Covidence and the Newcastle-Ottawa Scale. Based on the surveyed literature, several synovial pro-inflammatory cytokines, including interleukins (IL)-1β, IL-2, IL-6, IL-8, IL-12p70, interferon-y, and tumor necrosis factor-α, were significantly elevated in patients suffering from intra-articular fractures compared to the control groups. A simultaneous elevation of anti-inflammatory cytokines such as IL-10 and IL-1RA was also observed. In contrast, IL-13, CTX-II, and aggrecan concentrations did not differ significantly between the compared cohorts. Overall, intra-articular fractures are associated with an increase in inflammation-related synovial cytokines. However, more standardized studies which focus on the ratio of pro- and anti-inflammatory cytokines at different time points are needed.

摘要

关节内骨折是创伤后骨关节炎(PTOA)的主要原因。尽管进行了适当的手术治疗,但 PTOA 的长期风险仍然很高。先前的研究报告称,关节损伤会引发以滑膜促炎细胞因子升高为特征的炎症级联反应,从而导致软骨降解和 PTOA 的发展。本综述总结了关于关节内骨折患者关节损伤后促炎细胞因子和软骨破坏标志物的文献。我们检索了 Medline、Embase 和 Cochrane 数据库(1960 年-2020 年 2 月),纳入了在人类参与者中进行的研究,并纳入了对照组。两名调查员使用 Covidence 和纽卡斯尔-渥太华量表评估了纳入研究的质量。基于调查文献,与对照组相比,患有关节内骨折的患者的几种滑膜促炎细胞因子(包括白细胞介素[IL]-1β、IL-2、IL-6、IL-8、IL-12p70、干扰素-y 和肿瘤坏死因子-α)显著升高。同时也观察到抗炎细胞因子如 IL-10 和 IL-1RA 的升高。相比之下,比较队列之间的 IL-13、CTX-II 和聚集蛋白聚糖浓度没有显著差异。总体而言,关节内骨折与炎症相关的滑膜细胞因子增加有关。然而,需要更多针对不同时间点促炎和抗炎细胞因子比值的标准化研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adaf/8070895/1451738fa1b9/cells-10-00902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adaf/8070895/1451738fa1b9/cells-10-00902-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adaf/8070895/1451738fa1b9/cells-10-00902-g001.jpg

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