Schmal Hagen, Bernstein Anke, Feucht Matthias J, Erdle Benjamin, Pestka Jan M, Pham That Minh, Kubosch Eva Johanna
Department of Orthopaedics and Traumatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Department of Orthopedics and Trauma Surgery, Albert-Ludwigs University Medical Center Freiburg, Freiburg, Germany.
Mediators Inflamm. 2016;2016:5491971. doi: 10.1155/2016/5491971. Epub 2016 Sep 5.
. Intra-articular infections can rapidly lead to osteoarthritic degradation. The aim of this clinical biomarker analysis was to investigate the influence of inflammation on cartilage destruction and metabolism. . Patients with acute joint infections were enrolled in a prospective clinical trial and the cytokine composition of effusions ( = 76) was analyzed. Characteristics of epidemiology and disease severity were correlated with levels of cytokines with known roles in cartilage turnover and degradation. . Higher synovial IL-1 concentrations were associated with clinical parameters indicating a higher disease severity ( < 0.03) excluding the incidence of sepsis. Additionally, intra-articular IL-1 levels correlated with inflammatory serum parameters as leucocyte counts (LC) and C-reactive protein concentrations ( < 0.05) but not with age or comorbidity. Both higher LC and synovial IL-1 levels were associated with increased intra-articular collagen type II cleavage products (C2C) indicating cartilage degradation. Joints with preinfectious lesions had higher C2C levels. Intra-articular inflammation led to increased concentrations of typical cartilage metabolites as bFGF, BMP-2, and BMP-7. Infections with species induced higher IL-1 expression but less cartilage destruction than other bacteria. . Articular infections have bacteria-specific implications on cartilage metabolism. Collagen type II cleavage products reliably mark destruction, which is associated with upregulation of typical cartilage turnover cytokines. This trial is registered with DRKS00003536, MISSinG.
关节内感染可迅速导致骨关节炎性退变。本临床生物标志物分析的目的是研究炎症对软骨破坏和代谢的影响。急性关节感染患者被纳入一项前瞻性临床试验,并对积液(n = 76)的细胞因子组成进行了分析。流行病学特征和疾病严重程度与在软骨周转和降解中起已知作用的细胞因子水平相关。滑膜白细胞介素-1(IL-1)浓度较高与表明疾病严重程度较高的临床参数相关(P < 0.03),排除败血症的发生率。此外,关节内IL-1水平与炎症血清参数如白细胞计数(LC)和C反应蛋白浓度相关(P < 0.05),但与年龄或合并症无关。较高的LC和滑膜IL-1水平均与关节内II型胶原裂解产物(C2C)增加相关,表明软骨降解。有感染前病变的关节C2C水平较高。关节内炎症导致典型软骨代谢产物如碱性成纤维细胞生长因子(bFGF)、骨形态发生蛋白-2(BMP-2)和骨形态发生蛋白-7(BMP-7)的浓度增加。与其他细菌相比,[具体细菌名称]感染诱导更高的IL-1表达,但软骨破坏较少。关节感染对软骨代谢有细菌特异性影响。II型胶原裂解产物可靠地标记破坏,这与典型软骨周转细胞因子的上调相关。本试验在德国临床试验注册中心注册号为DRKS00003536,缺失。