Infrapatellar fat pad of patients with end-stage osteoarthritis inhibits catabolic mediators in cartilage
Infrapatellar fat pad of patients with end-stage osteoarthritis inhibits catabolic mediators in cartilage
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DOI：
10.1136/ard.2011.153858
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发表时间：
2012-02-01
影响因子：
27.4
通讯作者：
van Osch, Gerjo J. V. M.
中科院分区：
文献类型：
--
作者：
Bastiaansen-Jenniskens, Yvonne M.;Clockaerts, Stefan;van Osch, Gerjo J. V. M.
目的脂肪组织可释放炎性细胞因子和生长因子。在这项探索性研究中，作者研究了膝关节中与软骨紧密相关的髌下脂肪垫（IPFP）是否会影响软骨代谢。此外，作者分析了是否存在于IPFP中的巨噬细胞类型可以解释对软骨的影响。方法将29例骨关节炎（OA）患者全膝关节置换术中获得的IPFP外植体用于制备脂肪条件培养基（FCM）。牛软骨的外植体培养有或没有FCM。一氧化氮（NO）和糖胺聚糖释放和软骨基质降解酶的基因表达进行了分析。为了刺激软骨中的分解代谢过程，作者添加了白细胞介素1 β，并评估了六种FCM的效果。不同类型的巨噬细胞（CD68+，CD86+和CD206+）在OA IPFP的存在进行了比较，皮下脂肪组织样品和IPFP样品与前交叉韧带rupture.Results单独FCM减少NO和糖胺聚糖释放和基质金属蛋白酶（MMP）1基因表达的软骨。此外，当用白细胞介素1 β增强分解代谢条件时，FCM抑制NO产生以及MMP 1和MMP 3基因表达，并增加II型胶原基因表达。OA IPFP样品中的CD206+细胞显著多于皮下脂肪或前交叉韧带IPFP样品中的CD206+细胞。结论与作者的预期相反，终末期OA IPFP条件培养基抑制软骨的分解代谢过程。用于制备FCM的IPFP中存在的CD206+细胞可能有助于抑制软骨中的分解代谢过程。
Objective Adipose tissue is known to release inflammatory cytokines and growth factors. In this exploratory study, the authors examined whether the infrapatellar fat pad (IPFP) closely located to cartilage in the knee joint can affect cartilage metabolism. In addition, the authors analysed whether the macrophage types present in IPFP could explain the effect on cartilage.Methods IPFP explants obtained during total knee replacement of 29 patients with osteoarthritis (OA) were used to make fat-conditioned medium (FCM). Explants of bovine cartilage were cultured with or without FCM. Nitric oxide (NO) and glycosaminoglycan release and gene expression of matrix-degrading enzymes in cartilage were analysed. To stimulate catabolic processes in the cartilage, the authors added interleukin 1 beta, and the effect of six FCMs was evaluated. The presence of different types of macrophages (CD68+, CD86+ and CD206+) in OA IPFPs was compared with subcutaneous adipose tissue samples and IPFP samples from patients with an anterior cruciate ligament rupture.Results FCM alone reduced NO and glycosaminoglycan release and matrix metalloproteinase (MMP)1 gene expression by the cartilage. Moreover, when catabolic conditions were enhanced with interleukin 1 beta, FCM inhibited NO production as well as MMP1 and MMP3 gene expression and increased collagen type II gene expression. Significantly more CD206+ cells were present in OA IPFP samples than in subcutaneous fat or anterior cruciate ligament IPFP samples.Conclusion In contrast to the authors' expectations, medium conditioned by end-stage OA IPFP inhibited catabolic processes in cartilage. CD206+ cells present in the IPFPs used for making the FCM might have contributed to the inhibition of catabolic processes in the cartilage.