INSERM, UMR-S 926, CHU de Reims, IFR 53, URCA-1 avenue du Maréchal Juin, 51095 Reims, Cedex, France.
Biomaterials. 2010 Mar;31(8):2001-9. doi: 10.1016/j.biomaterials.2009.11.066. Epub 2009 Dec 5.
Hydroxyapatite (HA) is widely used as coating biomaterial for prosthesis metal parts and as bone substitute. The release of HA particles induces an inflammatory response and, if uncontrolled, could result in implant loss. At the inflamed site, the polymorphonuclear cells (PMNs) represent the earliest phagocytic cells that predominate the cellular infiltrate. We have recently proposed that HA wear debris activate polymorphonuclear cells (PMNs) initiating and/or amplifying thereby the acute inflammatory response. Previous studies have shown that activation of monocytes by HA could be modulated by supplementing this latter with the divalent cation, Zinc. The purpose of this work was to investigate the modulation of PMNs activation following exposure to zinc-substituted HA. Our study demonstrate that addition of zinc to HA particles resulted in decreased levels of the pro-inflammatory mediator interleukin-8 (IL-8) and the matrix metallo-proteinase-9. We also show that these changes involve IL-8 receptors (CXCR-1 and CXCR-2).
羟基磷灰石（HA）被广泛用作假体金属部件的涂层生物材料和骨替代物。HA 颗粒的释放会引起炎症反应，如果不受控制，可能导致植入物丢失。在发炎部位，多形核细胞（PMN）是最早的吞噬细胞，占细胞浸润的主要部分。我们最近提出，HA 磨损颗粒激活多形核细胞（PMN），从而引发和/或放大急性炎症反应。先前的研究表明，通过向 HA 中添加二价阳离子锌，可以调节 HA 对单核细胞的激活。这项工作的目的是研究暴露于锌取代的 HA 后 PMN 激活的调节。我们的研究表明，向 HA 颗粒中添加锌会降低促炎介质白细胞介素-8（IL-8）和基质金属蛋白酶-9 的水平。我们还表明，这些变化涉及白细胞介素-8 受体（CXCR-1 和 CXCR-2）。
