In vitro studies on the role of titanium in aseptic loosening.
In vitro studies on the role of titanium in aseptic loosening.
复制标题
钛在无菌松动中作用的体外研究。
DOI：
10.1097/00003086-199609000-00032
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发表时间：
1996
影响因子：
4.2
通讯作者：
Horowitz,SM
中科院分区：
文献类型：
--
作者：
Gonzales,JB;Purdon,MA;Horowitz,SM
本研究旨在确定钛碎片在无菌性松动中的作用。巨噬细胞暴露于商业纯钛（1-3微米）表现出与暴露于聚甲基丙烯酸甲酯相同的介质特征。这种反应包括肿瘤坏死因子的释放增加，而不是前列腺素e2或白细胞介素1的释放增加。当暴露于钛刺激巨噬细胞培养基时，成骨细胞增加前列腺素e2的产生，但不增加白细胞介素6或粒细胞巨噬细胞集落刺激因子。在器官培养中，暴露于钛的巨噬细胞培养基不导致骨吸收，通过钙45释放来测量。细胞对钛的反应以巨噬细胞释放肿瘤坏死因子和暴露于巨噬细胞条件培养基的成骨细胞释放前列腺素e2为特征。本研究结果与其他涉及组织培养中巨噬细胞暴露的研究结果的比较表明，钛可能不像无菌松动关节中的其他颗粒那样具有炎症性。
This study was designed to define the role titanium debris plays in aseptic loosening. Macrophages exposed to commercially pure titanium (1-3 microns) exhibit the same mediator profile as those exposed to polymethylmethacrylate. This response consists of increased release of tumor necrosis factor but not prostaglandin E 2 or interleukin-1. Osteoblasts increase production of prostaglandin E 2 when exposed to media from titanium stimulated macrophages but not interleukin-6 or granulocyte macrophage colony stimulating factor. Media from macrophages exposed to titanium did not lead to bone resorption, as measured by calcium 45 release, in organ culture. The cellular response to titanium is characterized by release of tumor necrosis factor from macrophages and prostaglandin E 2 from osteoblasts exposed to the macrophage conditioned medium. A comparison of the results of this study with those of others involving exposure of macrophages in tissue culture suggests that titanium may not be as inflammatory as other particles in the aseptically loose joint.