Revision joint replacement, wear particles, and macrophage polarization.
Revision joint replacement, wear particles, and macrophage polarization.
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DOI：
10.1016/j.actbio.2012.03.042
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发表时间：
2012-07
影响因子：
9.7
通讯作者：
Goodman, Stuart B.
中科院分区：
文献类型：
--
作者：
Rao, Allison J.;Gibon, Emmanuel;Ma, Ting;Yao, Zhenyu;Smith, R. Lane;Goodman, Stuart B.
目前，更年轻，更活跃的患者正在提供全关节置换术（TJR）的终末期关节炎疾病。尽管TJR的耐久性有所改善，但关节面的颗粒相关磨损仍与颗粒碎屑相关，颗粒碎屑可激活单核细胞/巨噬细胞。活化的巨噬细胞然后产生促炎因子和细胞因子，其诱导活化破骨细胞的炎症反应，导致骨分解和无菌性松动。我们假设，由于磨损颗粒相关的细胞活化，从翻修关节置换术中采集的组织中的活化巨噬细胞主要表达M1促炎表型，而不是M2促炎表型。我们进一步质疑是否有可能通过加入白细胞介素-4（IL-4）将未定型的单核细胞/巨噬细胞转化为M2表型，或者是否有必要首先通过M1中间阶段。使用免疫组织化学染色和Western印迹法，与未手术的骨关节炎滑膜组织相比，取出的假体周围组织显示M1/M2巨噬细胞比率增加。当细胞通过暴露于内毒素首先通过M1表型时，具有/不具有聚甲基丙烯酸甲酯颗粒的未定型单核细胞/巨噬细胞通过IL-4更有效地转化为M2表型。磨损颗粒诱导促进骨质溶解的促炎微环境;这些事件可能通过暴露于IL-4而有利地调节。
Currently, younger, more active patients are being offered total joint replacement (TJR) for end-stage arthritic disorders. Despite improved durability of TJRs, particle-associated wear of the bearing surfaces continues to be associated with particulate debris, which can activate monocyte/macrophages. Activated macrophages then produce pro-inflammatory factors and cytokines that induce an inflammatory reaction that activates osteoclasts leading to bone breakdown and aseptic loosening. We hypothesized that activated macrophages in tissues harvested from revised joint replacements predominantly express an M1 pro-inflammatory phenotype due to wear-particle-associated cell activation, rather than an M2 antiinflammatory phenotype. We further questioned whether it is possible to convert uncommitted monocyte/macrophages to an M2 phenotype by the addition of interleukin-4 (IL-4), or whether it is necessary to first pass through an M1 intermediate stage. Retrieved periprosthetic tissues demonstrated increased M1/M2 macrophage ratios compared to non-operated osteoarthritic synovial tissues, using immunohistochemical staining and Western blotting. Uncommitted monocyte/macrophages with/without poly-methyl-methacrylate particles were transformed to an M2 phenotype by IL-4 more efficiently when the cells were first passed through an M1 phenotype by exposure to endotoxin. Wear particles induce a pro-inflammatory microenvironment that facilitates osteolysis; these events may potentially be modulated favorably by exposure to IL-4.
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影响因子：
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作者：
Huang, Zhinong;Nelson, Ehren Robert;Goodman, Stuart B.
通讯作者：
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影响因子：
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