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Roles of Cellular and Molecular Targets of Wear Debris in Periprosthetic Osteolysis

机译:围骨质骨解中磨损碎片细胞和分子靶标的作用

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Wear-generated particulate debris is the main cause of initiating this destructive process. We present recent advances in understanding of how wear debris causes osteolysis in the aspect of cellular and molecular biological levels. Macrophages, the most important cellular target for wear debris, respond to particle challenge in two distinct ways of proinflammatory signaling and inhibition of the protective actions of anthosteociastogenic cytokines, finally leading to suppression of osteogenic activity as well as increased osteoclast activity. At a molecular level, such alterations of cellular activities occur through MAP kinase, transcription factors including NF-kB, Wnt/p-catenin signaling and cytokine signaling cascades in various kinds of cells.However, in spite of complex researches concerning periprosthetic osteolysis, no approved treatments are yet available. In addition, research to find new articulation materials that can minimize the production of wear debris is ongoing. Therefore, it will be of immense interest to see what will make rapid progress to the solution of periprosthetic osteolysis in the future.
机译:磨损的微粒碎片是发起这种破坏性过程的主要原因。我们提出了了解磨损碎片如何导致细胞和分子生物水平方面的骨解骨溶解的进步。巨噬细胞,磨损碎片最重要的细胞靶标,以两种明显的促炎信号传导方式响应粒子挑战,并抑制大脑细胞源细胞因子的保护作用,最终导致抑制骨质发生活性以及增加的破骨细胞活性。在分子水平时,这种细胞活性的改变通过Map激酶,转录因子,包括NF-Kb,Wnt / p-catenin信号传导和细胞因子信号传导级联的各种细胞。然而,尽管有关骨质增孔溶解的复杂研究,但没有批准的治疗方法尚无批准。此外,寻找能够最小化磨损碎片生产的新关节材料的研究正在进行中。因此,看看将来会对未来的植物骨质溶解溶液迅速进展,这将是巨大的兴趣。

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