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微损伤:一种基于骨细胞突起破裂的细胞转导机制。

Microdamage: a cell transducing mechanism based on ruptured osteocyte processes.

作者信息

Hazenberg Jan G, Freeley Michael, Foran Eilis, Lee Thomas C, Taylor David

机构信息

Trinity Centre for Bioengineering, Trinity College, Dublin 2, Ireland.

出版信息

J Biomech. 2006;39(11):2096-103. doi: 10.1016/j.jbiomech.2005.06.006. Epub 2005 Aug 19.

Abstract

As a result of underlying pathological diseases, such as osteoporosis, osteopenia, or due to altered loading after joint replacements, bones become more susceptible to microdamage accumulation than those of normal human beings, as are those of athletes who undertake strenuous exercise [Stromsoe, 2004. Fracture fixation problems in osteoporosis. Injury 35, 107-113]. Experimental evidence has linked bone adaptation to microdamage, and to increased cell activity. In this work, we investigated whether microcrack detection is related to rupturing of the cellular material itself due to crack face displacements. Using specific cell staining techniques, it was confirmed that relative crack displacements are capable of tearing cell processes between neighbouring osteocytes. No ruptured cell processes were found near the crack tip where the displacements are less. Rupturing of cell processes due to crack opening and shear displacement is a feasible new mechanism by which bone can detect and estimate the size of a microcrack. Ruptured cell processes may directly secrete passive and active components in the extracellular matrix, triggering a repair response.

摘要

由于潜在的病理疾病,如骨质疏松症、骨质减少,或由于关节置换后负荷改变,骨骼比正常人的骨骼更容易积累微损伤,从事剧烈运动的运动员的骨骼也是如此[斯特罗姆索伊,2004年。骨质疏松症中的骨折固定问题。《损伤》35卷,第107 - 113页]。实验证据表明骨骼适应性与微损伤以及细胞活性增加有关。在这项研究中,我们调查了微裂纹检测是否与由于裂纹面位移导致的细胞物质本身破裂有关。使用特定的细胞染色技术,证实了相对裂纹位移能够撕裂相邻骨细胞之间的细胞突起。在位移较小的裂纹尖端附近未发现破裂的细胞突起。由于裂纹张开和剪切位移导致的细胞突起破裂是一种可行的新机制,通过该机制骨骼能够检测并估计微裂纹的大小。破裂的细胞突起可能直接在细胞外基质中分泌被动和主动成分,触发修复反应。

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