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TISSUE STRAIN TRANSDUCTION AND AMPLIFICATION AT THE OSTEOCYTE AS A RESULT OF MICROSTRUCTURAL CHANGES IN THE BONE MATRIX

机译:由于骨基质的微观结构变化而导致骨细胞的组织菌株转导和扩增

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It is well known that bone adapts to changes in its mechanical environment and that this adaptation is controlled at the cellular level through the coordinated actions of osteoblasts, osteocytes, and osteoclasts. Osteocytes make up over 90% of all bone cells [1], and are hypothesized to be the mechanosensors in bone [2] that mediate the effects of bone loading through their extensive communication network. The application of force to the skeletal system produces several potential stimuli for osteocyte function including hydrostatic pressure, fluid flow-induced shear stress, and bone tissue strain. Previously, the basis used for studying the stimulatory effects of mechanical strain on bone cell biological responses in vitro has been the direct measurement of bone strain in humans during various physical activities [3,4]. The limitation of applying this strain magnitude data to cells in vitro, however, is that the in vivo strain gage measurements represent continuum measures of bone deformation. Clearly, at the spatial level of bone cells, cortical bone is not a continuum and microstructural inhomogeneities will result in inhomogeneous microstructural strain fields; local tissue strains will be magnified in association with microstructural features [5,6]. It is unclear as to how much of these magnified strains will be directly transmitted to the osteocyte itself. Additionally, if the osteocyte has the ability to alter its perilacunar environment [7], it is unknown what effect do these changes have on the strain that is transmitted to the osteocyte and cell process. The objective of this study was to investigate how microstructural bone tissue strains may be transmitted to an embedded osteocyte and its cell processes and to determine how changes to the perilacunar bone tissue structure and properties affect this strain and cell deformation.
机译:众所周知,骨骼适应其机械环境的变化,并且通过成骨细胞,骨细胞和破骨细胞的协调作用,在细胞水平下控制这种适应。骨细胞占所有骨细胞的90%超过90%[1],并假设是骨骼中的机械传感器[2]通过其广泛的通信网络介导骨负荷的影响。施力到骨骼系统的施加产生了骨细胞功能的几种潜在刺激,包括静压压力,流体流动引起的剪切应力和骨组织菌株。以前,用于研究机械菌株对体外骨细胞生物反应对骨细胞生物反应的刺激作用的基础一直是人类在各种物理活性期间的骨菌株[3,4]。然而,将该应变幅度数据施加到体外细胞的限制是体内应变计测量值代表骨骼变形的连续措施。显然,在骨细胞的空间水平下,皮质骨不是连续骨,微观结构的不均匀性会导致非均匀的微观结构应变场;局部组织菌株将与微观结构特征相关联的放大[5,6]。目前尚不清楚这些放大的菌株中的大约是多少将直接传递给骨细胞本身。另外,如果骨细胞具有改变其贫血清环境的能力[7],则未知这些变化对传输到骨细胞和细胞过程的菌株的效果。本研究的目的是研究微观结构骨组织菌株如何传递给嵌入的骨细胞和其细胞过程,并确定贫血骨组织结构和性能如何影响这种应变和细胞变形。

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