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表面微裂纹向成骨细胞发出信号,以调节排列和骨形成。

Surface microcracks signal osteoblasts to regulate alignment and bone formation.

作者信息

Shu Yutian, Baumann Melissa J, Case Eldon D, Irwin Regina K, Meyer Sarah E, Pearson Craig S, McCabe Laura R

机构信息

Chemical Engineering and Materials Science Department, Michigan State University, United States; The College of Materials Science and Engineering, Beijing University of Technology, Beijing 100124, People's Republic of China.

Chemical Engineering and Materials Science Department, Michigan State University, United States; Department of Mechanical Engineering, Auburn University, Auburn, AL 36849, United States.

出版信息

Mater Sci Eng C Mater Biol Appl. 2014 Nov;44:191-200. doi: 10.1016/j.msec.2014.08.036. Epub 2014 Aug 16.

DOI:10.1016/j.msec.2014.08.036
PMID:25280696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4186695/
Abstract

Microcracks are present in bone and can result from fatigue damage due to repeated, cyclically applied stresses. From a mechanical point, microcracks can dissipate strain energy at the advancing tip of a crack to improve overall bone toughness. Physiologically, microcracks are thought to trigger bone remodeling. Here, we examine the effect of microcracks specifically on osteoblasts, which are bone-forming cells, by comparing cell responses on microcracked versus non-microcracked hydroxyapatite (HA) specimens. Osteoblast attachment was found to be greater on microcracked HA specimens (p<0.05). More importantly, we identified the preferential alignment of osteoblasts in the direction of the microcracks on HA. Cells also displayed a preferential attachment that was 75 to 90 μm away from the microcrack indent. After 21 days of culture, osteoblast maturation was notably enhanced on the HA with microcracks, as indicated by increased alkaline phosphatase activity and gene expression. Furthermore, examination of bone deposition by confocal laser scanning microscopy indicated preferential mineralization at microcrack indentation sites. Dissolution studies indicate that the microcracks increase calcium release, which could contribute to osteoblast responses. Our findings suggest that microcracks signal osteoblast attachment and bone formation/healing.

摘要

微裂纹存在于骨骼中,可能由反复循环施加的应力导致的疲劳损伤引起。从力学角度来看,微裂纹可以在裂纹前端耗散应变能,从而提高骨骼的整体韧性。从生理学角度来看,微裂纹被认为会触发骨重塑。在这里,我们通过比较成骨细胞在有微裂纹和无微裂纹的羟基磷灰石(HA)标本上的细胞反应,专门研究微裂纹对成骨细胞(即骨形成细胞)的影响。发现成骨细胞在有微裂纹的HA标本上的附着更强(p<0.05)。更重要的是,我们确定了HA上成骨细胞在微裂纹方向上的优先排列。细胞还表现出在距离微裂纹凹痕75至90μm处的优先附着。培养21天后,有微裂纹的HA上的成骨细胞成熟明显增强,碱性磷酸酶活性和基因表达增加表明了这一点。此外,通过共聚焦激光扫描显微镜对骨沉积的检查表明,微裂纹凹痕部位有优先矿化现象。溶解研究表明,微裂纹会增加钙释放,这可能有助于成骨细胞的反应。我们的研究结果表明,微裂纹为成骨细胞的附着和骨形成/愈合提供信号。

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