Morphology, localization and accumulation of in vivo microdamage in human cortical bone
Morphology, localization and accumulation of in vivo microdamage in human cortical bone
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DOI：
10.1016/j.bone.2006.09.027
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发表时间：
2007-03-01
期刊：
影响因子：
4.1
通讯作者：
Vashishth, Deepak
中科院分区：
文献类型：
--
作者：
Diab, Tamim;Vashishth, Deepak
在体内，微损伤以线状微裂纹和弥漫性损伤的形式出现。然而，在体内加载过程中，骨质量的年龄相关变化是否会使骨形成一种类型的损伤形态，而不是另一种类型，目前尚不清楚。本研究通过对19 ~ 89岁衰老人骨胫骨横截面进行组织学和组织形态学分析，探讨损伤形态在体内的积累和定位。结果表明，老年供骨（83 +/- 13岁）的骨皮质线状微裂纹比年轻供骨多，其主要受压缩（p < 0.01）和拉伸载荷（p < 0.01）的影响。相比之下，年轻供体骨（40 +/- 10岁）在主要受拉伸载荷的皮质区比年老供体骨含有更多弥漫性损伤（p < 0.01）。损伤形态的形成与骨几何参数无关，与骨微观结构有明显的偏好。骨间隙形成线状微裂纹（p < 0.01），并被骨水泥线和骨板层界面捕获或阻滞（p < 0.05）。弥漫性损伤区域主要与继发性骨相关（p < 0.01），与微结构界面无关（p < 0.01）。基于这些发现，我们得出结论，在体内加载条件下，老年供体的骨微观结构的年龄相关变化，而不是骨几何形状的变化，在形成线状微裂纹而不是弥漫性损伤的倾向中起关键作用。(c) 2006爱思唯尔公司版权所有。
In vivo, microdamage occurs in the form of linear microcracks and diffuse damage. However, it is unknown whether the age-related changes in bone quality predispose bone to form one type of damage morphology over the other during in vivo loading. In this study, histological and histomorphometrical analyses were conducted on transverse cross sections, obtained from the tibiae of aging human bone (age 19 to 89), to investigate the in vivo accumulation and localization of damage morphologies. The results demonstrate that old donor bone (83 +/- 13 years) contains more linear microcracks than younger donor bone in the cortices predominantly subjected to compressive (p < 0.01) and tensile loading (p < 0.01). In contrast, young donor bone (40 +/- 10 years) contains more diffuse damage than older donor bone in the cortex predominantly subjected to tensile loading (p < 0.01). The formation of damage morphology showed no correlation with bone geometry parameters and exhibited distinct preferences with bone microstructure. Linear microcracks formed in the interstitial bone (p < 0.01) and were either trapped or arrested by the microstructural interfaces (cement line and lamellar interface) (p < 0.05). Areas of diffuse damage, however, were preferentially associated with secondary osteonal bone (p < 0.01) and had no relationship with the microstructural interfaces (p < 0.01). Based upon these findings, we conclude that age-related changes in bone microstructure, but not bone geometry, play a key role in the propensity of old donors to form linear microcrack over diffuse damage under in vivo loading conditions. (c) 2006 Elsevier Inc. All rights reserved.