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The importance of murine cortical bone microstructure for microcrack initiation and propagation

Voide, R; Schneider, P; Stauber, M; van Lenthe, G H; Stampanoni, M; Müller, R (2011). The importance of murine cortical bone microstructure for microcrack initiation and propagation. Bone, 49(6):1186-1193.

Abstract

In order to better understand bone postyield behavior and consequently bone failure behavior, this study aimed first to investigate cortical bone microstructure and second, to relate cortical bone microstructure to microdamage initiation and propagation in C57BL/6 (B6) and C3H/He (C3H) mice; two murine inbred strains known for their differences in bone phenotype. Murine femora of B6 and C3H were loaded axially under compression in a stepwise manner. For each loading step, 3D data sets at a nominal resolution of 700 nm were acquired by means of synchrotron radiation-based computed tomography. Cortical bone microstructure was divided into three phases: the canal network, the osteocyte lacunar system, and microdamage. Canal volume density and canal unit volume both correlated highly to crack number density (canal volume density: R(2)=0.64, p<0.005 and canal unit volume: R(2)=0.75, p<0.001). Moreover, the large canal units in C3H bone were responsible for more microdamage accumulation compared to B6 bones. This more pronounced microdamage accumulation due to large intracortical bone voids, which eventually leads to a fatal macrocrack (fracture), represents a potential contributing factor to the higher incidence of bone fractures in the elderly.

Copyright © 2011 Elsevier Inc. All rights reserved.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Biomedical Engineering
Dewey Decimal Classification:170 Ethics
610 Medicine & health
Scopus Subject Areas:Health Sciences > Endocrinology, Diabetes and Metabolism
Life Sciences > Physiology
Health Sciences > Histology
Language:English
Date:2011
Deposited On:30 Jan 2012 09:19
Last Modified:06 May 2025 01:39
Publisher:Elsevier
ISSN:1873-2763
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.bone.2011.08.011
PubMed ID:21884836
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