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In metabolic bone diseases, the alterations in fibrillar level bone-material quality affecting macroscopic mechanical competence are not well-understood quantitatively. Here, we quantify the fibrillar level deformation in cantilever bending in a mouse model for hereditary rickets (Hpr). Microfocus in-situ synchrotron small-angle X-ray scattering (SAXS) combined with cantilever bending was used to resolve nanoscale fibril strain in tensile- and compressive tissue regions separately, with quantitative backscattered scanning electron microscopy used to measure microscale mineralization. Tissue-level flexural moduli for Hpr mice were significantly (p < . 0.01) smaller compared to wild-type (~. 5 to 10-fold reduction). At the fibrillar level, the fibril moduli within the tensile and compressive zones were significantly (p < . 0.05) lower by ~. 3- to 5-fold in Hpr mice compared to wild-type mice. Hpr mice have a lower mineral content (24.2 ± 2.1. Ca. wt.% versus 27.4 ± 3.3. Ca wt.%) and its distribution was more heterogeneous compared to wild-type animals. However, the average effective fibril modulus did not differ significantly (p > . 0.05) over ages (4, 7 and 10. weeks) between tensile and compressive zones. Our results indicate that incompletely mineralized fibrils in Hpr mice have greater deformability and lower moduli in both compression and tension, and those compressive and tensile zones have similar moduli at the fibrillar level. © 2012 Elsevier Inc.

Original publication

DOI

10.1016/j.bone.2012.10.029

Type

Journal article

Journal

Bone

Publication Date

01/02/2013

Volume

52

Pages

689 - 698