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Altered lacunar and vascular porosity in osteogenesis imperfecta mouse bone as revealed by synchrotron tomography contributes to bone fragility

Altered lacunar and vascular porosity in osteogenesis imperfecta mouse bone as revealed by synchrotron tomography contributes to bone fragility
Altered lacunar and vascular porosity in osteogenesis imperfecta mouse bone as revealed by synchrotron tomography contributes to bone fragility
Osteogenesis imperfecta (brittle bone disease) is caused by mutations in the collagen genes and results in skeletal fragility. Changes in bone porosity at the tissue level indicate changes in bone metabolism and alter bone mechanical integrity. We investigated the cortical bone tissue porosity of a mouse model of the disease, oim, in comparison to a wild type (WT-C57BL/6), and examined the influence of canal architecture on bone mechanical performance.

High-resolution 3D representations of the posterior tibial and the lateral humeral mid-diaphysis of the bones were acquired for both mouse groups using synchrotron radiation-based computed tomography at a nominal resolution of 700 nm. Volumetric morphometric indices were determined for cortical bone, canal network and osteocyte lacunae. The influence of canal porosity architecture on bone mechanics was investigated using microarchitectural finite element (?FE) models of the cortical bone. Bright-field microscopy of stained sections was used to determine if canals were vascular.

Although total cortical porosity was comparable between oim and WT bone, oim bone had more numerous and more branched canals (p < 0.001), and more osteocyte lacunae per unit volume compared to WT (p < 0.001). Lacunae in oim were more spherical in shape compared to the ellipsoidal WT lacunae (p < 0.001). Histology revealed blood vessels in all WT and oim canals. ?FE models of cortical bone revealed that small and branched canals, typical of oim bone, increase the risk of bone failure. These results portray a state of compromised bone quality in oim bone at the tissue level, which contributes to its deficient mechanical properties.
osteogenesis imperfect, oim, bone, porosity, canal, osteocyte lacunae
8756-3282
116-124
Carriero, A.
6701911c-72c7-4ed2-96ed-191cef4d85e3
Doube, M.
98154832-9fc5-4f5a-a1ec-69cdf667f4f9
Vogt, M.
bd78edf9-30bb-4524-831a-d73ed3f2d18a
Busse, B.
4f761b9e-ecba-4064-aa7b-cdec326186f1
Zustin, J.
30049db8-2aa5-4f28-9b07-1846904e281b
Levchuk, A.
8ca2b3fd-e513-4207-9ba8-85c57e772c42
Schneider, P.
a810f925-4808-44e4-8a4a-a51586f9d7ad
Müller, R.
6524b971-59e6-4c83-868d-90dfc3c5b8b0
Shefelbine, S.J.
1153780e-939e-4658-9ebe-f03db4155188
Carriero, A.
6701911c-72c7-4ed2-96ed-191cef4d85e3
Doube, M.
98154832-9fc5-4f5a-a1ec-69cdf667f4f9
Vogt, M.
bd78edf9-30bb-4524-831a-d73ed3f2d18a
Busse, B.
4f761b9e-ecba-4064-aa7b-cdec326186f1
Zustin, J.
30049db8-2aa5-4f28-9b07-1846904e281b
Levchuk, A.
8ca2b3fd-e513-4207-9ba8-85c57e772c42
Schneider, P.
a810f925-4808-44e4-8a4a-a51586f9d7ad
Müller, R.
6524b971-59e6-4c83-868d-90dfc3c5b8b0
Shefelbine, S.J.
1153780e-939e-4658-9ebe-f03db4155188

Carriero, A., Doube, M., Vogt, M., Busse, B., Zustin, J., Levchuk, A., Schneider, P., Müller, R. and Shefelbine, S.J. (2014) Altered lacunar and vascular porosity in osteogenesis imperfecta mouse bone as revealed by synchrotron tomography contributes to bone fragility. Bone, 61, 116-124. (doi:10.1016/j.bone.2013.12.020). (PMID:24373921)

Record type: Article

Abstract

Osteogenesis imperfecta (brittle bone disease) is caused by mutations in the collagen genes and results in skeletal fragility. Changes in bone porosity at the tissue level indicate changes in bone metabolism and alter bone mechanical integrity. We investigated the cortical bone tissue porosity of a mouse model of the disease, oim, in comparison to a wild type (WT-C57BL/6), and examined the influence of canal architecture on bone mechanical performance.

High-resolution 3D representations of the posterior tibial and the lateral humeral mid-diaphysis of the bones were acquired for both mouse groups using synchrotron radiation-based computed tomography at a nominal resolution of 700 nm. Volumetric morphometric indices were determined for cortical bone, canal network and osteocyte lacunae. The influence of canal porosity architecture on bone mechanics was investigated using microarchitectural finite element (?FE) models of the cortical bone. Bright-field microscopy of stained sections was used to determine if canals were vascular.

Although total cortical porosity was comparable between oim and WT bone, oim bone had more numerous and more branched canals (p < 0.001), and more osteocyte lacunae per unit volume compared to WT (p < 0.001). Lacunae in oim were more spherical in shape compared to the ellipsoidal WT lacunae (p < 0.001). Histology revealed blood vessels in all WT and oim canals. ?FE models of cortical bone revealed that small and branched canals, typical of oim bone, increase the risk of bone failure. These results portray a state of compromised bone quality in oim bone at the tissue level, which contributes to its deficient mechanical properties.

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More information

Accepted/In Press date: 17 December 2013
e-pub ahead of print date: 26 December 2013
Published date: April 2014
Keywords: osteogenesis imperfect, oim, bone, porosity, canal, osteocyte lacunae
Organisations: Bioengineering Group

Identifiers

Local EPrints ID: 381909
URI: http://eprints.soton.ac.uk/id/eprint/381909
ISSN: 8756-3282
PURE UUID: 8d40f449-6998-4f2b-8ad0-86cd4d31a116
ORCID for P. Schneider: ORCID iD orcid.org/0000-0001-7499-3576

Catalogue record

Date deposited: 01 Oct 2015 08:46
Last modified: 29 Oct 2019 01:37

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