Altered lacunar and vascular porosity in osteogenesis imperfecta mouse bone as revealed by synchrotron tomography contributes to bone fragility |
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| Affiliation: | 1. Department of Bioengineering, Imperial College London, UK;2. Institute for Biomechanics, ETH Zürich, Switzerland;3. Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Germany;4. Institute of Pathology, University Medical Center Hamburg-Eppendorf, Germany;1. Ludwig Boltzmann Institute of Osteology at Hanusch Hospital of WGKK and AUVA Trauma Center Meidling, 1st Med. Dept. Hanusch Hospital, 1140 Vienna, Austria;2. Max Planck Institute of Colloids and Interfaces, Dept. of Biomaterials, 14424 Potsdam, Germany;3. Genetics Unit, Shriners Hospital for Children, McGill University, Montreal H3G 1A6, Canada;1. Orthopaedic Research Laboratories, Department of Orthopaedic Surgery, University of Michigan, Ann Arbor, MI, United States;2. Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, United States;3. Department of Metabolic Disorders, Amgen, Inc., Thousand Oaks, CA, United States;4. Bone and Extracellular Matrix Branch, National Institute of Child Health and Human Development, NIH, Bethesda, MD, United States;1. LTDS UMR CNRS 5513, Ecole Centrale Lyon, 36 avenue Guy de Collongue, 69134 Ecully, France;2. Department of Pediatric Orthopedics, Necker — Enfants Malades Hospital, AP-HP, Paris Descartes University, 145 rue de Sèvres, 75014 Paris, France;3. B2OA UMR CNRS 7052, University Paris-Diderot, 10 avenue de Verdun, 75010 Paris, France;1. Ludwig Boltzmann Institute of Osteology, Hanusch Hospital of WGKK and AUVA Trauma Center Meidling, 1st Med. Dept., Hanusch Hospital, Vienna, Austria;2. Shriners Hospital for Children, Montreal, Quebec, Canada;3. McGill University, Montreal, Quebec, Canada;4. Musculoskeletal Disease Area, Novartis Institutes for Biomedical Research, Basel, Switzerland |
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| 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 (μFE) 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. μFE 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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