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1.
J Bone Miner Res ; 29(6): 1392-1401, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24420672

ABSTRACT

The multiscale hierarchical structure of bone is naturally optimized to resist fractures. In osteogenesis imperfecta, or brittle bone disease, genetic mutations affect the quality and/or quantity of collagen, dramatically increasing bone fracture risk. Here we reveal how the collagen defect results in bone fragility in a mouse model of osteogenesis imperfecta (oim), which has homotrimeric α1(I) collagen. At the molecular level, we attribute the loss in toughness to a decrease in the stabilizing enzymatic cross-links and an increase in nonenzymatic cross-links, which may break prematurely, inhibiting plasticity. At the tissue level, high vascular canal density reduces the stable crack growth, and extensive woven bone limits the crack-deflection toughening during crack growth. This demonstrates how modifications at the bone molecular level have ramifications at larger length scales affecting the overall mechanical integrity of the bone; thus, treatment strategies have to address multiscale properties in order to regain bone toughness. In this regard, findings from the heterozygous oim bone, where defective as well as normal collagen are present, suggest that increasing the quantity of healthy collagen in these bones helps to recover toughness at the multiple length scales.


Subject(s)
Bone and Bones/physiopathology , Osteogenesis Imperfecta/physiopathology , Animals , Biomechanical Phenomena , Bone Density , Bone and Bones/pathology , Bone and Bones/ultrastructure , Computer Simulation , Fibrillar Collagens/metabolism , Fractures, Bone/pathology , Fractures, Bone/physiopathology , Glycation End Products, Advanced/metabolism , Mice , Mice, Inbred C57BL , Osteogenesis Imperfecta/pathology , Scattering, Small Angle , Spectroscopy, Fourier Transform Infrared , Tomography, X-Ray Computed , X-Ray Diffraction
2.
Phys Rev E Stat Nonlin Soft Matter Phys ; 84(5 Pt 2): 056301, 2011 Nov.
Article in English | MEDLINE | ID: mdl-22181492

ABSTRACT

A second order in space accurate implicit scheme for time-dependent advection-dispersion equations and a discrete fracture propagation model are employed to model solute transport in porous media. We study the impact of the fractures on mass transport and dispersion. To model flow and transport, pressure and transport equations are integrated using a finite-element, node-centered finite-volume approach. Fracture geometries are incrementally developed from a random distributions of material flaws using an adoptive geomechanical finite-element model that also produces fracture aperture distributions. This quasistatic propagation assumes a linear elastic rock matrix, and crack propagation is governed by a subcritical crack growth failure criterion. Fracture propagation, intersection, and closure are handled geometrically. The flow and transport simulations are separately conducted for a range of fracture densities that are generated by the geomechanical finite-element model. These computations show that the most influential parameters for solute transport in fractured porous media are as follows: fracture density and fracture-matrix flux ratio that is influenced by matrix permeability. Using an equivalent fracture aperture size, computed on the basis of equivalent permeability of the system, we also obtain an acceptable prediction of the macrodispersion of poorly interconnected fracture networks. The results hold for fractures at relatively low density.


Subject(s)
Geology/methods , Physics/methods , Algorithms , Computer Simulation , Finite Element Analysis , Models, Theoretical , Movement , Permeability , Porosity , Risk Assessment/methods , Stress, Mechanical , Time Factors
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