Abstract
Summary
Canals are the preferential sites for failure in cortical bone and their architecture is able to dictate the mechanical behaviour of the bone: smaller and branched canals generate a high volume of bone failure even at low apparent tissue strain.
Introduction
Osteogenesis imperfecta (OI), or brittle bone disease, is caused by mutations in the collagen genes and results in skeletal fragility. We recently showed that a mouse model of osteogenesis imperfecta (oim) has smaller and denser intracortical canals with a branched architecture compared to healthy wild type (WT) bones with similar cortical porosity [1]. We hypothesise this abnormal intracortical structure contributes to the increased fracture risk of the oim bones.
Methods
Micro-architecture finite element (µFE) models of WT and oim cortical bone with the canals explicitly modelled as voids were developed (Mimics, Materialise) from 10 high resolution (700 nm) synchrotron-radiated computed tomography images previously collected at the Swiss Light Source, Switzerland. Bone was modelled as linear elastic, isotropic and homogeneous tissue with same material properties for WT and oim (E=17GPa, ν=0.3) in order to account for the solely contribute of the intracortical architecture to the mechanical properties of the bone. We estimated stresses and strains within the bone structure when under compression (0.1–0.5% apparent strain) (Abaqus, Simulia) and determined the bone failure per each element when the effective strain (
Results
Visualization of the failure within the bone revealed that the high risk tissue is mainly located around the canals in both oim and WT bone structure. However, oim intracortical bone architecture presented a higher amount of bone strained at more than 0.7% than WT one.
Discussion and Conclusions
Our μFE models of cortical bone showed that preferential site for bone failure is near canals, in agreement with previous experimental studies. However, our findings demonstrated that cortical bone with high canal density and branched canal architecture, as in oim, increases the volume of bone failure density and the chances for the entire bone to fail at a lower apparent tissue strain (when same material properties were used for WT and oim bone). Because cracks in mouse bone originate at the canal surface and propagate through osteocyte lacunae, it is possible that the increased lacunar porosity in oim bone additionally contributes to its fragility. Oim bone has also reduced stiffness compared to WT bone, which increases the strain around pores and may promote damage. Intracortical architecture and material properties can help explain why brittle bone fracture at a much smaller ultimate load and lower apparent tissue strain than WT bone.
These findings are broader than just oim bone as provide an estimate of the influence of the intracortical canal structure on the strain distribution within the bone and a relationship with its mechanical integrity. Future treatment strategies should aim to reduce the number of canals and their braches within the cortical bone in order to reduce risk of fracture.
