Osteoporosis is a degenerative bone disease that causes an increase of fracture risk. The present method of diagnosing the disease is through a bone mineral density (BMD) scan which neglects bone quality. Due to the complexity of bone, experimental testing is difficult;​ hence the use of finite element models can assist in understanding deformation behaviour and failure mechanisms. The aim of this study is to construct specimen specific-finite element models to investigate stiffness sharing and axial strain distributions of cortical versus trabecular bone of rat L4 vertebral bodies with and without the inclusion of vascular apertures.

In a previous experimental study, healthy (SHAM), osteoporotic (OVX) and treated osteoporotic (OVX+E) rat vertebrae underwent uniaxial compression while synchronously imaged with a micro-CT machine [1]. For the present study, these images have been processed into 3D FE models. The ratio of cortical shell stiffness to total vertebral body apparent stiffness was 70.1 ± 4.5% across all models with no significant difference across health conditions. However, since this value is significantly (P<0.01) higher than previously reported values in humans, caution should be taken when extrapolating rat vertebrae behaviour to those of humans. When viewing the axial strain, it was found that in the OVX models, the trabeculae had statistically significantly lower mean strains but a larger proportion of high strain elements creating more strain heterogeneity. Another confounding issue in these rat vertebrae is the presence of large vascular apertures in the dorsal surface of the cortical shell, that have been shown to be associated with cracks [2]. Additional models were created that removed these holes by virtually filling them in. The apparent stiffness of the cortical shell was found to increase by only 0.5%. Looking at the average axial strain distributions with the removal of the vascular apertures, the trabeculae strains showed minimal change, but the cortical shell experienced a significant (P<0.01) increased average axial strain across all health conditions. These results suggest that failure likely originates in the cortical shell and is affected by the presence of the vascular apertures, before progressing into the reduced trabecular network in the region adjacent to the vascular apertures.