No abstract

When studying bone fragility diseases, it is difficult to identify which factors reduce bone’s resistance to fracture because these diseases alter bone at many length scales. Here, we investigate the contribution of nanoscale collagen behavior on macroscale toughness and microscale toughening mechanisms using a bovine heat-treatment fragility model. This model is assessed by developing an in situ toughness testing technique for synchrotron radiation micro-computed tomography to study the evolution of microscale crack growth in 3D. Low-dose imaging is employed with deep learning to denoise images while maintaining bone’s innate mechanical properties. We show that collagen damage significantly reduces macroscale toughness and post-yield properties. We also find that bone samples with a compromised collagen network have reduced amounts of crack deflection, the main microscale mechanism of fracture resistance. This research demonstrates that collagen damage at the nanoscale adversely affects bone’s toughening mechanisms at the microscale and reduces the overall toughness of bone.

No abstract

Type 2 diabetes mellitus (T2DM) is associated with an increased fracture risk independent of bone mass. The exact origin of this increased fracture risk still needs to be better understood. Using a polygenic diabetic ZDSD rat model, synchrotron radiation micro-computed tomography imaging (SRuCT), and in situ scanning electron microscope (SEM) fracture toughness test, we related the changes at the microscale to toughness and material properties of diabetic rat femurs. As expected, the diabetic rat model displayed overnight fasting hyperglycemia, increased AGEs content, and reduced crack-growth toughness. At the microscale level, our data revealed deficits in the canal and osteocyte lacunar structure. Type 2 diabetes significantly decreased the canal density by 31%, the lacunar density by 16%, and the lacunar volume by 14%. These microstructural deficits can explain the 55% reduction in crack-growth fracture resistance; these extrinsic toughening mechanisms use microstructural features to dissipate energy. This drop in fracture resistance can also be attributed to decreased post-yield properties with AGEs concentration in diabetes. Reduction in osteocyte density is an indicator of alteration of bone remodeling and bone quality. In conclusion, we showed that changes in lacunae and canal density, combined with loss of material properties, decreased toughness in T2DM rat bone.

No abstract