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.
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