Abstract

Because areal bone mineral density and bone structure do not necessarily explain the elevated fracture risk that occurs with both type 1 diabetes (T1D) and type 2 diabetes (T2D), there is a need to understand how diabetes is possibly affecting the material properties of bone. Such apparent-level properties as modulus, strength, toughness, fatigue life, and fracture toughness are, by definition, independent of bone structure. They are measured from mechanical tests of uniform cortical bone specimens of known geometry or estimated from mechanical tests of rodent long bones in which the contribution of structure, as typically determined by micro-computed tomography (μCT), is factored out leaving the material contribution. There is a dearth of information about how diabetes affects the material properties of human bone, and so a working hypothesis is that diabetes affects bone similar to aging effects on bone but on a shorter time scale. If true, diabetes decreases post-yield toughness, the ability of bone to dissipate energy after the onset of damage, and fracture toughness, the ability of bone to resist crack propagation. In rodent studies measuring fracture resistance of bone, structural strength of cortical bone is consistently less for mice with T1D or T2D than for nondiabetic, control rodents. However, a difference in material strength of bone is not always statistically significant across studies suggesting strain, gender, age of diabetes onset, and duration of diabetes influence the degree to which there is a diabetes-related decrease in material strength. Likewise, a significant loss in bone toughness with diabetes appears to be dependent on the duration that the rodent was diabetic. Along with mechanical testing, indentation techniques are described because there is emerging evidence that diabetes affects tissue-level properties.

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