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Bone fracture is a severe health concern; therefore, understanding the causes of bone fracture are crucial. This paper investigates the microstructure and fracture behaviour of cadaveric cortical bone of two different groups (Young, n= 6; Aged, n=7). The microstructure is obtained from µ-CT images, and the material parameters are measured with nanoindentation. Fracture behaviour in transverse and longitudinal orientations is investigated experimentally and numerically. The results show that the Haversian canal (HC) size increases and the osteon wall thickness (OWT) decreases significantly in the aged group, whereas a nonsignificant difference is found in tissue properties. The crack initiation (J ic) and crack growth (J grow) toughness of the aged group are found to be significantly lower (p<0.01) than the young group in the transverse orientation; however, for the longitudinal orientation, only the value of J ic in the aged group is found significantly lower. Further, a 4-phase XFEM (based on micro-CT image) model is developed to investigate the crack propagation behaviour in both orientations. For the transverse orientation, results show that in the aged group, the crack initially follows the cementline and then penetrates the osteon, whereas, in the young group, it propagates along the cementline. These results are in agreement with experimental results where the decrease in J grow is more significant than the J ic in the aged group. This study suggests that ageing leads to a larger HC and reduced OWT, which weakens the crack deflection ability and causes fragility fracture. Further, the XFEM results indicate that the presence of a small microcrack in the vicinity of a major crack tip causes an increase in the critical stress intensity factor. [ABSTRACT FROM AUTHOR]

• This study investigates the effect of type 2 diabetes on time dependent properties of trabecular bone using stress relaxation and dynamic mechanical analysis under compression loading. • Correlation of viscoelastic properties with microstructural parameters and biochemical properties are established. • Type 2 diabetes causes degradation storage modulus and initial stress as compared non type 2 diabetes. • The viscoelastic properties are independent of type 2 diabetes. • Amount of stress relaxed during the hold period is related to its mineral and matrix content. Type 2 diabetes (T2D) is a well-known disease that impaired bone mechanical properties and increases the risk of fragility fracture. The bone tissue is a viscoelastic material that means the loading rate determines its mechanical properties. This study investigates the impact of T2D on the viscoelastic properties of human bone and its association with microstructure and biochemical properties. Viscoelasticity is an important mechanical property of bone and for this the interaction of individual constituents of bone plays an important role. The viscoelastic nature of bone can be affected by aging and diseases, which can further influence its deformation and damage behavior. The present study investigated the effects of T2D on the viscoelastic behavior of trabecular bone. The femoral heads of T2D (n = 26) and non-T2D (n = 40) individuals with hip fragility fractures were collected for this investigation. Following the micro-CT scanning of all bone samples, the stress relaxation and dynamic mechanical analysis (DMA) tests were performed to quantify the viscoelasticity of bone. Further, a correlation analysis was performed to investigate the effects of alteration in bone microstructural and biochemical parameters on viscoelasticity. The stress relaxation and frequency sweep responses of T2D and non-T2D trabecular bone specimens were not found significantly different. However, the storage modulus, initial stiffness, and initial stress were found lower in T2D bone. The significant correlation of percentage stress relaxed is obtained between the mineral content (r = - 0.52, p-value = 0.003), organic content (r = 0.40, p-value = 0.02), and mineral-to-matrix ratio (r = - 0.43, p-value = 0.009). Further, storage and loss modulus were correlated with bone volume fraction (BV/TV) for both groups. The stress relaxation and frequency sweep characteristics were not found significantly connected with the other chemical, structural, or clinical parameters. This study suggests that T2D does not affect the time-dependent response of human femoral trabecular bone. The viscoelastic properties are positively correlated with organic content and negatively correlated with mineral content. [ABSTRACT FROM AUTHOR]

Type-2 diabetic (T2D) and osteoporosis (OP) suffered patients are more prone to fragile fracture though the nature of alteration in areal bone mineral density (aBMD) in these two cases are completely different. Therefore, it becomes crucial to compare the effect of T2D and OP on alteration in mechanical and structural properties of femoral trabecular bone. This study investigated the effect of T2D, OP, and osteopenia on bone structural and mechanical properties using micro-CT, nanoindentation and compression test. Further, a nanoscale finite element model (FEM) was developed to predict the cause of alteration in mechanical properties. Finally, a damage-based FEM was proposed to predict the pathological related alteration of bone's mechanical response. The obtained results demonstrated that the T2D group had lower volume fraction (−18.25%, p = 0.023), young's modulus (−23.47%, p = 0.124), apparent modulus (−37.15%, p = 0.02), and toughness (−40%, p = 0.001) than the osteoporosis group. The damage-based FE results were found in good agreement with the compression experiment results for all three pathological conditions. Also, nanoscale FEM results demonstrated that the elastic and failure properties of mineralised collagen fibril decreases with increase in crystal size. This study reveals that T2D patients are more prone to fragile fracture in comparison to OP and osteopenia patients. Also, the proposed damage-based FEM can help to predict the risk of fragility fracture for different pathological conditions. [ABSTRACT FROM AUTHOR]