Diabetes is associated with increased fracture risk in human tissues, especially in the elderly population. One important factor indicating the fracture risk in hard tissues with diabetes is the elevated advanced glycation end-products (AGEs) crosslinks. This increase in AGEs in tissues such as cortical bone and dentin can deteriorate their properties and consequently, lead to a high fracture risk rate. There are limited data on fracture behavior and crack formation rate in cortical bone and dentin with increased AGEs levels. In addition to elevated AGEs, the microstructural features of these hard tissues undergo changes with aging. The combined influence of increased AGEs and age-related changes in cortical bone and dentin have not been fully understood, and more in-depth investigations are required to discover such effects. The main objective of the present work is to evaluate how AGEs and materials heterogeneity along with age-related changes can alter crack growth trajectory in human hard tissues such as cortical bone and dentin at the microscale level. In addition to this, this thesis aims to explore how fracture behavior in such hard tissues with elevated AGEs varies under different types of loading conditions (e.g., quasi-static, dynamic, and cyclic loading). To discover such effects at the microscale, an advanced numerical tool, phase field framework, is used to simulate fracture and crack growth trajectory in cortical bone and human dentin. To create cortical bone models, tibia cross sections have been cut and stained by a silver-nitrate method, and microscopic images were taken from the sections. To construct the microstructure of dentin, morphological and geometrical parameters are gathered from other studies in the literature. The relationships between AGEs and the fracture properties of the microstructural features in cortical bone and dentin are also assumed based on experimental observations. The fracture simulations show how the mismatch between the fracture properties of the microstructural features due to elevated AGEs in cortical bone and dentin can alter the post-yielding properties under different loading conditions (e.g., quasi-static, dynamic, and cyclic loading). The bone and dentin fragility are discussed based on crack formation rate, brittle behavior of samples after yielding, and the crack-microstructure interactions. Furthermore, the role of materials heterogeneity of microstructural features in the activation of toughening mechanisms such as crack merging and branching is investigated in more detail. The findings of the present thesis show that cortical bone and dentin tissues become more fragile with increased AGEs content and all cracks growth trajectories at the microscale level depend on how AGEs disrupt the fracture properties of the microstructural features.