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Due to the increase in the average age of the population, the projections on the number of age-dependent bone fractures appear to be constantly increasing. They are mainly due to bone pathologies, including osteoporosis. The latter leads to a reduction in bone mineral density and deterioration of the micro-architecture, with a consequent increase in bone fragility. However, the mechanisms of damage at the micro-scale have not yet been elucidated and there is no universally recognized damage criterion. Recent research has evaluated the importance of implementing computational models to study the influence of bone gaps, canaliculi and microporosities on the propagation of damage. These models need to be validated through experimental tests, still lacking, in particular on human bones, in the current scientific landscape. Once the experimental validation of computational models has been de
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