The fracture of bone is a health concern of increasing significance as the population ages. It is therefore of importance to understand the mechanics and mechanisms of how bone fails, both from a perspective of outright (catastrophic) fracture and from delayed/time‐dependent (subcritical) cracking. To address this need, there have been many in vitro studies to date that have attempted to evaluate the relevant fracture and fatigue properties of human cortical bone;​ despite these efforts, however, a complete understanding of the mechanistic aspects of bone failure, which spans macroscopic to nanoscale dimensions, is still lacking. This paper seeks to provide an overview of the current state of knowledge of the fracture and fatigue of cortical bone, and to address these issues, whenever possible, in the context of the hierarchical structure of bone. One objective is thus to provide a mechanistic interpretation of how cortical bone fails. A second objective is to develop a framework by which fracture and fatigue results in bone can be presented. While most studies on bone fracture have relied on linear‐elastic fracture mechanics to determine a single‐value fracture toughness (e.g., K_c or G_c), more recently, it has become apparent that, as with many composites or toughened ceramics, the toughness of bone is best described in terms of a resistance‐curve (R‐curve), where the toughness is evaluated with increasing crack extension. Through the use of the R‐curve, the intrinsic and extrinsic factors affecting its toughness are separately addressed, where ‘intrinsic’ refers to the damage processes that are associated with crack growth ahead of the tip, and ‘extrinsic’ refers to the shielding mechanisms that primarily act in the crack wake. Furthermore, fatigue failure in bone is presented from both a classical fatigue life (S/N) and fatigue‐crack propagation (da/dN) perspective, the latter providing for an easier interpretation of fatigue micromechanisms. Finally, factors, such as age, species, orientation, and location, are discussed in terms of their effect on fracture and fatigue behaviour and the associated mechanisms of bone failure.