As one of the most important natural materials, cortical bone is a composite material comprising assemblies of tropocollagen molecules and nanoscale hydroxyapatite mineral crystals, forming an extremely tough, yet lightweight, adaptive and multi-functional material. Bone has evolved to provide structural support to organisms, and therefore its mechanical properties are vital physiologically. Like many mineralized tissues, bone can resist deformation and fracture from the nature of its hierarchical structure, which spans molecular to macroscopic length-scales. In fact, bone derives its fracture resistance with a multitude of deformation and toughening mechanisms that are active at most of these dimensions. Here we examine ways to quantity the quality of bone in terms of its basic mechanical properties of strength, ductility and most importantly resistance to fracture (toughness). We show that bones strength and ductility originates primarily at the scale of the nano to submicron structure of its mineralized collagen fibrils and fibers, whereas bone toughness is additionally generated at much larger, micro- to near-millimeter, scales from crack-tip shielding associated with interactions between the crack path and the microstructure. We further how the effectiveness with which bones structural features can resist fracture at small to large length-scales can become degraded by biological factors such as aging and disease, which affect such features as the collagen cross-linking environment, the homogeneity of mineralization, and the density of the osteonal structures. In this regard, we specifically examine the effects of various diseases, such as vitamin D deficiency, osteogenesis imperfecta, and Pagets disease, on bone quality, and present the results of preliminary experiments on the effects of bisphosphonate treatments as a possible cause of atypical femoral fractures.