Every hip fracture begins with a microscopic crack that enlarges explosively. Most hip fractures in the elderly occur on falling from standing height, usually sideways or backwards. The typically moderate level of trauma very rarely causes fracture in younger people. This growing fragility may follow the decline of multiple protective mechanisms at many length scales from nanometres to that of the whole femur. With normal aging, the femoral neck asymmetrically and progressively loses bone tissue precisely where the cortex is already thinnest and is compressed in a fall. At the microscopic scale of the basic remodelling unit (BMU), increased numbers of actively remodelling BMUs associated with reduced mechanical loading in a typically inactive old age augments the numbers of mechanical flaws in the structure potentially capable of initiating cracking. Menopause and over-deep osteoclastic resorption are associated with incomplete BMU refilling leading to excessive porosity, cortical thinning, and disconnection of trabeculae. In the femoral cortex, replacement of damaged bone or bone containing dead osteocytes is inefficient, impeding the homeostatic mechanisms that match strength to mechanical usage. In consequence the participation of healthy osteocytes in crack-impeding mechanisms is impaired. Observational studies demonstrate that protective crack deflection in the elderly is reduced. At the most microscopic levels attention now centres on the role of tissue aging, which may alter the relationship between mineral and matrix that optimises the inhibition of crack progression, on the role of osteocyte aging and death that impedes tissue maintenance and repair and on one newly revived and one quite new topic: the potentially key role of citrate in binding crystal to matrix and regulating crystal growth; and the potential role of repeated moderate trauma to cause de-lamination of cortical bone.