Role of cortical bone in hip fracture

In this review, I consider the varied mechanisms in cortical bone that help preserve its integrity and how they deteriorate with aging. Aging affects cortical bone in two ways: extrinsically through its effects on the individual that modify its mechanical loading experience and 'milieu interieur'; and intrinsically through the prolonged cycle of remodelling and renewal extending to an estimated 20 years in the proximal femur. Healthy femoral cortex incorporates multiple mechanisms that help prevent fracture. These have been described at multiple length scales from the individual bone mineral crystal to the scale of the femur itself and appear to operate hierarchically. Each cortical bone fracture begins as a sub-microscopic crack that enlarges under mechanical load, for example, that imposed by a fall. In these conditions, a crack will enlarge explosively unless the cortical bone is intrinsically tough (the opposite of brittle). Toughness leads to microscopic crack deflection and bridging and may be increased by adequate regulation of both mineral crystal size and the heterogeneity of mineral and matrix phases. The role of osteocytes in optimising toughness is beginning to be worked out; but many osteocytes die in situ without triggering bone renewal over a 20-year cycle, with potential for increasing brittleness. Furthermore, the superolateral cortex of the proximal femur thins progressively during life, so increasing the risk of buckling during a fall. Besides preserving or increasing hip BMD, pharmaceutical treatments have class-specific effects on the toughness of cortical bone, although dietary and exercise-based interventions show early promise.