The basic morphology of the skeleton is determined genetically, but its fin
al mass and architecture are modulated by adaptive mechanisms sensitive to
mechanical factors. When subjected to loading, the ability of bones to resi
st fracture depends on their mass, material properties, geometry and tissue
quality. The contribution of altered bone geometry to fracture risk is una
ppreciated by clinical assessment using absorptiometry because it fails to
distinguish geometry and density. For example, for the same bone area and d
ensity, small increases in the diaphyseal radius effect a disproportionate
influence on torsional strength of bone. Mechanical factors are clinically
relevant because of their ability to influence growth, modeling and remodel
ing activities that can maximize, or maintain, the determinants of fracture
resistance. Mechanical loads, greater than those habitually encountered by
the skeleton, effect adaptations in cortical and cancellous bone, reduce t
he rate of bone turnover, and activate new bone formation on cortical and t
rabecular surfaces. In doing so, they increase bone strength by beneficial
adaptations in the geometric dimensions and material properties of the tiss
ue. There is no direct evidence to demonstrate anti-fracture efficacy for m
echanical loading, but the geometric alterations engendered undoubtedly inc
rease the structural properties of bone as an organ, increasing the resista
nce to fracture. Like all interventions, issues of safety also arise. Physi
cal activities involving high strain rates, heavy lifting or impact loading
may be detrimental to the joints, leading to osteoarthritis; may stimulate
fatigue damage leading with some to stress fractures; or may interact phar
maceutical interventions to increase the rate of microdamage within cortica
l or trabecular bone.