pathogenesis of age-related bone loss show that most bone loss with age is cortical, not trabecular, and is the result of intracortical remodelling on the surfaces of the myriads of haversian canals traversing the cortex. These excavated canals increase in number, size and coalesce, particularly in the cortex adjacent to the marrow space leaving a layer of chaotically connected cortical remnants that look like trabeculae. Half of the total bone loss that occurs during ageing is produced during the process of formation of cortical remnants; indeed, the ratio of the thickness of the layer of cortical remnants to the thickness of the entire cortical mass (proportion compact remnants; PCR) appears to be a more reliable indicator of age-related bone loss than the cortical thickness. The calculation of porosity in the compactappearing cortex without including porosity produced by cortical remnants underestimates the true age related increase in porosity by three-fold. Moreover, the true decline with age is underestimated fourfold when cortical remnants are erroneously included in the trabecular compartments as is commonly done in standard bone structure analyses. Thus, overlooking intracortical porosity producing cortical remnants has resulted in a significant underestimation of agerelated cortical decay and loss.Contrary to prevailing notions, most bone loss is cortical, occurs by intracortical remodelling, causes most structural decay, and occurs after 60 years of age, not in the decade after menopause. Intracortical remodelling is a neglected target for preventing and reversing bone fragility in old age.