Bone modelling and remodelling are the final common pathways expressing all genetic and environmental factors affecting the attainment, maintenance, and decay of bone’s material and structural strength.’ During growth, this cellular machinery assembles the size, shape, and architecture of bone by depositing and removing material from the outer (periosteal) surface and the three (endocortical, intracortical, and trabecular) components of the inner (endosteal) surface
At completion of growth, periosteal apposition slows and remodelling of the three inner surfaces maintains bone strength by removing and replacing old or damaged bone with an identical volume of new bone. Around midlife, remodelling becomes unbalanced so that every time bone matrix is remodelled, whether initiated for damage repair or adaptation to loading, more bone is removed than is replaced by cells of the basic multicellular unit, producing one loss and structural decay. Although this negative balance of a few percent can worsen as age advances, the driving force producing bone loss and structural decay is the remodelling intensity, the birth rate of the many new basic multicellular units arising on these surfaces after menopause in women and in both sexes late in life.
The amount of bone loss and structural decay also relies on accessibility of the bone matrix to remodelling. This accessibility depends in part oft how a volume of bone is designed in space. Remodelling is initiated on a bone surface. A volume of bone with a large exposed surface will be remodelled rapidly by the large number of basic multicellular units that can access and erode bone matrix beneath the surface.’ A volume of trabecular or spongy bone has a larger surface than does an equal volume of cortical or compact bone and is thus exposed to more remodelling and is lost more rapidly than is cortical bone.’ For this reason, trabecular bone loss and fractures of the vertebral body, which is a structure containing large amounts of trabecular bone, have dominated thinking and research into the structural basis of bone fragility for almost 70 years.”
Which neglects the role of decay of cortical bone in pathogenesis of bone fragility, which is an omission that is difficult to reconcile with the epidemiology of fractures. About 80% of all fractures in old age are non-vertebral, arise at sites that are mainly cortical, and occur after age 60 years when the rate of trabecular bone loss decelerates.” Moreover, only 20% of bone is trabecular-80% is cortical.
Zebaze et al 2010 Intracortical remodelling and porosity. in the distal radius and post-mortem femurs of women: a cross-sectional study . The Lancet vol 375 pp 1729-1736

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