Bone modeling adapts structure to loading by changing bone size and shape and removes damage and so maintains bone strength. Remodeling is initiated by damage producing osteocyte apoptosis, which signals the location of damage via the osteocyte-canalicular system to endosteal lining cells that form the canopy of a bone remodeling compartment (BRC). Molecular signalling within the BRC between precursors, mature cells, cells of the immune system, and products of the resorbed matrix titrate the birth, work, and lifespan of this remodeling machinery to either remove or form a net volume of bone. Advancing age is associated with a reduction in the volume of bone resorbed by each basic multicellular unit (BMU), an even greater reduction in the volume of bone formed by each BMU producing a net negative BMU balance, and an increased remodeling rate in midlife in women and late in life in both sexes so that now many remodeling events erode bone while an age-related decline in periosteal apposition results in net bone loss and bone fragility. A better understanding of the mechanisms responsible for structural decay is likely to reveal new approaches to the prevention and reversal of bone fragility.