The vicious cycle of remodeling↔microdamage→fracturing which is the engine that drives postmenopausal bones to osteoporotic hyperfragility and fracturing. With advancing age, remodeling and the remodeling hole-refilling deficit rise, which increases microarchitectural deterioration, fragility, and microdamage at load-bearing sites. The signals from the damage sites increase remodeling. When the estrogen level drops during menopause, the cycle accelerates, and the microdamage level and weakening escalates toward "spontaneous" fracturing by the impacts of normal muscle pulling. Breaking the circle by reducing remodeling with osteoclast-killing antiresorptives reduces microdamage, permits the existing remodeling holes that have been dug out of damaged patches to be more or less refilled with more prolongedly mineralized, hence stronger, bone matrix. This reduces the probability of refracturing. But the prevalent microarchitecural deterioration and attendant fragility can only be reversed by an anabolic drug that can stimulate osteoblast generation and bone-making activity.