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Microdamage, small crack in bone, is a product of bone fatigue. Burden of microdamage in vivo bone is determined by balance of generation and repair of microdamage. It has been reported that aging, bone loss, coarse osteocyte network, reduced bone remodeling cause accumulation of microdamage in bone. It is suspected that insufficiency fractures of subtrochanteric femur in patients under long term bisphophonate treatment are caused by severely suppressed bone turnover.

In tissue level turnover of bone cells, bone remodeling shows a sequential events of activation, resorption, reversal and formation. This may be observed as secondary osteons in the cortical bone and trabecular packets in the cancellous bone. Microcracks are repaired by targeted remodeling, and calcium is released by non-targeted remodeling. In macromodeling, a macroscopic size of a bone increases with growth, without changing its basic figure. In micromodelimg, a shift of trabecula, a minishift, is biomechnically controlled. New lamellar bone is added parallel to compressive and tensile force, and bone resorption occurs at the opposite surface of formation. In minimodeling new lamellar bone is formed with a sequence of activation, then directly formation, without scalloping at the cement line between newly formed bone and its basic bone.