As mechanical usage (MU) of a bone changes from complete disuse towards maximal vigor, the biologic mechanisms that can adapt it to its MU tend to react predictably. Acute disuse can increase BMU (Basic Multicellular Unit, the remodeling ‘packet’) creations but reduces how much bone they form, to increase bone loss next to marrow. Normal usage reduces those creations to normal and tends to equalize their resorption and formation;​ this conserves bone. In mild overloading, BMUs still conserve existing bone, while modeling drifts can begin adding to and/or reshaping it. Severe overloading can increase microdamage alarmingly, its repair by BMUs too, and can cause woven bone formation, anarchic resorption and a regional acceleratory phenomenon.

Those ranges of MU vigor can define four ‘windows’. An adapted window should apply to healthy, normally active adult mammals, and a mild overload window to healthy, normally active growing ammals. The biologic responses in the pathologic window could explain among other things some total joint and internal fixation failures, some pathologic fractures and some bone healing and sports medicine problems.