Models for the pathogenesis of stress fractures in athletes.

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Abstract
It would seem that the development of a stress fracture results from unsuccessful adaptation of bone to a change in its mechanical environment caused by repetitive loading. It involves the physiological processes of microdamage production and remodelling. Whether the initiating factor is microdamage production or activation of remodelling through direct effects of strain is unclear. The remodelling process involves both the removal of bone which has become fatigue damaged or is extraneous to the requirements of the new loading environment, and the addition of new bone in an manner that is best suited to withstand the new mechanical strain. Normally this process is well modulated and does not cause symptoms. If the amount of bone removed is not sufficient to unduly weaken bone structure and the addition of new bone occurs sufficiently rapidly to correct any weakness before failure occurs or to repair microdamage, the process will successfully lead to a bone with appropriate material strength and geometry to withstand the new strain environment. However, if there is imbalance between bone removal and replacement, together with accumulation of microdamage, signs and symptoms of a stress fracture may result. Any factors which influence bone load, bone strength, or remodelling have the potential to result in a stress fracture. Attention should be paid to the identification of these factors in an attempt to prevent this overuse injury in athletes.