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Models for the pathogenesis of stress fractures in athletes.

机译:运动员应力性骨折的发病机理模型。

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摘要

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.
机译:应力性骨折的发展似乎是由于骨骼未能成功适应因重复载荷导致的机械环境变化而引起的。它涉及微损伤产生和重塑的生理过程。尚不清楚引发因素是微损伤产生还是通过应变的直接作用激活重塑。重塑过程包括去除已经疲劳损坏或不符合新加载环境要求的骨骼,以及以最适合承受新机械应力的方式添加新骨骼。通常,此过程是经过良好调制的,不会引起症状。如果去除的骨量不足以过度削弱骨骼结构,并且新骨的添加足够迅速地发生,以在出现故障之前修复任何弱点或修复微损伤,则该过程将成功地导致具有适当材料强度和几何形状的骨骼承受新的应变环境。但是,如果在取骨和置换之间不平衡,并伴有微损伤的累积,可能会导致应力性骨折的体征和症状。任何影响骨负荷,骨强度或重塑的因素都有可能导致应力性骨折。应该注意识别这些因素,以防止运动员过度使用这种伤害。

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