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Stress fractures (SF) are one of the most common and potentially serious overuse injuries.This study aimed to develop a computational biomechanical model of strain in human tibial bone that will facilitate better understanding of the pathophysiology of SF.The MRI of a healthy, young male was used for full anatomical segmentation of the calf tissues, which considered hard–soft tissues biomechanical interactions. From the undeformed coronal MR images, the geometry of bones, muscles, connecting ligaments, and fat were reconstructed in three dimensions and meshed to a finite element model. A force that simulated walking was applied on the tibial plateaus. The model was then analyzed for strains in the tibia under various conditions: unloaded walking, walking with a load equivalent to 30% of bodyweight, and walking under conditions of muscular fatigue. In addition, the effect of tibia robustness on strain was analyzed.The model showed that the tibia is mostly loaded by compression, with maximal strains detected in the distal anterior surface: 1241 and 384 microstrain, compressive and tensile, respectively. Load carriage resulted in ~30% increase in maximal effective strains. Muscle fatigue has a complex effect; fatigued calf muscles (soleus) reduced the maximal effective strains up to 9%, but fatigued thigh muscles increased those strains by up to 3%. It had also been shown that a slender tibia is substantially prone to higher maximal effective strains compared with an average (22% higher) or robust tibia (39% higher).Thigh muscle fatigue, load carriage, and a slender tibia were detected as factors that may contribute to the development of SF. The methodology presented here is a novel tool for investigating the pathophysiology of SF.