Tibial Morphology, Muscle Strength and Stress Fractures - A Computational Model

Amir Hadid 1 Amit Gefen 1 Nogah Shabshin 2 Yoram Epstein 3,4
1Biomedical Engineering, Tel Aviv University, Israel
2Diagnostic Imaging, Haemek Medical Center, Israel
3Heller Institute of Medical Research, Sheba Medical Center, Israel
4Sackler Faculty of Medicine, Tel Aviv University, Israel

Background: Stress fractures (SFs) are one of the most common and potentially serious overuse injuries. There is a large volume of literature regarding SFs, but most studies have been designed as clinical observations with limited control of the underlying risk factors.

Aims: To develop a computational model of SFs in humans that enables a better understanding of their pathophysiology.

Methods: Magnetic resonance scan protocol, which was specially developed for the purpose of this research, was used for a full anatomical segmentation of the calf tissues that were reconstructed in 3D, and meshed to construct a finite element computational model. A force that represents walking, equivalent to 3.5 times body weight, was applied and the stresses and strains that develop in the tibia were analyzed. The analysis was applied on bone models that represent robust and average tibial geometries. Additionally, a model was constructed to evaluate the effect of muscle forces on tibial strains.

Results: Computational simulations showed that for an individual with a body weight of 82 kg, the maximal tensile strain during walking peaks at ~500 microstrain, and the maximal compressive strain peaks at ~1600 microstrain. Robust tibial morphology was more sustainable to deformations; average tibia resulted in a more than 100% increase in the effective strain compared to robust geometry. Muscle forces resulted in a 30% reduction in maximal tibial strain.

Conclusion: By applying computational models we can provide evidence that anatomical variance (slenderness/robustness) within healthy individuals, and muscle forces variations (e.g., optimal vs. fatigue), may significantly affect SF susceptibility.









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