Biomechanical factors affecting metatarsal fatigue and bone stress injury risk

项目摘要 近50%的骨应激损伤(BSI)诊断发生在20岁以下的人， 青少年BSI在过去十年中增加了两倍。BSI是骨骼重复超负荷的结果， 超过骨的重塑，导致微损伤的积累。足部解剖学、生物力学、肌肉 功能，和外部因素决定了在行走或跑步时传递到跖骨上的力。反过来, 合力会产生机械应变，这种应变会因跖骨结构和局部骨密度而异。这里, 我们提出了一种机械测试、计算建模和定量图像的新组合 足部肌力、跖骨结构和跖骨之间相互作用的分析 损害累积。我们假设支撑足弓的肌肉减少了背部弯曲，增加了 跖骨压缩(目标1)。我们相信这可以减少疲劳过程中的损伤积累。 加载，由于骨的各向异性材料属性(目标2)。我们还预计受损的肌肉 功能和骨骼结构将通过增加骨骼应变的机制与BSI(目标3)相关。 这些假说是基于足部肌肉无力、足部解剖变异和 患有BSI的跑步者骨密度降低的观察。为了更好地了解 在跑步过程中，我们提出了三个目标：跖骨损伤和肌肉激活。目标1：确定如何 在跑步过程中，肌肉的激活会影响跖骨的负荷，通过模拟分析 足部内在和外在肌肉的生物力学贡献。目标2：比较弯曲和弯曲的效果。 通过实验测试对整个跖骨疲劳破坏/损伤累积的轴向载荷。目标3： 比较女性跑步者和新近跑步者的足部肌肉力量和跖骨结构(4 数周的测试)，而不是没有跖骨BSI。 如果我们的假设得到支持，这表明，通过加强治疗可以降低跖骨BSI的风险。 和激活足部肌肉，通过改变跖骨加载方向和减少应变的机制。 这可能直接为临床干预提供信息，如步态再训练、足部强化或 鞋类。这项研究将为导致跖骨疲劳失效的机制和 识别有跖骨BSI风险的个体。我们的研究团队包括骨科专家 生物力学(特洛伊)，跑步损伤生物力学(戴维斯)，骨健康和运动损伤(Tenforde)， 使我们独一无二地有资格从事这一多学科项目。此外，我们的计划展示了我们的 持续致力于通过本科生和研究生的融合来培养学生 参与项目的方方面面。

Project Summary Nearly 50% of all bone stress injury (BSI) diagnoses occur in individuals under age 20 and the prevalence of adolescent BSI has tripled over the past decade. A BSI is the result of repetitive overload of the skeleton that exceeds bone remodeling, resulting in accumulation of microdamage. Foot anatomy, biomechanics, muscle function, and external factors dictate forces transmitted onto the metatarsals during walking or running. In turn, resulting forces create mechanical strain that varies by metatarsal structure and regional bone density. Here, we propose a novel combination of mechanical testing, computational modeling, and quantitative image analysis to characterize the interactions between foot muscle forces, metatarsal bone structure, and metatarsal damage accumulation. We hypothesize that muscles supporting the arch reduce dorsal bending and increase compression of the metatarsals (Aim 1). We believe this may reduce damage accumulation during fatigue loading, due to the anistropic material properties of bone (Aim 2). We also expect that impaired muscle function and bone structure will be associated with BSI (Aim 3) through mechanisms of increased bone strain. These hypotheses are based on clinical reports of foot muscle weakness, variations in foot anatomy, and observations of low bone density in runners with a BSI. To better understand the interactions between metatarsal damage and muscle activation during running, we propose three aims. Aim 1: Determine how muscle activation can influence metatarsal loading during running, by using simulation to analyze the biomechanical contribution of intrinsic and extrinsic foot muscles. Aim 2: Compare the effect of bending vs. axial loading on whole metatarsal fatigue failure/damage accumulation using experimental testing. Aim 3: Compare foot muscle strength and metatarsal bone structure between female runners with recent (within 4 weeks of testing) versus no metatarsal BSI. If our hypotheses are supported, it suggests that the risk of metatarsal BSI may be reduced via strengthening and activation of foot muscles, through mechanisms of altered metatarsal loading direction and reduced strain. This may directly inform clinical interventions such as gait retraining, foot strengthening, or changes in footwear. This research will provide evidence for the mechanisms contributing to metatarsal fatigue failure and the identification of individuals at risk for metatarsal BSI. Our research team includes experts in orthopaedic biomechanics (Troy), running injury biomechanics (Davis), and bone health and sports injury (Tenforde), making us uniquely qualified to pursue this multidisciplinary project. Additionally, our plan demonstrates our ongoing commitment to student training through integration of both undergraduate and graduate student involvement in all aspects of the project.