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[论文解读] A Computational Model of Force within the Ligaments and Tendons in Progressive Collapsing Foot Deformity

Hamed Malakoutikhah, Erdogan Madenci|arXiv (Cornell University)|Dec 13, 2021
Foot and Ankle Surgery参考文献 46被引用 10
一句话总结

本研究开发了一种经过验证的足部有限元模型,以探究韧带或胫后肌腱(PTT)功能不全如何改变剩余软组织稳定结构中的力。研究发现,韧带破裂会导致其余韧带的过度负荷——但特定配对除外——而恢复足部对线则需要PTT力量达到体重的30%,主要减少后足外翻和前足外展。

ABSTRACT

Progressive collapsing foot deformity results from degeneration of the ligaments and the posterior tibial tendon (PTT). Our understanding of the relationship between the failures of them remains incomplete. We sought to improve this understanding through computational modeling of force in these soft tissues. The impact of PTT and ligament tears on force changes in the remaining ligaments was investigated using a previously validated finite element model of the foot. The ability of the PTT to restore foot alignment in a collapsed foot was evaluated by increasing the PTT force in a foot with attenuated ligaments and comparing the alignment angles to the intact foot. Rupture of any one of the ligaments led to overloading the remaining ligaments, except for the plantar naviculocuneiform, first plantar tarsometatarsal, and spring ligaments, where removing one led to unloading the other two. The attenuation of the plantar fascia, long plantar, short plantar, and spring ligaments significantly overloaded the deltoid and talocalcaneal ligaments. Isolated PTT rupture had no effect on foot alignment, but did increase the force in the deltoid and spring ligaments. Increasing the force within the PTT to 30% of body weight was effective at restoring foot alignment during quiet stance, primarily through reducing hindfoot valgus and forefoot abduction as opposed to improving arch height. The attenuation of any one ligament often leads to overload of the remaining ligaments which may lead to progressive degeneration. The PTT can maintain alignment in the collapsing foot, but at an increased load which could lead to its injury. Early intervention, in the form of ligament repair or reconstruction, might be used to prevent the progression of deformity. Moreover, strengthening the PTT through therapeutic exercise might improve its ability to restore foot alignment.

研究动机与目标

  • 了解单个韧带或PTT功能障碍如何改变剩余软组织稳定结构中的力分布。
  • 评估PTT在韧带受损的塌陷足中恢复足部对线的能力。
  • 通过计算模拟识别进行性塌陷足畸形(PCFD)的生物力学机制。
  • 为早期干预策略(如韧带修复或PTT强化)提供依据,以防止疾病进展。

提出的方法

  • 采用基于尸体足部CT扫描重建的个体化、经过验证的足部有限元模型。
  • 将韧带和肌腱建模为仅承受拉力的弹簧单元,材料属性基于已有文献数据。
  • 模拟韧带和PTT的切断,以量化剩余软组织中张力的变化。
  • 施加生理负荷(重心处50%体重,跟腱附着处25%体重)以模拟安静站立状态。
  • 评估PTT力量从0%至30%体重的增加,以评估对线恢复效果。
  • 对中立位和塌陷足两种形态的模型进行验证。

实验结果

研究问题

  • RQ1单个韧带破裂如何影响其余韧带和肌腱的张力?
  • RQ2在韧带受损的塌陷足中,需要多大的PTT力量才能恢复足部对线?
  • RQ3增加PTT力量对足部畸形的哪些组成部分(后足外翻、前足外展、足弓高度)最有效?
  • RQ4韧带和肌腱的力学行为如何影响PCFD中的代偿性负荷模式?
  • RQ5先前研究中的模型简化在多大程度上限制了其生理准确性?

主要发现

  • 单个韧带破裂通常导致其余韧带的过度负荷,但足底骰状骨-楔状骨、第一足底跗跖、以及弹簧韧带这组配对除外,其中移除一个会导致另一对的减荷。
  • 足底筋膜、长屈肌、短屈肌和弹簧韧带的减弱显著增加了三角韧带和距下关节韧带的负荷。
  • 单独PTT破裂对足部对线无影响,但增加了三角韧带和弹簧韧带的负荷。
  • 将PTT力量提高至体重的30%可恢复安静站立时的足部对线,主要通过减少后足外翻和前足外展实现。
  • PTT恢复对线的能力在减少矢状面和冠状面畸形方面最为有效,这是由于其在距舟关节处的解剖力臂。
  • 该模型表明,剩余稳定结构的代偿性过度负荷可能驱动进行性退变,支持通过韧带修复或PTT强化进行早期干预。

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