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软组织缺陷导致的成年人获得性平足早期的腓骨长肌过载:有限元分析。

Peroneus Longus overload caused by soft tissue deficiencies associated with early adult acquired flatfoot: A finite element analysis.

机构信息

Biomedical Engineering Deparment, Universidad de los Andes, Colombia; Universidad Espíritu Santo - Ecuador.

Queen Elizabeth Hospital, Kings Lynn, Norfolk, UK.

出版信息

Clin Biomech (Bristol). 2021 Jun;86:105383. doi: 10.1016/j.clinbiomech.2021.105383. Epub 2021 May 11.

Abstract

BACKGROUND

Peroneus Longus tendinopathy has been related to overload from cavus and ankle instability. The etiology of isolated Peroneus Longus tendon synovitis has not been elucidated. Loss of foot arch integrity as a cause of isolated Peroneus Longus overload is difficult to establish using cadaver modeling. Our objective was to analyze Peroneus Longus stress changes in pathological scenarios related to flatfoot development.

METHODS

A three-dimensional finite element foot model which included the foot bones and main soft tissues that maintain the arch was used. Simulations were performed in midstance of gait. Tendon's maximum principal stress and von Mises were calculated in scenarios where the plantar fascia, spring ligament and the posterior tibial tendon were weakened.

FINDINGS

Decreasing plantar fascia stiffness thus weakening arch integrity increases Peroneus Longus stresses by over three times. Additional failure of tissues that support arch, such as the spring ligament and tibialis posterior tendon further overloads this tendon. The absence of Peroneus Longus also affects stresses in tissues that maintain the arch. Stress concentrations increase in the plantar component of the Peroneus Longus.

INTERPRETATION

Results offer an explanation into isolated Peroneus Longus overload synovitis. Recognition of failing medial arch structures that occur in early acquired flatfoot as a cause of Peroneus Longus overload could help in its treatment. We caution the practice of transfer of peroneus brevis to longus in surgical treatment of flatfoot as it may further overload an overloaded tendon and focus should be on restoration of arch stability to offload stresses within it.

摘要

背景

腓骨长肌腱病与高弓足和踝关节不稳定引起的超负荷有关。孤立性腓骨长肌腱滑膜炎的病因尚未阐明。使用尸体建模很难确定足弓完整性丧失是否是孤立性腓骨长肌腱超负荷的原因。我们的目的是分析与平足发展相关的病理情况下腓骨长肌的应力变化。

方法

使用包括维持足弓的足骨和主要软组织的三维有限元足模型。在步态的中间阶段进行模拟。在足底筋膜、弹簧韧带和胫骨后肌腱减弱的情况下,计算肌腱的最大主应力和 von Mises。

结果

降低足底筋膜的刚度从而削弱足弓的完整性会使腓骨长肌的应力增加三倍以上。支撑足弓的组织(如弹簧韧带和胫骨后肌腱)的进一步失效会进一步加重该肌腱的负荷。腓骨长肌的缺失也会影响维持足弓的组织的应力。腓骨长肌的足底部分的应力集中增加。

结论

结果为孤立性腓骨长肌超负荷滑膜炎提供了解释。认识到早期获得性扁平足中内侧足弓结构的失效是腓骨长肌超负荷的原因,可以帮助治疗。我们警告在扁平足的手术治疗中转移腓骨短肌到长肌的做法,因为这可能会进一步加重超负荷的肌腱,并且应该注重恢复足弓的稳定性以减轻其内部的应力。

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