Saw Kenneth Kai Wei, Gurney Ziki, Noel-Barker Natasha, Boote Leia, Pasapula Chandra, Norrish Alan R
University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK.
School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.
Foot (Edinb). 2025 Jun;63:102174. doi: 10.1016/j.foot.2025.102174. Epub 2025 Jun 3.
The progressive ligament instability associated with flatfoot deformity may result in altered foot biomechanics and represent a risk factor for the development of Achilles Tendinopathy (AT). The aim of this study was to determine whether an increased tendo-Achilles (TA) force was required to generate a set heel lift in a cadaveric flatfoot model. Thirteen fresh (previously frozen) cadavers, with no previous foot pathology and sectioned from the knee were mounted on a testing frame. The frame maintained a dorsiflexed ankle position, to simulate the terminal stance phase of gait, and allowed a constant axial load to be applied through the tibia. The heel was elevated 3 cm by a measured traction force through the TA to a pre-determined laser mark. The flatfoot model was created by sequential sectioning of the medial arch supporting structures, creating progressive midfoot instability and flatfoot deformity, from mild to severe. The force (N) required to generate heel lift was recorded at each stage of the development of the flatfoot. Initially, following Spring ligament and Tibialis Posterior sectioning, the force required to generate heel lift decreased. However, as the flatfoot deformity progressed the force required for heel lift increased. A severe flat foot deformity, characterised by medial ray destabilisation significantly increased the force required to generate a heel lift (5.1 ± 7.2 N, p = 0.02) as did sectioning of the (ii) short and long plantar ligaments (5.5 ± 8.7 N, p = 0.03). Progressive ligament failure associated with acquired flatfoot deformity may be a risk for AT overload due to increased TA force required for heel lift, resulting in TA overload symptoms. The paradoxical decrease in force required to generate heel lift with isolated SL sectioning has not been previously described. This biomechanical study raises the possibility that interventions that support the medial longitudinal arch, such as orthotics, may protect against TA overload.
与扁平足畸形相关的渐进性韧带不稳定可能导致足部生物力学改变，并成为跟腱病（AT）发生的一个风险因素。本研究的目的是确定在尸体扁平足模型中，产生一定程度的足跟抬起是否需要增加跟腱（TA）力。13具新鲜（之前冷冻）、无既往足部病变且从膝关节处截断的尸体被安装在测试框架上。该框架保持踝关节背屈位置，以模拟步态的终末支撑期，并允许通过胫骨施加恒定的轴向负荷。通过TA施加测量好的牵引力，将足跟抬高3厘米至预先确定的激光标记处。通过依次切断内侧足弓支撑结构来创建扁平足模型，从而产生从轻度到重度的渐进性中足不稳定和扁平足畸形。在扁平足发展的每个阶段，记录产生足跟抬起所需的力（牛顿）。最初，在切断弹簧韧带和胫后肌腱后，产生足跟抬起所需的力下降。然而，随着扁平足畸形的进展，足跟抬起所需的力增加。以内侧射线不稳定为特征的严重扁平足畸形显著增加了产生足跟抬起所需的力（5.1±7.2牛顿，p = 0.02），切断（ii）长短跖韧带时也是如此（5.5±8.7牛顿，p = 0.03）。与后天性扁平足畸形相关的渐进性韧带失效可能是AT过载的一个风险因素，因为足跟抬起需要增加TA力，从而导致TA过载症状。之前尚未描述过孤立切断弹簧韧带时产生足跟抬起所需力的反常下降情况。这项生物力学研究提出了一种可能性，即诸如矫形器等支持内侧纵弓的干预措施可能预防TA过载。
