Abstract
Category:
Hindfoot; Basic Sciences/Biologics
Introduction/Purpose:
The posterior tibialis muscle (PTm) could be a contributing factor in progressive collapsing foot deformity (PCFD), but the extent to which the function of PTm is related to PCFD progression is debated. The morphology of the PTm is most often evaluated through oversimplified cross-sectional measurements of CT, MRI, or ultrasound images. Recently, statistical shape models (SSM), built from three-dimensional segmentations of volumetric images, have been shown to provide more accurate and comprehensive morphological evaluations of musculoskeletal tissue. To enhance understanding of the PTm in patients with PCFD, herein, we used a 3D SSM to test the hypothesis that both the shape of the PTm and alignment of the PTm relative to the hindfoot bones is different in patients with PCFD when compared to asymptomatic controls.
Methods:
In this retrospective comparative study, 12 female patients presenting with PCFD with an intact PTm, and 19 female asymptomatic individuals underwent simulated weight-bearing CT (SW-CT) from above the knee to the sole. For each participant, SW-CT images were segmented to create 3D models of distal tibia, talus, calcaneus, navicular, and PTm. We developed two SSMs to compare morphological differences. One compared only the shape of the PTm and the other compared the relative position and alignment of the PTm with the hindfoot bones. The PTm 3D model was also used to measure volume, tendon normalized length, and percentage fat of the PTm. Each measurement and SSM were compared between PCFD and asymptomatic controls. For all statistical measures and comparisons an alpha value of 0.05 was used (p < 0.05).
Results:
The SSM did not identify significant differences in the isolated shape of the PTm between groups. However, the SSM showed significant differences in the alignment of PTm with respect to the hindfoot bones. Within PCFD, the PTm course shifted the lateral side of the tibia, increasing the distance to the navicular bone. Also, within the PCFD group, the tibia was more internally rotated, but the PTm was not. Tendon normalized length was significantly lower in PCFD than in asymptomatic controls, and there was no difference in muscle length, whereas tendon normalized length was shorter in the PCFD group. Percent fat content was significantly higher in PCFD compared to asymptomatic controls. No significant differences were found for PTm volume and tibia torsion angle between both groups.
Conclusion:
In PCFD with an intact PTm, alignment differences of PTm and hindfoot bones suggest that PCFD progression may be a cause of PTm rupture. Tibia internal rotation and PTm altered course in PCFD could mechanically alter PTm function and should be further investigated. Additionally, low PTm tendon normalized length may be a factor contributing to PCFD, but our evidence suggests that primary PTm morphology differences are likely caused by PCFD. It may suggest that PTm does not handle the progression of PCFD. In the future, we need to evaluate morphologies of PCFD with and without PTM rupture.
This figure showed results of each measurement for PTm, and the alignment variation (mean and ± standard deviation) and P-values for each model represent a group-wise comparison. Arrows indicated focal locations of morphological differences/changes.