TY - JOUR
T1 - An ex vivo sequential ligament transection model of flatfoot
AU - Renfree, Sean
AU - Malakoutikhah, Hamed
AU - Borgstrom, Mark
AU - Latt, Leonard Daniel
N1 - Publisher Copyright:
© 2023
PY - 2024/8
Y1 - 2024/8
N2 - Background: The ligaments implicated in the earliest stages of developing a progressive collapsing foot deformity are poorly understood. Commonly employed cadaveric flatfoot models are created from simultaneous transection of multiple ligaments, making it difficult to assess early changes in pressure distribution from ligaments critical for maintaining load distribution. A serial transection of ligaments may provide insight into changes in pressure distribution under the foot to identify a potential combination of ligaments that may be involved in early deformities. Methods: Specimens were loaded using a custom designed axial and tendon loading system. Plantar pressure data for the forefoot and hindfoot were recorded before and after six sequential ligament complex transections. Findings: Sectioning the plantar fascia (first) and short/long plantar ligaments (second) failed to generate appreciable differences in load distribution. Dividing the spring ligament (third) led to changes in hindfoot load distribution with a shift towards the lateral column indicative of hindfoot valgus angulation. All subsequent conditions resulted in similar patterns in hindfoot plantar load distribution. An anterior shift in the center of pressure only occurred after transection of all six ligament complexes. Interpretation: Loss of the plantar fascia and short/long plantar ligaments are not critical in maintaining plantar load distribution or contact area. However, the additional loss of the spring ligament caused notable changes in hindfoot load distribution, indicating the combination of these three ligament complexes is particularly critical for preventing peritalar subluxation. Minimal changes in load distribution occurred when performing additional transections to reach a complete flatfoot deformity.
AB - Background: The ligaments implicated in the earliest stages of developing a progressive collapsing foot deformity are poorly understood. Commonly employed cadaveric flatfoot models are created from simultaneous transection of multiple ligaments, making it difficult to assess early changes in pressure distribution from ligaments critical for maintaining load distribution. A serial transection of ligaments may provide insight into changes in pressure distribution under the foot to identify a potential combination of ligaments that may be involved in early deformities. Methods: Specimens were loaded using a custom designed axial and tendon loading system. Plantar pressure data for the forefoot and hindfoot were recorded before and after six sequential ligament complex transections. Findings: Sectioning the plantar fascia (first) and short/long plantar ligaments (second) failed to generate appreciable differences in load distribution. Dividing the spring ligament (third) led to changes in hindfoot load distribution with a shift towards the lateral column indicative of hindfoot valgus angulation. All subsequent conditions resulted in similar patterns in hindfoot plantar load distribution. An anterior shift in the center of pressure only occurred after transection of all six ligament complexes. Interpretation: Loss of the plantar fascia and short/long plantar ligaments are not critical in maintaining plantar load distribution or contact area. However, the additional loss of the spring ligament caused notable changes in hindfoot load distribution, indicating the combination of these three ligament complexes is particularly critical for preventing peritalar subluxation. Minimal changes in load distribution occurred when performing additional transections to reach a complete flatfoot deformity.
KW - Adult acquired flat foot
KW - Cadaveric study
KW - Foot biomechanics
KW - Pedobarography
KW - Posterior tibial tendon dysfunction
KW - Progressive collapsing foot deformity
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U2 - 10.1016/j.clinbiomech.2024.106302
DO - 10.1016/j.clinbiomech.2024.106302
M3 - Article
AN - SCOPUS:85199184314
SN - 0268-0033
VL - 118
JO - Clinical Biomechanics
JF - Clinical Biomechanics
M1 - 106302
ER -