Anterior talofibular ligament laxity restricts deep deltoid ligament strain in a cadaveric model of acquired planus 'The deep deltoid paradoxical intact sign'.

Abstract

The Deep Deltoid Ligament (DDL) laxity development and subsequent rupture can occur in pes planus. Anteromedial drawer tests reveal reduced anteromedial anteroposterior (AP) ankle laxity with concurrent anterior talofibular ligament (ATFL) laxity. The paradoxical protection conferred by ATFL laxity to the DDL in progressive collapsing foot deformity (PCFD) warrants further investigation. Investigate the effect of ATFL laxity on DDL laxity development in an experimental flat-foot model. 18 cadaveric feet were assigned to three experimental protocols: (1) control, (2) induced flat-foot, and (3) induced flat-foot with ATFL sectioned. The flat-foot model was induced by sectioning the plantar fascia, spring ligament (SL), and the plantar first tarsometatarsal ligament. Sectioning the SL due to the interconnectedness would result in defunctioning of the superficial deltoid. Positional markers were placed on the medial malleolus, fibula, and talus. Jig-mounted feet underwent 2000 loading cycles. Every 200 cycles, images were taken before and after antero-posterior force application and the markers used to determine anteromedial and anterolateral AP separation, modelled as a linear function of cycle number. In ATFL-intact flat feet, antero-posterior force-induced anteromedial separation and thus DDL laxity increased by 3.45 ± 0.34 mm per 1000 cycles (mean ± SD), whereas in ATFL-sectioned and control feet, this was 0.64 ± 0.59 and 0.59 ± 0.32 mm per 1000 cycles respectively. Minimal cycle-induced change occurred in anterolateral separation in the three conditions. ATFL-sectioned feet had greater antero-posterior force-induced anterolateral separation (9.33 ± 1.42 mm) before cyclic loading than control (1.85 ± 0.85 mm) and ATFL-intact flat feet (1.85 ± 0.31 mm). Sectioning ATFL in experimentally induced flat feet paradoxically reduces anteromedial separation/DDL laxity.