Introduction. The arch of the foot has been described as a truss where the plantar fascia (PF) acts as the tensile element. Its role in maintaining the arch has likely been underestimated because it only rarely torn in patients with progressive collapsing foot deformity (PCFD). We hypothesized that elongation of the plantar fascia would be a necessary and sufficient precursor of arch collapse. Method. We used a validated finite element model of the foot reconstructed from CT scan of a female cadaver. Isolated and combined simulated ligament transection models were created for each combination of the ligaments. A collapsed foot model was created by simulated transection of all the arch supporting ligaments and unloading of the posterior tibial tendon. Foot alignment angles, changes in force and displacement within each of the ligaments were compared between the intact, isolated ligament transection, and complete collapse conditions. Result. Isolated release of the PF did not cause deformity, but lead to increased force in the long (142%) and short plantar (156%), deltoid (45%), and spring ligaments (60%). The PF was the structure most able to prevent arch collapse and played a secondary role in preventing hindfoot valgus and forefoot abduction deformities. Arch collapse was associated with substantial attenuation of the spring (strain= 41%) and interosseous talocalcaneal ligaments (strain= 27%), but only a small amount in the plantar fascia (strain= 10%). Conclusion. Isolated PF release did not cause arch collapse, but arch collapse could not occur without at least 10% elongation of the PF. Simulated transection of the PF led to substantial increase in the force in the other arch supporting ligaments, putting the foot at risk of arch collapse over time. Chronic degeneration of the PF leading to plantar fasciitis may be an early sign of impending PCFD

The anatomy of the first metatarsophalangeal (MTP) joint and, in particular, the metatarsosesamoid articulation remains poorly understood. Its effect on sesamoid function and the pathomechanics of this joint have not been described. Fresh frozen cadaveric specimens without evidence of forefoot deformity were dissected to assess the articulating surfaces throughout a normal range of motion. The dissections were digitally reconstructed in various positions of dorsiflexion and plantarflexion using a MicroScribe, enabling quantitative analyses in a virtual 3D environment. In 75% of specimens, there was some degree of chondral loss within the metatarsosesamoid articulation. The metatarsal surface was more commonly affected. These changes most frequently involved the tibial metatarsosesamoid joint. The tibial sesamoid had an average excursion of 14.2 mm in the sagittal plane when the 1st MTP joint was moved from 10 degrees of plantarflexion to 60 degrees of dorsiflexion; the average excursion of the fibular sesamoid was 8.7 mm. The sesamoids also move in a medial to lateral fashion when the joint was dorsiflexed. The excursion of the tibial sesamoid was 2.8 mm when the joint was maximally dorsiflexed while that of the fibular sesamoid was 3.2 mm. There appears to be differential tracking of the hallucal sesamoids. The tibial sesamoid has comparatively increased longitudinal excursion whilst the fibular sesamoid has comparatively greater lateral excursion. This greater excursion of the tibial sesamoid could explain the higher incidence of sesamoiditis in this bone. The differential excursion of the 2 metatarsosesamoid articulations is also a factor that should be considered in the design and mechanics of an effective hallux MTP joint arthroplasty

A cavovarus foot deformity was simulated in cadaver specimens by inserting metallic wedges of 15° and 30° dorsally into the first tarsometatarsal joint. Sensors in the ankle joint recorded static tibiotalar pressure distribution at physiological load.

The peak pressure increased significantly from neutral alignment to the 30° cavus deformity, and the centre of force migrated medially. The anterior migration of the centre of force was significant for both the 15° (repeated measures analysis of variance (ANOVA), p = 0.021) and the 30° (repeated measures ANOVA, p = 0.007) cavus deformity. Differences in ligament laxity did not influence the peak pressure.

These findings support the hypothesis that the cavovarus foot deformity causes an increase in anteromedial ankle joint pressure leading to anteromedial arthrosis in the long term, even in the absence of lateral hindfoot instability.