The arch of the human foot is an important adaptation to our way of walking. Its part-dome transmits forces to and from the ground through relatively limited areas under the calcaneal tuberosity and the metatarsal heads, into the proximal skeleton. The work of Stainsby and Briggs is beginning to unravel the subtle control systems that keep these parts of the foot applied to the ground in many positions of the foot.
The arch provides shock absorption in the early stance phase of gait, and a stiff lever for propulsion forward by the triceps surae in the late stance.
Unlike many arches which are made stable by a locked capstone, the arch of the foot is capped by part of a universal joint, the talonavicular joint, which with the subtalar joint translates between leg and foot rotations. As it does so, it introduces distortions into the arch. Thus the arch of the foot is not entirely stable, but rather flexible with restraints to limit distortion.
Arch stability
The main stabilisers of the arch are:
- The plantar fascia, which stretches from the medial calcaneal tuberosity to the bases of the toes, and across the metatarsal area. By binding the base of the arch together, it limits spreading of the base and, secondarily, collpse of the apex. The plantar fascia is the most important passive stabiliser of the arch Kitaoka 1994).
- The spring ligament (superior and inferior plantar calcaneonavicular ligaments), which limits descent of the talar head. It is continous with…
- The medial talonavicular capsule and superficial deltoid ligament, which limit medial deviation of the talar head
- The interosseous talocalcaneal ligament, which limits descent and medial deviation of the talus
- The long and short plantar ligaments and the plantar ligaments of the individual joint capsules
- The tibialis posterior tendon, inserted primarily into the navicular tuberosity, with slipd into every tarsal bone except the talus. It has little or no function in standing. It fires in early stance, mainly eccentrically, to limit midfoot abduction and provide some support for the spring ligament.
In every gait cycle, these stabilisers are called into action.
At first contact, the arch is raised by tibialis anterior, which dorsiflexes the ankle in swing phase to prevent tripping. This pull also supinates the subtalar joint and adducts the midfoot, drawing the arch into its most stable configuration.
As heel contact is established, the tibia internally rotates, the subtalar joint pronates and the talar head descends and deviates medially. The navicular and the rest of the midfoot abduct, evert and slightly dorsiflex, as do the metatarsals to a slightly lesser extent.
All of these changes have the effect of moving the apex of the arch downwards and medially. Normally, the restraints control talar movement and arch descent.
By midstance the tibia is externally rotating, the subtalar joint is beginning to supinate and the talus rises up the calcaneum and rotates externally. The arch becomes stiffer, to act as a propulsive lever in late stance.
If the restraints are not competent, internal rotation and descent of the talus, with balancing forefoot abduction, may continue beyond its normal phase of the gait cycle. The “temporary flatfoot” of early stance becomes permanent. Initially the foot is late in supinating. Later it may be flattened throughout the stance phase. Propulsion becomes less efficient.
Incompetence of the restraints may be produced by:
- Generalised joint laxity
- Hypermobility syndromes such as Ehlers-Danlos, Marfan’s or Down’s syndromes
- Inflammatory arthritis, especially rheumatoid, in which ligament attachements and joint surfaces are destroyed by pannus
- Degenerative joint disease with instability of the naviculocuneiform or metatarsocuneiform joints. It may be difficult to know whether this is independent of degenerative failure of the arch stabilisers or consequent upon this. However, Suneja’s findings suggest these patients may, to some extent, represent a distinct population within adult acquired flatfoot.
- Muscular imbalance in neurological diseases such as cerebral palsy or myelomeningocoele, when unbalanced muscle activity can overcome the passive restraints
- Degenerative changes in the ligaments and tibialis posterior tendon, which render them less effective in controlling talar movement. A vicious cycle amy then be set up in which restraint weakness leads to more abnormal movement, which in turn stretches the weakened restraints still further.
It is the latter syndrome which is described as adult acquired flatfoot. Since Kettlecamp and Alexander’s paper in 1969, the tibialis posterior abnormalities were emphasised and the syndrome often referred to as “tibialis posterior insufficiency”. More recent work has recognised the abnormalities in other structures. X carried out MRI of adult acquired flatfeet and found that abnormalities of the spring ligament were almost as common as those of tibialis posterior tendon, with the superficial deltoid and ITCL not far behind.
It should be noticed that other structural abnormalities of the arch may cause a lowered arch, sometimes with a normal profile in the coronal plane, sometimes with medial deviation and lowering of the talar head and/or midfoot abduction:
- Congenital vertical talus
- Tarsal coalition
- Charcot arthropathy
- Trauma
- Bony or ligamentous disruption by infection or tumour