Foot Ankle Clin N Am

8 (2003) 419 – 430

Biomechanics and pathophysiology of f lat foot

Drew H. Van Boerum, MDa,b, Bruce J. Sangeorzan, MDa,b,*
a
Department of Orthopaedics and Sports Medicine, Harborview Medical Center,
P.O. Box 359798, Seattle, WA 98104, USA
b
School of Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA

Many terms have been used to describe the flat foot. Some of the more
common ones are pes planus, planovalgus, calcaneo-valgus, and fallen arches.
The human foot has 26 bones, 10 major extrinsic tendons and their respective
muscles, numerous intrinsic musculotendinous units, and more than 30 joints.
These musculoskeletal structures work together with the neurovascular elements,
fat pads, and skin to provide a mobile, sensate, adaptive foundation during
standing and to provide a means of balance and locomotion during gait. flat foot
describes the common end point of any abnormality that causes the medial
longitudinal arch to collapse. Flatfeet can cause severe symptoms or be asymp-
tomatic. flat foot is now considered a normal variant assuming it functions in its
normal capacity without symptoms.
Children have developmental flat foot. Developmental flat foot has many
causes and may be symptomatic or asymptomatic, flexible or rigid. The cause
may be abnormal bone and joint development like with a tarsal coalition,
a congenital vertical talus, or an accessory navicular bone. Soft tissue of
generalized ligamentous laxity from Marfan’s or Ehlers Danlos can also lead to
a flat foot deformity [1].
Adult flat foot may be categorized as either residual flat foot deformity from a
developmental cause or as an acquired flat foot. Acquired flat foot is associated
with a tight triceps surae or isolated gastrocnemeus tightness, posterior tibial
tendon (PTT) dysfunction, midfoot laxity, abduction of the forefoot, external
rotation of the hindfoot, subluxation of the talus, traumatic deformities, ruptured
plantar fascia, Charcot’s foot, and neuromuscular imbalance (polio, cerebral
palsy, closed head injury, or following a cerebrovascular accident) [1].
It is difficult to define the exact cause of flat foot in every situation
because of the multiple factors, which can contribute to the deformity. To

* Corresponding author. Department of Orthopaedics and Sports Medicine, Harborview Medical

Center, P.O. Box 359798, Seattle, WA 98104.
E-mail address: bsangeor@u.washington.edu (B.J. Sangeorzan).

1083-7515/03/$ – see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S1083-7515(03)00084-6
420 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430

understand the pathologic biomechanics of flat foot it is important to

understand normal foot biomechanics.

Normal foot biomechanics

The normal gait cycle is normally divided into a stance phase and a swing
phase as it affects each limb. The stance phase is the weight-bearing portion of
the cycle and begins at heel-strike and ends at toe-off. It is further subdivided into
three segments: heel-strike, flat foot (mid-stance and terminal stance), and heel-
rise [2].
During the normal gait cycle, weight bearing on the limb begins with the
initial contact of heel-strike. The tibia rotates inwardly and the hindfoot or triple
joint complex (subtalar, talonavicular, and calcaneocuboid) moves into a more
everted or valgus position whereas the tibiotalar or ankle joint plantar flexes [2].
The posterior tibialis muscle acts eccentrically as a shock absorber by controlling
the arch collapse and eversion of the foot [3]. When the calcaneus moves into this
everted position, the cuboid follows which abducts the forefoot and flattens out
the medial longitudinal arch. The ground-reaction force that is associated with
heel-strike changes the contraction of the muscles of the anterior crural com-
partment from concentric to eccentric. This eccentric contraction provides control
and cushioning as the foot approaches the mid-stance or the flat foot phase of gait
by preventing the foot from slapping down at heel-strike [2]. This eccentric
control of the ankle and hindfoot from the anterior and posterior crural muscles
lessens the impact of bearing weight during the transition from heel-strike to flat
foot. During the flat foot mid-stance phase of the gait cycle, the weight centers
over the middle of the foot at the level of the second metatarsal. As the body’s
center of gravity moves forward over the foot and heel-rise is approached, the
tibia outwardly rotates as the ankle dorsiflexes. The hindfoot or triple joint
complex actively inverts and comes to a slight varus position by way of the pull
from the PTT [3]. This locking of the triple joint in a slight varus position creates
a rigid lever out of the medial column by reconstituting the medial longitudinal
arch. The rigid lever is then used for push-off during gait propulsion. This
complex motion and function predisposes the foot to a certain shape, one that has
a partially collapsible medial arch to absorb the impact of bearing weight and an
arch that can be reconstituted to provide rigid lever for efficient propulsion during
ambulation. Form follows function. This allows us to walk, run, jump, climb, and
move over variable terrain. Multiple factors can lead to dysfunction of this
biomechanically elaborate function.
The medial longitudinal arch is composed of the medial column of bones and
their joints connected by strong plantar ligaments, especially the plantar calca-
neonavicular or spring ligament which supports the head of the talus. The bones
of the medial longitudinal arch are the calcaneus and its sustentaculum tali, the
talus, the navicular, the medial, middle and lateral cuneiforms, and the medial
metatarsals, especially the first metatarsal. The plantar ligaments allow mini-
 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430 421

mal stretching and are taut when the arch is loaded. The plantar fascia contributes
significantly to the support of the arch [4]. Huang et al [4] demonstrated in ca-
daveric feet that the plantar fascia contributed the greatest to arch stability
followed by the plantar ligaments and spring ligament. Crary et al [5] showed that
release of the plantar fascia increased the strain in the spring and long plantar
ligaments by 52% and 94%, respectively in a cadaveric foot model. Thordarson
et al [6] showed that the plantar aponeurosis was the most siginificant supporter
of the arch in cadaveric feet with dorsiflexed metatarsal phalangeal joints. The
posterior tibial, flexor hallicus longus, flexor digitorum longus, peroneus longus,
and brevis tendons had lesser supporting roles of the arch. The PTT is the main
tendon that inserts in the midfoot with the exception of some fibers from the
peroneus longus and anterior tibial tendons. The peroneus longus and the tibialis
anterior insert primarily at the base of the first metatarsal, but also have
attachments to the medial cuneiform.
Many studies demonstrated that the PTT is the main dynamic stabilizer of the
arch (see references [3,6,7]) with lesser contributions from the peroneus longus,
flexor digitorum longus, and flexor hallicus longus [6]. Passive supporting
ligaments and fascia, as well as muscles, play important roles in supporting the
medial longitudinal arch [8]. Functionally, the medial longitudinal arch goes from
the weight-bearing portion of the calcaneal tuber up through the sustentaculum
tali and across the subtalar joint into the talus and down through the talar head,
naviculuar, cuneiforms, and first ray through the sesamoids to the ground. The
weight-bearing surface of the tibiotalar joint lies anterior to the weight-bearing
portion of the calcaneal tuber. Thus, the medial arch functions much like an upside
down leaf spring and cushions the impact of weight bearing during walking and
running. The structures that act plantar to the arch (plantar ligaments, PTT,
peroneus longus, plantar fascia) help prevent the arch from collapsing during
increased weight bearing and provide the spring in the arch during gait. Increased
tension from the triceps surae and increased weight across the tibiotalar joint lead to
flattening of the arch [6,9].

Flat foot biomechanics

Triceps surae tension

The triceps surae attaches to the posterior portion of the calcaneal tuber. The
gastrocnemius and soleus muscles make up about two thirds of the posterior calf
muscles. The other one third consists of the posterior tibialis, flexor hallicus
longus, and flexor digitorum longus [2]. The soleus originates from the posterior
portion of the tibia and fibula. The gastrocnemius originates proximal to the
medial and lateral condyles of the posterior femur. Inman et al [2] showed that
with the knee straight, thus increasing the mechanical advantage of the gas-
trocnemius, the ankle flexion moment is increased by about 30%. Flexing the knee
shortens the gastrocnemius so it can no longer exert its maximum tension on the
422 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430

Achilles tendon. Bending the knee to 90° significantly decreases the upward pull
of the Achilles tendon against gravity [2]. Because this is closed system, (ie, the
origins of the triceps are directly or indirectly attached to the tibia), simple
biomechanics shows us that any increase in pull from the Achilles tendon
increases the force across the tibiotalar joint. The tibiotalar joint is posterior to
the center of the longitudinal arch but lies between the main weight-bearing
portions of the foot (ie, the forefoot under the metatarsal heads) and the weight-
bearing portion of the calcaneal tuber. The longitudinal arch spans this distance.
The increase of pull from the triceps and the commensurate increase of force
across the tibiotalar joint shifts the weight bearing toward the forefoot by way of
the medial longitudinal arch. This is not surprising because the insertion of the
Achilles tendon lies posterior to the axis of rotation of the ankle joint; therefore,
any increase in force from the triceps surae will result in a force directed in the
opposite direction anterior to the fulcrum or tibiotalar joint [6]. As this process
proceeds, less weight is borne by the heel and the heel will eventually lift off the
ground. This is exactly what happens during jumping when the heel always leaves
the ground before any other portion of the foot. The same forces apply during
normal gait. The heel-rise portion of the terminal stance phase of gait precedes toe-
off. Just before toe-off, the entire weight is borne under the metatarsal heads with
some under the toes. A stiff or inflexible medial longitudinal arch is necessary for
normal forward propulsion to occur. The force transmission travels by way of the
longitudinal arch and to the metatarsal heads. Any weakening of the arch or its
supporting structures will cause the arch to collapse because of the repetitive loads
and will make the transfer of force less efficient.
During the later portion of stance phase, the body’s center of gravity moves
forward and the knee extends. The triceps surae eccentrically controls the forward
progression (dorsiflexion) of the tibia in mid-stance to terminal stance. As the
knee extends, the gastrocnemius exerts an increasing force on the foot by way of
the Achilles tendon. With a normal PTT, this initiates heel-rise. With a normal
functioning arch this proceeds to toe-off. With PTT dysfunction and a weakened
arch, there is a decrease in the inversion during midstance. This prevents the medial
longitudinal arch from forming a rigid lever arm for efficient gait. The forward
propulsion generated by of the triceps surae acts on the midfoot instead of the
metatarsal heads. This increases midfoot stress leading to more collapse and
abduction [8]. With a collapsed arch, the foot rolls forward like a rocker bottom
and loses the force that is needed for efficient gait.

Midfoot laxity
If the soft tissue supporting structures of the arch are weak or lax then the
normal triceps surae complex could become tighter or shorter to accommodate
the plantarflexed position of the talus and calcaneus because the triceps surae
would not be stretched during gait. If the triceps surae complex is too tight or
short then this increase in force through the normal supporting structures of the
arch will weaken and the midfoot will become lax and begin to collapse. In either
 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430 423

case, the arch collapses and the triceps complex becomes shorter, and, therefore,
tighter. On a weight-bearing lateral radiograph of the foot, the collapse can be
easily seen through either the talonavicular, naviculocuneiform, or tarsal meta-
tarsal joints (Figs. 1 – 3).
If the gastrocnemius or soleus are too tight, too short, or too strong, the arch
can become weaker and collapse. In a cadaveric study, Thordarson et al [6]
showed that the triceps surae had the most significant arch flattening effect in the
sagittal plane. The triceps surae also contributes significantly to abduction of the
forefoot in the transverse plane [6,10].

Forefoot displacement
As the arch collapses, the normal curve of the arch becomes straighter, and,
therefore, functionally longer. As the arch collapses, the talus plantar flexes, the
calcaneus subluxates posteriorly, and the anterior process of the calcaneus no
longer supports the talar head. To accommodate this change in foot posture, the
midfoot and forefoot subluxate dorsally and laterally around the talus. This
happens because the lateral column cannot flatten out for commensurate
lengthening. Were the lateral column able to accommodate this deformity,
primarily of the medial column, the foot would not drift laterally and the forefoot
would not be abducted. With this in mind, Evans [11] advocated lengthening of
the lateral column through the anterior process of the calcaneus, whereas others
reported results on lengthening the lateral column with the use of a distraction
arthrodesis of the calcaneocuboid joint [12]. The progressive deformity that is
seen when the midfoot and forefoot pivot dorsally and laterally around the head
of the talus is termed dorsilateral peritalar subluxation [13].

Posterior tibial tendon

The dorsilateral displacement of the navicular and midfoot puts excessive
stress on the normal PTT because the PTT is the strongest tendon that inserts on
the midfoot and counteracts the collapse of the arch and abduction of the midfoot
or forefoot [6]. Chronic stress on the PTT from a flexible flat foot and a tight
Achilles tendon could lead to a chronic overuse injury leading to microtrauma
and degeneration of the PTT [8]. This excessive strain on the PTT from the
powerful arch-flattening effect of the triceps surae [6] can lead to PTT tendonosis
and eventual rupture [8]. Mosier et al [8] showed in a histologic study that PTT
dysfunction is not a result of acute or chronic tendonitis because there is no
histologic evidence of an inflammatory response. They did demostrate histo-
pathologic evidence of mucinous degeneration, fibroblast hypercellularity, chon-
droid metaplasia, and neovascularization. These findings support a degenerative
tendinosis with a nonspecific repair response to tissue injury. It is unclear whether
this precedes or postdates the PTT dysfunction [8]. Weakening of the PTT from
tendonosis or rupture will lead to progressive dorsilateral peritalar subluxation
and collapse of the normal arch. Niki et al [14] examined the role of the PTT in
424 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430

Fig. 1. (A) Anterioposterior (AP) radiograph of a 63-year-old woman showing abduction primarily
through the talonavicular joint. (B) Lateral radiograph demonstrating collapse almost exclusively
through the talonavicular joint.
 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430 425

Fig. 2. (A) AP radiograph of a 61-year-old male showing abduction primarily through the talonavicular
joint. (B) Lateral radiograph of the same man demonstrating collapse primarily through the navicu-
locuneiform joint.
426 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430

Fig. 3. (A) AP radiograph showing the foot of a 66-year-old nondiabetic man with a normal neurologic
examination with abduction primarily through the tarsometatarsal joints. (B) Lateral radiograph of the
same man demonstrating collapse primarily through the tarsometatarsal joints.
 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430 427

arch dysfunction and collapse. They showed that directional changes of the
hindfoot bones, as a result of releasing the PTT, were consistent with those of
acquired flat foot deformity; however, the magnitude of change was much
smaller. This supports the theory that gradual attenuation of the plantar ligaments
over time from ambulation on an unlocked valgus hindfoot leads to adult
acquired flat foot deformity. They also demonstrated that acute restoration of
PTT function had little effect on overcoming the soft tissue laxity that ensues
from gradual attrition of the static plantar stabilizers. Adult acquired flat foot is
too complex to be classified as a simply different stage of PTT dysfunction.

Calcaneal drift
The medial and lateral constraints of the normal intact ankle prevent the talus
from assuming either a varus or valguS compensatory position. As the flat foot
deformity progresses and the medial column collapses, the talus plantar flexes in
relation to the tibia and the angle between the talus and the first metatarsal
assumes an increasing apex plantar position (Figs. 4, 5). The apex of the
deformity can be at the talonavicular, naviculocuneiform, or tarsal metatarsal
joints (see Figs.1 – 3). As the talus plantar flexes with respect to the calcaneus,
the calcaneonavicular ligament or spring ligament lengthens or ruptures. As the
head of the talus drops plantarward, the calcaneus drifts laterally and posteriorly.

Fig. 4. Lateral views of wire-mesh models of the talus and first metatarsal from the weight-bearing CT
scans of a normal patient (top) and a patient with a painful fallen arch (bottom). Note the difference in
the talar-first metatarsal angle.
428 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430

Fig. 5. AP views of wire-mesh models of the talus and first metatarsal from the same weight-bearing
CT scans of a normal patent (left) and one with acquired flat foot deformity (right). Note the difference
in the talar-first metatarsal angle.

The cuboid follows the calcaneus and the forefoot follows the cuboid thus
abducting the forefoot. As the abduction deformity increases, the angle between
the talus and the first metatarsal progresses to an increasing apex medial position
(see Figs. 4, 5). As the medial arch collapses, it lengthens. This increase in length
is tethered by the fixed lengths of the lateral column and the plantar fascia.
Therefore, the forefoot abducts toward the lateral column. The abduction of the
forefoot and the collapse of the medial longitudinal arch can occur through the
talonavicular, naviculocuneiform, or tarsalmetatarsal joints. Sometimes, most of
the longitudinal collapse occurs through the naviculocuneiform joint, whereas the
most of the abduction occurs through the talonavicular joint (see Figs. 1 –3).
When the posterior facet of the talus bottoms out and impinges in the sinus
tarsi, the medial arch is completely collapsed. Degenerative changes can ensue in
the subtalar, talonavicular, and other involved joints of the midfoot [15]. Over
 D.H. Van Boerum, B.J. Sangeorzan / Foot Ankle Clin N Am 8 (2003) 419–430 429

time the deformity can become fixed. This can put undue pressure on the ankle
joint and degenerative changes can develop. Beals et al [16] classified these
degenerative changes in the ankle as stage IV PTT dysfunction.

Summary
When the foot works properly it is an amazing, adaptive, powerful aid during
walking, running, jumping, and in locomotion up or down hill and over uneven
ground. Dysfunction of the foot can often arise from the foot losing its normal
structural support, thus altering is shape. An imbalance in the forces that tend to
flatten the arch and those that support the arch can lead to loss of the medial
longitudinal arch. An increase in the arch-flattening effects of the triceps surae or
an increase in the weight of the body will tend to flatten the arch [6,9]. Weakness
of the muscular, ligamentous, or bony arch supporting structures will lead to
collapse of the arch (see references [6– 8,10,14]). The main factors that contribute
to an acquired flat foot deformity are excessive tension in the triceps surae [6,9],
obesity, PTT dysfunction [6,8], or ligamentous laxity in the spring ligament,
plantar fascia, or other supporting plantar ligaments. Too little support for the
arch or too much arch flattening effect will lead to collapse of the arch. Acquired
flat foot most often arises from a combination of too much force flattening the
arch in the face of too little support for the arch.
Treatment of the adult acquired flat foot is often difficult. The clinician should
remember the biomechanics of the normal arch and respond with a treatment that
strengthens the supporting structures of the arch or weakens the arch-flattening
effects on the arch. After osteotomies or certain hindfoot fusions, the role of the
supporting muscles of the arch, in particular the PTT, play less of a role in
supporting the arch [17]. Rebalancing the forces that act on the arch can improve
function and lessen the chance for further or subsequent development of deformity.

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