Anatomic and Biomechanical

Considerations of Flatfoot
Deformity
Michael H. Theodoulou, DPM, Madison Ravine, DPM*

KEYWORDS
 Pes planus  Flat foot  Collapsed foot  Posterior tibial tendon dysfunction
 Spring ligament  Equinus

KEY POINTS
 Anatomy of pediatric/adolescent versus adult.
 Static versus dynamic anatomy.
 Anatomy in the progression of the disease.
 Pathomechanics related to anatomic change.

INTRODUCTION

Pes planus, also known as pes planovalgus or colloquially termed flat foot or fallen
arches, comprises a spectrum of deformities with many possible causes. This postural
presentation may be developmental, such as a congenital pediatric flat foot, or ac-
quired, as is the adult case acquired flat foot deformity. In simplistic terms, the flat
foot deformity describes the common end-point of any abnormality that causes the
medial longitudinal arch to collapse.1 In its continuum, individuals may have symptom-
atic deformity from congenital pes planus deformity, which was previously asymptom-
atic. However, symptoms may progress to an adult acquired pes planus deformity,
which results in the failure of various ligaments and tendons. As the degree of defor-
mity progresses along a spectrum so does the clinical significance. This deformity may
be relatively asymptomatic or lead to profound symptoms and dysfunction. Although
some patients may compensate adequately to address the symptoms, others develop
symptoms that are functionally debilitating. The most common subset of this defor-
mity is adult acquired flat foot due to posterior tibial tendon dysfunction. The following
article aims to provide a comprehensive review of flatfoot deformity, with a focus on

Cambridge Health Alliance, Harvard Medical School, 1493 Cambride Street, Cambridge, MA
02139, USA
* Corresponding author.
E-mail address: [email protected]

Clin Podiatr Med Surg 40 (2023) 239–246

https://doi.org/10.1016/j.cpm.2022.11.001 podiatric.theclinics.com
0891-8422/23/ª 2022 Elsevier Inc. All rights reserved.

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
240 Theodoulou & Ravine

up-to-date anatomic and biomechanical considerations involved in the management

of this deformity.

A REVIEW OF FUNCTIONAL ANATOMY

Three identified arches contribute to the inherent stability of the foot: the medial lon-
gitudinal arch, lateral longitudinal arch, and transverse arch. The medial longitudinal
arch is composed of the bones and joints of the medial column, connected by strong
plantar ligaments, namely the plantar calcaneonavicular or spring ligament.1 The
lateral longitudinal arch is composed of the lateral column, whereas the transverse
arch runs transversely across the foot at the tarsometatarsal region of the foot.2
Although in a flat foot deformity, the medial longitudinal arch is generally unstable,
leading to flattening or collapse, it is essential to understand that all 3 arches of the
foot are interconnected. The failure at 1 arch will inevitably lead to structural compro-
mise at the other arches. Although the skeletal pedal architecture contributes to the
overall stability of the foot, the extrinsic and intrinsic muscular and ligamentous struc-
tures are critical to maintaining this arch. We can further separate these components
into static versus dynamic stabilizers, as discussed below and summarized in Table 1.

Dynamic Stabilizers
One of the most critical dynamic stabilizers of the hindfoot and medial column is the
tibialis posterior tendon. Originating from the proximal tibia, fibula, and interosseous
membrane, the tendon forms within the deep posterior compartment and passes pos-
terior to the medial malleolus. It then trifurcates into its primary insertion along the
navicular tuberosity and medial cuneiform. It also broadly and extensively inserts
along the plantar aspect of the foot, across metatarsals 2 through 4, all 3 cuneiforms,
the sustentaculum tali, and the cuboid, which further contributes to the extensive liga-
mentous support of the arch.3,4 This tendon passes medial to the subtalar joint axis,
thereby functioning as a supinatory force: inverting the subtalar joint, stabilizing the
medial longitudinal arch, and plantarflexing the ankle joint. It serves throughout the
gait cycle, decelerating subtalar joint pronation, preventing excess hindfoot eversion
at heel contact, accelerating subtalar joint supination at midstance, and locking the
midtarsal joint.5 It also decelerates the lower leg’s internal rotation.3
There are other extrinsic musculatures that provide dynamic support to the arch.
Flexor digitorum longus also passes on the supinatory side of the subtalar joint axis.
It spans the entire length of the plantar foot, inserting on the distal phalanges of the
lesser digits. As the leg rotates during gait, tension generates on this tendon, which

Table 1
Anatomic summary, stratified by dynamic versus static stabilizers as they function across the
medial longitudinal arch

Stabilization Class Structure

Dynamic Tibialis posterior
Flexor digitorum longus
Peroneus longus
Tibialis anterior
Peroneus brevis
Static Spring ligament
Deltoid ligament
Dynamic and Static Plantar fascia
Plantar intrinsics

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
 Biomechanical Considerations of Flatfoot Deformity 241

contracts and supports the arch.3 Furthermore, peroneus longus works to support the
arch via plantarflexion of the first ray. As the tendon courses around the lateral malleo-
lus, this creates a pulley mechanism through midstance into heel off, stabilizing the arch.
An assessment of functional anatomy would not be complete without mention of the
appropriate muscular antagonists. The tibialis anterior, the antagonist to the peroneus
longus, works to dorsiflex the first ray and also has a supinatory moment about the
subtalar joint axis.3 Peroneus brevis, the antagonist to the tibialis posterior, everts
the subtalar joint and has a pronatory moment about the subtalar joint axis.3

Static Stabilizers
Although the extrinsic musculature provides necessary dynamic stabilization of the
arch, there are static soft tissue stabilizers that work in concert to reinforce and main-
tain this arch. Because the posterior tibial tendon is the principal dynamic stabilizer,
the spring ligament (or plantar calcaneonavicular ligament) is the primary static stabi-
lizer of the medial longitudinal arch.2,3,5 This ligament consists of the superomedial,
medioplantar oblique, and inferoplantar longitudinal bundles (listed from medial to
lateral). The superomedial bundle is the largest and most important of the three. It orig-
inates from the sustentaculum tali, passing below the talus, and finally inserts into the
distal medial aspect of the navicular. This structure forms hammock-like support for
the talar head, supporting the talonavicular joint.2
Forming a soft tissue confluence with the spring ligament and posterior tibial tendon
is the deltoid ligament. This confluence works to prevent excessive talar head
descent.2 The deltoid ligament is further separated into deep and superficial compo-
nents. The deep deltoid ligament stabilizes the tibiotalar articulation, resisting ankle
valgus. The superficial deltoid ligament spans the subtalar and tibionavicular joints,
limiting hindfoot eversion and medial talar head displacement.2
Other specific structures act as both dynamic and static stabilizers. The plantar fas-
cia is considered both a static and dynamic stabilizer of the longitudinal arch. It orig-
inates from the tuberosity of the calcaneus and is composed of medial, central, and
lateral bands spanning the entire length of the foot and inserting into the proximal pha-
langes. In a static sense, it prevents elongation of the plantar foot—much like a tie rod
holding the anterior strut (lesser tarsus and metatarsals) and posterior strut (talus and
calcaneus) together. As a dynamic stabilizer, it functions in the Windlass mechanism
during the end of late stance. As the digits dorsiflex and the heel begins to leave the
ground, the plantar fascia tenses, drawing the calcaneus and metatarsal heads toward
one another to maintain the height of the medial longitudinal arch.2,4 Although the
plantar intrinsic musculature’s role in stabilization is ill-defined, Basmajian and Stecko
demonstrated through electromyographic studies that the intrinsic musculature is
increasingly active in the static phase of gait in a pes planus foot as compared with
a rectus foot.3,6 Further hypotheses include that the intrinsics may work to sense
deformation and provide local stabilization.2 Other authors have hypothesized that
the inherent orientation of the musculature, parallel to the long axis of the foot, pro-
vides support to the arch with contraction throughout gait.3,5

DEVELOPMENTAL CONSIDERATIONS

It is important to recall that flatfoot deformity may be congenital or acquired. Although

there exists a period of skeletal development in which a certain degree of flatfoot is a
normal finding. This postural presentation usually spontaneously resolves by ages 3 to
6 years, with the development of the pedal arches.2 When this persists past the above-
defined developmental period, it may be more characteristic of a congenital flatfoot

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
242 Theodoulou & Ravine

deformity. In the congential deformity, specific malformations such as congenital cal-

caneovalgus or congenital convex pes valgus, also known as vertical talus, may result
in flexible and rigid flatfoot deformities.
There are many potential causes for pediatric flatfoot deformity whether congenital
or acquired. This deformity may result from collagen disorders leading to ligamentous
laxity, muscle-tendon imbalances, central and peripheral nerve pathologic condition,
or even trauma. These may be due to congenital deformities, including the tarsal coa-
lition, although this is typically asymptomatic until later in childhood or adolescence.7,8
From a structural perspective, this may result from faulty biomechanical alignment of
the lower extremity as the principal cause for a compensatory deformity of the foot.
Suprapedal reasons include femoral anteversion, internal genicular position, internal
tibial torsion, or equinus. Intrapedal causes for this may consist of forefoot varus lead-
ing to compensatory pronation of the subtalar joint, flexible forefoot valgus, or meta-
tarsus adductus to name a few.3,7
It is difficult to predict which of these pediatric flatfeet will progress to the symptom-
atic pes planovalgus condition in the adult.3 Literature reports that only approximately
7% to 15% of those with developmental flatfoot will eventually develop symptoms as
adults that lead them to seek medical attention.2,9 Regardless, a thorough under-
standing of the developmental flatfoot is essential to distinguish the pathophysiology
from the adult acquired flatfoot.

DETAILED DEVELOPMENT OF PATHOPHYSIOLOGY

The adult acquired flat foot deformity is the most common subset of pes planus defor-
mity, with a reported incidence of greater than 3% in women aged older than 40 years
and greater than 10% in all adults aged older than 65 years.8,10,11 As previously
mentioned, the posterior tibial tendon is the principal stabilizer of the medial longitu-
dinal arch. Therefore, tendinopathy or dysfunction of this tendon is the most common
cause of adult-acquired flatfoot. There is recognition of 4 stages of adult-acquired flat-
foot. The classification was initially described in the 1980s by Johnson and Strom, later
modified by Myerson to include Stage 4, and Stage 2 was further subdivided by
Deland and colleagues.10,12–16

Stage 1
Stage 1 is characterized by posterior tibial tendon tenosynovitis or tendinosis in its
mildest form, rather than frank degeneration of the tendon. The posterior tibial tendon
is still intact with maintained motor function, able to invert the heel with the heel raise
test. In this stage, pain or tenderness presents throughout the tendon; however, at this
point, the length of the tendon is normal, and there may be minimal degeneration pre-
sent. There may be mild weakness and minimal, flexible deformity appreciated as well.
As such, treatment is generally conservative.15

Stage 2
As the pathologic condition advances, dysfunction and degeneration of the posterior
tibial tendon progress, thereby leading to evident deformity and functional abnormal-
ities. The posterior tibial tendon may be elongated or torn, and patients may or may not
be able to perform a heel raise test on the affected side. Because the posterior tibial
tendon degenerates and attenuates, its ability to actively invert the subtalar joint is
weakened, compromising the ability to lock the midtarsal joint. Peroneus brevis, the
muscular antagonist to the tibialis posterior, gains a mechanical advantage over the
compromised posterior tibial tendon. This antagonism leads to eversion of the

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
 Biomechanical Considerations of Flatfoot Deformity 243

subtalar joint, midfoot pronation, and forefoot abduction at the transverse tarsal joint.
The medial longitudinal arch further collapses as the heel begins to assume a valgus
position and the forefoot abducts at the talonavicular joint.15 There is a varying degree
of forefoot supination resulting from an accommodation of the foot, permitting the
medial and lateral column to remain in contact with the ground. At the same time,
the hindfoot is in a valgus position. This medial instability will lead to sinus tarsi pain
associated with subtalar impingement as the disease progresses.14,15 With the talus
now unsupported and plantarflexed and the dynamic stabilizers compromised, the
spring ligament then undergoes a secondary attenuation. Furthermore, once the
heel becomes lateralized and assumes a more valgus position, the pull of the triceps
surae complex is also lateralized and begins to evert the calcaneus because it de-
velops a pronatory moment across the subtalar joint axis.15 This increased pronation
is accentuated in underlying equinus deformity as well. It is essential to note the defor-
mation remains supple and manually reducible on the physical examination at this
point; however, standard weight-bearing radiographs will demonstrate a structural
deformity.
In 2006, Deland and colleagues subdivided stage 2 into stage 2A and stage 2B.
Stage 2A was described as increased heel valgus but minimal abduction through
the midfoot as determined by clinical and radiographic examination. In contrast,
stage 2B was described as increased heel valgus with greater than 30% uncovering
of the talonavicular head as seen on weight-bearing anteroposterior radiographs of
the foot.16 Deland and colleagues noted that due to this distinction, stage 2A might
benefit from the medial calcaneal slide procedure, whereas stage 2B may benefit
from lateral column lengthening as well.16 Operative treatment in this stage generally
depends on the severity of the deformity seen. Commonly joint-sparing procedures
are used. Depending on the amount of pathologic condition to the posterior tibial
tendon, an adjunct tendon transfer may be performed, most commonly, transfer of
the flexor digitorum longus tendon to the navicular tuberosity. Further, depending
on the degree of forefoot supinatus, a medial cuneiform opening wedge may be
used.14

Stage 3
A Stage 3 deformity signifies a more rigid deformity, which generally develops as a
function of time. At this point, the deformation is no longer flexible and manually reduc-
ible. There is commonly complete disruption of the posterior tibial tendon. The static
stabilizers, namely the spring ligament, are attenuated or even disrupted at this point.
The hindfoot is in a fixed valgus position, with the forefoot abducted. Pain is generally
due to degenerative changes at the triple joint complex (talonavicular, calcaneocu-
boid, subtalar joint). Patients may begin to develop secondary pain laterally, near
the sinus tarsi or subfibular region due to impingement because the foot is rigidly
valgus. In this presentation, joint destructive procedures, including double or triple
arthrodesis, are frequently used. A Stage 3 deformity is demonstrated in Fig. 1.

Stage 4
The final most severe stage of deformity is characterized by valgus angulation and
talar tilt of the ankle joint with associated deltoid ligament insufficiency. This malalign-
ment may lead to early degeneration of the ankle joint.15 In nonpathological functional
anatomy, the deltoid ligament provides significant stabilization to the medial aspect of
the tibiotalocalcaneal joint complex; however, because the deformity progresses, this
becomes attenuated valgus malalignment. Damage to the deltoid ligament is usually
limited to the superficial component. However, damage to the deep ligaments can be

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
244 Theodoulou & Ravine

Fig. 1. Clinical images of a Stage 3 adult acquired pes planovalgus deformity demonstrating
hindfoot valgus and complete collapse of the medial longitudinal arch.

Fig. 2. Radiographic images of a Stage 4 adult acquired pes planovalgus deformity demon-
strating ankle valgus and degenerative changes at the ankle joint.

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
 Biomechanical Considerations of Flatfoot Deformity 245

seen in the late process.2 This stage is further subdivided into a flexible ankle defor-
mity with minimal arthritic changes versus advanced, rigid, and degenerative. A severe
Stage 4 deformity is seen in Fig. 2. The early deformity may be amenable to deltoid
ligament reconstruction with a triple arthrodesis. However, treatment is complex in
a fixed ankle valgus deformity and may be limited to a tibiotalocalcaneal fusion versus
total ankle arthroplasty with an implant.14

CLINICAL CARE POINTS

 The anatomy of the pediatric and adult flatfoot deformity are important in understanding its
biomechanics and pathology of deformity.
 As the pathology progresses, it is important to distinguish between the static and dynamic
contributors of the flatfoot deformity.
 As the flatfoot deformity, it is important to understand the anatomic changes as it relates to
the pathomechanics.

SUMMARY

The appreciation of pathoanatomy as it presents in pediatric/adolescent and acquired

collapsed foot remains crucial in understanding the disease process and its progres-
sion through secondary pathomechanics. The reader can enjoy a more significant
experience of used diagnostic and treatment measures in its management with this
understanding.

REFERENCES

1. Van Boerum DH, Sangeorzan BJ. Biomechanics and pathophysiology of flat foot.
Foot Ankle Clin N Am 2003;8:419–30.
2. Flores DV, Gomez CM, Davis MA, et al. Adult acquired flatfoot deformity: anat-
omy, biomechanics, staging, and imaging findings. Radiographics 2019;39(5):
1437–60.
3. Mahan KT, Flanigan KP. Chapter 44: flexible valgus deformity. McGlamry’s
comprehensive textbook of foot and ankle surgery. 4th edition. Philadelphia: Lip-
pincott Williams & Wilkins; 2012. p. 585–97.
4. Lever CJ, Hennessy MS. Adult flat foot deformity. J Orthop Trauma 2016;30(1):
41–50.
5. Catanzariti AR, Mendicino RW, Maskill MP. Chapter 46: posterior tibial tendon
dysfunction. McGlamry’s comprehensive textbook of foot and ankle surgery.
4th edition. Philadelphia: Lippincott Williams & Wilkins; 2012. p. 636–69.
6. Basmajian JV, Stecko G. The role of muscles in arch support of the foot. J Bone
Joint Surg Am 1963;45:1184–90.
7. Rodriguez N, Volpe RG. Clinical diagnosis and assessment of the pediatric pes
planovalgus deformity. Clin Podiatr Med Surg 2010;27:43–58.
8. Cowell HR, Elener V. Rigid painful flatfoot secondary to tarsal coalition. Clin Or-
thop Relat Res 1983;177:54–60.
9. Ling SKK, Lui TH. Posterior tibial tendon dysfunction: an overview. Open Orthop J
2017;11:714–23.
10. Henry JK, Shakked R, Ellis SJ. Adult-acquired flatfoot deformity. Foot Ankle Int
2019;4(1):1–17.

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.
246 Theodoulou & Ravine

11. Kohls-Gatzoulis J, Woods B, Angel JC, et al. The prevalence of symptomatic pos-
terior tibialis tendon dysfunction in women over the age of 40 in England. Foot
Ankle Surg 2009;15:75–81.
12. Johnson KA. Tibialis posterior tendon rupture. Clin Orthop Relat Res 1983;177:
140–7.
13. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Relat
Res 1989;14(239):196–206.
14. Bluman EM, Title CI, Myerson MS. Posterior tibial tendon rupture: a refined clas-
sification system. Foot Ankle Clin N Am 2007;12:233–49.
15. Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the
posterior tibial tendon. J Bone Joint Surg Am 1996;78-A(5):780–92.
16. Deland JT, Page A, Sung IH, et al. Posterior tibial tendon insufficiency results at
different stages. HSS J 2006;2:157–60.

Downloaded for Anonymous User (n/a) at Gadjah Mada University from ClinicalKey.com by Elsevier on September 09,
2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.