SYMPOSIUM: CLUBFOOT: ETIOLOGY AND TREATMENT
Update on Clubfoot: Etiology and Treatment
Matthew B. Dobbs MD, Christina A. Gurnett MD, PhD
Published online: 18 February 2009
? The Association of Bone and Joint Surgeons 2009
congenital abnormalities affecting the lower limb, it
remains a challenge not only to understand its genetic
origins but also to provide effective long-term treatment.
This review provides an update on the etiology of clubfoot
as well as current treatment strategies. Understanding the
exact genetic etiology of clubfoot may eventually be
helpful in determining both prognosis and the selection of
appropriate treatment methods in individual patients. The
primary treatment goal is to provide long-term correction
with a foot that is fully functional and pain-free. To achieve
this, a combination of approaches that applies the strengths
of several methods (Ponseti method and French method)
may be needed. Avoidance of extensive soft-tissue release
operations in the primary treatment should be a priority,
Although clubfoot is one of the most common
and the use of surgery for clubfoot correction should be
limited to an ‘‘a la carte’’ mode and only after failed
Level of Evidence: Level V, therapeutic study. See
Guidelines for Authors for a complete description of levels
Congenital talipes equinovarus, also referred to as clubfoot,
occurs in one in 1000 live births  and is one of the most
common birth defects involving the musculoskeletal sys-
tem. Although clubfoot is recognizable at birth, the severity
of the deformity can vary from mild to an extremely rigid
foot that is resistant to manipulation. Two classification
systems are widely used in the initial evaluation of clubfoot
deformities. One of these classification systems was
developed by Dimeglio et al.  and the second by Pirani
. Both systems apply a point score based on a number
of different physical findings, which when totaled lead to a
score that correlates with clubfoot severity. Good correla-
tion between the two systems has been demonstrated .
Idiopathic clubfoot is an isolated deformity of the foot
and leg that is identifiable in utero and consists of four
components: equinus, hindfoot varus, forefoot adductus,
and cavus. When untreated, children with clubfoot walk on
the sides and/or tops of their feet, resulting in callus for-
mation, potential skin and bone infections, inability to wear
standard shoes, and substantial limitations in mobility and
The first aim of this review is to provide the readers with
an overview of what is known regarding the etiology of
clubfoot. Because of recent advances in terms of under-
standing clubfoot on a genetic level, emphasis will be
The authors are supported by NIH NINDS K12 Award (NS01690),
the Children’s Discovery Institute, and March of Dimes Basil
O’Connor Award (CAG); and by the Shriners Hospital for Children,
the Saint Louis Children’s Hospital Foundation, and the Pediatric
Orthopaedic Society of North America (MBD).
Each author certifies that his or her institution has approved the
human protocol for this investigation and that all investigations were
conducted in conformity with ethical principles of research, and that
informed consent for participation in the study was obtained.
M. B. Dobbs (&), C. A. Gurnett
Department of Orthopaedic Surgery, Washington University
School of Medicine, One Children’s Place, Suite 4S60, St. Louis,
MO 63110, USA
M. B. Dobbs
St. Louis Shriners Hospital for Children, St. Louis, MO, USA
C. A. Gurnett
Department of Neurology, Washington University School of
Medicine, St. Louis, MO, USA
Clin Orthop Relat Res (2009) 467:1146–1153
placed on reviewing these advances and discussing the
implications of how a genetic classification could lead to
improved and individualized treatment strategies. The
second aim is to give a historical perspective on the evo-
lution of treatment strategies for clubfoot emphasizing how
predominantly non-surgical strategies have become the
gold standard [18, 43]. The poor long-term results of
extensive soft-tissue release surgery for clubfoot will be
discussed as well as what the role for surgery is in the
modern day treatment of clubfoot.
Clubfoot deformity may be associated with myelodyspla-
sia, arthrogryposis, or multiple congenital abnormalities,
but is most commonly an isolated birth defect and con-
sidered idiopathic . The prevalence of additional
congenital anomalies or chromosomal abnormalities in
patients with clubfoot varies substantially across studies,
depending on the population and ranges from 24% to 50%
[3, 30]. Of the known etiologies for clubfoot, disorders
specifically involving the nervous system comprise the
greatest number. The most common known etiologies are
distal arthrogryposis and myelomeningocele. Given the
vastly different etiologies of this condition, clubfoot likely
represents a final common pathway for disruption any-
where along the neuromuscular unit, including the brain,
spinal cord, nerve, or muscle .
Many theories have been proposed to explain the eti-
ology of idiopathic clubfoot including vascular deficiencies
, environmental factors, in utero positioning ,
abnormal muscle insertions , and genetic factors [28,
30]. While it is becoming more clear that clubfoot is
multifactorial in origin, genetic factors clearly play a role
as suggested by the 33% concordance of identical twins
and the fact that nearly 25% of all cases are familial .
Additional evidence for a genetic etiology is provided by
differences in clubfoot prevalence across ethnic popula-
tions with the lowest prevalence in Chinese (0.39 cases per
1000 live births) and the highest in Hawaiians and Maoris
(seven per 1000) [5, 13]. Though the exact genetic mech-
anism of clubfoot has not yet been determined, a
multifactorial and possibly polygenic causation has been
suggested [44, 75]. Earlier studies using complex segre-
gation analyses suggested a single incompletely dominant
disease gene with unmeasured factors contributing to
incomplete penetrance [56, 71]. In a different study, seg-
regation analysis suggested a recessive mixed model ,
and a complex segregation analysis in Pacific and Maori
people demonstrated a single dominant gene with 33%
penetrance . A polygenic threshold model was also
supported by the finding of the Carter effect, in which
females require a greater genetic load in order to inherit the
disorder than males . However, the physiological cause
of this sex dimorphism, in which males are twice as likely
to be affected as females, is currently unknown.
Environmental factors may play a role in some cases of
clubfoot. Early amniocentesis (\13 weeks gestation) was
associated with an increased risk in talipes equinovarus
compared to midgestational amniocentesis or chorionic
villus sampling . Increased risk of clubfoot was par-
tially associated with amniotic fluid leakage, suggesting
that oligohydramnios occurring at a critical gestational
period may be detrimental to foot development .
However, amniocentesis is an uncommon risk factor
among patients with idiopathic clubfoot. Unlike positional
foot deformities, such as metatarsus adductus, that occur at
increased frequency in twin pregnancies, there are little
data to support an association of clubfoot with late gesta-
tional uterine compression .
Environmental exposure to cigarette smoke in utero is
another independent risk factor for clubfoot. In a study of
over 3000 patients, Honein et al. reported an association of
smoking with clubfoot, with an adjusted odds ratio of
clubfoot of 1.34 for smoking only, 6.52 for family history
only, and 20.30 for combined exposure to smoking and
family history . Variants in genes responsible for the
metabolism of tobacco , seasonal viral infections ,
elevated maternal homocysteine , and methylenetetra-
hydrofolate reductase (MTHFR) gene polymorphisms 
have also been associated with an increased risk of
It is not yet known to what degree clubfoot will result
from the inheritance of common genetic variants (such as
single nucleotide polymorphisms which, by definition, are
present at an allele frequency of[5%) or rare mutations in
susceptibility genes. Using a candidate gene approach,
common genetic variants have been associated with club-
foot including variants in homeodomain transcription
factors HOXD12 and HOXD13 , and several apoptotic
genes including the caspase genes . However, these
genetic variants are all of relatively small effect, contribute
only slightly to an individual’s risk of clubfoot, and will
require replication in larger cohorts to confirm their
importance. Future genome-wide association studies will
provide an unbiased approach to the identification of
clubfoot susceptibility genes and with the use of large
sample sizes, will be able to identify both major and minor
susceptibility genes if they are present.
The importance of genes involved in early limb devel-
opment was recently shown by the identification of a rare
mutation in the transcription factor PITX1 in a large family
with idiopathic clubfoot . PITX1 is the first gene
of the foot, since PITX1 is expressed nearly exclusively in
Volume 467, Number 5, May 2009Update on Clubfoot: Etiology and Treatment1147
the hindlimb and is responsible for rapid evolutionary
changes in pelvic morphology in lower vertebrates .
Specific involvement of the foot also appears to exclude
many of the skeletal muscle contractile genes that are
responsible for distal arthrogryposis [62, 63, 65, 70] in the
causation of idiopathic clubfoot, as mutations in these genes
cause bothupper andlower extremityinvolvement andwere
not identified in idiopathic clubfoot patients .
There is increasing evidence that clubfoot severity and
treatment outcomes may vary by etiology [8, 30]. Thus,
identification of the exact etiology of clubfoot may even-
tually be helpful in determining both prognosis and the
selection of appropriate treatment methods in an individual
Treatment of Clubfoot
Surgeons have struggled over the years to identify the best
method of treatment for the congenital clubfoot deformity.
This struggle has lessened over the last decade as the
Ponseti method of clubfoot manipulation and casting,
Achilles tendon tenotomy, and foot abduction bracing has
become the primary treatment for idiopathic clubfoot
around the world . This is due to both the excellent
short-term results reproduced at multiple centers as well as
the long-term results published from the University of Iowa
using this method [14, 43]. In addition, there is increasing
evidence that extensive surgical releases for clubfoot result
in painful, arthritic feet in adulthood .
Early attempts at primarily nonoperative strategies relied
on forceful manipulations . One of the most notable
devices for forceful clubfoot manipulation was the Thomas
wrench developed by Hugh Owen Thomas (1834–1891)
who studied medicine at Edinburgh and University College,
London . These types of manipulations often resulted in
incomplete corrections as well as iatrogenic deformities. As
a result, Kite in 1939 introduced a more gentle method of
manipulation that primarily involved serial manipulations
and casting [40, 41]. Kite attempted to correct each com-
ponent of the clubfoot deformity separately instead of
simultaneously. Correction of the heel varus was attempted
by abducting the foot at the midtarsal joints and by applying
direct pressure on the calcaneocuboid joint. However, by
abducting the forefoot in this manner, the calcaneus was
actually blocked from adducting under the talus and the heel
varus persisted. Therefore, because of this fundamental flaw
in technique, this method of correction was often quite
lengthy with children being casted for up to 2 years. In
addition, 50% to 75% of patients still required soft tissue
release surgery because of incomplete corrections .
With the introduction of anesthesia and aseptic tech-
niques in the late 1800’s, surgical treatments for clubfoot
were developed. Most of the surgeries involved different
types of soft-tissue release operations but the reported good
results with these techniques were around 45% [24, 50].
During this same time period, surgeons were also experi-
menting with different osteotomy procedures for the
correction of clubfoot but, again, with disappointing results
In the 1970s, extensive soft-tissue release surgery for
clubfoot again became popular in part due to the efforts of
Turco [67, 68]. In his single-stage release procedure,
emphasis was placed on the medial release of the subtalar
joint, ankle and talonavicular joint. Release of the pos-
terolateral aspect of the ankle and subtalar joint was not
performed and, as a result, one of the complications of this
procedure was the development of hindfoot valgus defor-
mity due to lateral translation of the hindfoot. Many
variations of extensive soft tissue release operations were
promoted in the 1980s and 1990s [35, 47, 60]. Even though
extensive soft tissue release operations can provide defin-
itive correction, there are many reported short-term
complications including incomplete corrections, overcor-
rections, as well as neurovascular injuries [2, 73]. The few
long-term followup studies that are available on clubfeet
treated with extensive soft tissue releases illustrate that the
results often deteriorate with time [1, 21, 36, 37]. Reported
long-term complications include stiffness of the ankle and
subtalar joints [21, 37], arthritis [21, 37], muscle weakness
[1, 21, 37], pain [21, 37], and residual deformity [1, 21,
37]. Because of these poor long-term results, intraarticular
soft tissue release surgery as primary treatment for clubfoot
deformity should be avoided.
Ignacio Ponseti developed and refined his treatment
method for clubfoot in the late 1940s. The method was
developed in part as a response to the observation that
patients treated with extensive surgeries for clubfoot often
developed painful feet with residual deformities over time.
Ponseti was convinced there should be a more effective and
less invasive way of correcting clubfoot. As a result, he
studied extensively to better understand the functional and
pathological anatomy of both the normal foot and the
clubfoot. His studies led to the development of the Ponseti
method of clubfoot correction.
The Ponseti method is a specific method of serial
manipulation, casting, and tenotomy of the Achilles tendon
to achieve correction of the clubfoot . Included in the
method is the use of a foot abduction brace to prevent
relapses as well as strategies to treat relapses once they
occur based on age of the child. The importance of com-
munication with the family early in the treatment process
1148 Dobbs and Gurnett Clinical Orthopaedics and Related Research
as to what is involved in terms of casting and brace wear
cannot be overemphasized. Parents need to be aware that
this treatment method lasts for at least 4 years and requires
a serious commitment from the parents to make it
In general, treatment is ideally started within the first
few weeks of life and consists of gentle manipulation of the
foot in an office setting followed by serial application of a
long leg cast as described by Ponseti [43, 54]. Though
Ponseti advocates the use of plaster for the cast material as
it is easier to mold, there are reports on the successful use
of fiberglass materials for achieving clubfoot correction
[15, 53]. Regardless of the casting material used, the casts
are changed every 5 to 7 days . As the Ponseti method
has spread around the world there is increasing experience
and success with the use of this method in children older
than 1 year of age with neglected clubfoot [22, 45, 61, 64].
The upper age limit to which this method can be applied
remains a moving target. In some children older than
15 months of age, serial casting may need to be performed
under sedation because of the difficulty in keeping the child
still enough to apply a good cast .
Although the Ponseti method has traditionally been
applied only to individuals with idiopathic clubfoot, the
Ponseti method is now being used successfully for the
treatment of severe nonidiopathic clubfoot deformities
such as clubfoot occurring with arthrogryposis , mye-
lomeningocele , a host of different genetic syndromes
, as well as neuromuscular disorders [8, 30]. The
method is also being applied to the treatment of complex
clubfeet recently defined by Ponseti  and for clubfeet
that have been previously treated with extensive soft tissue
release surgery but have suffered a relapse .
In all patients, the cavus deformity is corrected first by
supinating the forefoot with direct pressure under the first
metatarsal. The cavus deformity is corrected with a single
cast in most cases. The hindfoot varus, forefoot adduction,
and hindfoot equinus are simultaneously corrected in the
next three to four casts by gently abducting the foot in
supination while counterpressure is applied to the head of
the talus. In most cases, after the fourth clubfoot cast all
deformities are corrected with the exception of some
remaining hindfoot equinus. The foot should be able to be
abducted to 50? at this point and the hindfoot varus should
be corrected. A tenotomy of the Achilles tendon is per-
formed at this point to correct the remaining equinus
contracture. In the author’s experience a tenotomy is
required in over 90% of cases. The tenotomy is performed
in the clinic setting under a local anesthesia for patients
under 1 year of age and under formal sedation in the
operating room for those children over 1 year of age. The
authors prefer to use a topical anesthetic before the tenot-
omy and an injectable local anesthetic only after the
tenotomy is performed. If local anesthetic is injected prior
to the tenotomy, the surgeon may have difficulty palpating
the tendon which makes the risk of damaging the neuro-
vascular bundles more likely . The Achilles tenotomy
is a complete sectioning of the tendon and not a length-
ening procedure. The final long leg cast is applied after the
tenotomy and the foot is positioned in 70? of abduction and
only 5? to 10? of dorsiflexion. One ultrasound study sug-
gests the tendon heals within 3 weeks of casting .
After the final cast is removed, the patient goes directly
into a foot abduction brace to prevent relapse. Many dif-
ferent braces are available today that all share the same
principle with shoes attached to a bar of approximately the
length between the child’s shoulders. Many improvements
have been made based on parental reports of difficulties
with earlier braces. One example is the development of a
dynamic bar that allows independent movement of each leg
rather than a solid bar. The dynamic bar has the potential to
improve patient comfort thus resulting in improved bracing
tolerance [8, 12, 30]. The rotation of the shoes on the bar is
set at around 70? of external rotation for the clubfeet and
around 40? of external rotation for the normal feet. The
brace is worn full time (23 hours a day) for 3 months and
then at sleeping time (12 to 14 hours a day) until the age of
4 years. To improve compliance with brace wear, the
authors have a designated nurse educator who instructs
parents on brace wear and makes followup phone calls
during the first week the child goes into the brace to trou-
bleshoot any problems that may occur [12, 22, 30]. If the
parents are having trouble with the brace, they are brought
back into the clinic for a potential brace adjustment and re-
education. If parents are doing well with the brace, the child
is seen back in clinic 1 month after initiating brace wear and
then at 3-month intervals. The nurse educator also instructs
parents on range-of-motion exercises to be performed on
the ankle and foot several times a day to improve flexibility.
Clubfoot relapses continue to be a problem in caring for
the child with clubfoot. Brace intolerance is the primary
reason for recurrence [10, 22, 49], though it may also occur
with successful brace wear in some patients. Most early
relapses occur in the hindfoot and are clinically evident by
the development of equinus and varus deformities of the
heel. Early relapses can usually be treated with repeat
casting followed by the use of the foot abduction brace. If
there is less than 15? of ankle dorsiflexion after casting,
then a repeat tenotomy of the Achilles tendon may be
needed. Children over 3 years of age who present with
hindfoot varus in combination with a dynamic supination
of the forefoot observed while walking require a different
approach. The varus of the heel and adduction of the foot
are first corrected with serial casting. Once these defor-
mities are corrected a full tibialis anterior tendon transfer to
the third cuneiform is performed. The child is casted for
Volume 467, Number 5, May 2009Update on Clubfoot: Etiology and Treatment1149
6 weeks postoperatively, but there is no need for use of the
foot abduction brace after this procedure. The authors
incorporate formal physical therapy into the postcasting
regime for these patients to help with gait training and
Another popular method of clubfoot treatment that also
avoids extensive surgical treatment is the French or func-
tional method . This method requires daily manipulations
of the newborn clubfoot by a skilled physiotherapist fol-
lowed by immobilization with adhesive taping to maintain
the correction achieved with stretching. The taping holds
the foot in the corrected position but also allows some
motion, unlike the casting used by Ponseti. The French
method also focuses on peroneal muscle strengthening as a
way to maintain long-term correction. A continuous passive
motion machine was added to the treatment regimen in the
1990s to help with further stretching during sleeping hours.
Daily treatments are continued for the first 2 months. The
treatment frequency then decreases to three times a week
until the child is 6 months of age. Once the program is
successful in achieving correction, parents continue both
the home exercises and night splints until the child reaches
The reported success rate with the French method has
varied. Dimeglio et al. in 1996 reported that 74% of
patients were successfully treated with the French method,
without the need for surgical intervention . Others have
reported a much higher need for surgical intervention fol-
lowing application of the French method [57, 69]. Most of
the surgery required was posterior release operations for
residual equinus. Another potential disadvantage of the
French method is the large time commitment for the par-
ents as the children undergo daily formal physical therapy
for 2 months.
Role of Surgery in Clubfoot Correction Today
The use of surgery for primary clubfoot correction today
should be limited to an ‘‘a la carte’’ approach , where
structures are released only as needed to obtain correction
as an adjunct to a more conservative treatment approach.
The vast majority of idiopathic clubfeet should be treated
with casting and a percutaneous Achilles tendon tenotomy
alone . For those resistant idiopathic cases, as well as
some syndromic and neurogenic clubfeet, more extensive
soft tissue releases may be necessary [8, 30] if casting and
bracing are not sufficient. This can usually be limited to a
posterior release operation as the tight medial structures
even in severe clubfeet typically respond to serial casting
. Another indication for surgery in the clubfoot cor-
rection is for recurrent clubfoot deformities that do not
respond to casting alone. Many recurrent deformities, in
both clubfeet that were initially treated with casting 
and clubfeet that were treated initially with extensive soft
tissue release operations, can be corrected with casting
alone or casting followed by limited ‘‘a la carte’’ proce-
dures . The final role for surgery in clubfoot treatment
is for those feet that have been initially treated with
extensive soft tissue release operations and have residual
deformities either from an incomplete correction, an
overcorrection, or from residual muscle imbalance.
Despite the fact that clubfoot is one of the most common
musculoskeletal birth defects there is still much unknown
regarding its etiology and continued controversy regarding
optimal treatment strategies. This purpose of this review
was to provide an update on the recent advances made in
understanding the genetic etiology of clubfoot and explore
what future studies are needed to arrive at a genetic clas-
sification system for this disorder. The second purpose was
to review the history of clubfoot treatment and explain how
the Ponseti method has revolutionized the care of children
with clubfoot around the world.
While multiple theories have been proposed to explain
the etiology of clubfoot [9, 23, 34], it is becoming
increasingly clear that genetic factors play a major role [28,
30]. A recent study points toward a polygenic threshold
model for clubfoot inheritance where multiple genes and
environmental factors will be found to play a role .
Variants in genes responsible for a variety of environmental
factors have been associated with an increase risk of club-
foot [31, 39, 44, 59]. In addition, using a candidate gene
approach, other genetic variants have been associated with
clubfoot including variants in homeodomain transcription
factors HOXD12 and HOXD13 , and several apoptotic
genes including the caspase genes . Of note, however, is
the fact that these genetic variants are all of relatively small
effect, contribute only slightly to an individual’s risk of
clubfoot, and will require replication in larger cohorts to
confirm their importance. The next step in unraveling the
genetic etiology of clubfoot will be a genome-wide asso-
ciation study. This type of study will provide an unbiased
approach to the identification of clubfoot susceptibility
genes and, with the use of large sample sizes, will be able to
identify both major and minor susceptibility genes.
The ideal treatment of clubfoot has been a matter of
debate for hundreds of years. There are historical reports of
both primarily operative and nonoperative strategies
1150 Dobbs and Gurnett Clinical Orthopaedics and Related Research
utilized . In more recent times, Kite introduced his
method of primarily cast correction of clubfoot in the
1940s . His method in most surgeon’s hands resulted in
incomplete corrections and a high rate of surgery for
residual deformities . Turco then popularized a single-
stage extensive soft tissue release operation for clubfoot
correction in the 1970s [67, 68]. While this surgery could
result in initial correction of the clubfoot deformity
reported long-term results were not good with a high rate of
ankle stiffness and arthritis [21, 37]. The French method is
primarily nonoperative and involves daily manipulations
and splinting. Though this method can be successful , it
has been reported to result in a substantial amount of
residual equinus requiring posterior release operations .
Though Ponseti published on his primarily nonoperative
method of clubfoot correction in the 1960s , it did not
become the gold standard until the last 10 years. His
method of treatment has excellent long-term results
reported for idiopathic clubfeet . In addition, his
method is being used with a high rate of success in very
stiff clubfeet associated with distal arthrogryposis ,
myelomeningocele , and a host of different genetic
syndromes and genetic disorders . Success has also
been reported in treating older children with neglected
clubfoot [45, 61] and clubfeet that have relapsed after
initial treatment with extensive soft-tissue release surgery
. There is a report combining the principles of
stretching emphasized in the French method  with the
casting and bracing method of Ponseti . The stretching
exercises are taught to the parents and are performed three
to four times a day while out of the foot abduction brace,
emphasizing dorsiflexion of the ankle. A long-term study is
needed to see if the addition of therapy can reduce the
number of relapses seen with the Ponseti method.
Although current treatment methods appear to be
effective for most patients irrespective of etiology,
knowledge of etiology may be helpful for prognosis, risk of
comorbidities (ie, hip dysplasia), and response to treatment.
Personalized treatment based on etiology may also allow
reduced brace wear if risk of relapse correlates with eti-
ology or genetic profile. The primary treatment goal is to
provide long-term correction with a foot that is fully
functional and pain-free. To achieve this, a combination of
approaches that applies the strengths of several methods
(Ponseti method and French method) may be needed.
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