The aetiology of congenital club foot is unclear. Although studies on populations, families and twins suggest a genetic component, the mode of inheritance does not comply with distinctive patterns. The Odense-based Danish Twin Registry contains data on all 73 000 twin pairs born in Denmark over the last 130 years. In 2002 all 46 418 twins born between 1931 and 1982 received a 17-page questionnaire, one question of which was ‘Were you born with club foot?’ A total of 94 twins answered ‘Yes’, giving an overall self-reported prevalence of congenital club foot of 0.0027 (95% confidence interval (CI) 0.0022 to 0.0034). We identified 55 complete twin pairs, representing 12 monozygotic, 22 dizygotic same sex (DZ. ss. ), 18 dizygotic other sex (DZ. os. ) and three unclassified. Two monozygotic and 2 DZ. ss. pairs were concordant. The pairwise concordance was 0.17 (95% CI 0.02 to 0.48) for monozygotic, 0.09 (95% CI 0.01 to 0.32) for DZ. ss. and 0.05 (95% CI 0.006 to 0.18) for all dizygotic (DZ. tot. ) twins. We have found evidence of a genetic component in congenital club foot, although non-genetic factors must play a predominant role

Aims. To assess if older symptomatic children with club foot deformity differ in perceived disability and foot function during gait, depending on initial treatment with Ponseti or surgery, compared to a control group. Second aim was to investigate correlations between foot function during gait and perceived disability in this population. Methods. In all, 73 children with idiopathic club foot were included: 31 children treated with the Ponseti method (mean age 8.3 years; 24 male; 20 bilaterally affected, 13 left and 18 right sides analyzed), and 42 treated with primary surgical correction (mean age 11.6 years; 28 male; 23 bilaterally affected, 18 left and 24 right sides analyzed). Foot function data was collected during walking gait and included Oxford Foot Model kinematics (Foot Profile Score and the range of movement and average position of each part of the foot) and plantar pressure (peak pressure in five areas of the foot). Oxford Ankle Foot Questionnaire, Disease Specific Index for club foot, Paediatric Quality of Life Inventory 4.0 were also collected. The gait data were compared between the two club foot groups and compared to control data. The gait data were also correlated with the data extracted from the questionnaires. Results. Our findings suggest that symptomatic children with club foot deformity present with similar degrees of gait deviations and perceived disability regardless of whether they had previously been treated with the Ponseti Method or surgery. The presence of sagittal and coronal plane hindfoot deformity and coronal plane forefoot deformity were associated with higher levels of perceived disability, regardless of their initial treatment. Conclusion. This is the first paper to compare outcomes between Ponseti and surgery in a symptomatic older club foot population seeking further treatment. It is also the first paper to correlate foot function during gait and perceived disability to establish a link between deformity and subjective outcomes. Cite this article: Bone Joint Open 2020;1-7:384–391

The Ponseti method of treating club foot has been shown to be effective in children up to two years of age. However, it is not known whether it is successful in older children. We retrospectively reviewed 17 children (24 feet) with congenital idiopathic club foot who presented after walking age and had undergone no previous treatment. All were treated by the method described by Ponseti, with minor modifications. The mean age at presentation was 3.9 years (1.2 to 9.0) and the mean follow-up was for 3.1 years (2.1 to 5.6). The mean time of immobilisation in a cast was 3.9 months (1.5 to 6.0). A painless plantigrade foot was obtained in 16 feet without the need for extensive soft-tissue release and/or bony procedures. Four patients (7 feet) had recurrent equinus which required a second tenotomy. Failure was observed in five patients (8 feet) who required a posterior release for full correction of the equinus deformity. We conclude that the Ponseti method is a safe, effective and low-cost treatment for neglected idiopathic club foot presenting after walking age

We have compared the density of nerve fibres in the synovium in club foot with that of specimens obtained from the synovium of the hip at operations for developmental dysplasia. The study focused on the sensory neuropeptides substance P; calcitonin gene-related peptide; protein gene product 9.5, a general marker for mature peripheral nerve fibres; and growth associated protein 43, a neuronal marker for new or regenerating nerve fibres. In order to establish whether there might be any inherent difference we analysed the density of calcitonin gene-related peptide-positive nerve fibres in the hip and ankle joints in young rats. Semi-quantitative analysis showed a significant reduction in the number of sensory and mature nerve fibres in the synovium in club foot compared with the control hips. Calcitonin gene-related peptide (CGRP) positive fibres were reduced by 28%, substance P-positive fibres by 36% and protein gene product 9.5-positive fibres by 52% in club foot. The growth associated protein 43-positive fibres also seemed to be less in six samples of club foot. No difference in the density of CGRP-positive nerve fibres was observed in the synovium between ankle and hip joints in rats. The lack of sensory input may be responsible for the fibrosis and soft-tissue contractures associated with idiopathic club foot

Continuous passive motion has been shown to be effective in the conservative treatment of idiopathic club foot. We wished to determine whether its use after operation could improve the results in resistant club feet which required an extensive soft-tissue release. There were 50 feet in the study. Posteromedial lateral release was performed in 39 feet but two were excluded due to early relapse. The mean age at surgery was eight months (5 to 12). Each foot was assigned a Dimeglio club foot score, which was used as a primary outcome measure, before operation and at 6, 12, 18 and 44 months after. Nineteen feet were randomly selected to receive continuous passive motion and 18 had standard immobilisation in a cast. After surgery and subsequent immobilisation in a cast the Dimeglio club foot score improved from 10.3 before to 4.17 by 12 months and to 3.89 at 48 months. After operation followed by continuous passive motion the score improved from 9.68 before to 3.11 after 12 months, but deteriorated to 4.47 at 48 months. Analysis of variance adjusted for baseline values indicated a significantly better score in those having continuous passive motion up to one year after surgery, but after 18 and 48 months the outcomes were the same in both groups

Most cases of club foot (congenital talipes equinovarus) respond to non-operative treatment but resistant cases may need surgery. It is broadly accepted that lengthening of tendo Achillis, the tendon of tibialis posterior and capsulotomy of the ankle and subtalar joints are necessary during surgical release, but there is no consensus as to whether lengthening of the tendons of flexor hallucis longus and flexor digitorum longus is required. We randomised 13 children with severe bilateral club foot deformities to undergo lengthening of the flexor hallucis longus and flexor digitorum longus tendons on one side and simple decompression on the other. We found no difference in the deformities of the toes between the lengthened and non-lengthened sides at a mean follow-up of four years (2 to 6). We conclude that routine lengthening of the tendons of flexor hallucis longus and flexor digitorum longus during soft-tissue surgery for resistant club foot is not necessary

We investigated the pathogenesis of soft-tissue contracture in club foot, using immunohistochemistry to study 41 biopsy specimens and 12 normal deltoid ligaments from cadavers. Five biopsy specimens were studied by electron microscopy (EM) to determine the presence of myofibroblasts. All 41 specimens of club foot stained positively for vimentin as against only one of the 12 control specimens. By contrast, there was no difference in staining for desmin or α-smooth muscle actin. EM showed some variability in the appearance of ligamentous cells. Most contained bundles of microfilaments in the cytoplasm and many had abundant pinocytotic vesicles, but no basal lamina or plasmalemmal attachment plaques. Cells of the medial ligamentous tissue in patients with club foot contain vimentin and others have myofibroblastic characteristics. Both features may contribute to recurrence after soft-tissue release

Club foot can be diagnosed by ultrasound of the fetus in more than 60% of cases. We have correlated the accuracy of the prenatal findings in 281 ultrasound surveys with the physical findings after birth and the subsequent treatment in 147 children who were born with club foot. The earliest week of gestation in which the condition was diagnosed with a high degree of confidence was the 12th and the latest was the 32nd. Not all patients were diagnosed at an early stage. In 29% of fetuses the first ultrasound examination failed to detect the deformity which subsequently became obvious at a later examination. Club foot was diagnosed between 12 and 23 weeks of gestation in 86% of children and between 24 and 32 weeks of gestation in the remaining 14%. Therefore it can be considered to be an early event in gestation (45% identified by the 17th week), a late event (45% detected between 18th and 24th weeks) or a very late event (10% recognised between 25th and 32nd weeks). We cannot exclude, however, the possibility that the late-onset groups may have been diagnosed late because earlier scans were false-negative results. The prenatal ultrasonographic findings were correlated with the physical findings after birth and showed that bilateral involvement was more common than unilateral. There was no significant relationship between the prenatal diagnosis and the postnatal therapeutic approach (i.e., conservative or surgical), or the degree of rigidity of the affected foot

We studied in vivo the talonavicular alignment of club foot in infants using MRI. We examined 26 patients (36 feet) with congenital club foot. The mean age at examination was 9.0 months (4 to 12). All analyses used MRI of the earliest cartilaginous development of the tarsal bones in the transverse plane, rather than the ossific nucleus. The difference in the mean talar neck angle (44.0 ± 8.1°) in club foot was statistically significant (p < 0.001) when compared with that of the normal foot (30.8 ± 5.5°). The difference between the mean angles in the group treated by operation (47.9 ± 6.7°) and those treated conservatively (40.1 ± 7.5°) was also statistically significant. The anatomical relationship between the head of the talus and the navicular was divided into two patterns, based on the position of the mid-point of the navicular related to the long axis of the head. In the operative group, 18 feet were classified as having a medial shift of the navicular and none had a lateral shift. In the conservative group, 12 showed a medial shift of the navicular and six a lateral shift. All nine unaffected normal feet in which satisfactory MRI measurements were made showed a lateral shift of the navicular. Club feet had a larger talar neck angle and a more medially deviated navicular when compared with normal feet. This was more marked in the surgical group than in the conservative group

We report our initial experience of using the Ponseti method for the treatment of congenital idiopathic club foot. Between November 2002 and November 2004 we treated 100 feet in 66 children by this method. The standard protocol described by Ponseti was used except that, when necessary, percutaneous tenotomy of tendo Achillis were performed under general anaesthesia in the operating theatre and not under local anaesthesia in the out-patient department. The Pirani score was used for assessment and the mean follow-up time was 18 months (6 to 30). The results were also assessed in terms of the number of casts applied, the need for tenotomy of tendo Achillis and recurrence of the deformity. Tenotomy was required in 85 of the 100 feet. There was a failure to respond to the initial regimen in four feet which then required extensive soft-tissue release. Of the 96 feet which responded to initial casting, 31 (32%) had a recurrence, 16 of which were successfully treated by repeat casting and/or tenotomy and/or transfer of the tendon of tibialis anterior. The remaining 15 required extensive soft-tissue release. Poor compliance with the foot-abduction orthoses (Denis Browne splint) was thought to be the main cause of failure in these patients

We performed electrophysiological studies on both legs of 52 children, aged from 3 months to 15 years, with idiopathic club foot. In only nine (17%) was no abnormality found. Isolated peroneal nerve damage was seen in 14 (27%). Abnormality of both peroneal and posterior tibial nerves was found in five (10%). Four patients (8%) had evidence of isolated spinal-cord dysfunction, whereas combined spinal-cord and peripheral-nerve lesions were seen in 14 (27%). Six patients (11%) had variable neurogenic electrophysiological patterns. In 13 patients in whom the studies were repeated neither progression nor improvement of the electrophysiological parameters was observed. Pathological electrophysiological findings were found in 66% of conservatively-treated patients. In the 43 patients treated surgically, all 16 with fair and poor results had pathological electrophysiological findings and 12 required further operations. Multiplicity of the pathological findings was related to the severity of the deformity of the foot; normal studies represent a good prognostic sign. Electrophysiological studies are useful in idiopathic club foot with residual deformities after conservative or operative treatment. Our findings support the theory that muscle imbalance is an aetiological factor in idiopathic club foot

Treatment by continuous passive movement at home is an alternative to immobilisation in a cast after surgery for club foot. Compliance with the recommended treatment, of at least four hours daily, is unknown. The duration of treatment was measured in 24 of 27 consecutive children with a mean age of 24 months (5 to 75) following posteromedial release for idiopathic club foot. Only 21% (5) of the children used the continuous passive movement machine as recommended. The mean duration of treatment at home each day was 126 minutes (11 to 496). The mean range of movement for plantar flexion improved from 15.2° (10.0° to 20.6°) to 18.7° (10.0° to 33.0°) and for dorsiflexion from 12.3° (7.4° to 19.4°) to 18.9° (10.0° to 24.1°) (both, p = 0.0001) when the first third of therapy was compared with the last third. A low level of patient compliance must be considered when the outcome after treatment at home is interpreted

In 12 infants aged under 16 months with unilateral club foot we used MRI in association with multiplanar reconstruction to calculate the volume and principal axes of inertia of the bone and cartilaginous structures of the hindfoot. The volume of these structures in the club foot is about 20% smaller than that in the normal foot. The reduction in volume of the ossification centre of the talus (40%) is greater than that of the calcaneus (20%). The long axes of both the ossification centre and the cartilaginous anlage of the calcaneus are identical in normal and club feet. The long axis of the osseous nucleus of the talus of normal and club feet is medially rotated relative to the cartilaginous anlage, but the angle is greater in club feet (10° v 14°). The cartilaginous structure of the calcaneus is significantly medially rotated in club feet (15°) relative to the bimalleolar axis. The cartilaginous anlage of the talus is medially rotated in both normal and club feet, but with a smaller angle for club feet (28° v 38°). This objective technique of measurement of the deformity may be of value preoperatively

Primary skin closure after surgery for club foot in children can be difficult especially in revision operations. Between 1990 and 1996 a soft-tissue expander was implanted in 13 feet before such procedures. Two were primary operations and 11 were revisions. A standard technique was used for implantation of the expander. Skin augmentation was successful in 11 cases. There was failure of one expander and one case of wound infection. Sufficient stable skin could be gained at an average of five weeks. Primary skin closure after surgery was achieved in 12 cases. We conclude that soft-tissue expansion can be used successfully before extensive surgery for club foot. The method should be reserved for revision procedures and for older children. The technique is not very demanding, but requires experience to achieve successful results

The Pirani scoring system, together with the Ponseti method of club foot management, was assessed for its predictive value. The data on 70 idiopathic club feet successfully treated by the Ponseti method and scored by Pirani’s system between February 2002 and May 2004 were analysed. There was a significant positive correlation between the initial Pirani score and number of casts required to correct the deformity. A foot scoring 4 or more is likely to require at least four casts, and one scoring less than 4 will require three or fewer. A foot with a hindfoot score of 2.5 or 3 has a 72% chance of requiring a tenotomy. The Pirani scoring system is reliable, quick, and easy to use, and provides a good forecast about the likely treatment for an individual foot but a low score does not exclude the possibility that a tenotomy may be required

1. An operation which can correct congenital club foot deformity in older children is described. 2. The operation is based on the assumption that the essential element in a complex tarsal deformity is a displacement of the navicular bone on the talus and that all other elements of the deformity are secondary and adaptive. 3. The results of the operation are noted and the implications of some of its effects are discussed

1. An anatomical study of congenital club foot in various stages of foetal development is presented, and the literature is reviewed. 2. The most striking finding was deformity of the talus and in particular a change in its angle of declination. 3. That deformity was present in feet whose deformity could not be corrected by gentle manipulation; it was absent in feet whose deformity could be so corrected. 4. Abnormality of the tendon and insertion of the tibialis posterior muscle was found in most cases. 5. Speculations are advanced concerning the nature and cause of the talar deformity

Talectomy was performed on 10 patients (15 feet) for club foot deformity in arthrogryposis multiplex congenita. These were reviewed after an average follow-up of eight years. At follow-up nine feet were plantigrade, and six had less than 15 degrees residual equinus at the ankle. All the feet were asymptomatic but had mild residual adduction of the forefoot and marked stiffness of the hindfoot. Seven feet developed spontaneous bony ankylosis in the tibiotarsal joint. The common technical errors were incomplete removal of the talus and incorrect positioning of the calcaneus in the ankle mortise

1. The results of seventy-six transfers of the tibialis anterior tendon to the outer side of the foot to prevent relapse of congenital club foot are reviewed. 2. There were relapses in fifty-two of the seventy-six feet on which the operation had been performed. 3. The equinus component of the deformity is the dominant feature in all the relapses. 4. A test for occult equinus is described. 5. The factors contributing to the high relapse rate are discussed

A histochemical analysis was made of 103 muscle biopsies taken from 62 patients with idiopathic club feet. Any reduction in the diameter of the muscle fibres associated with wasting of the calf muscle was recorded. Histochemical abnormalities existing in these biopsies were revealed by comparison with normal biopsies obtained from the normal legs of 13 children with unilateral deformities. No significant difference was found between the diameter of the muscle fibres taken from normal and affected legs aged under six months. This indicates that wasting of the calf muscle is due to a reduction in the number of fibres rather than their size. The muscle structure was normal excluding denervation and reinnervation. The soleus muscle in patients aged under six months contained 61 per cent Type 1 fibres in the affected legs, compared to 44.3 per cent in normal legs. Similar values were found in the normal and abnormal tibialis posterior muscles, long flexors of the toe and peroneal muscles. The change in composition of the soleus muscle and the reduction in the number of fibres may be caused by a defective neural influence on the development of the limb in club foot