SciELO - Scientific Electronic Library Online

vol.19 issue3Prospective-comparative study between pseudarthrosis and bone fusion in lumbar stenosis author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand




Related links


Acta Ortopédica Brasileira

Print version ISSN 1413-7852

Acta ortop. bras. vol.19 no.3 São Paulo  2011 



Congenital Clubfoot



Daniel Augusto Carvalho Maranho; José Batista Volpon

Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo, Brazil

Mailing address




The clubfoot is one of the most common congenital deformities affecting the lower limbs, it still presents controversial aspects regarding etiology and treatment. In spite of its relatively high frequency, the treatment is still challenging, since the long-term aim is achieving an everlasting flexible, plantigrade, pain-free and totally functional foot. The Ponseti method has gained attention and popularity because of its satisfactory results and surgery avoidance. Presently, surgical treatment is indicated only after failure of conservative methods, avoiding extensive soft-tissue release, but performing localized corrections of the deformities, a technique also know as "a la carte" release. The future perspective is based on the knowledge about long-term results and new understanding of the clubfoot etiology, especially in the genetic field, which may eventually be helpful for prognostic and treatment. Level of Evidence: Level II, systematic review.

Keywords Clubfoot. Foot deformities. Congenital abnormalities.




The treatment of idiopathic congenital clubfoot (CC) has presented important evolution, since ample surgical releases were the rule a few years ago, in view of the unsatisfactory results of the manipulation techniques used at that time. Today, the Ponseti method is highly acclaimed due to the more satisfactory results and the reduction in the need for extensive surgical releases.

In the sector of Pediatric Orthopedics and Foot Disorders of Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto, the Ponseti method was introduced 10 years ago by the senior author (JBV), after discussion of treatment details with the creator of the method.

In comparison with Kite's method there has been a complete change of the prognosis and results of the deformity, which were confirmed over the years not only in local experience, but also in other national and international centers.

It is the proposal of this review to present and discuss the main ideas about the disorder, based on literature and the authors' experience, with the purpose of increasing the understanding and disclosure of modern concepts of etiology, anatomopathology and treatment of congenital clubfoot.



CC is defined as a deformity characterized by complex poor alignment of the foot that involves soft and bony parts, with hindfoot equinus and varus deformity (talipes equinovarus) besides midfoot and forefoot cavus and adduction.1-5

With approximate incidence of one in every 1,000 live births, it predominates in males, in the proportion of 2:1, with bilateral involvement in 50% of cases.6-9 Population variations are found in relation to incidence, whereas in the Chinese, there are around 0.39 cases in every 1,000 live births, in Caucasians one to three cases per 1,000 live births, while in Hawaiians it occurs in about seven in every 1,000 live births.6



With etiology still unknown, several theories were proposed to explain the origin of CC, considering intrinsic or extrinsic causes, including: intrauterine position of the fetus, mechanical compression or increase of intrauterine hydraulic pressure10,11; interruption in fetal development12; viral infections13; vascular deficiencies14,15; muscular alterations16-20; neurological alterations21-27; defect in the development of bones structures3,28,29 and genetic defects.7,30-39

The discovery of the existence of fibrotic tissue in the muscles, fasciae, ligaments and tendon sheaths of the posteromedial region of the ankle and hindfoot18,20 corroborates the hypothesis of primary defect of soft parts and neuromuscular units that lead to bone alterations.16,18,21,22,24,26,40

The cytocontractile proteins and myofibroblasts identified in the posteromedial contractured tissues of the hindfoot30,34 are structurally similar to those present in palmar fibromatosis and express high levels of type III collagen and certain growth factors, when compared to the non-contractured tissues.41,42

Shortening, fibrosis and retraction of the muscles and ligaments in CC are said to be genetically induced, resulting in abnormal retraction capacity that could possibly be related to primary congenital deformities and also to relapses that occur, even after adequate treatment.

Genetic factors may be involved in the origin of CC as suggested by studies that evidenced an increase in family incidence and in identical twins.7,43 Several investigations identified genes with evidence of association with CC.33,36-38,44-46.On the other hand, external factors related to development were also considered6,31,35 and the deformity appears not to develop before the 12th week of gestation, pursuant to a fetal ultrasonographic study.47

The consensus concerning the true genetic inheritance pattern has not yet been established, but a multifactorial polygenic inheritance pattern that can be influenced by external factors is suggested48,49, with incomplete dominance and variable penetrance.35



Three-dimensional bone connectivity is altered in a complex manner and, according to Ponseti4, the most severe deformities are located in the hindfoot, where the talus and the calcaneus are in accentuated equinus, the calcaneus is positioned medially and angulated in varus, and the navicular exhibits accentuated medial deviation. Moreover, the posterior ligaments of the ankle, such as those from the medial and plantar region, are shortened and thickened. The triceps surae, tibialis posterior and flexor muscles of the toes are shortened.

The talus presents morphological malformation, and the neck is angulated medially and plantarly, in comparison to a normal foot.12,17,18,20,28,29,50,52 Moreover, the talar neck is shortened and, in some cases, absent28. The calcaneus is directed medially on the horizontal plane,3,50 in equinus, adduced and inverted, with the anterior tuberosity facing the lateral malleolus and under the talar head (varus).18,20,51-55 In more severe cases, there is medial angulation of the long axis of calcaneus.20,28 The navicular is in extreme inversion, medialized and displaced over the talar head12,52,54 so as to articulate with the medial portion of the talar head, and is not infrequently in contact with the medial malleolus.18,20,28,50,56 The cuboid is displaced medially in relation to the calcaneus.52-54 The tarsometatarsal joints and the metatarsal diaphyses are medialized and cause adduction of the forefoot20,53, which is pronated in relation to the hindfoot, since the first and the second metatarsals are angulated plantarly in relation to the fifth, which, in general, is aligned with the hindfoot. Such a relationship gives rise to cavus.53

There are complex and extensive anomalies in the posterior ligaments of the ankle and posteromedial ligaments of the hindfoot12,50,55,57,58, such as retractions that exercise deforming forces and resistance to corrections. The deltoid ligament and the plantar calcaneonavicular ligament ("spring ligament") are shortened and thickened.42,55,58,59

Moreover, in CC, the calf muscles are smaller1,12,28,50,56,57,60,61, the foot size, as a whole, and that of the bones, individually, is also smaller50. Thus, the triceps surae muscle is invariably contractured and shortened16-18, 50, 55-58, although it is not clear whether the shortening is primary or secondary.

Anomalous or accessory muscles are more frequent in idiopathic congenital clubfoot58,62-67 and there are also variations in the tendon insertions9,16, including more medial insertion of the calcaneal (Achilles) tendon, which contributes to the varus angle.58

Vascular malformations were described in CC whose origin can be congenital, or otherwise adaptive to severe and prolonged deformity.14 The most frequent anomaly is absence or hypoplasia of the anterior tibial artery, which is present proximally in the leg, but ends abruptly in the ankle or in the calf, with deficient or absent anastomotic network.14,68-73 The absence of pedis pulse is more frequent in CC of greater severity and in older children.74 In rarer situations, there can be more accentuated vascular insufficiencies, which also compromise the perfusion provided by the posterior tibial artery.71,75-78 In these cases, the blood supply occurs separately through the fibular artery.73



Kite's method

In 1932, Kite,79,80 in opposition to the methods then used, published a gentler manipulation method aimed at correcting each component of CC separately, and not simultaneously. Adduction correction consisted of foot abduction with fulcrum in the midfoot and support in the calcaneocuboid joint. Varus correction was performed with hindfoot eversion, with wedges or plaster cast changes. The manipulations successively forced abduction and pronation of the forefoot. After adduction and inversion correction, the forefoot and hindfoot equinus deformities were corrected with progressive dorsiflexion.

However, neither Kite's method or other predecessor techniques of manipulation and plaster cast change techniques allowed complete correction of the deformities, and they resulted in feet with residual cavus, "rocker-bottom" feet, lateral torsion of the ankle, flattening and deformation of the upper side of the talar body, navicular subluxation, ligament and capsular rigidity, among other alterations.4 As other authors did not manage to reproduce the same rate of good results described by Kite81,82, they resumed surgical treatment when there was resistance to correction by the conservative technique. Codivilla's classical medial release was performed often.83

The posteromedial release

In the 70s, based on the studies of Turco58,59, the extensive release of soft parts became popular, with emphasis on posteromedial release. However, the complication of hypercorrection with hindfoot valgus was a common occurrence. Consequently, variations on the technique arose in the 80s and 90s.84-87 However, the long-term results continued unsatisfactory, with joint and ligament rigidity, ankylosis, weakness of the triceps and of the dorsiflexors, residual deformity due to hypocorrection or hypercorrection, navicular displacement, flattening and necrosis of the talus, skin necrosis, infections, scars with hypersensitivity, gait disorders, pain and late onset arthrosis.4,51,54,60,82,88-91 The current tendency is to avoid surgery with extensive joint releases1,5 and the use of surgery as a primary correction method is limited to the customized procedure, where just the structures required to achieve correction are released.92 (Figure 1)



Ponseti's method

Ponseti, after in-depth studies on the pathological and functional anatomy of CC, starting in the 40s, developed and refined his own treatment method, in view of the poor results obtained with surgical and non-surgical treatments then in practice. He established details of manipulation and casting maneuvers, as well as follow-up after sectioning of the calcaneal tendon and strategies for prevention of relapses, based on the child's age and on the parents' cooperation. In addition, he identified and announced the most common mistakes.93

Other initial treatment methods such as the use of the Denis Browne splint, physiotherapy, stretching and taping (French method) may have relative success, when adequately applied, but failure to achieve complete correction of the deformity is common.94

The Ponseti method1,4,53, composed basically of manipulations and serial plaster cast changes, percutaneous sectioning of the calcaneal tendon and use of abduction orthosis, has become the preferential method for the treatment of idiopathic CC in many countries, in the last ten years (Bor; Coplan, Herzenberg, 2009; Dobbs, Gurnett, 2009; Dobbs et al., 2004b; Herzenberg; Radler, Bor, 2002). With widespread acceptance, it was extended for use on older children95-98; complex and resistant feet99; relapsed feet100, including relapses after extensive surgical release101, and also, in non-idiopathic cases, such as in myelomeningocele102,103 and distal arthrogryposis104,105.

The grounds of the manipulation technique consist of correcting deformities by means of the plastic change of the contractured and shortened elements, which have a high elastic capacity in the younger child. Pirani, Zeznik and Hodges52 confirmed, with the use of magnetic nuclear resonance imaging that, with the Ponseti method, there is not just correction of foot bone connectivity, but also bone remodeling guided by mechanical stimuli, according to Wolff's classical theory.

The treatment, according to Ponseti1, should be started in the first days of life, with gentle manipulations, performed at intervals of five to seven days, followed by the application of a plaster cruropodalic cast, with the knee flexed ~90º. Cavus is the first deformity to be corrected with forefoot supination and plantar support on the head of the first metatarsal. Adduction and varus are corrected simultaneously in the next three or four casts, with counter-support on the lateral surface of the talar head and forefoot abduction, in supination. In achieving abduction of ~70º, varus should be corrected. Equinus correction should only be started after the correction of adduction and varus, with modeled plaster cast in the posterior part of the foot, with dorsal flexion. Ponseti gave the name "Kite's error" to the support performed in the calcaneocuboid joint and the attempt to correct varus with pronation, as there is, respectively, blocking of the adduced calcaneus below the talar head (which prevents lateral rotation of the calcaneus and maintains the varus deformity) and cavus accentuation.93,94,106 Figure 2 illustrates a case treated by the Ponseti method.



The Ponseti method is being widely publicized, both in developed countries and in those under development107-112, on account of the good correction rates achieved, which are close to 90%4,60,95,113,114, while in Kite's technique, around 50% of cases require surgical intervention and around 40% present residual deformity.115 Another important factor is that the treatment time with Kite's technique is approximately twenty-two months, while with the Ponseti method, the time is from two to four months.116 Herzenberg, Radler and Bor117 reported that the Ponseti method was able to significantly reduce the need for posteromedial surgical release (3% against 94% by the traditional technique of that time).

However, most cases treated by the Ponseti method present residual equinus and require percutaneous sectioning of the calcaneal tendon, originally performed with an ophthalmic scalpel blade, through a small incision in the skin. Tenotomy is indicated when the hindfoot does not attain 15º of dorsiflexion, after achieving varus and adduction correction, and is necessary in 70 to 90% of patients.1,4,95,114,117-119 Attempts at forced correction of equinus with plaster produces the classical "rocker-bottom" deformity.

Furthermore, relapses after treatment can be frequent and are part of the actual natural history of the disease. They are caused by the same pathological factors that initiated the deformity.93 The use of abduction orthosis and daily manipulation at home should be encouraged, as they can act preventively. Relapses can be treated fast with two or three plaster cast changes, but cases with a strong tendency for dynamic supination are candidates for transfer of the tibialis anterior tendon to the third cuneiform bone.93 Surgery can prevent future relapses and correct the talocalcaneal angle60. The occurrence of varus and/or residual adduction can also be treated with localized surgical corrections, such as osteotomies on the midfoot (cuboid subtraction wedge or combined wedges) or in the calcaneus (Dwyer), which avoid surgical joint releases.1

Calcaneal tendon sectioning

Percutaneous sectioning of the calcaneal tendon was performed widely for a long time, although without any descriptions of the complications and risk of the procedure. However, those in the orthopedic field express misgivings about the possibility of injury to the adjacent structures and concern regarding the quality of tendon healing.

Complications were reported recently after percutaneous tenotomy of the Achilles tendon. These include excessive bleeding, attributed to lesion of the posterior fibular artery or saphenous vein118 and formation of pseudoaneurysm.73

Clinical studies with late follow-up showed that tenotomy does not cause late onset effects such as tendon weakening and ruptures.53,60,113,120,121 Previous studies on other types of disease showed that there is complete repair of the calcaneal tendon after its total sectioning at the myotendineous junction122, or more distally.123,124 The tendon appears to undergo complete repair within six weeks after the sectioning.120 Repair of the calcaneal tendon after percutaneous tenotomy in the CC was studied more recently verifying fast healing, with recovery of the mechanical transmission of movements in all the cases three weeks after the sectioning. At six months after sectioning, the repair tissue was similar to the normal tendon.125,126

Several instruments were used for percutaneous sectioning of the calcaneal tendon. Ponseti initially advocated the use of the ophthalmic scalpel blade. As it is long and pointed, the use of a shorter ophthalmic blade with a rounded end was suggested.118 Common scalpel blades such as no. 11 and 15 are widely used. The 1.6mm caliber needle has been employed more recently.125-128

The surgical technique of tenotomy is more important than the instrument used. The entry point should be on the level of the medial edge of the calcaneal tendon, about 1.0 cm above the insertion, in order to avoid the posterior tibial neurovascular bundle. The section should be assessed by palpation, with the extremity of the instrument. Ultrasonography can be used for transoperative evaluation of the tenotomy125,126,128, in order to ensure that it is complete and that the equinus is corrected.



CC has variable expression and there are classifications that consider only clinical aspects, while others also take into account the radiographic aspects. However, no classification system has prevailed until now, but the main classifications are those of Dimeglio129 and of Pirani.110,130,131

Pirani's classification is simpler and more recent, yet it is still in the validation phase (personal information). It is based on a simple scaling system, composed of three variables in the hindfoot and three in the midfoot.110 Each variable can receive a score of zero, half a point and one point. (Figure 3)




Some feet are not correctable by Ponseti's classic manipulative technique, and the incorrect application of the method can even iatrogenically produce more complex deformities. Clinically, these feet are characterized by accentuated rigid equinus, severe plantar flexion of all the metatarsals, with appearance of a more shortened foot. There is a deep transverse plantar fold both medially and laterally, besides shortening and hyperextension of the hallux. The calcaneal tendon is under more tension than usual, is long, fibrotic, and palpable up to the proximal half of the calf and produces accentuated equinus, with deep posterior fold in the ankle. The forefoot, besides adduction, is in accentuated plantar flexion, both medially and laterally. The lateral malleolus is more protuberant. The talus appears smaller and its head is not easily palpable, as in habitual CC, and it is frequently confused with the anterior calcaneal tuberosity.99

Attempts at correction by the habitual technique do not work as support occurs in the anterior calcaneal tuberosity, with hyperabduction in the Lisfranc joint and deterioration of plantar flexion of the metatarsals. There are a large number of plaster cast changes and the casts slip easily. For this reason, many orthopedists opt for surgical treatment.

In these cases, Ponseti himself99 recommended a modified manipulation technique. Correction initially requires correct identification of the talar head, which is smaller than usual, in front of the malleoli, with dynamic perception of the navicular and of the anterior calcaneal tuberosity. At the time of the counter-support, for manipulation and casting, it is necessary to make sure the procedure is performed in the talar head, and not in the prominent anterior calcaneal tuberosity. The abduction should reach around ~40º, after two or three plaster cast changes. Afterwards cavus correction is started with support under the head of the first and fifth metatarsals, for correction of forefoot plantar flexion, with an assistant providing counter-support at the knee. (Figure 4) The cast should be very well molded to avoid slipping, and the knee is immobilized in flexion of ~110º.



After cavus correction, the calcaneal tendon is sectioned in the habitual manner and equinus correction is generally performed with weekly plaster cast changes for gain of dorsiflexion, up to around 10º. Afterwards, the use of orthosis with abduction of ~40º is prescribed for the patient.



The Ponseti method has been used in older children100, including above two years96,98 of age, as an initial treatment method, with satisfactory results. In older children modifications were suggested in the method, such as the obtainment of ~40º of abduction and not ~70º like in the younger children. Moreover, the manipulations and plaster cast changes are performed every two weeks, to allow greater accommodation and remodeling of the soft and bony parts. If residual equinus remains after tenotomy, there can be posterior release of the tibiotarsus and subtalar joint.

However, the upper age limit, both for treatment using the Ponseti method, and for the performance of percutaneous tenotomy, is not well established.

The use of the Ponseti method was also extended to relapsed feet, including after surgical releases, with reports of good outcomes101.



The Ponseti method has been used for the treatment of CC in arthrogryposis with satisfactory short-term results104,105,132, although with modifications such as performing percutaneous sectioning of the calcaneal tendon as a first corrective measure104 or even accepting abduction gain of 40-50º132, including in the abduction orthosis. Apparently, flexibility of the foot improves with the evolution of treatment and a lower degree of surgical correction is necessary, yet relapses are common.132

The method has also been applied in cases of myelomeningocele102,103, but it is worth remembering that in diseases with foot sensitivity alterations, treatment with plaster cast may be dangerous and provoke severe skin lesions, stress fractures and plastic deformation, especially after acute corrections, such as calcaneal tendon sectioning.103

In general, when compared to idiopathic CC, the Ponseti method in the treatment of syndromic CC results in a higher average number of plaster cast changes and greater frequency of failures, relapses and the need for additional surgical procedures. However, the correction produced is satisfactory in most cases.133

The use of the abduction orthosis should also be encouraged in spite of the tendency for reduced family participation and higher incidence of skin lesions. Abduction should be the same as that achieved at the end of the treatment with plaster cast.103



To guarantee that patients with CC are adequately treated in a progressively less invasive manner, with functional, flexible, painless feet, without deformities or callosities and that do not need special footwear, it will be necessary not only to know the disease pathogenesis and other technicalities, but also the late functional results of the various types of treatment. Most related surveys are still of short and medium terms and compare the Ponseti method with other surgical or non-surgical methods. Thus in the future, new evidence will help to clear up the current uncertainties and controversies related to the treatment of CC.



1. Ponseti IV. Congenital clubfoot: fundamentals of treatment. Oxford: Oxford University Press; 1996.         [ Links ]

2. Song HR, Carroll NC, Neyt J, Carter JM, Han J, D'Amato CR. Clubfoot analysis with three-dimensional foot models. J Pediatr Orthop B. 1999;8(1):5-11.         [ Links ]

3. Cahuzac JP, Baunin C, Luu S, Estivalezes E, Sales de Gauzy J, Hobatho MC. Assessment of hindfoot deformity by three-dimensional MRI in infant club foot. J Bone Joint Surg Br. 1999;81(1):97-101.         [ Links ]

4. Ponseti IV. Treatment of congenital club foot. J Bone Joint Surg Am. 1992;74(3):448-54.         [ Links ]

5. Dobbs MB, Gurnett CA. Update on clubfoot: etiology and treatment. Clin Orthop Relat Res. 2009;467(5):1146–53.         [ Links ]

6. Lochmiller C, Johnston D, Scott A, Risman M, Hecht JT. Genetic epidemiology study of idiopathic talipes equinovarus. Am J Med Genet. 1998;79(2):90-6.         [ Links ]

7. Wynne-Davies R. Family studies and the cause of congenital club foot. Talipes equinovarus, talipes calcaneo-valgus and metatarsus varus. J Bone Joint Surg Br. 1964;46(3):445-63.         [ Links ]

8. Barker SL, Macnicol MF. Seasonal distribution of idiopathic congenital talipes equinovarus in Scotland. J Pediatr Orthop B. 2002;11(2):129-33.         [ Links ]

9. Stewart SF. Club-foot: its incidence, cause, and treatment; an anatomical-physiological study. J Bone Joint Surg Am. 1951;33(3):577-90.         [ Links ]

10. Farrell SA, Summers AM, Dallaire L, Singer J, Johnson JA, Wilson RD. Club foot, an adverse outcome of early amniocentesis: disruption or deformation? CEMAT. Canadian Early and Mid-Trimester Amniocentesis Trial. J Med Genet. 1999;36(11):843-6.         [ Links ]

11. Browne D. Congenital deformities of mechanical origin. Arch Dis Child. 1955;30(149):37-41.         [ Links ]

12. Böhm M. The embriologic origin of club-foot. J Bone Joint Surg Am. 1929;11(2):229-59.         [ Links ]

13. Robertson WW, Jr., Corbett D. Congenital clubfoot. month of conception. Clin Orthop Relat Res. 1997(338):14-8.         [ Links ]

14. Hootnick DR, Levinsohn EM, Crider RJ, Packard DS, Jr. Congenital arterial malformations associated with clubfoot. A report of two cases. Clin Orthop Relat Res. 1982(167):160-3.         [ Links ]

15. Atlas S, Menacho LC, Ures S. Some new aspects in the pathology of clubfoot. Clin Orthop Relat Res. 1980(149):224-8.         [ Links ]

16. Flinchum D. Pathological anatomy in talipes equinovarus. J Bone Joint Surg Am. 1953;35(1):111-4.         [ Links ]

17. Bechtol CO, Mossman HW. Clubfoot: an embryological study of associated muscle abnormalities. J Bone Joint Surg Am. 1950;32(4):827-38.         [ Links ]

18. Ippolito E, Ponseti IV. Congenital club foot in the human fetus. A histological study. J Bone Joint Surg Am. 1980;62(1):8-22.         [ Links ]

19. Gray DH, Katz JM. A histochemical study of muscle in club foot. J Bone Joint Surg Br. 1981;63(3):417-23.         [ Links ]

20. Ippolito E. Update on pathologic anatomy of clubfoot. J Pediatr Orthop B. 1995;4(1):17-24.         [ Links ]

21. Feldbrin Z, Gilai AN, Ezra E, Khermosh O, Kramer U, Wientroub S. Muscle imbalance in the aetiology of idiopathic club foot. An electromyographic study. J Bone Joint Surg Br. 1995;77(4):596-601.         [ Links ]

22. Isaacs H, Handelsman JE, Badenhorst M, Pickering A. The muscles in club foot - a histological histochemical and electron microscopic study. J Bone Joint Surg Br. 1977;59(4):465-72.         [ Links ]

23. Nadeem RD, Brown JK, Lawson G, Macnicol MF. Somatosensory evoked potentials as a means of assessing neurological abnormality in congenital talipes equinovarus. Dev Med Child Neurol. 2000;42(8):525-30.         [ Links ]

24. Handelsman JE, Badalamente MA. Neuromuscular studies in clubfoot. J Pediatr Orthop. 1981;1(1):23-32.         [ Links ]

25. Macnicol MF, Nadeem RD. Evaluation of the deformity in club foot by somatosensory evoked potentials. J Bone Joint Surg Br. 2000;82(5):731-5.         [ Links ]

26. Dittrich RJ. Pathogenesis of congenital club-foot (pes equinovarus): an anatomical study. J Bone Joint Surg Am. 1930;12:373-99.         [ Links ]

27. Edmonds EW, Frick SL. The drop toe sign: an indicator of neurologic impairment in congenital clubfoot. Clin Orthop Relat Res. 2009;467(5):1238–42.         [ Links ]

28. Irani RN, Sherman MS. The pathological anatomy of club foot. J Bone Joint Surg Am. 1963;45(1):45-52.         [ Links ]

29. Shapiro F, Glimcher MJ. Gross and histological abnormalities of the talus in congenital club foot. J Bone Joint Surg Am. 1979;61(4):522-30.         [ Links ]

30. Zimny ML, Willig SJ, Roberts JM, D'Ambrosia RD. An electron microscopic study of the fascia from the medial and lateral sides of clubfoot. J Pediatr Orthop. 1985;5(5):577-81.         [ Links ]

31. Wang JH, Palmer RM, Chung CS. The role of major gene in clubfoot. Am J Hum Genet. 1988;42(5):772-6.         [ Links ]

32. Poon R, Li C, Alman BA. Beta-catenin mediates soft tissue contracture in clubfoot. Clin Orthop Relat Res. 2009;467(5):1180–5.         [ Links ]

33. Wang LL, Fu WN, Li-Ling J, Li ZG, Li LY, Sun KL. HOXD13 may play a role in idiopathic congenital clubfoot by regulating the expression of FHL1. Cytogenet Genome Res. 2008;121(3-4):189-95.         [ Links ]

34. Sano H, Uhthoff HK, Jarvis JG, Mansingh A, Wenckebach GF. Pathogenesis of soft-tissue contracture in club foot. J Bone Joint Surg Br. 1998;80(4):641-4.         [ Links ]

35. Rebbeck TR, Dietz FR, Murray JC, Buetow KH. A single-gene explanation for the probability of having idiopathic talipes equinovarus. Am J Hum Genet. 1993;53(5):1051-63.         [ Links ]

36. Karakurt L, Yilmaz E, Serin E, Bektas B, Cikim G, Gursu F. Plasma total homocysteine level in mothers of children with clubfoot. J Pediatr Orthop. 2003;23(5):658-60.         [ Links ]

37. Heck AL, Bray MS, Scott A, Blanton SH, Hecht JT. Variation in CASP10 gene is associated with idiopathic talipes equinovarus. J Pediatr Orthop. 2005;25(5):598-602.         [ Links ]

38. Ester AR, Tyerman G, Wise CA, Blanton SH, Hecht JT. Apoptotic gene analysis in idiopathic talipes equinovarus (clubfoot). Clin Orthop Relat Res. 2007(462):32-7.         [ Links ]

39. Dietz FR, Cole WG, Tosi LL, Carroll NC, Werner RD, Comstock D, et al. A search for the gene(s) predisposing to idiopathic clubfoot. Clin Genet. 2005;67(4):361-2.         [ Links ]

40. Lichtblau S. Etiology of clubfoot. Clin Orthop Relat Res. 1972;84:21-4.         [ Links ]

41. Li C, Nguyen Q, Cole WG, Alman BA. Potential treatment for clubfeet based on growth factor blockade. J Pediatr Orthop. 2001;21(3):372-7.         [ Links ]

42. Fukuhara K, Schollmeier G, Uhthoff HK. The pathogenesis of club foot. A histomorphometric and immunohistochemical study of fetuses. J Bone Joint Surg Br. 1994;76(3):450-7.         [ Links ]

43. Wynne-Davies R. Genetic and environmental factors in the etiology of talipes equinovarus. Clin Orthop Relat Res. 1972(84):9-13.         [ Links ]

44. Gurnett CA, Alaee F, Kruse LM, Desruisseau DM, Hecht JT, Wise CA, et al. Asymmetric lower-limb malformations in individuals with homeobox PITX1 gene mutation. Am J Hum Genet. 2008;83(5):616-22.         [ Links ]

45. Shyy W, Dietz F, Dobbs MB, Sheffield VC, Morcuende JA. Evaluation of CAND2 and WNT7a as candidate genes for congenital idiopathic clubfoot. Clin Orthop Relat Res. 2009;467(5):1201–5.         [ Links ]

46. Sharp L, Miedzybrodzka Z, Cardy AH, Inglis J, Madrigal L, Barker S, et al. The C677T polymorphism in the methylenetetrahydrofolate reductase gene (MTHFR), maternal use of folic acid supplements, and risk of isolated clubfoot: A case-parent-triad analysis. Am J Epidemiol. 2006;164(9):852-61.         [ Links ]

47. Mammen L, Benson CB. Outcome of fetuses with clubfeet diagnosed by prenatal sonography. J Ultrasound Med. 2004;23(4):497-500.         [ Links ]

48. Brand RA. 50 years ago in CORR: Dural and intradural compression as a cause of clubfoot NJ Giannestras MD CORR 1953;1:28-32 calcaneovalgus foot in the newborn and Its relationship to developmental flatfoot CF Ferciot MD CORR 1953;1:22-27. Clin Orthop Relat Res. 2009;467(5):1385–6.         [ Links ]

49. Kruse LM, Dobbs MB, Gurnett CA. Polygenic threshold model with sex dimorphism in clubfoot inheritance: the Carter effect. J Bone Joint Surg Am. 2008;90(12):2688-94.         [ Links ]

50. Settle GW. The anatomy of congenital talipes equinovarus: sixteen dissected specimens. J Bone Joint Surg Am. 1963;45(7):1341-54.         [ Links ]

51. Ponseti IV, Campos J. Observations on pathogenesis and treatment of congenital clubfoot. Clin Orthop Relat Res. 1972(84):50-60.         [ Links ]

52. Pirani S, Zeznik L, Hodges D. Magnetic resonance imaging study of the congenital clubfoot treated with the Ponseti method. J Pediatr Orthop. 2001;21(6):719-26.         [ Links ]

53. Ponseti IV, Smoley EN. Congenital club foot: the results of treatment. J Bone Joint Surg Am. 1963;45(2):261-344.         [ Links ]

54. McKay DW. New concept of and approach to clubfoot treatment: section I - principles and morbid anatomy. J Pediatr Orthop. 1982;2(4):347-56.         [ Links ]

55. Da Paz ACJ, de Souza V. Talipes equinovarus: pathomechanical basis of treatment. Orthop Clin North Am. 1978;9(1):171-85.         [ Links ]

56. Wiley AM. Club foot: an anatomical and experimental study of muscle growth. J Bone Joint Surg Br. 1959;41:821 - 35.         [ Links ]

57. Waisbrod H. Congenital club foot. An anatomical study. J Bone Joint Surg Br. 1973;55(4):796-801.         [ Links ]

58. Turco VJ. Surgical correction of the resistant club foot. One-stage posteromedial release with internal fixation: a preliminary report. J Bone Joint Surg Am. 1971;53(3):477-97.         [ Links ]

59. Turco VJ. Resistant congenital club foot - one-stage posteromedial release with internal fixation. A follow-up report of a fifteen-year experience. J Bone Joint Surg Am. 1979;61(6):805-14.         [ Links ]

60. Laaveg SJ, Ponseti IV. Long-term results of treatment of congenital club foot. J Bone Joint Surg Am. 1980;62(1):23-31.         [ Links ]

61. De Maio F, Orefice A, Ippolito E, Mancini F, Potenza AD, editors. Leg muscle atrophy in idiopatic congenital clufoot: is it primitive or acquired? Scientific programme and abstracts of 27th Annual Meeting of European Paediatric Orthopaedic Society; 2008 2008; Warsaw. Heidelberg: J Child Orthop.         [ Links ]

62. Porter RW. An anomalous muscle in children with congenital talipes. Clin Anat. 1996;9(1):25-7.         [ Links ]

63. Windisch G, Anderhuber F, Haldi-Brandle V, Exner GU. Additional muscle in idiopathic club foot. Eur J Pediatr Surg. 2006;16(4):294-6.         [ Links ]

64. Rambani R, Shahid MS. Accessory soleus muscle as a cause of congenital talipes equino varus. A case report. Acta Orthop Belg. 2006;72(5):644-6.         [ Links ]

65. Sodré H. Músculos anômalos no pé torto eqüinovaro congênito. Rev Bras Ortop. 1994;29(1):24-8.         [ Links ]

66. Salomão O, Carvalho AEd, Fernandes TD, Romano D, Adachi PP, Neto RS. Músculo solear acessório: aspectos clínicos e achados cirúrgicos. Rev Bras Ortop. 1994;29(4):251-5.         [ Links ]

67. Karapinar L, Kaya A, Altay T, Ozturk H, Surenkok F. Congenital clubfoot associated with an accessory soleus muscle. J Am Podiatr Med Assoc. 2008;98(5):408-13.         [ Links ]

68. Ben-Menachem Y, Butler JE. Arteriography of the foot in congenital deformities. J Bone Joint Surg Am. 1974;56(8):1625-30.         [ Links ]

69. David RH, Packard DS, Jr., Levinsohn EM, Berkowitz SA, Aronsson DD, Crider RJ, Jr. Ischemic necrosis following clubfoot surgery: the purple hallux sign. J Pediatr Orthop B. 2004;13(5):315-22.         [ Links ]

70. Greider TD, Siff SJ, Gerson P, Donovan MM. Arteriography in club foot. J Bone Joint Surg Am. 1982;64(6):837-40.         [ Links ]

71. Kruse L, Gurnett CA, Hootnick D, Dobbs MB. Magnetic resonance angiography in clubfoot and vertical talus: a feasibility study. Clin Orthop Relat Res. 2009;467(5):1250–5.         [ Links ]

72. Sodré H, Bruschini S, Mestriner LA, Miranda F, Jr., Levinsohn EM, Packard DS, Jr., et al. Arterial abnormalities in talipes equinovarus as assessed by angiography and the Doppler technique. J Pediatr Orthop. 1990;10(1):101-4.         [ Links ]

73. Burghardt RD, Herzenberg JE, Ranade A. Pseudoaneurysm after Ponseti percutaneous Achilles tenotomy: a case report. J Pediatr Orthop. 2008;28(3):366-9.         [ Links ]

74. Edelson JG, Husseini N. The pulseless club foot. J Bone Joint Surg Br. 1984;66(5):700-2.         [ Links ]

75. Dobbs MB, Gordon JE, Schoenecker PL. Absent posterior tibial artery associated with idiopathic clubfoot. A report of two cases. J Bone Joint Surg Am. 2004;86(3):599-602.         [ Links ]

76. Hootnick DR, Packard DS, Jr., Levinsohn EM, Crider RJ, Jr. Confirmation of arterial deficiencies in a limb with necrosis following clubfoot surgery. J Pediatr Orthop B. 1999;8(3):187-93.         [ Links ]

77. Quillin SP, Hicks ME. Absent posterior tibial artery associated with clubfoot deformity: an unusual variant. J Vasc Interv Radiol. 1994;5(3):497-9.         [ Links ]

78. Kitziger K, Wilkins K. Absent posterior tibial artery in an infant with talipes equinovarus. J Pediatr Orthop. 1991;11(6):777-8.         [ Links ]

79. Kite JH. Principles involved in the treatment of congenital club-foot. J Bone Joint Surg Am. 1939;21(3):595-606.         [ Links ]

80. Kite JH. Principles involved in the treatment of congenital clubfoot. Clin Orthop Relat Res. 1972(84):4-8.         [ Links ]

81. Karski T, Wosko I. Experience in the conservative treatment of congenital clubfoot in newborns and infants. J Pediatr Orthop. 1989;9(2):134-6.         [ Links ]

82. Aronson J, Puskarich CL. Deformity and disability from treated clubfoot. J Pediatr Orthop. 1990;10(1):109-19.         [ Links ]

83. Santin RAL, Hungria Filho JS. Pé torto congênito. Rev Bras Ortop. [Revisão]. 1977;12:1-15.         [ Links ]

84. McKay DW. New concept of and approach to clubfoot treatment: Section III - evaluation and results. J Pediatr Orthop. 1983;3(2):141-8.         [ Links ]

85. Hudson I, Catterall A. Posterolateral release for resistant club foot. J Bone Joint Surg Br. 1994;76(2):281-4.         [ Links ]

86. Simons GW. Complete subtalar release in club feet. Part II - Comparison with less extensive procedures. J Bone Joint Surg Am. 1985;67(7):1056-65.         [ Links ]

87. Carroll NC. Surgical technique for talipes equinovarus. Oper Tech Orthop. 1993;3(2):115-20.         [ Links ]

88. Ippolito E, Farsetti P, Caterini R, Tudisco C. Long-term comparative results in patients with congenital clubfoot treated with two different protocols. J Bone Joint Surg Am. 2003;85(7):1286-94.         [ Links ]

89. Dobbs MB, Nunley R, Schoenecker PL. Long-term follow-up of patients with clubfeet treated with extensive soft-tissue release. J Bone Joint Surg Am. 2006;88(5):986-96.         [ Links ]

90. Hutchins PM, Foster BK, Paterson DC, Cole EA. Long-term results of early surgical release in club feet. J Bone Joint Surg Br. 1985;67(5):791-9.         [ Links ]

91. Kite JH. Nonoperative treatment of congenital clubfoot. Clin Orthop Relat Res. 1972(84):29-38.         [ Links ]

92. Bensahel H, Csukonyi Z, Desgrippes Y, Chaumien JP. Surgery in residual clubfoot: one-stage medioposterior release "a la carte". J Pediatr Orthop. 1987;7(2):145-8.         [ Links ]

93. Ponseti IV. Common errors in the treatment of congenital clubfoot. Int Orthop. 1997;21(2):137-41.         [ Links ]

94. Ponseti IV. Clubfoot management. J Pediatr Orthop. 2000;20(6):699-700.         [ Links ]

95. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV. Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method. Pediatrics. 2004;113(2):376-80.         [ Links ]

96. Lourenco AF, Morcuende JA. Correction of neglected idiopathic club foot by the Ponseti method. J Bone Joint Surg Br. 2007;89(3):378-81.         [ Links ]

97. Alves C, Escalda C, Fernandes P, Tavares D, Neves MC. Ponseti method: does age at the beginning of treatment make a difference ? Clin Orthop Relat Res. 2009;467(5):1271–7.         [ Links ]

98. Spiegel DA, Shrestha OP, Sitoula P, Rajbhandary T, Bijukachhe B, Banskota AK. Ponseti method for untreated idiopathic clubfeet in Nepalese patients from 1 to 6 years of age. Clin Orthop Relat Res. 2009;467(5):1164-70.         [ Links ]

99. Ponseti IV, Zhivkov M, Davis N, Sinclair M, Dobbs MB, Morcuende JA. Treatment of the complex idiopathic clubfoot. Clin Orthop Relat Res. 2006(451):171-6.         [ Links ]

100. Bor N, Herzenberg JE, Frick SL. Ponseti management of clubfoot in older infants. Clin Orthop Relat Res. 2006(444):224-8.         [ Links ]

101. Nogueira MP, Ey Batlle AM, Alves CG. Is it possible to treat recurrent clubfoot with the Ponseti technique after posteromedial release? A preliminary study. Clin Orthop Relat Res. 2009;467(5):1298–305.         [ Links ]

102. Chen RC, Gordon JE, Luhmann SJ, Schoenecker PL, Dobbs MB. A new dynamic foot abduction orthosis for clubfoot treatment. J Pediatr Orthop. 2007;27(5):522-8.         [ Links ]

103. Gerlach DJ, Gurnett CA, Limpaphayom N, Alaee F, Zhang Z, Porter K, et al. Early results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele. J Bone Joint Surg Am. 2009;91(6):1350-9.         [ Links ]

104. van Bosse HJ, Marangoz S, Lehman WB, Sala DA. Correction of arthrogrypotic clubfoot with a modified Ponseti technique. Clin Orthop Relat Res. 2009;467(5):1283–93.         [ Links ]

105. Boehm S, Limpaphayom N, Alaee F, Sinclair MF, Dobbs MB. Early results of the Ponseti method for the treatment of clubfoot in distal arthrogryposis. J Bone Joint Surg Am. 2008;90(7):1501-7.         [ Links ]

106. Ponseti IV. The Ponseti technique for correction of congenital clubfoot. J Bone Joint Surg Am. 2002;84(10):1889-91.         [ Links ]

107. Pirani S, Naddumba E, Mathias R, Konde-Lule J, Penny JN, Beyeza T, et al. Towards effective Ponseti clubfoot care: the Uganda sustainable clubfoot care project. Clin Orthop Relat Res. 2009;467(5):1154-63.         [ Links ]

108. Siapkara A, Duncan R. Congenital talipes equinovarus: a review of current management. J Bone Joint Surg Br. 2007;89(8):995-1000.         [ Links ]

109. Sud A, Tiwari A, Sharma D, Kapoor S. Ponseti's vs. Kite's method in the treatment of clubfoot -- a prospective randomised study. Int Orthop. 2008;32(3):409-13.         [ Links ]

110. Pirani S, Naddumba E. Ponseti clubfoot management: teaching manual for heatlh-care providers in Uganda: Global-HELP Organization; 2008. Available from: Disponível em: <>.Acesso em: 11/abril/2010.         [ Links ]

111. Gupta A, Singh S, Patel P, Patel J, Varshney MK. Evaluation of the utility of the Ponseti method of correction of clubfoot deformity in a developing nation. Int Orthop. 2008;32(1):75-9.         [ Links ]

112. Zwick EB, Kraus T, Maizen C, Steinwender G, Linhart WE. Comparison of Ponseti versus surgical treatment for idiopathic clubfoot: a short-term preliminary report. Clin Orthop Relat Res. 2009;467(10):2668-76.         [ Links ]

113. Cooper DM, Dietz FR. Treatment of idiopathic clubfoot. A thirty-year follow-up note. J Bone Joint Surg Am. 1995;77(10):1477-89.         [ Links ]

114. Bor N, Coplan JA, Herzenberg JE. Ponseti treatment for idiopathic clubfoot: minimum 5-year followup. Clin Orthop Relat Res. 2009;467(5):1263–70.         [ Links ]

115. Segev E, Keret D, Lokiec F, Yavor A, Wientroub S, Ezra E, et al. Early experience with the Ponseti method for the treatment of congenital idiopathic clubfoot. Isr Med Assoc J. 2005;7(5):307-10.         [ Links ]

116. Cummings RJ, Davidson RS, Armstrong PF, Lehman WB. Congenital clubfoot. J Bone Joint Surg Am. 2002;84(2):290-308.         [ Links ]

117. Herzenberg JE, Radler C, Bor N. Ponseti versus traditional methods of casting for idiopathic clubfoot. J Pediatr Orthop. 2002;22(4):517-21.         [ Links ]

118. Dobbs MB, Gordon JE, Walton T, Schoenecker PL. Bleeding complications following percutaneous tendoachilles tenotomy in the treatment of clubfoot deformity. J Pediatr Orthop. 2004;24(4):353-7.         [ Links ]

119. Scher DM, Feldman DS, van Bosse HJ, Sala DA, Lehman WB. Predicting the need for tenotomy in the Ponseti method for correction of clubfeet. J Pediatr Orthop. 2004;24(4):349-52.         [ Links ]

120. Barker SL, Lavy CB. Correlation of clinical and ultrasonographic findings after Achilles tenotomy in idiopathic club foot. J Bone Joint Surg Br. 2006;88(3):377-9.         [ Links ]

121. Goksan SB, Bursali A, Bilgili F, Sivacioglu S, Ayanoglu S. Ponseti technique for the correction of idiopathic clubfeet presenting up to 1 year of age. A preliminary study in children with untreated or complex deformities. Arch Orthop Trauma Surg. 2006;126(1):15-21.         [ Links ]

122. Weigl D, Copeliovitch L, Itzchak Y, Strauss S. Sonographic healing stages of Achilles tendon after tenomuscular lengthening in children with cerebral palsy. J Pediatr Orthop. 2001;21(6):778-83.         [ Links ]

123. Berg EE. Percutaneous Achilles tendon lengthening complicated by inadvertent tenotomy. J Pediatr Orthop. 1992;12(3):341-3.         [ Links ]

124. Maranho DAC. Avaliação ultrassonográfica da reparação do tendão calcâneo após secção percutânea para a correção do equino residual do pé torto congênito idiopático [tese de mestrado]. Ribeirão Preto: Universidade de São Paulo; 2009.         [ Links ]

125. Maranho DAC, Nogueira-Barbosa MH, Simão MN, Volpon JB. Ultrasonographic evaluation of Achilles tendon repair after percutaneous sectioning for the correction of congenital clubfoot residual equinus. J Pediatr Orthop. 2009;29(7):804-10.         [ Links ]

126. Minkowitz B, Finkelstein BI, Bleicher M. Percutaneous tendo-Achilles lengthening with a large-gauge needle: a modification of the Ponseti technique for correction of idiopathic clubfoot. J Foot Ankle Surg. 2004;43(4):263-5.         [ Links ]

127. Dimeglio A, Bensahel H, Souchet P, Mazeau P, Bonnet F. Classification of clubfoot. J Pediatr Orthop B. 1995;4(2):129-36.         [ Links ]

128. Dyer PJ, Davis N. The role of the Pirani scoring system in the management of club foot by the Ponseti method. J Bone Joint Surg Br. 2006;88(8):1082-4.         [ Links ]

129. Flynn JM, Donohoe M, Mackenzie WG. An independent assessment of two clubfoot-classification systems. J Pediatr Orthop. 1998;18(3):323-7.         [ Links ]

130. Morcuende JA, Dobbs MB, Frick SL. Results of the Ponseti method in patients with clubfoot associated with arthrogryposis. Iowa Orthop J. 2008;28:22-6.         [ Links ]

131. Janicki JA, Narayanan UG, Harvey B, Roy A, Ramseier LE, Wright JG. Treatment of neuromuscular and syndrome-associated (nonidiopathic) clubfeet using the Ponseti method. J Pediatr Orthop. 2009;29(4):393-7.         [ Links ]



Mailing address:
Av. Caramuru, 2100, apto 1424
Ribeirão Preto-SP, Brazil, CEP 14030-000

Article received on 10/14/09, and aproved on 11/10/09



Study conducted in the Sector of Pediatric Orthopedics and Foot Disorders of the Department of Biomechanics, Medicine and Musculoskeletal Rehabilitation of Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo – USP – Ribeirão Preto. SP. Brazil.
All the authors declare that there is no potential conflict of interest referring to this article.

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License