Is clubfoot due to a reduction in fetal movement?

NewsBot · Oct 1, 2009

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A hypothesis and model of reduced fetal movement as a common pathogenetic mechanism in clubfoot.
Hester TW, Parkinson LC, Robson J, Misra S, Sangha H, Martin JE.
Med Hypotheses. 2009 Sep 26. [Epub ahead of print]

BACKGROUND: Clubfoot or Talipes equinovarus is characterised by an adducted forefoot, hindfoot varus, and ankle equinus deformity, varying in severity and ease of correction. It is one of the most common congenital defects, with a prevalence of around 1 per 1000. Ambiguity still surrounds the classification and pathogenesis of clubfoot.

METHODS: A literature search was performed using Pubmed, Ovid, and the Cochrane Databases, using search terms in isolation or combination: clubfoot, Talipes equinovarus, congenital foot deformities and joint development, identified articles were further hand searched and relevant references identified.

CONCLUSION: We propose that the underlying unifying factor in all cases of clubfoot is a lack of fetal movement. Fetal movement is a key developmental signal in the development of joints, and we suggest that this applies to the morphogenesis of the forefoot. Theories exist to explain specific individual features of clubfoot in certain cases and to explain experimental studies, however no common final pathway has been described. We believe that our hypothesis brings together key elements of these and will simplify understanding and classification of clubfoot.
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Admin2 · Oct 1, 2009

Related threads:
Other threads tagged with talipes equino varus and clubfoot

Stanley · Oct 1, 2009

In 1977, I heard a lecture by Mr. Appley, a British orthopedic surgeon on his research on club foot. He used chicks in eggs. He would tie up the foot and put it back in the egg. He found that if he did it for a few weeks prior to hatching, the chicks would be born with a malpositioned foot, that would reduced on its own. If it were for a longer time, the malpositioned foot would maintain its deformity.
He said that this is what you see in clubfoot, and related his findings to intrinsic vs. extrinsic clubfoot.

regards,

Stanley

NewsBot · Aug 23, 2021

Clubfoot pathology in fetus and pathogenesis. A new pathogenetic theory based on pathology, imaging findings and biomechanics-a narrative review
Ernesto Ippolito, Giulio Gorgolini
Ann Transl Med. 2021 Jul;9(13):1095

Several studies have described the pathology of idiopathic congenital clubfoot (ICCF) in fetus. Numerous pathogenetic theories have been postulated on ICCF, but many of them lack any objective evidence. Pathologic studies in fetus together with MRI studies in patients with ICCF seem to favor the theory of a muscular imbalance of the foot activators during fetal growth as the main pathogenetic factor of ICCF. Our objectives were: (I) To support the theory of muscular imbalance as the primary pathogenetic factor of ICCF; (II) To clarify why atrophy and shortening affect the activator muscles of the foot unevenly, as reported by literature. A literature search based on MEDLINE and the COCHRANE database was performed to identify all published studies from 1929 to 2020 which report ICCF pathology in fetus, its etiopathogenesis, and imaging and biomechanical studies showing how the basic pathology may be addressed by Ponseti treatment. A manual search was also performed of the references cited in studies, reviews, and university libraries. Altered size, shape and articular relationships of the tarsal bones, and uneven atrophy and shortening of the leg muscles together with capsule and ligament abnormalities were the main pathologic findings reported in fetus with ICCF. Regarding ICCF pathogenesis, the main debate is between the advocators of a primitive blastemal defect of the tarsal bones leading to the skeletal abnormalities and those who hold that the latter are secondary to a deforming force generated by the soft tissues. Imaging studies have shown that the Ponseti method is able to address the skeletal abnormalities, the correction of which is maintained until adulthood, whereas leg muscle atrophy is not improved but tends to worsen with growth. Preliminary histochemical studies of the soleus-Achilles tendon junction have shown a decrease of the growth factors and the presence of myostatin, both down-regulators of muscle growth in patients with ICCF. The authors postulate that a defect of both the radial and the longitudinal growth unevenly affecting the leg muscles with a consequent imbalance of the foot activators might be the main pathogenetic factor of ICCF. Further studies are needed to confirm this theory.
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