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A hypothesis and model of reduced fetal movement as a common pathogenetic mechanism in clubfoot
T W Hester1, L C Parkinson, J Robson
1Neuroscience Centre and Pathology Group, Institute of Cell and Molecular Sciences, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, The Royal London Hospital, Whitechapel, London E1 1BB, United Kingdom.
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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