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Pathogenesis of Idiopathic Clubfoot

Pathogenesis of Idiopathic Clubfoot During embryonic development the foot passes consecutively into three different positions: (1) when the embryo is in the 15-mm stage the foot is in a straight line with the leg (initial position); (2) by 30 mm the foot passes to a marked equinovarus-adductus position (embryonic position); and (3) finally, by 50 mm, the foot changes to a slightly equinovarus adductus position (fetal position). The morphologic and structural changes of the foot from the initial to the embryonic position result from the growth of the distal ends of the fibula and of the skeletal elements of the lateral foot during the “fibular phase” of rapid growth (from 21 to 30 mm). The changes form the embryonic to the fetal posistion are due to the growth of the distal ends of the tibia and of the skeletal rays of the medical foot during the “tibial phase” of rapid growth. Many known noxious industrial chemicals (and probably many more yet to be recognized) have antimitotic and antimetabolic action. Depending on the characteristics of the chemical, some produce permanent arrest and therefore congenital malformation, while others cause temporary growth arrest, e.g., Harris transverse lines, which is frequently unnoticed. Finally, some substances, e.g., glucocorticoids, cause a growth delay. Depending on the developmental stage of the embryo and the duration of the action of the noxious substance, growth arrest of the foot occurs in an attitude close to the embryonic position. If it occurs at the end of the fibular phase and during the first half of the tibial phase, the foot will remain in a permanent and marked equinovarus-adductus position, and a severe clubfoot will result. When a noxious chemical acts only during the last half of the tibial phase, a mild, flexible clubfoot will result because by this stage most parts of the embryonic components have been corrected. If it occurs at the end of the tibial phase, a simple metatarsus adductus deformity will persist. As soon as the growth arrest phase ends, all of the skeletal elements begin to grow again, but only from a a later point in development. If the growth disturbance occupies the entire tibial phase, neither the tibia nor the skeletal elements of the foot would be able to complete a rapid growth spurt, since by that stage the moment genetically programmed for such growth has already passed. The morphology of the deformities existing in the clubfoot corresponds to the morphologic program of the embryonic foot. Other more accentuated deformities arise from soft tissue contractures or from the growth of skeletal elements in an abnormal position. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Orthopaedic and Related Research (CORR) Wolters Kluwer Health

Pathogenesis of Idiopathic Clubfoot

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ISSN
0009-921X
eISSN
1528-1132

Abstract

During embryonic development the foot passes consecutively into three different positions: (1) when the embryo is in the 15-mm stage the foot is in a straight line with the leg (initial position); (2) by 30 mm the foot passes to a marked equinovarus-adductus position (embryonic position); and (3) finally, by 50 mm, the foot changes to a slightly equinovarus adductus position (fetal position). The morphologic and structural changes of the foot from the initial to the embryonic position result from the growth of the distal ends of the fibula and of the skeletal elements of the lateral foot during the “fibular phase” of rapid growth (from 21 to 30 mm). The changes form the embryonic to the fetal posistion are due to the growth of the distal ends of the tibia and of the skeletal rays of the medical foot during the “tibial phase” of rapid growth. Many known noxious industrial chemicals (and probably many more yet to be recognized) have antimitotic and antimetabolic action. Depending on the characteristics of the chemical, some produce permanent arrest and therefore congenital malformation, while others cause temporary growth arrest, e.g., Harris transverse lines, which is frequently unnoticed. Finally, some substances, e.g., glucocorticoids, cause a growth delay. Depending on the developmental stage of the embryo and the duration of the action of the noxious substance, growth arrest of the foot occurs in an attitude close to the embryonic position. If it occurs at the end of the fibular phase and during the first half of the tibial phase, the foot will remain in a permanent and marked equinovarus-adductus position, and a severe clubfoot will result. When a noxious chemical acts only during the last half of the tibial phase, a mild, flexible clubfoot will result because by this stage most parts of the embryonic components have been corrected. If it occurs at the end of the tibial phase, a simple metatarsus adductus deformity will persist. As soon as the growth arrest phase ends, all of the skeletal elements begin to grow again, but only from a a later point in development. If the growth disturbance occupies the entire tibial phase, neither the tibia nor the skeletal elements of the foot would be able to complete a rapid growth spurt, since by that stage the moment genetically programmed for such growth has already passed. The morphology of the deformities existing in the clubfoot corresponds to the morphologic program of the embryonic foot. Other more accentuated deformities arise from soft tissue contractures or from the growth of skeletal elements in an abnormal position.

Journal

Clinical Orthopaedic and Related Research (CORR) – Wolters Kluwer Health

Published: May 1, 1984

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