The muscles in club foot--a histological histochemical and electron microscopic study

Abstract

In talipes equino-varus the diminished bulk of the calf muscle suggests a neuromuscular defect. Accordingly, biopsies were taken from the postero-medial and peroneal muscle groups, and occasionally from abductor hallucis, in sixty patients mostly under the age of five years; 111 were studied histochemically and histologically, and a further fifty-three by electron-microscopy. Histochemical anomalies were revealed in ninety-two specimens; the muscle fibres in the other nineteen varied in size but were abnormal at the ultramicroscopic level, as were all specimens examined with the electron microscope. Evidence of neurogenic disease was seen in most instances and was more obvious in the older patients. The pattern of abnormality was similar in both muscle groups. It is thought that shortening of the postero-medial muscles may result from a small increase of fibrosis due to minor innervation changes occurring in intra-uterine life. There is evidence that immobilisation, stretching or relaxation of muscles does not account for the anomalies observed. This study of the extrinsic muscles in talipes equino-varus indicates a dominant neurogenic factor in its causation.

Tibialis Anterior Tendon Transfer after Clubfoot Surgery

“…Recent biopsy studies of the extrinsic muscles of the calf during clubfoot surgery have demonstrated fiber type disproportion, reduction in the number of muscle fibers, increased neuromuscular junctions, and electron microscopic abnormalities [22,24,33]. The normal ratio of type I to type II fibers is 1:2 but in clubfeet the relationship is approximately 7:1.…”

Copy number analysis of 413 isolated talipes equinovarus patients suggests role for transcriptional regulators of early limb development

“…Despite the frequency of talipes equinovarus in neurological disorders, no consistent neuromuscular abnormalities have been identified in isolated talipes equinovarus patients using muscle biopsy or electrophysiological examinations. [4][5][6][7] Most cases of clubfeet (80%) occur as isolated birth defects and are considered idiopathic. 8 Approximately 25% of patients with isolated talipes equinovarus report a family history of talipes equinovarus, suggesting a genetic basis for this disorder.…”

Pé torto congênito

“…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 pressure 10,11 ; interruption in fetal development 12 ; viral infections 13 ; vascular deficiencies 14,15 ; muscular alterations [16][17][18][19][20] ; neurological alterations [21][22][23][24][25][26][27] ; defect in the development of bones structures 3,28,29 and genetic defects. 7,[30][31][32][33][34][35][36][37][38][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 hindfoot 18,20 corroborates the hypothesis of primary defect of soft parts and neuromuscular units that lead to bone alterations.…”

“…7,[30][31][32][33][34][35][36][37][38][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 hindfoot 18,20 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 hindfoot 30,34 are structurally similar to those present in palmar fibromatosis and express high levels of type III collagen and certain growth fac-tors, 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.…”