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Orthopaedic Proceedings
Vol. 85-B, Issue SUPP_III | Pages 278 - 278
1 Mar 2003
Guida P Esposito M Esposito A Costabile T Sorrentino B Esposito V De Rosa M Riccio V Riccardi G
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Objective: Starting from results of studies made in the last ten years about the presence of myofibroblasts as the main cells involved into fibro-contractile disease, we investigated if this cells were also involved into pathogenesis of club foot deformities.

Methods: Specimens removed surgically from five patients affected by congenital club foot were investigated. Each specimen was cut in three parts: the first, was fixed for optical microscopy in formalin; the second was fixed for trasmission electron microscopy (TEM) in glutaraldehyde and postfixed in osmium tetroxide; the third was immediately placed in cold (4°C) tissue culture medium. We have stained the first part of each specimen with: haematoxylineosin, Pasini, Masson, Congo red, Van Gieson, Martius scarlet blue and immunostaining for a-smooth muscle actin (a-SM actin). The third part of each specimen, dissected into 2mm. cubes, was place in standard medium and cultured at 37°C. On the cultured cells, we have valued metalloproteinases and a-SM actin expressions. Moreover, a part of culture cells, when reached confluence, were detached with trypsin-EDTA and centrifuged for 10 min. at 2000 rpm. to obtain a pellet, subsequently fixed for TEM.

Results: Optical and electron microscopy have showed, only in one of our cases, the presence of myofibroblast’s clusters in the Henry’s nodule and in the medial and lateral fibrous nodules, that are characteristic nodule of congenital club foot.

Conclusions: Starting from the results of our studies, we would like to study in detail the role of myofibroblast in the pathogenesis of club foot.