Different Expression of Fibronectin and Tgf-Beta in Adhesion and Adhesion Free Tendon Repairs
Flexor tendon healing is often complicated by the formation of adhesions despite early active motion protocols. It is well known that migrating fibroblasts are responsible for adhesion formation, however, the pathophysiology of adhesion formation is not well understood. Fibronectin (FN) and TGF-beta are major contributions of adhesion formation. Our aim in this study was to compare the expression of FN and TGF-beta type I receptor (RI) in tendons healing with and without adhesions. Histology & Immunohistochemistry were performed on specimens from a canine study of flexor tendon healing 21 days after repair. We subdivided the specimens into groups that had no adhesions, significant adhesions, and contralateral control. Immunohistochemical analysis consistently demonstrated positive staining for FN and RI.
A large amount of FN was observed in the thick epitenon and in the epitenon cells in the group with no adhesions and in the control group (Fig. 1). Epitenon cells and fibroblasts were labeled for FN and RI in group with significant adhesions. It appears that FN and RI are upregulated in the epitenon in those tendons with heavy adhesion formation (Fig. 2).
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