IMMUNOHISTOCHEMICAL PROFILE OF VEGF, PGE2 AND TGF-β IN INFLAMMATORY TENOSYNOVITIS OF CARPAL TUNNEL SYNDROME

Inflammatory tenosynovitis is an inflammation that involves the tendons and synovial sheaths caused by minor trauma repeated for a long period of time. This inflammatory disease may be involved in the onset of tunnel carpal syndrome (CTS), because of the thickening of the tendon sheath that may produce an increase in the carpal canal pressure and damage of the median nerve in the wrist. Recent studies suggest that in patients with CTS pathological changes occur in the subsynovial connective tissue, such as vascular proliferation and non-inflammatory synovial fibrosis. However, little is known about the pathological mechanism of tenosynovial thickening. The aim of this study is to evaluate the potential role of vascular endothelial growth factor (VEGF), prostaglandin E2 (PGE2) and trasforming growth factor-beta (TGF-β) in the modifications of connective synovial tissue of CTS specimens in order to determine whether these factors play a role in the development of this disease. Ten specimens from patients with CTS and four control tissues (cadavers) were analyzed by immunohistochemistry using specific antibodies against these growth factors. A temporary increase in the production of these molecules was found in cells within the vessels and synovial lining during the intermediate phase of the syndrome, when the histology of the tenosynovium changes from oedematous to fibrotic. Our data confirm a close correlation between the expression of PGE2 and VEGF. Recent histological examinations have shown a marked increase in vascular proliferation and reduction of fibroblast density in specimens from CTS patients during the intermediate phase. Our study indicates that the expression of TGF-β in fibroblasts and vascular endothelial cells of synovial connective tissues of CTS patients was significantly higher than in those of controls. These findings suggest that angiogenesis appears to take place as a part of a regenerative reaction that results in fibrosis. We believe that VEGF, TGF-β and PGE2 may be potential therapeutic targets in the treatment of this disease although proof of this evidence requires further studies.