Oxidative stress in subsynovial connective tissue of idiopathic carpal tunnel syndrome.

Abstract

Ischemic-reperfusion injury is thought to be a cause of idiopathic carpal tunnel syndrome (CTS). The purpose of this study was to determine whether oxidative stress caused by ischemia-reperfusion injury in subsynovial connective tissue is associated with idiopathic CTS and its symptoms. Bioptic samples of tenosynovial tissue were collected from 20 idiopathic CTS patients during surgery. Control specimens of tenosynovial tissue were collected from eight non-CTS patients. Analysis included histological and immunohistochemical examination for the distribution of endothelial nitric oxide synthase (eNOS), nuclear factor (NF)-κβ, and transforming growth factor (TGF)-β RI in subsynovial connective tissues. Histological examinations showed a marked increase in fibroblast density and vascular proliferation in specimens from CTS patients. The expressions of eNOS, NF-κβ, and TGF-β RI in fibroblasts and vascular endothelial cells of subsynovial connective tissues of patients were significantly higher than in those of controls. A significant positive correlation was found between the subjective symptom severity of CTS, and the immunoreactivities of eNOS and NF-κβ. This study suggests that oxidative stress in subsynovial connective tissue is related to CTS and its symptoms.