Abstract
Carpal tunnel syndrome (CTS) is an idiopathic disease that results from increased fibrosis of the subsynovial connective tissue (SSCT). A recent study found overexpression of both transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) in the SSCT of CTS patients. This study investigated TGF-β and CTGF expression in a rabbit model of CTS, in which SSCT fibrosis is induced by a surgical injury. Levels of TGF-β1 and CTGF at 6, 12, 24 weeks after injury were determined by immunohistochemistry A significant increase in TGF-β1 and a concomitant significant increase in CTGF were found at 6 weeks, in addition to higher cell density compared to normal (all p<0.05), Interestingly, CTGF expression was reduced at 12 and 24 weeks, suggesting that an initial insult results in a time limited response. We conclude that this rabbit model mimics the fibrosis found in human CTS, and may be useful to study pathogenetic mechanisms of CTS in vivo.
Highlights
Idiopathic Carpal tunnel syndrome (CTS) [1,2] is characterized as well by non-inflammatory fibrosis of the (SSCT) within the carpal tunnel
In an animal model of subsynovial connective tissue (SSCT) fibrosis, we have demonstrated that TGF-b1 and connective tissue growth factor (CTGF) are increased at 6 weeks, with higher cell density compared to normal
CTGF is expressed in fibroblasts during the wound healing process [18]
Summary
Idiopathic CTS [1,2] is characterized as well by non-inflammatory fibrosis of the (SSCT) within the carpal tunnel. While the presence of TGF-b and a downstream cytokine, CTGF, suggests strongly that TGF-b signaling is implicated in SSCT fibrosis, clinical data from the SSCT of CTS patients is limited, due to the need for biopsy, which is most commonly accomplished at the time of surgery, when the CTS is well advanced. The model is created by surgically stretching SSCT, thereby disrupting the normal elasticity of the tissue. Pathological alterations in this model include increased fibroblast proliferation and overexpression of TGF-b receptors [11,12,13], suggesting that the shearing injury activates TGF-b signaling
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