Evaluation of the material properties of the subsynovial connective tissue in carpal tunnel syndrome
Introduction
The subsynovial connective tissue (SSCT) is the most characteristic structure in the carpal tunnel. It consists of multiple thin layers of collagenous fibers, in which blood and lymphatic vessels are richly represented (Guimberteau, 2001, Ettema et al., 2004). The SSCT plays an important role as a gliding unit to diminish friction and protect the vascular system within the SSCT. Noninflammatory fibrosis of the tenosynovium is the most common finding in idiopathic carpal tunnel syndrome (CTS), but its relationship to the neuropathy is unknown. Some have suggested that the changes in the SSCT might cause the neuropathy, through altered mechanics and vascularity in the carpal tunnel (Lluch, 1992, Sud et al., 2002).
Recent studies have demonstrated alterations in the gliding mechanism of the SSCT in patients with CTS (Ettema et al., 2004), as well as increased collagen type III, TGF-beta and abnormal angiogenesis (Ettema et al., 2004, Oh et al., 2004, Oh et al., 2005, Oh et al., 2006). These changes support the hypothesis that idiopathic CTS may be caused primarily by an injury to the SSCT, with secondary nerve involvement, rather than by direct damage of the nerve itself.
If CTS is caused, or can be caused, by an injury to the SSCT, then the mechanism of that injury must be plausible. One such mechanism could be a shearing injury of the SSCT, due to excessive differential tendon motion. There are many reports describing highly repetitive work as one of the risk factors for idiopathic CTS (Finkel, 1985, Atcheson et al., 1998, Chin and Jones, 2002). One biomechanical study has reported that differential finger motion with the wrist flexed elevated the tendon gliding resistance in the carpal tunnel (Zhao et al., 2007). The thickening of the fibers, noted by Ettema et al., 2004, Oh et al., 2006 could be the result of healing of such an injury. To date, there have been no reports describing the mechanical properties of the SSCT in the carpal tunnel. The purpose of this study was to compare the mechanical properties of the SSCT of normal human cadavers in response to shear stress with those of patients with CTS.
Section snippets
Specimen preparation
This study was approved by our Institutional Review Board, and all patients gave informed consent for the use of their tissue in the study. Ten SSCT samples were obtained from 10 wrists of eight adult patients (2 males and 6 females) with idiopathic CTS undergoing open carpal tunnel release surgery. The patients’ ages ranged from 24 to 71 years (mean, 45 years). A full thickness SSCT biopsy, 5 mm wide by 10 mm long, was taken from the visceral synovium on the anterior middle finger flexor
Results
There were no surgical complications as a result of the synovial biopsy.
The mean SSCT thickness for the carpal tunnel patients; 1.46 mm (SD 0.56 mm) was significantly greater than the normal control, 0.48 mm (SD 0.12 mm) (P < 0.05).
Fig. 2 shows representative shear stress–shear strain curves. Typically, no load (i.e., a “toe” region) was observed during the initial strain phase. The failure mode during testing included mid-substance rupture (n = 5 patients, n = 9 controls) or avulsion from the plastic
Discussion
Recently, several immunohistological (Ettema et al., 2004, Oh et al., 2005) and biochemical studies (Freeland et al., 2002, Hirata et al., 2004, Hirata et al., 2005, Tsujii et al., 2006) have been reported describing the SSCT in carpal tunnel syndrome patients. The SSCT of CTS patients is fibrotic, with increased amounts of type III collagen, tenascin-C, versican, VEGF, PGE-2, MMP-2, IL-6, and TGF-beta, and decreased elastin. Sud et al. (2002) have shown that the in vitro tenosynovial
Acknowledgement
This study was funded by grants from NIH (NIAMS AR49823) and Mayo Foundation.
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