Study of Flexor Tenosynovium and Carpal Tunnel Syndrome
Principal Investigator: Peter C. Amadio, M.D.
Project Coordinator: Chunfeng Zhao, M.D. — zhao.chunfeng@mayo.edu
In most cases, the etiology of carpal tunnel syndrome (CTS) is considered to be idiopathic. It is our hypothesis that the subsynovial connective tissue (SSCT), a part of the tendon sheath in the carpal tunnel (Figure 4), is affected by repetitive activity, and that the resulting changes in the SSCT may contribute to development of CTS. Our current studies have focused on the vascular and morphological properties of the SSCT in CTS patients and cadaver controls.
Figure 4: Structure of subsynovial connective tissue intrasynovial tendon (SM: synovial membrane; SF: synovial fluid) extrasynovial tendon (PT: paratenon) flexor tendons in carpal tunnel (SSCT: sybsynovial connective tissue).
Vascular and Morphological Changes to the SSCT
A Verhoeff-van Gieson stain method was used to identify histopathology and to localize elastin in the SSCT of the middle finger FDS tendon within the carpal tunnel (Figure 5). Compared to the control, the density of vessels was greater in the CTS group, as was the average vessel thickness. In CTS, although there is no infiltration of inflammatory cells in the SSCT, elastin was decreased around and within vessels. These changes may be important in the development of the chronic fibrosis and ischemia that are characteristic of idiopathic CTS. Using transmission electron microscopy (TEM), SSCT from CTS patients showed larger collagen fibril diameter and decreased fibril density compared to control. This evidence suggests that the dynamic equilibrium of the extracellular matrix in the SSCT in CTS is shifted to a pattern of fibrosis, which could affect the mechanical properties of the SSCT. Our continued work will examine the mechanical properties of the SSCT.
Figure 5: Pathohistology in SSCT
A. Normal -whole image of SSCT showing uneven distribution of lastin, lesser mount of elastin in non-vascular site, and larger amount of elastin within and around vessels.
B. Pathologic-increased number of vessels, decreased elastin within and around vessels, obstructed lumen of vessels and Thickened vessel wall, and decreased reddish color intensity of stained collagen.
Collagen Type in SSCT
In this study, we used immunogold labeling and TEM to localize collagen types within the SSCT CTS patients and controls. In the control SSCT there were many striated collagen bundles with D-periodicity, elastin, and thin filaments between collagen fibrils, between collagen bundles, between elastin and collagen bundles and between collagen bundles and cells. Anti-type I and anit-type III collagen antibodies labeled with immunogold particle stained the striated collagen fibrils in both control and CTS specimens . However, collagen type VI was ubiquitous in the SSCT of both CTS and control specimens.
