Effect of TGF-beta Inducible Early Gene Deficiency on Flexor Tendon Healing

Principal Investigator: Peter C. Amadio, M.D.
Project Coordinator: Chunfeng Zhao, M.D. — zhao.chunfeng@mayo.edu

Figure 1: Cadaver control SSCT close to the tendon (SEM) x 1.00K)

The tenosynovium in the carpal tunnel is part of the visceral synovial layer of the wrist bursa. It is connected to the flexor tendons and the medial nerve by the subsynovial connective tissue (SSCT). While fibrosis of the tissue is nearly universally noted in patients with carpal tunnel syndrome (CTS), the relationship, if any, between the fibrosis and the nerve pathology is unknown. In this observational study, we used light and scanning electron microscope imaging of the SSCT to gather information about the construction of this functional structure, and to help formulate hypotheses as to how the known changes to this tissue might be causally associated with the typical nerve compression of carpal tunnel syndrome. The SSCT consists of collagenous bundles parallel to the tendon, interconnected by smaller microfibrillar collagenous fibers. During tendon motion the loose collagenous fibers between adjacent layers are stretched. Our control tissue showed interconnections between all the parallel layers (Fig. 1), while in the patients the interconnections disappear, leaving thicker parallel collagenous bundles (Fig. 2).

Figure 1: Patient SSCT close to the tendon

The changes in the patient specimens were most marked close to the tendon, and became progressively less severe in more superficial layers. Our observation that the most severe changes to the SSCT in the patients were close to the tendon, suggest that these changes may be the result of a shearing injury. Our ongoing hypothesis is that this resulting thickening of the SSCT alters its gliding and nutritional function, and thereby affects the median nerve, resulting in the characteristic findings of carpal tunnel syndrome.