Subsynovial connective tissue is sensitive to surgical interventions in a rabbit model of carpal tunnel syndrome.
The most common histological finding in carpal tunnel syndrome (CTS) is non-inflammatory fibrosis and thickening of the subsynovial connective tissue (SSCT) in the tunnel. While the cause of SSCT fibrosis and the relationship of SSCT fibrosis and CTS are unknown, one hypothesis is that SSCT injury causes fibrosis, and that the fibrosis then leads to CTS. We investigated the sensitivity of the SSCT to injuries. Two types of surgical interventions were performed in a rabbit model: A skin incision with tendon laceration and SSCT stretching sufficient to damage the SSCT, and skin incision alone. Twelve weeks after surgery, the rabbit carpal tunnel tissues were studied with immunochemistry for TGF-β receptors 1, 2, and 3, collagen III, and collagen VI. All TGF-β receptors were expressed. The percentages of the TGF-β receptors' expressions were less in the control SSCT fibroblasts than in the fibroblasts from rabbits with surgical interventions. The surgical interventions did not result in any alteration of collagen III expression. However, both surgical interventions resulted in a significant decrease in collagen VI expression compared to the control group. The two surgical interventions achieved similar expression of TGF-β receptors and collagens. Our results provide evidence that the SSCT is sensitive to surgical interventions, even when these are modest. Since SSCT fibrosis is a hallmark of CTS, these data also suggest that such fibrosis could result from relatively minor trauma.
Biomechanics Laboratory, Division of Orthopedic Research, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA.
Yu-Long
YL
Sun
Tamami
T
Moriya
Chunfeng
C
Zhao
Ramona L
RL
Kirk
Takako
T
Chikenji
Sandra M
SM
Passe
Kai-Nan
KN
An
Peter C
PC
Amadio
D000818:Animals; D002349:Carpal Tunnel Syndrome / Q000601:surgery*; D024061:Collagen Type III / Q000378:metabolism; D024142:Collagen Type VI / Q000378:metabolism; D003238:Connective Tissue / Q000378:metabolism / Q000473:pathology* / Q000601:surgery*; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis / Q000378:metabolism / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism; D011817:Rabbits; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism; D033081:Shear Strength / Q000502:physiology; D000074402:Synovectomy; D013583:Synovial Membrane / Q000378:metabolism / Q000473:pathology*; D014945:Wound Healing / Q000502:physiology
D024061:Collagen Type III; D024142:Collagen Type VI; D011509:Proteoglycans; D018125:Receptors, Transforming Growth Factor beta; C071736:betaglycan; D017346:Protein Serine-Threonine Kinases; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II