Abstract
Introduction
Degenerative articular disc perforations of the triangular fibrocartilage (TFC) of the wrist are characterized by fibrocartilage cell loss and are often associated with ulna-plus situations. Apoptosis has been found to play a crucial role in fibrocartilage cell loss, however, the molecular mechanism and mediators are still poorly understood.
Aim
The purpose of this study was to identify receptors to apoptosis in degenerative disc lesions.
Patients
Included in the study were 17 patients with degenerative articular disc tears of the TFC (Palmer type 2C). Following arthroscopic debridement of the TFC, histological sections were examined to assess the presence of apoptosis. Apoptosis was determined using TRAIL and death receptor DR4 agonists for immunohistochemical analyses. The number of cells positive for apoptosis was then correlated with ulna length.
Results
Cells positive for TRAIL and DR4 were found in all specimens. The number of cells positive for TRAIL was significantly increased in specimens of patients with an ulna positive variance (P = 0.040). However, DR4 was not significantly increased in ulna plus (P > 0.05). Both, TRAIL and DR4 positive cells were found to be evenly distributed throughout each specimen. There was no accumulation of any type of cells in any particular zone of the biopsies.
Conclusion
This is the first study that shows that TFCC cells express TRAIL and DR4, which suggests that apoptosis, as well as, mechanical trauma are involved in the development of disc perforation. The TRAIL/DR4 receptor system is a molecular mediator of apoptosis induction in TFC cells and therefore plays a role in cell loss in degenerative disc lesions.
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The study was supported by the ELAN Fonds, University of Erlangen, Germany.
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F. Unglaub and S. B. Thomas contributed equally to this work.
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Unglaub, F., Thomas, S.B., Kroeber, M.W. et al. Expression of TRAIL and death receptor DR4 in Palmer type 2 TFCC lesions. Arch Orthop Trauma Surg 130, 1215–1220 (2010). https://doi.org/10.1007/s00402-009-0988-4
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DOI: https://doi.org/10.1007/s00402-009-0988-4