title: Expression of TRAIL and death receptor DR4 in Palmer type 2 TFCC lesions.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  The purpose of this study was to identify receptors to apoptosis in degenerative disc lesions.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Plastic and Hand Surgery, University Erlangen, Krankenhausstrasse 12, Erlangen, Germany. Frank.Unglaub@uk-erlangen.de
authors.forename: Frank
authors.initials: F
authors.lastname: Unglaub
authors.forename: Susanne B
authors.initials: SB
authors.lastname: Thomas
authors.forename: Markus W
authors.initials: MW
authors.lastname: Kroeber
authors.forename: Adrian
authors.initials: A
authors.lastname: Dragu
authors.forename: Jörg
authors.initials: J
authors.lastname: Fellenberg
authors.forename: Thomas
authors.initials: T
authors.lastname: Mittlmeier
authors.forename: Maya B
authors.initials: MB
authors.lastname: Wolf
authors.forename: Raymund E
authors.initials: RE
authors.lastname: Horch
mesh_terms: D000328:Adult; D017209:Apoptosis; D001182:Arthroscopy; D003646:Debridement; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand / Q000096:biosynthesis*; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000096:biosynthesis*; D051478:Triangular Fibrocartilage / Q000293:injuries / Q000378:metabolism* / Q000601:surgery
chemical_list: D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D053221:TNF-Related Apoptosis-Inducing Ligand; C105190:TNFRSF10A protein, human; C505653:TNFSF10 protein, human