Apoptotic pathways in degenerative disk lesions in the wrist.
OBJECTIVE
Degenerative articular disk perforations of the triangular fibrocartilage (TFC) of the wrist could result from chronic loading of the ulnocarpal joint. Apoptosis played a crucial role in fibrocartilage cell loss, and the purpose of this study was to clarify which apoptotic pathway was involved in the development of degenerative disk lesions. We also investigated whether ulna length played an etiologic role in the occurrence of fibrocartilage cell loss.


METHODS
Included in the study were 17 patients with degenerative articular disk tears of the TFC (Palmer type 2C). After arthroscopic debridement of the TFC, histologic sections were examined to assess the presence of apoptosis. Apoptosis was determined by use of caspase 3, caspase 8, and caspase 9 immunohistochemistry. Furthermore, Fas ligand and BID (BH3 interacting domain death) agonist were applied for immunohistochemical analysis.


RESULTS
Cells positive for caspase 3, caspase 8, caspase 9, Fas ligand, and BID were found in all specimens. The number of cells positive for caspase 3 and BID was significantly increased in specimens from patients with an ulna-positive variance. In contrast, for cells positive for caspase 8, caspase 9, and Fas ligand, no significant difference was found between specimens from patients with an ulna-positive variance and those from patients with an ulna-neutral/ulna-negative variance.


CONCLUSIONS
The extrinsic and intrinsic apoptotic pathways are involved in the development of degenerative disk lesions. Fibrocartilage cell loss occurs mainly through the intrinsic apoptotic pathway. The accumulation of apoptotic cells is not significantly different between the 3 zones of the TFC. It could be verified that ulna length is correlated with fibrocartilage cell loss.


CONCLUSIONS
Ulnar shortening is a valuable treatment option for degenerative TFC lesions. Knowledge of the specific apoptotic pathway that is causing degenerative disk lesions is critical in selecting the appropriate and most beneficial therapeutic treatment to halt further cell loss and the degeneration of the TFC.
Unglaub
Frank
F
Department of Plastic and Hand Surgery, University of Erlangen, Erlangen, Germany. Frank.Unglaub@uk-erlangen.de
Thomas
Susanne B
SB
Kroeber
Markus W
MW
Dragu
Adrian
A
Fellenberg
Jörg
J
Wolf
Maya B
MB
Horch
Raymund E
RE
D000328:Adult; D017209:Apoptosis / Q000502:physiology*; D001182:Arthroscopy; D051023:BH3 Interacting Domain Death Agonist Protein / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D003646:Debridement / Q000379:methods; D053222:Fas Ligand Protein / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D007592:Joint Diseases / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D008297:Male; D011379:Prognosis; D051478:Triangular Fibrocartilage / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D014955:Wrist Joint / Q000473:pathology* / Q000601:surgery
D051023:BH3 Interacting Domain Death Agonist Protein; C494814:BID protein, human; D053222:Fas Ligand Protein; D020169:Caspases