Abstract
Central traumatic injuries of the triangular fibrocartilage are frequent sources of ulnar wrist pain. It is unknown whether the fibrocartilage cells survive this trauma in the central part of the triangular fibrocartilage. The goal of this study was to determine the viability of cells in traumatic triangular fibrocartilage complex (TFCC) Palmer 1A lesions to estimate the role of apoptosis for the fate of fibrocartilage cells. Twenty-two patients with a symptomatic central traumatic tear in the triangular fibrocartilage were included in this study. The cartilage was debrided arthroscopically, and histologic sections were used for the analysis of cell viability and apoptosis. Cell viability was quantified by terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and apoptotic cells were visualized by poly(ADP-ribose) polymerase (PARP) p85 immunohistochemistry. The number of apoptotic cells was correlated with the total number of cells. In contrast with the control patients with only minimal amounts of TUNEL-positive cells, cell viability was markedly reduced in all analyzed patients with TFCC Palmer 1A lesion. Likewise, the number of PARP p85-positive cells was significantly increased in all patients. This indicates that the observed cell death is attributed to apoptosis. Concerning the distribution of apoptotic cells, the inner zone of the biospy showed much higher numbers of apoptotic cells than the outer zone in both PARP and TUNEL staining. In contrast to the analyzed patients, no apoptosis could be detected in the controls. High amounts of apoptotic cartilage cells could be detected within the inner part of the triangular fibrocartilage suggesting that fibrocartilage cells died in response to trauma and were not quickly replaced by new viable cells. PARP p85-positive cells indicate that the apoptotic cascade plays a crucial role in the TFCC Palmer 1A disorder.
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