Object: The nucleus pulposus has been reported to be an immunologically privileged site. The expression of Fas ligand (FasL) on normal and herniated lumbar disc cells has been reported. The relationship between a physiological barrier and the role of FasL has not yet been addressed. To clarify this relationship and to investigate a possible pathogenesis of intervertebral disc degeneration (IDD), the expression of Fas and FasL (a mean apoptosis index) on normal and stabbed-disc cells was examined in a rabbit model of IDD.
Methods: Using defined needle gauges and depths, the anular puncture model of IDD was established in rabbits. The normal and stabbed discs were harvested at 3, 6, and 10 weeks after surgery. Immunohistochemical staining of these discs for Fas and FasL was performed using standard procedures. The mean apoptosis indices of the disc cells were determined using flow cytometry analysis. The nucleus pulposus cells from the normal discs exhibited relatively weak immunopositivity, whereas the nucleus pulposus cells from the stabbed discs exhibited strong immunopositivity. There was a significant difference (p < 0.001) in the percentage of FasL-positive nucleus pulposus cells between the normal discs and the stabbed discs. The mean apoptosis indices of the stabbed-disc cells at 3, 6, and 10 weeks poststab were significantly higher than those in normal disc cells (p < 0.001, 0.002, and 0.006, respectively). There was a significant correlation between the degree of FasL-positive expression and the degree of Fas-positive expression of the nucleus pulposus cells poststab (r = 0.571, p = 0.0036).
Conclusions: These observations indicate that the nucleus pulposus is an immunologically privileged site. This immunological privilege is maintained by FasL and the physiological barrier together. When the physiological barrier was damaged (by stabbing the disc), the role of FasL changed, and FasL was coexpressed with Fas to induce apoptosis of disc cells. These results indicate that an autoimmune reaction may be a possible pathogenesis of IDD.