Postlaminectomy Osteopontin Expression and Associated Neurophysiological Findings in Rat Peridural Scar Model

Abstract

Study Design. Experimental study. Objective. To evaluate the postlaminectomy osteopontin expression in peridural scar tissue and structures within the vertebral canal as well as to correlate these findings with peridural scar extent, scar vascularity, and neurophysiological findings. Summary of Background Data. Postoperative peridural scar formation may be a cause of failed back surgery syndrome; however, the exact mechanism is unknown. Osteopontin (OPN) may play important role in this process, as it is involved in wound healing, organ fibrosis, and nerve tissue response to injury. Methods. The experiment was carried out in 2 experimental groups: group I—laminectomy, group II—sham. Six weeks after surgery animals' neurologic status was evaluated by spinal somatosensory-evoked potentials. Histologic assessment include the following: scar extent, thickness of dura, presence of the arachnoid adhesions was performed on hematoxylin and eosin stained transversal sections of the operated level. OPN expression in peridural scar, dorsal root ganglions (DRG) and within vertebral canal was studied using immunohistochemistry. In addition, scar vascularity was assessed with CD31 mAb. Obtained results were analyzed statistically. Results. Laminectomy resulted in significant loss of somatosensory-evoked potentials amplitudes and thicker dura compared to sham surgery. Sham group physiologically expressed OPN in bone tissue. We found significant increase in OPN immunoreactivity in meninges, arachnoid adhesions, and tissue surrounding DRG in group I when compared with group II. Significant postlaminectomy increase in percentage of OPN positive DRG neurons (P = 0.0002, 43.041 ± 3.706 vs. 21.227 ± 3.481), which correlated with scar extent, and scar OPN immunoreactivity was also noted. Conclusion. This study identifies OPN as a major player in formation of epidural fibrosis and a marker of DRG response to peridural scar formation. We confirm previous neurophysiological findings and provide new evidence supporting the theory of DRG involvement in peridural scar-related recurrent radiculopathy. Further studies are warranted to fully assess the relevance of these findings.