The Role of Cyclooxygenase-2 in Lumbar Disc Herniation

Abstract

Study Design. The expression of cyclooxygenase-2 was studied immunohistologically in specimens from lumbar disc herniation. The cultured disc cells also were examined to evaluate the significance of cyclooxygenase-2, which might be involved in the pathogenesis of lumbar disc herniation. Objective. To investigate whether cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation. Summary of Background Data. Prostaglandin E2 is one of the most important mediators contributing to pathogenetic components of lumbar disc herniation. Cyclooxygenase-2, the rate-limiting enzyme of prostaglandin E2 synthesis, has been identified and extensively investigated in other inflammatory diseases. However, the role of cyclooxygenase-2 in lumbar disc herniation has never been addressed. Methods. Fifteen specimens from patients with lumbar disc herniation and five control discs from traumatic burst fracture were harvested. The expression of cyclooxygenase-2 was evaluated immunohistologically. The ability of cultured disc cells to produce prostaglandin E2 with inflammatory stimulus in the presence or absence of a selective inhibitor of cyclooxygenase-2 was investigated. At the same time, the induction of cyclooxygenase-2 mRNA of these cells by reverse transcriptase–polymerase chain reaction was detected. The manner in which this prostaglandin E2 production could be suppressed by various doses of a cyclooxygenase-2 inhibitor also was investigated. Results. Immunohistologically, the expression of cyclooxygenase-2 was observed only in the lumbar disc herniation specimens. The cultured cells had a strong ability to produce prostaglandin E2 coinciding with cyclooxygenase-2 mRNA induction. A selective inhibitor of cyclooxygenase-2 inhibited this prostaglandin E2 production in a dose-dependent manner. Conclusion. Cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation through upregulation of prostaglandin E2 production.