The role of cyclooxygenase-2 in lumbar disc herniation

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.

To investigate whether cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation.

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.

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.

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.

Cyclooxygenase-2 might be involved in the pathogenesis of lumbar disc herniation through upregulation of prostaglandin E2 production.