PATHOMECHANISM OF PAIN-RELATED BEHAVIOR PRODUCED BY ALLOGRAFTS OF INTERVERTEBRAL DISC IN THE RAT

Study Design. This study was designed to evaluate whether allografts o f intervertebral disc materials produce hyperalgesia in the rat and wh ether an immune response, pH, or chemicals correlate with the induced hyperalgesia. Objective. To elucidate the pathomechanisms of radicular pain secondary to lumbar disc herniation. Summary of Background Data. It has been reported that a low pH, an autoimmune reaction, or chemic al radiculitis is likely responsible for radicular pain associated wit h lumbar disc herniation. In animal studies, it has been shown that hy peralgesia (an increased sensitivity to painful stimuli) involves acti vation of phospholipase A(2) and nitric oxide synthase. Methods. Fat, nucleus pulposus, and anulus fibrosus were allografted into the epidur al space at L6 in the rat. Withdrawal response thresholds to mechanica l stimuli and withdrawal response latencies to thermal stimuli on the tail and pH in the applied tissues were measured after surgery. Interl eukin-1, phospholipase A(2), and nitric oxide synthase were examined i n the applied tissues using immunohistochemistry, nicotineamide adenin e dinucleotide phosphate-diaphorase histochemistry, and in situ hybrid ization. Results. Allografted fat did not produce hyperalgesia. Allogr afts of nucleus pulposus and nucleus pulposus plus anulus fibrosis sho wed evidence of mechanical and thermal hyperalgesia, respectively. The re were no observed changes in pH over time. Although interleukin-1 wa s demonstrated in all applied tissues, phospholipase A(2) ws only obse rved around the applied nucleus pulposus and nucleus pulposus plus anu lus fibrosus. Nitric oxide synthase was only markedly increased around the applied tissues. Conclusion. The nucleus pulposus and anulus fibr osus produced different forms of hyperalgesia (mechanical vs. thermal) associated with different and distinct immunohistochemical changes. I t is possible that radicular pain of a lumbar disc herniation results from chemicals, such as phospholipase A(2) and nitric oxide.