[A mechanism for sciatic pain caused by lumbar disc herniation--involvement of inflammatory cytokines with sciatic pain].

We have investigated the role, if any, of inflammatory cytokines in herniated tissues in the development of sciatic pain resulting from lumbar disc herniation. In histological examination of herniated discs, granulation tissue was observed in 16.7% of protrusion type herniation,69.6% of extrusion type, and in 77.9% of sequestration type herniation. In homogenates of the herniated tissues. IL-1 alpha, IL-1 beta, IL-6, TNF-alpha and GM-CSF were detected in all types of lumbar disc herniation. Cells producing these cytokines were detected in the tissues after immunohistological staining In the protrusion type, cells producing these cytokines were detected in chondrocytes, and in extrusion or sequestration type, most of these cytokines producing cells were histiocytes or fibroblasts which constituted granulation tissue. The herniated tissue in culture produced these cytokines and prostaglandin E2, which ws remarkable decreased by the addition of betamethasone. The production of prostaglandin E2 in vitro was dramatically increased by the addition of IL-1 alpha and decreased by the addition of TNF-alpha. Furthermore, IL-1 alpha receptors and TNF-alpha were detected in cultured herniated tissue using radioimmunoassay techniques. The affinity of the IL-1-alpha receptor was higher than that of the TNF-alpha receptor. Based on these findings, it was suggested that inflammatory cytokines, such as IL-1 alpha, are produced in herniated tissue, which increased prostaglandin E2 production and caused in sciatic pain.