Study Design
Tissues in the area of herniated lumbar discs were examined for inflammatory cytokines to elucidate the causes of sciatic pain in lumbar disc herniation.
Objectives
To determine the role of inflammatory cytokines in the stimulation of sciatic pain in lumbar disc herniation.
Summary of Background Data
It is postulated that in addition to mechanical compression of lumbar nerve roots and sensory root ganglia by herniated discs, there is a chemical stimulus to the production of sciatic leg pain. The exact mechanisms of chemical stimulation are not clearly defined.
Methods
During surgery, cases of lumbar disc herniation in 77 patients were classified macroscopically into protrusion, extrusion, and sequestration types. Tissues adjacent to nerve roots at the herniation were excised and analyzed biochemically and immunohistochemically for the presence of inflammatory cytokines and for the production of these cytokines and prostaglandin E2 in vitro.
Results
The homogenates of samples were analyzed for interleukin-1α, interleukin-1β, interleukin-6, tumor necrosis factor-α, and granulocyte-macrophage colony stimulating factor, which were detectable. Most of the cytokine-producing cells were histiocytes, fibroblasts, or endothelial cells in extrusion and sequestration types, and chondrocytes in protrusion type. The secretion of these cytokines and prostaglandin E2 was decreased by the addition of betamethasone. The prostaglandin E2 production was dramatically enhanced by additional interleukin-1α, but decreased by the addition of tumor necrosis factor-α.
Conclusion
The results demonstrate that at the site of lumbar disc herniation, inflammatory cytokines such as interleukin-1α are produced, which increases prostaglandin E2 production. Further studies are required to elucidate the role of inflammatory cytokines in causing sciatic pain.
