The nucleus pulposus can set off an immune-mediated inflammatory process. The proteoglycan component of the nucleus is largely isolated from the immune system after birth. Herniation of a fragment of the nucleus pulposus may trigger an autoimmune reaction and generate an inflammatory process whose cellular component is mainly supported by macrophages. A non-immune-mediated mechanism of inflammation may be created by the nucleus, which reacts with surrounding histiocytes, fibroblasts, and chondrocytes to produce cytokines (interleukin 1a, interleukin-6, and tumor necrosis factor a) with an increase in phospholipase A2 leading to the release of prostaglandin E2, leukotrienes, and thromboxanes. In small amounts, prostaglandins enhance sensitivity of the nerve roots and other pain-producing substances like bradykinin. Experimental studies have shown that an oxygen-ozone gas mixture at the concentrations used for intradiscal treatment has the same effect as steroids on inhibiting cytokine production and hence the pain induced by the same.24
The oxygen-ozone mechanisms of action are currently being investigated and include the following25:
1. Enhanced oxygenation and reduced inflammation in the disease site due to the oxidizing effect on pain-producing chemical mediators
2. Direct effect of ozone on the mucopolysaccharides making up the nucleus pulposus with shrinkage of the disc herniation
3. Improved microcirculation and resolution of venous stasis, which results in better supply of oxygenated blood in the area of the compression
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