Ozone therapy has been used to treat disc herniation for more than four decades. There are several papers describing results and mechanism of action. However, it is very important to define the characteristics of extruded disc herniation. Although ozone therapy showed excellent results in the majority of spinal diseases, it is not yet fully accepted within the medical community. Perhaps it is partly due to the fact that, sometimes, indications are not appropriately made. The objective of our work is to explain the mechanisms of action of ozone therapy on the extruded disc herniation. Indeed, these mechanisms are quite different from those exerted by ozone on the protruded disc herniation and on the degenerative disc disease because the inflammatory response is very different between the various cases. Extruded disc herniation occurs when the nucleus squeezes through a weakness or tear in the annulus. Host immune system considers the nucleus material to be a foreign invader, which triggers an immune response and inflammation. We think ozone therapy modulates this immune response, activating macrophages, which produce phagocytosis of extruded nucleus pulposus. Ozone would also facilitate the passage from the M1 to M2 phase of macrophages, going from an inflammatory phase to a reparative phase. Further studies are needed to verify the switch of macrophages.
Degeneration of the intervertebral disc is one of the most frequent causes of lumbar pain, and it puts an extreme strain on worldwide healthcare systems. Finding a solution for this disease is an important challenge as current surgical and conservative treatments fail to bring a short-term or long-term solution to the problem. Medical ozone has yielded excellent results in intervertebral disc pathology. When it comes to extruded disc herniation, ozone is the only etiological treatment because it stimulates the immune system to absorb the herniated portion of the nucleus pulposus, thus resolving discal extrusion. This work aims to examine the biomolecular mechanisms that lead to intervertebral disc degeneration while highlighting the significance of oxidative stress and chronic inflammation. Considering that ozone is a regulator of oxidative stress and, therefore, of inflammation, we assert that medical ozone could modulate this process and obtain inflammatory stage macrophages (M1) to switch to the repair phase (M2). Consequently, the ozone would be a therapeutic resource that would work on the etiology of the disease as an epigenetic regulator that would help repair the intervertebral space.
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