ABSTRACT
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.
