Carbon Dioxide Therapy Eases the Pain of Osteoarthritis and Revitalizes Tissue In Joints

Osteoarthritis is a leading cause of pain, lost training and competition days, and abandonment seen by veterinarians across the industry. Because there is no cure for osteoarthritis, the best we can do is prevent its onset and slow its progression. DioxyfinTM transdermal carbon dioxide is an ideal way to ease pain in animals with this condition and spur the growth of healthy new tissue.

Osteoarthritis is a disease of the joints that involves an injury to cartilage, a highly specialized and unique tissue that lines the bones where they meet and allows the smooth, frictionless movement between one bone and another. Cartilage consists mostly of collagen that is produced from underlying cells and is continuously revitalized. A change in the revitalization process leads to a loss of cartilage and, eventually, failure of the joint. This change can be caused by direct traumatic injury to the joint, simple strain from overuse, or spillover from nearby inflamed tendons.

To heal the injured cartilage, the body activates an inflammatory process that attracts white blood cells and other substances called mediators,1 to the damaged site. One side effect of the inflammatory process is the overproduction of reactive oxygen species (ROS),2 which are chemical that can be destructive under certain conditions. Together, inflammation and ROS accelerate the breakdown of cartilage and stall its production. As a consequence, the cartilage slowly begins to degrade, causing pain and dysfunction in the joint.

Given this process, the goals of therapy are to (1) reduce the inflammation, (2) counteract the ROS, and (3) increase the formation of collagen so that the revitalization of joint tissue can begin again.

Dioxyfin transdermal carbon dioxide is ideal for this therapy because it reduces inflammation and neutralizes the destructive actions of ROS when it is applied directly to the affected tissue and joints. The result is a reduction in pain and swelling as well as a healthy environment for the formation of new tissue and collagen.

REFERENCES

  1. Marcu KB, Otero M, Olivotto E, Borzi RM, Goldring MB. NF-kappaB signaling: Multiple angles to target OA. Current drug targets. 2010;11(5):599. https://www.ncbi.nlm.nih.gov/pubmed/20199390.

  2. Lepetsos P, Papavassiliou AG. ROS/oxidative stress signaling in osteoarthritis. Biochimica et biophysica acta. Molecular basis of disease. 2016;1862(4):576-591. http://dx.doi.org/10.1016/j.bbadis.2016.01.003. doi: 10.1016/j.bbadis.2016.01.003.

  3. Keogh CE, Scholz CC, Rodriguez J, Selfridge AC, von Kriegsheim A, Cummins EP. Carbon dioxide-dependent regulation of NF-kappaB family members RelB and p100 gives molecular insight into CO2-dependent immune regulation. J Biol Chem. 2017;292(27):11561-11571. doi: 10.1074/jbc.M116.755090 [doi].

  4. Bolevich S, Kogan A, Zivkovic V, et al. Protective role of carbon dioxide (CO2) in generation of reactive oxygen species. Mol Cell Biochem. 2016;411(1):317-330. http://www.ncbi.nlm.nih.gov/pubmed/26541754. doi: 10.1007/s11010-015-2594-9.

Serendi Medical