酸化ストレスと歯周病

Periodontitis is a term used to describe a chronic inflammatory disease, caused by subgingival plaque biofilm, that leads to the loss of tissues supporting the root surfaces and adjacent alveolar bone, which ultimately results in tooth loss. It is believed that while the primary etiological agent is specific, a majority of periodontal tissue destruction is caused by an inappropriate host response to those microorganisms and their products. More specifically, a loss of homeostatic balance between reactive oxygen species (ROS) and antioxidant defense systems, which protect and repair vial tissues, cells, and molecular components, are believed to be responsible. A paradigm shift in our understanding of the importance of ROS and antioxidant power to human biology over the last decade came from the realization of vial and ubiquitous transcription factors. ROS are products of normal cellular metabolism; however, excessive products of ROS oxidize proteins, lipids, and DNA, resulting in tissue damage. Studies have shown that systemic increases in ROS are involved in the pathogenesis of periodontitis. When periodontitis develop, ROS produced in the periodontal lesion diffuse into the blood stream, resulting in the oxidation of circulating oxidative stress. For instance, previous animal studies in a rat periodontal model suggested that experimental periodontitis induced oxidative damage by increasing circulating oxidative stress. In addition, a positive association has been shown to exist between oxidative status and clinical attachment level in the maintenance phase of chronic periodontitis patients. These results suggest that high oxidative status in plasma could have affected the rate of progression of periodontal disease in the past. Furthermore, patients with chronic periodontitis showed higher levels of circulating oxidized low-density lipoproteins, C-reactive proteins, and oxidative stress than healthy subjects. Non-surgical periodontal treatment was effective in improving periodontal health and decreasing oxidized low-density lipoprotein and C-reactive protein, which were positively associated with a reduction in circulating oxidative stress. In patients with chronic periodontitis, a reduction in periodontal inflammation by non-surgical periodontal treatment might be beneficial in preventing systemic disease by decreasing circulating oxidative stress. Furthermore, increased serum levels of ROS following periodontitis may influence the rate of progression of systemic diseases. Hepatocellular carcinoma patients with chronic periodontitis had a higher circulating ROS level and progression of cancer than patients without periodontitis. Therefore, increased ROS levels following periodontitis may be detrimental to hepatic health.