[P-060] SOD2 is upregulated in chronic periodontitis to reduce further inflammation progression
研修コード：2504
Keywords:Chronic periodontitis、Inflammatory mediator、Gene expression
Chronic periodontitis is a highly prevalent chronic inflammatory disease which results in destruction of tooth-supporting structures followed by tooth-loss. Although the progression of chronic periodontitis is relatively slow, periodontal tissue disruption is irreversible. Therefore, identification of genes which can affect the advancement of periodontitis would be helpful for fundamental pathological understanding of the disease and development of new drugs. Chronic periodontitis is initiated by gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive tissue destruction are matrix metalloproteinases （MMPs）, cathepsins, and other osteoclast-derived enzymes. Superoxide dismutase-2 （SOD2） which is one of the inflammatory mediators related to bacteria increasing as the chronic periodontitis progresses. Here, we computationally and biochemically analyzed that SOD2 expression is significantly increased in advanced periodontitis. We also confirmed that SOD2 expression is upregulated when inflammatory signal is stronger and extended. Gene manipulation against SOD2 through the CRISPR system showed that absence of SOD2 caused higher inflammasome production. This study demonstrates that SOD2 contributes to protection during periodontitis progression by inhibiting excessive inflammation.