Periodontitis: possible role of mitochondrial DNA mutations

Abstract

Periodontal diseases are inflammatory disorders that give rise to tissue damage and loss, as a result of complex interactions between pathogenic bacteria and the host's immune response. There is an increasing body of evidence available to implicate Reactive Oxygen Species (ROS) in the pathogenesis of a variety of inflammatory disorders, of which periodontal disease is no exception. Mammalian cells can generate ROS by different biologic mechanisms, such as mitochondrial respiratory chain and Polymorphonuclear (PMN) activation in inflammation. It might be expected that ROS-mediated damage to mitochondria may inactivate electron transport complexes or inhibit mtDNA transcription thereby altering normal mitochondrial function. Any cellular insult that leads to disruption of the electron transport chain could lead to an increase in mitochondrial-generated ROS which may lead to the destruction of extracellular matrix components as seen in periodontitis. As there is no comprehensive study on the impact of mtDNA mutations in Periodontotitis, this study was initiated to understand the possible association of mtDNA in causing Periodontitis.