Int Poster J Dent Oral Med 10 (2008), No. 4 15. Dec. 2008
Int Poster J Dent Oral Med 10 (2008), No. 4 (15.12.2008)
Poster 429, Language: English
Periodontitis: Possible role of Mitochondrial DNA Mutations
Chandra, Rampalli Viswa/Govindaraj, Periyasamy/Vanniarrajan, Ayyasamy/Reddy, Aileni Amarendhar/Singh, Lalji/Thangaraj, Kumarasamy
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.
Keywords: periodontitis, mitochondrial DNA, mutations
December 6-8, 2007
International Symposium on Dissecting the Role of Genes and Environment in Complex diseases
Centre for Cellular and Molecular Biology, Hyderabad, India.