IADR Abstract Archives
Treponema denticola Promotes Pro-atherosclerotic Extracellular Matrix Remodeling In Aortic Endothelium
Objectives: Treponema denticola (Td) is a prominent periodontal pathogen also associated with atherosclerotic plaques in patients with cardiovascular disease and periodontitis. Despite the clear clinical association between these conditions, knowledge of how Td contributes to plaque formation is severely lacking. The protease dentilisin is a virulence factor that allows Td to translocate through gingival tissue. Decorin is an important component of healthy endothelium while matrix metalloproteinases (MMPs) are host factors important for maintaining tissue homeostasis but also contribute to inflammation and destruction of extracellular matrix (ECM). Our objectives were to characterize the ability of Td to cleave decorin and stimulate MMP activity in aortic endothelium.
Methods: Bovine aortic endothelial cells were exposed to wild type Td or a protease mutant (K1) (MOI 100) for 24 hours. Cleavage of ECM proteins by Td was assessed by immunoassay and immunofluorescence microscopy. MMP production, activity (zymography, ELISA) and transcription (RT-PCR) in cells exposed to Td was quantified.
Results: Decorin is cleaved from cells by dentilisin, which also disrupts the tight junctions on the endothelial cell layer. MMP transcription and activation are also stimulated by exposure to Td.
Conclusions: T. denticola disrupts endothelial cell matrix stability and increases damaging host protease activity. These events are known to stimulate immune cell recruitment and together can promote formation of an atherosclerotic plaque. Understanding how oral bacteria contribute to systemic inflammatory conditions is critical to developing targeted therapeutic approaches to improve both oral and overall health
Methods: Bovine aortic endothelial cells were exposed to wild type Td or a protease mutant (K1) (MOI 100) for 24 hours. Cleavage of ECM proteins by Td was assessed by immunoassay and immunofluorescence microscopy. MMP production, activity (zymography, ELISA) and transcription (RT-PCR) in cells exposed to Td was quantified.
Results: Decorin is cleaved from cells by dentilisin, which also disrupts the tight junctions on the endothelial cell layer. MMP transcription and activation are also stimulated by exposure to Td.
Conclusions: T. denticola disrupts endothelial cell matrix stability and increases damaging host protease activity. These events are known to stimulate immune cell recruitment and together can promote formation of an atherosclerotic plaque. Understanding how oral bacteria contribute to systemic inflammatory conditions is critical to developing targeted therapeutic approaches to improve both oral and overall health
