Modified LDL has been suggested to initiate the formation of atherosclerosis by inducing an inflammatory reaction in the vessel wall.

We have previously shown that incubation of human whole blood with the periodontal pathogen Porphyromonas gingivalis causes leukocyte/platelet aggregate formation and ROS production, and that the bacteria via its cysteine proteases (gingipains) markedly modifies plasma lipoproteins, by fragmentation of apoE and apoB-100, and oxidation.

Consequently, our findings together with others suggest that P. gingivalis during translocation in circulating blood modifies LDL and HDL to an atherogenic form which supports a role of periodontal disease in the development of atherosclerosis.

In agreement, by using 2D gel electrophoresis and MALDI TOF- and nano LC-mass spectrometry, we have found significant changes in the expression of several proteins in LDL and HDL of patients with periodontitis compared to healthy controls. For example; increased expression of Lp –PLA2, apoM, apoC3, apoA2 and apoL1, and decreased expression of apoA1, ApoJ, LCAT and PTP as well as increased oxidation- effects that are associated with defective removal of cholesterol from blood and tissues and reduced reverse cholesterol transport.

Except to increase our understanding of the pathogenesis of periodontitis and its association with cardiovascular disease the intention with this project is also to identify key virulence factors, as well as host mediators, involved in disease development and find biomarkers as targets for diagnostic and therapeutic approaches for periodontal and cardiovascular disease.