Cellular responses to oral pathogens

Several previous epidemiological studies, along with the results of more recent animal model approaches, have suggested a role for periodontitis in atherosclerosis. Such an association could be mediated by direct interactions of periodontopathic bacteria with host vascular tissues.

The interactions of Porphyromonas gingivalis with endothelial cells and macrophages in vitro were investigated relative to modification of low-density lipoproteins (LDL).

P. gingivalis 381, its outer membrane vesicles, and the lipopolysaccharide (LPS) derived from these organisms were all shown to induce modification of LDL in the presence of the murine macrophage J774.A.1. Such alterations led to an increase in the migration of the particles through agarose gels. In addition, direct modification of LDL by strain 381 was demonstrated in the absence of macrophages. This latter property appears to be related to the potent protease activities of the bacterium. These properties may contribute to modification of LDL to forms which have been strongly implicated in cholesterol lipid accumulation in vascular tissues. P. gingivalis 381 also appears to induce cyclooxygenase-2 expression in endothelial cells as determined with human umbilical vascular endothelial cells (HUVEC).

These in vitro results with vascular cells in culture suggest a molecular basis for a potential role for periodontopathic bacteria such as P. gingivalis in augmenting foam cell formation characteristic of atherosclerotic lesions.