Department of Oral Biology, University at Buffalo, Buffalo, NY 14214, USA.
BACKGROUND: Recent epidemiological studies have suggested a contribution of periodontitis in atherosclerotic diseases. Two mechanisms have been proposed to explain such a connection involving general inflammatory responses and/or specific effects of periodontal bacteria on host tissues. METHODS: The role of the periodontopathogen Porphyromonas gingivalis as a potential contributor to atherosclerosis has been investigated in model systems using human umbilical vein endothelial cells (HUVEC) and murine J774 macrophage cell cultures. RESULTS: P. gingivalis 381 was demonstrated to induce foam cell formation in J774 macrophage cell cultures in the presence of low-density lipoproteins. The active bacterial component involved in this process appears to be lipopolysaccharide. This effect was not limited to these organisms as several other Gram-positive and Gram-negative oral bacteria exhibited the same property. In addition, in a more specific manner, P. gingivalis induced monocyte chemoattractant protein-1 secretion in HUVEC cultures. CONCLUSIONS: The fimbriae of strain 381 are important, but are not required, for this inductive effect. Taken together, these results suggest a potential role for P. gingivalis in several steps involved in atherosclerotic lesion formation.
