Wild‐type isolates of Porphyromonas gingivalis derived from periodontitis patients display major variability in platelet activation

Abstract In vitro studies revealed tha t Porphyromonas gingivalis (Pg), a pathogen intimately associated with the onset and progression of periodontitis, is able to activate platelets, thus linking periodontal inflammation with the endangerment of vascular health. As wild‐type Pg strains are characterized by major genetic heterogeneity, the commonness of platelet‐activating Pg strains in periodontitis patients is unknown as of yet. Therefore, this study evaluated the platelet activation capacity of wild‐type Pg isolates sampled from patients with aggressive periodontitis. Methods Extent and velocity of platelet aggregation were determined by light transmission aggregometry. Platelet surface expression of P‐selectin was measured by flow cytometry, activation of p38 MAP kinase, and protein kinase C by Western blot using phospho‐specific antibodies. Results Pg isolates displayed high variability regarding extent and velocity of platelet activation, as well as the involved activating pathways. Corresponding results were observed for platelet P‐selectin expression, activation of p38 MAP kinase, or protein kinase C. Inhibitors of platelet immune receptor Fcγ RIIA and protease‐activated receptors revealed several, diverging pathways of activation. Some isolates induced platelet aggregation even in the presence of potent therapeutical platelet inhibitors. Conclusions Chronic bacteremia involving specific, platelet‐activating Pg strains may constitute a substantial hazard for the integrity of cardiovascular health.