Decreased phosphorylation of platelet vasodilator-stimulated phosphoprotein in periodontitis – a role of periodontal pathogens

IntroductionEpidemiological studies indicate an association between periodontitis and cardiovascular disease, but the underlying mechanisms are poorly understood. Vasodilator-stimulated phosphoprotein (VASP) in its phosphorylated form represents a regulator of platelet function and an indicator for the sensitivity of platelets towards physiologically relevant antagonists of platelet function.As platelets and their activation state play a central role in the development of cardiovascular disease, this study aimed to investigate the influence of periodontal disease and periodontal pathogens on intraplatelet VASP-phosphorylation and platelet function.Material and MethodsBesides several markers of platelet activation, basal and PGE1 induced intracellular VASP-phosphorylation were determined in platelets of periodontitis patients (n = 26) and healthy donors (n = 19). Furthermore, platelets from healthy donors were incubated with distinct periodontal pathogens and basal and PGE1 induced VASP-phosphorylation was determined.ResultsCompared to controls, platelets of periodontitis patients showed a significant decrease in basal and PGE1 induced VASP-phosphorylation. VASP-phosphorylation in platelets from periodontitis patients positive for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis or Tannerella forsythia was significantly decreased compared to patients that were negative for these bacteria. Furthermore, VASP-phosphorylation in platelets isolated from healthy donors was affected by incubation with these periodontal pathogens.ConclusionsOur results provide evidence that periodontitis interferes with VASP-phosphorylation in human platelets, presumably as a consequence of a direct effect of periodontitis-associated bacteria. Decreased basal and PGE1 induced VASP-phosphorylation might represent a mechanism responsible for enhanced platelet activation in periodontitis.