Mechanisms of oral bacteria-induced platelet activation

Abstract

The oral cavity is inhabited by over 500 different bacterial species that normally exist in ecological balance both with each other and with the host. When this equilibrium is disturbed, an overgrowth of individual organisms can occur, which, in turn, can lead to the onset of pathological processes, notably dental caries and periodontitis. Generally, bacteraemias occur more frequently in individuals with periodontal disease, and these bacteraemias have been implicated in the development of a range of systemic diseases, including atherothrombotic disorders. The mechanism underlying this relationship remains to be precisely defined, although studies have shown a link between bacteria of oral origin and platelet activation. Several orally derived species of bacteria interact with platelets, including those of the Streptococcus (Streptococcus sanguinis, Streptococcus mutans, Streptococcus agalactiae, Streptococcus pyogenes, Streptococcus gordonii, Streptococcus pneumoniae, Streptococcus mitis) and Staphylococcus (Staphylococcus epidermidis, Staphylococcus capitis) genera, as well as Pseudomonas aeruginosa and Porphyromonas gingivalis. In addition, some members of both the Streptococcus and the Staphylococcus genera, as well as Porphyromonas gingivalis, can activate platelets in vitro. The current review describes the heterogeneous mechanisms of platelet activation employed by individual bacterial species. The pathological and clinical implications of platelet activation by orally derived bacteria are discussed.