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Elevated platelet and leukocyte response to oral bacteria in periodontitis
Author(s) -
NICU E. A.,
VAN DER VELDEN U.,
NIEUWLAND R.,
EVERTS V.,
LOOS B. G.
Publication year - 2009
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2008.03219.x
Subject(s) - platelet , periodontitis , aggregatibacter actinomycetemcomitans , medicine , platelet activation , immunology , phagocytosis , neutrophil extracellular traps , monocyte , microbiology and biotechnology , inflammation , biology , porphyromonas gingivalis
Summary. Background: Periodontitis is associated with an increased risk for cardiovascular diseases (CVD), but the underlying mechanisms are poorly understood. Recently, we showed that platelets from periodontitis patients are more activated than those from controls. Objective: Given the regularly occurring bacteremic episodes in periodontitis patients, we hypothesized that platelets and/or leukocytes from periodontitis patients are more sensitive to stimulation by oral bacteria, in particular the known periodontal pathogens, than platelets from control subjects. Methods: Three‐color flow cytometry analysis was performed to quantify activation of platelets (P‐selectin, PAC‐1, CD63) and leukocytes (CD11b) in whole blood from patients with periodontitis ( n = 19) and controls ( n = 18), with and without stimulation by oral bacteria. Phagocytosis was assessed by using green‐fluorescent protein (GFP)‐expressing Aggregatibacter actinomycetemcomitans ( Aa ). Results: Neutrophils and monocytes were activated by all species of oral bacteria tested, but no differences were observed between patients and controls. In response to several species of oral bacteria, platelets from periodontitis patients showed, compared with controls, increased exposure of P‐selectin ( P = 0.027) and increased formation of platelet‐monocyte complexes ( P = 0.040). Platelet‐leukocyte complexes bound and/or phagocytosed more GFP‐ Aa than platelet‐free leukocytes (for neutrophils and monocytes, in both patients and controls, P < 0.001). Conclusions: In periodontitis, increased platelet response to oral bacteria is paralleled by increased formation of platelet‐leukocyte complexes with elevated capacity for bacterial clearance. We speculate that activated platelets and leukocytes might contribute to increased atherothrombotic activity.