title: Elevated platelet and leukocyte response to oral bacteria in periodontitis.
abstract: 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.
authors.affiliation: Department of Periodontology, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, Amsterdam, The Netherlands. e.nicu@acta.nl
authors.forename: E A
authors.initials: EA
authors.lastname: Nicu
authors.forename: U
authors.initials: U
authors.lastname: Van der Velden
authors.forename: R
authors.initials: R
authors.lastname: Nieuwland
authors.forename: V
authors.initials: V
authors.lastname: Everts
authors.forename: B G
authors.initials: BG
authors.lastname: Loos
mesh_terms: D000328:Adult; D001419:Bacteria / Q000276:immunology*; D001792:Blood Platelets / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000209:etiology; D016022:Case-Control Studies; D002448:Cell Adhesion; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology; D019007:P-Selectin; D010518:Periodontitis / Q000473:pathology* / Q000503:physiopathology; D010587:Phagocytosis; D015539:Platelet Activation
chemical_list: D019007:P-Selectin