title: Association of endodontic infection with detection of an initial lesion to the cardiovascular system.
abstract: BACKGROUND
  Dental infections might predispose toward the onset of cardiovascular disease (CVD). To date, only a few studies, yielding inconclusive findings, have investigated the potential correlation between apical periodontitis (AP) and CVD. The aim of this study (as the first part of a prospective study) was to evaluate, in the absence of CV risk factors, whether subjects with AP were more exposed to the pathogenetic indices of an atherosclerotic lesion.
  
  
  METHODS
  Forty men between the ages of 20 and 40 years who were free from periodontal disease, CVD, and traditional CV risk factors were enrolled in the study; 20 subjects had AP, and 20 acted as controls. All subjects underwent dental examination and complete cardiac assessment: physical examination, electrocardiogram, conventional and tissue Doppler echocardiography, and measurement of endothelial flow reserve (EFR). The following laboratory parameters were tested: interleukins -1, -2, and -6 (IL-1, IL-2, IL-6), tumor necrosis factor alpha, and asymmetrical dimethylarginine (ADMA). Data were analyzed by using the 2-tailed Student's t test, Pearson t test (or Spearman t test for nonparametric variables), and multivariate linear regression analysis.
  
  
  RESULTS
  Echocardiography revealed no abnormalities in any of the subjects studied. ADMA levels were inversely correlated with EFR (P < .05) and directly correlated with IL-2 (P < .001). Patients with AP presented with significantly greater blood concentrations of IL-1 (P < .05), IL-2 (P < .01), IL-6 (P < .05), and ADMA (P < .05) and a significant reduction of EFR (P < .05).
  
  
  CONCLUSIONS
  Increased ADMA levels and their relationship with poor EFR and increased IL-2 might suggest the existence of an early endothelial dysfunction in young adults with AP.
authors.affiliation: Department of Conservative Dentistry and Endodontics, School of Dentistry, University of Cagliari, Cagliari, Italy. cottiend@tin.it
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Cotti
authors.forename: Cristina
authors.initials: C
authors.lastname: Dessì
authors.forename: Alessandra
authors.initials: A
authors.lastname: Piras
authors.forename: Giovanna
authors.initials: G
authors.lastname: Flore
authors.forename: Martino
authors.initials: M
authors.lastname: Deidda
authors.forename: Clelia
authors.initials: C
authors.lastname: Madeddu
authors.forename: Angela
authors.initials: A
authors.lastname: Zedda
authors.forename: Giorgio
authors.initials: G
authors.lastname: Longu
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mercuro
mesh_terms: D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D002318:Cardiovascular Diseases / Q000150:complications* / Q000175:diagnosis; D002851:Chromatography, High Pressure Liquid; D003326:Coronary Circulation / Q000502:physiology; D003430:Cross-Sectional Studies; D003788:Dental Pulp Diseases / Q000150:complications / Q000175:diagnosis; D015150:Echocardiography, Doppler; D018619:Echocardiography, Doppler, Pulsed; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D010485:Periapical Periodontitis / Q000150:complications*; D010808:Physical Examination; D011446:Prospective Studies; D016300:Radiography, Bitewing; D011862:Radiography, Panoramic; D012307:Risk Factors; D013318:Stroke Volume / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D016277:Ventricular Function, Left / Q000502:physiology; D055815:Young Adult
chemical_list: D007375:Interleukin-1; D007376:Interleukin-2; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C487735:dimethylarginine; D001120:Arginine