title: Severity of periodontal disease correlates to inflammatory systemic status and independently predicts the presence and angiographic extent of stable coronary artery disease.
abstract: BACKGROUND
  Periodontal disease (PD) has been recognized as a risk factor for systemic diseases, but its involvement in the pathogenesis of coronary artery disease (CAD) remains debated.
  
  
  OBJECTIVE
  We sought to evaluate the potential relations between severity of the PD, inflammatory response and angiographic lesions extent in patients with stable CAD.
  
  
  METHODS
  A total of 131 subjects referred to our centre for coronary angiography were evaluated for presence and extension of CAD, then divided into two groups, one with presence of lesions (cases, n = 85) and other one with absence of lesions (controls, n = 46). Mean periodontal pocket depth (PPkD), high sensitivity C reactive protein (hs-CRP), serum amyloid A protein (SAA) and fibrinogen levels were measured in all patients.
  
  
  RESULTS
  Cases and controls did not differ according to their baseline characteristics and prevalence of traditional cardiovascular risk factors. PPkD was greater in patients with CAD than in controls (2.24 +/- 1.28 mm vs 1.50 +/- 0.93 mm, P < 0.001 by Student's t-test). Systemic inflammatory response was more pronounced in cases than in controls, with higher values of hs-CRP, SAA and fibrinogen. Furthermore, PPkD values correlated with hs-CRP (r = 0.80, P < 0.001), SAA (r = 0.71, P < 0.001), fibrinogen levels (r = 0.72, P < 0.001) and the American College of Cardiology/American Heart Association angiographic score (r = 0.68, P < 0.001) in cases. Multivariate analysis indicated a persistent independent correlation between PPkD and angiographic score after adjustment for inflammatory markers levels.
  
  
  CONCLUSIONS
  In the present study, PD lesions predicted presence of CAD stenosis in patients with cardiovascular risk factors. PD severity was correlated to angiographic extent of coronary lesions, independent of systemic inflammatory status. Those results suggest that these patients might benefit from an intensive periodontal therapy to prevent CAD progression.
authors.affiliation: Department of Cardiology, University of Marseille, Hôpital Nord, Marseille, France. nicolas.amabile@mail.ap-hm.fr
authors.forename: N
authors.initials: N
authors.lastname: Amabile
authors.forename: G
authors.initials: G
authors.lastname: Susini
authors.forename: I
authors.initials: I
authors.lastname: Pettenati-Soubayroux
authors.forename: L
authors.initials: L
authors.lastname: Bonello
authors.forename: J-M
authors.initials: JM
authors.lastname: Gil
authors.forename: S
authors.initials: S
authors.lastname: Arques
authors.forename: J J
authors.initials: JJ
authors.lastname: Bonfil
authors.forename: F
authors.initials: F
authors.lastname: Paganelli
mesh_terms: D000328:Adult; D000368:Aged; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000209:etiology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D010514:Periodontal Pocket / Q000473:pathology; D010518:Periodontitis / Q000097:blood / Q000150:complications* / Q000473:pathology; D012307:Risk Factors; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects
chemical_list: D018836:Inflammation Mediators