title: Oral infection-inflammatory pathway, periodontitis, is a risk factor for endothelial dysfunction in patients with coronary artery disease.
abstract: OBJECTIVE
  Several studies have shown that periodontitis is a risk factor for cardiovascular diseases. There is an association between inflammation and endothelial dysfunction. The purpose of this study was to evaluate endothelial function in patients with coronary artery disease (CAD) who had periodontitis.
  
  
  RESULTS
  We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, in 101 CAD patients with periodontitis (37 men and 11 women, 63+/-12 yr) and without periodontitis (36 men and 17 women, 62+/-13 yr). FBF was measured by using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the non-periodontitis group. FBF response to ACh was significantly smaller in the periodontitis group than in the non-periodontitis group. SNP-stimulated vasodilation was similar in the two groups. Periodontal therapy reduced serum concentrations of C-reactive protein from 2.7+/-1.9 to 1.8+/-0.9mg/L (P<0.05) and interleukin-6 from 2.6+/-3.4 to 1.6+/-2.6ng/L (P<0.05) and augmented ACh-induced vasodilation from 14.7+/-5.2 to 20.1+/-6.1mL/(min100mL) tissue (P<0.05) in patients with periodontitis. The SNP-stimulated vasodilation was similar before and after treatment. After administration of N(G)-monomethyl-l-arginine, a nitric oxide synthase inhibitor, FBF response to ACh was similar before and after treatment.
  
  
  CONCLUSIONS
  These findings suggest that periodontitis is associated with endothelial dysfunction in patients with CAD through a decrease in nitric oxide bioavailability. Systemic inflammation may be, at least in part, a cause and predictor of progression of endothelial dysfunction.
authors.affiliation: Department of Cardiovascular Physiology and Medicine, Hiroshima University, Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. yhigashi@hiroshima-u.ac.jp
authors.forename: Yukihito
authors.initials: Y
authors.lastname: Higashi
authors.forename: Chikara
authors.initials: C
authors.lastname: Goto
authors.forename: Takayuki
authors.initials: T
authors.lastname: Hidaka
authors.forename: Junko
authors.initials: J
authors.lastname: Soga
authors.forename: Shuji
authors.initials: S
authors.lastname: Nakamura
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Fujii
authors.forename: Takaki
authors.initials: T
authors.lastname: Hata
authors.forename: Naomi
authors.initials: N
authors.lastname: Idei
authors.forename: Noritaka
authors.initials: N
authors.lastname: Fujimura
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Chayama
authors.forename: Yasuki
authors.initials: Y
authors.lastname: Kihara
authors.forename: Akira
authors.initials: A
authors.lastname: Taguchi
mesh_terms: D000109:Acetylcholine; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000150:complications / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005542:Forearm / Q000098:blood supply; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D009599:Nitroprusside; D010518:Periodontitis / Q000150:complications* / Q000503:physiopathology; D012039:Regional Blood Flow / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D019323:omega-N-Methylarginine
chemical_list: D015850:Interleukin-6; D009599:Nitroprusside; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D002097:C-Reactive Protein; D000109:Acetylcholine