title: Experimental periodontitis promotes transient vascular inflammation and endothelial dysfunction.
abstract: OBJECTIVE
  This study aimed to evaluate the systemic inflammatory response and cardiovascular changes induced by experimental periodontitis in rats.
  
  
  METHODS
  Experimental periodontitis was induced by placing a cotton ligature around the cervix of both sides of mandibular first molars and maxillary second molars in each male rat. Sham-operated rats had the ligature removed immediately after the procedure. Seven, 14 or 28 days after procedure, the effects of acetylcholine, sodium nitroprusside and phenylephrine were evaluated on blood pressure, aortic rings and isolated and perfused mesenteric bed. The blood was obtained for plasma Interleukin-6 (IL-6), C-reactive protein (CRP) and lipid evaluation. The mesenteric vessels were obtained to evaluate superoxide production and nitric oxide synthase 3 (NOS-3) expression.
  
  
  RESULTS
  Ligature induced periodontitis reduced endothelium-dependent vasodilatation, a hallmark of endothelial dysfunction. This effect was associated with an increase in systemic inflammatory markers (IL-6 and CRP), worsens on lipid profile, increased vascular superoxide production and reduced NOS-3 expression. It is interesting to note that many of these effects were transitory.
  
  
  CONCLUSIONS
  Periodontitis induced a transient systemic and vascular inflammation which leads to endothelial dysfunction, an initial step for cardiovascular diseases. Moreover, the animal model of periodontitis used here may represent a valuable tool for studying the relationship between periodontitis and endothelial dysfunction.
authors.affiliation: Department of Pharmaceutical Sciences, Universidade Estadual de Ponta Grossa, PR, Brazil.
authors.forename: Lorena C W
authors.initials: LC
authors.lastname: Brito
authors.forename: Silvia
authors.initials: S
authors.lastname: DalBó
authors.forename: Tatiane M
authors.initials: TM
authors.lastname: Striechen
authors.forename: Jéssica M
authors.initials: JM
authors.lastname: Farias
authors.forename: Luiz R
authors.initials: LR
authors.lastname: Olchanheski
authors.forename: Reila T
authors.initials: RT
authors.lastname: Mendes
authors.forename: José C R
authors.initials: JC
authors.lastname: Vellosa
authors.forename: Giovani M
authors.initials: GM
authors.lastname: Fávero
authors.forename: Regina
authors.initials: R
authors.lastname: Sordi
authors.forename: Jamil
authors.initials: J
authors.lastname: Assreuy
authors.forename: Fábio A
authors.initials: FA
authors.lastname: Santos
authors.forename: Daniel
authors.initials: D
authors.lastname: Fernandes
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D016301:Alveolar Bone Loss / Q000503:physiopathology; D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D004727:Endothelium / Q000187:drug effects* / Q000378:metabolism; D007249:Inflammation / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000503:physiopathology; D008856:Microscopy, Fluorescence; D019001:Nitric Oxide Synthase / Q000032:analysis; D009599:Nitroprusside / Q000494:pharmacology; D010518:Periodontitis / Q000209:etiology* / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013481:Superoxides / Q000032:analysis; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D013481:Superoxides; D009599:Nitroprusside; D010656:Phenylephrine; D002097:C-Reactive Protein; D019001:Nitric Oxide Synthase; D000109:Acetylcholine
keywords: Cholesterol; Endothelial dysfunction; Inflammation; Nitric oxide; Periodontitis; Superoxide