title: Periodontitis increases vascular cyclooxygenase-2: potential effect on vascular tone.
abstract: OBJECTIVE
  It has been demonstrated that periodontitis induces a systemic inflammation, which may impair endothelial function. Cyclooxygenase-2 (COX-2) is an important enzyme in the inflammatory process and is responsible for prostacyclin production. We hypothesised that in periodontitis, an increase in vascular COX-2 expression may occur, which in turn may have a role in vascular homeostasis. Thus, we evaluated the vascular effects of COX-2 inhibition in an experimental rat model of periodontitis.
  
  
  METHODS
  Experimental periodontitis was induced in rats by placing a cotton ligature around the cervix of both sides of the mandibular first molars and maxillary second molars. Sham-operated rats had the ligature removed immediately after the procedure. Mesenteric vessels were obtained for the study of COX-2 expression, and blood samples were collected for nitric oxide quantification. In another set of experiments, animals received etoricoxib (10 mg/kg/d, v.o.) or vehicle, and alveolar bone loss and cardiovascular parameters were evaluated.
  
  
  RESULTS
  We observed an increase in COX-2 expression in mesenteric vessels harvested from animals with periodontitis, which was accompanied by a reduction in nitric oxide content. Etoricoxib treatment impaired the endothelium-dependent reduction in blood pressure in rats with periodontitis.
  
  
  CONCLUSIONS
  Periodontitis increases vascular COX-2 expression, which is important in the maintenance of vascular homeostasis in this model. Despite the limitations of an animal study, these findings may have important implications regarding the safety of using selective COX-2 inhibitors in patients with periodontitis.
authors.affiliation: Department of Dentistry, Universidade Estadual de Ponta Grossa, Ponta Grossa, PR, Brazil.
authors.forename: R T
authors.initials: RT
authors.lastname: Mendes
authors.forename: R
authors.initials: R
authors.lastname: Sordi
authors.forename: L R
authors.initials: LR
authors.lastname: Olchanheski
authors.forename: W M
authors.initials: WM
authors.lastname: Machado
authors.forename: C P
authors.initials: CP
authors.lastname: Stanczyk
authors.forename: J
authors.initials: J
authors.lastname: Assreuy
authors.forename: F A
authors.initials: FA
authors.lastname: Santos
authors.forename: D
authors.initials: D
authors.lastname: Fernandes
mesh_terms: D016301:Alveolar Bone Loss / Q000201:enzymology / Q000517:prevention & control; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D062186:Arterial Pressure / Q000187:drug effects / Q000502:physiology*; D051546:Cyclooxygenase 2 / Q000187:drug effects / Q000502:physiology*; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000201:enzymology; D000077613:Etoricoxib; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D008638:Mesenteric Arteries / Q000201:enzymology; D009569:Nitric Oxide / Q000097:blood; D010518:Periodontitis / Q000201:enzymology* / Q000517:prevention & control; D011725:Pyridines / Q000494:pharmacology; D011897:Random Allocation; D017208:Rats, Wistar; D013450:Sulfones / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D052246:Cyclooxygenase 2 Inhibitors; D011725:Pyridines; D013450:Sulfones; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000077613:Etoricoxib
keywords: blood pressure; cardiovascular diseases; cyclooxygenase-2; periodontitis