title: Role of systemic and local administration of selective inhibitors of cyclo-oxygenase 1 and 2 in an experimental model of periodontal disease in rats.
abstract: OBJECTIVE
  Periodontal disease is an inflammatory condition of tooth-supporting tissues. Arachidonic acid metabolites have been implicated in development of periodontal disease, especially those derived from the cyclo-oxygenase (COX) pathway. This study investigated the role of inhibitors of cyclo-oxygenases (COX-1 and COX-2) in a model of periodontal disease in rats.
  
  
  METHODS
  A ligature was placed around the molar of rats. Losses of fiber attachment and of alveolar bone were measured morphometrically in histologically prepared sections. Infiltration of cells into gingival tissue surrounding the ligated tooth was also determined.
  
  
  RESULTS
  Systemic and local administration of non-selective and selective COX-2 inhibitors, preventively, resulted in significant reduction of the losses of fiber attachment and alveolar bone, as well as decreased leukocyte numbers in gingival tissue. Preventive selective inhibition of COX-1 was as effective as COX-2 inhibition in reducing local fiber attachment loss and cell migration, but did not prevent alveolar bone loss.
  
  
  CONCLUSIONS
  Our results provide evidence for participation of COX-1 and COX-2 in early stages of periodontal disease in rats. Furthermore, local administration of COX inhibitors reduced the signs of periodontal disease to the same extent as systemic treatment. Therapeutic approaches incorporating locally delivered anti-inflammatory drugs could be of benefit for patients suffering from periodontal disease.
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.
authors.forename: C M
authors.initials: CM
authors.lastname: Queiroz-Junior
authors.forename: C M F
authors.initials: CM
authors.lastname: Pacheco
authors.forename: K L M
authors.initials: KL
authors.lastname: Maltos
authors.forename: M V
authors.initials: MV
authors.lastname: Caliari
authors.forename: I D G
authors.initials: ID
authors.lastname: Duarte
authors.forename: J N
authors.initials: JN
authors.lastname: Francischi
mesh_terms: D016301:Alveolar Bone Loss / Q000188:drug therapy / Q000201:enzymology*; D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D000068579:Celecoxib; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D017622:Periodontal Attachment Loss / Q000188:drug therapy / Q000201:enzymology*; D010513:Periodontal Ligament / Q000187:drug effects; D010518:Periodontitis / Q000188:drug therapy / Q000201:enzymology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013449:Sulfonamides / Q000494:pharmacology; D000096926:Benzenesulfonamides
chemical_list: D016718:Arachidonic Acid; D000068579:Celecoxib; D016861:Cyclooxygenase Inhibitors; D007213:Indomethacin; D011451:Prostaglandin-Endoperoxide Synthases; D011720:Pyrazoles; D013449:Sulfonamides; C119130:4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; D000096926:Benzenesulfonamides