title: The overexpression of cyclo-oxygenase-2 in chronic periodontitis.
abstract: BACKGROUND
  The objective of this prospective cross-sectional study was to determine if cyclo-oxygenase-2, or COX-2, is overexpressed in the inflamed gingival tissue of patients diagnosed as having moderate-to-severe chronic periodontitis, or CP.
  
  
  METHODS
  The authors evaluated clinical measures, crevicular fluid and gingival biopsy specimens from patients with moderate or severe CP (n = 16) and from healthy volunteers (n = 8). Patients were diagnosed as having CP based on clinical attachment loss, or CAL, of at least 5 millimeters at two sites in each quadrant and on evidence of alveolar bone loss as assessed from standard periapical or bite-wing radiographs. Healthy patients exhibited no sites with CAL of more than 2 mm and no evidence of alveolar bone loss. The authors used standard techniques to perform biochemical measures.
  
  
  RESULTS
  Levels of interleukin-1 beta, or IL-1beta, in crevicular fluid were more than doubled in the CP group (P < .05). The amounts of COX-2 mRNA and protein also were elevated in gingival tissues from subjects with CP compared with those from healthy subjects. To gain further mechanistic insights, the authors conducted in vitro studies. The results showed that lipopolysaccharide and tumor necrosis factor alpha, or TNF-alpha, induced COX-2 in macrophages, while IL-1beta and TNF-alpha induced COX-2 in oral epithelial cells.
  
  
  CONCLUSIONS
  Taken together, these results suggest that levels of COX-2 in gingivae reflect clinical measures of periodontitis and gingival inflammation.
  
  
  CONCLUSIONS
  The discovery of increased levels of COX-2 in inflamed gingival tissue suggests that COX-2 represents a pharmacological target for the prevention or treatment of CP.
authors.affiliation: Department of Genetic Medicine, Weill Medical College of Cornell University, New York City, NY 10021, USA.
authors.forename: Fan
authors.initials: F
authors.lastname: Zhang
authors.forename: Steven P
authors.initials: SP
authors.lastname: Engebretson
authors.forename: Rakhi S
authors.initials: RS
authors.lastname: Morton
authors.forename: Paul F
authors.initials: PF
authors.lastname: Cavanaugh
authors.forename: Kotha
authors.initials: K
authors.lastname: Subbaramaiah
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Dannenberg
mesh_terms: D000328:Adult; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D051546:Cyclooxygenase 2; D004847:Epithelial Cells / Q000187:drug effects; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000235:genetics; D005881:Gingiva / Q000201:enzymology; D005883:Gingival Crevicular Fluid / Q000201:enzymology; D005891:Gingivitis / Q000201:enzymology; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis / Q000494:pharmacology; D007527:Isoenzymes / Q000032:analysis* / Q000235:genetics; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects; D008297:Male; D008565:Membrane Proteins; D010518:Periodontitis / Q000201:enzymology*; D010544:Peroxidases / Q000032:analysis* / Q000235:genetics; D011446:Prospective Studies; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis* / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D007375:Interleukin-1; D007527:Isoenzymes; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha; D010544:Peroxidases; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases