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Effects of Selective Cyclooxygenase‐2 Inhibition on Gingival Tissue Levels of Prostaglandin E 2 and Prostaglandin F 2α and Clinical Parameters of Chronic Periodontitis
Author(s) -
Vardar Saynur,
Baylas Haluk,
Huseyinov Afig
Publication year - 2003
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2003.74.1.57
Subject(s) - nimesulide , medicine , scaling and root planing , chronic periodontitis , naproxen , prostaglandin , cyclooxygenase , naproxen sodium , placebo , periodontitis , prostaglandin e2 , prostaglandin e , radioimmunoassay , gastroenterology , chemistry , pathology , enzyme , biochemistry , alternative medicine
Background: The purpose of the present study was to evaluate the effect of a relatively selective cyclooxygenase (COX)‐2 inhibitor (nimesulide) and non‐selective COX‐1/COX‐2 inhibitor (naproxen) used as an adjunct to non‐surgical (scaling and root planing [SRP]) periodontal therapy in chronic periodontitis patients on the gingival tissue (GT) levels of prostaglandin (PG)E 2 and PGF 2α . Methods: Thirty patients with chronic periodontitis were divided into 3 groups of 10 each. One group received 100 mg of nimesulide; one received 275 mg of naproxen sodium; and the third group received placebo tablets in a 2 × 1 regimen for 10 days as an adjunct to SRP. GT samples were obtained before drug intake and on day 10. Plaque index (PI) and papillary bleeding index (PBI) scores were recorded at baseline, day 10, and at 3 months; probing depth (PD) and clinical attachment level (CAL) were recorded at baseline and at 3 months. The levels of PGE 2 were detected using an enzyme immunoassay (EIA), and the levels of PGF 2α were analyzed by radioimmunoassay (RIA). Differences among and within the groups were assessed using non‐parametric statistical analysis. Ten periodontally healthy individuals served as controls. Results: All 3 groups showed statistically significant reductions in PBI and PI on day 10 and at 3 months ( P <0.02), and in PD and CAL at 3 months ( P <0.02, P <0.05, respectively). In the naproxen group, GT PGE 2 levels exhibited a significant decrease ( P <0.05). However, the decrease of GT PGE 2 levels in the nimesulide group was insignificant ( P >0.05), while a significant increase was observed in the placebo group ( P <0.05) on day 10. Both the nimesulide and naproxen groups showed a significant decrease ( P <0.05) in PGF 2α level, while the placebo group showed a significant increase ( P <0.05). Conclusions: Nimesulides, relatively selective COX‐2 inhibitors, may have additional inhibitory effects on GT PGF 2α levels in the first week following non‐surgical periodontal treatment. However, nimesulide has an insignificant effect on reducing PGE 2 levels in gingival tissue. The determination of GT levels of COX‐1 and COX‐2 enzymes as well as PGE 2 and PGF 2α in long‐term studies may provide further support for the adjunctive use of selective COX‐2 inhibitors in treatment of chronic periodontitis. J Periodontol 2003;74:57‐63.