FLURBIPROFEN IN THE PREVENTION AND TREATMENT OF EXPERIMENTAL GINGIVITIS

A clinical trial was undertaken to examine the effects of a potent cyc looxygenase inhibitor, flurbiprofen, on both developing and establishe d gingivitis in humans. 21 subjects with healthy gingiva abstained fro m all oral hygiene procedures for 21 days. 7 subjects were prescribed flurbiprofen, 50 mg b.d. beginning from baseline and a control group ( C1, n = 14) were given placebo. Gingival redness and bleeding on probi ng were assessed at baseline, 7, 14 and 21 days. Crevicular fluid (GCF ) samples were also taken to determine concentrations of PGE2, TxB2 an d LTB4 at baseline and at 21 days. Results show that flurbiprofen sign ificantly inhibited the development of redness and bleeding (p < 0.001 ) effects which were associated with a significant inhibition of TxB2 (p < 0.05). There were no apparent flurbiprofen effects on GCF-PGE, or GCF-LTB4 during this 21-day gingivitis model. To assess the effects o f flurbiprofen on established experimental gingivitis, the model was e xtended to 28 days. On day 21, the C1 group was subdivided into 2 grou ps of 7 subjects. One group was prescribed flurbiprofen (50 mg b.d.) f or 7 days and controls (C2) continued to take placebo. All subjects co ntinued to abstain from tooth cleaning. Pretreatment (day 21) and post -treatment (day 28) comparisons showed that flurbiprofen again signifi cantly inhibited bleeding (p < 0.001), but did not affect redness. Con trol subjects demonstrated a significant elevation in gingival bleedin g on day 28, and this was associated with significant rises in GCF-PGE 2 (p < 0.001), GCF-TxB2 (p < 0.01) and GCF-LTB4 (p < 0.05). Flurbiprof en suppressed the increases in these 3 mediators that occurred between 21 and 28 days. It is concluded that flurbiprofen controls gingival i nflammation with both preventive and therapeutic properties in the exp erimental gingivitis model, an action that is associated with an inhib ition in the production of both cyclooxygenase metabolites and indirec tly affects GCF-LTB4 levels.