Gingival crevicular fluid prostaglandin E(2) and thiobarbituric acid reactive substance levels in smokers and non-smokers with chronic periodontitis following phase I periodontal therapy and adjunctive use of flurbiprofen.

BACKGROUND

It has been established that smoking is an important risk factor for the initiation and progression of chronic periodontitis (CP). This study investigates the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on prostaglandin E(2) (PGE(2)) and thiobarbituric acid reactive substance (TBARS) levels in gingival crevicular fluid (GCF) samples from smoker and non-smoker patients with CP.

METHODS

Twenty-one non-smoker and 21 smoker patients with CP were divided into four groups according to treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 x 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 x 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded and GCF samples were collected at baseline and on day 10 of drug intake from each sampling area by a single examiner who was unaware of the treatment modality. Assays for GCF PGE(2) and TBARS were carried out by an enzyme-linked immunosorbent assay and fluorometric method, respectively.

RESULTS

All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment on day 10 (P <0.05), but no statistical differences were observed in PD and CAL scores after the therapy. In groups 1 and 2, the reduction of GCF PGE(2) and TBARS levels were not significant after the therapy compared to baseline levels. In group 3, GCF PGE(2) and TBARS levels exhibited a statistically significant decrease (P <0.05) after the therapy. Group 4 showed significant reductions (P <0.05) in GCF PGE(2) levels after the therapy. No statistically significant reductions were observed in group 4 with regard to GCF TBARS levels. When groups 1 and 3 were compared according to GCF TBARS levels after the therapy, a more statistically significant reduction was observed in group 3 (P = 0.001).

CONCLUSION

These results suggest that additional flurbiprofen administration may have more inhibitory effects on GCF levels of PGE(2) and TBARS in the groups of smokers compared to non-smokers with CP.