THE EFFECT OF TETRACYCLINE FIBER THERAPY ON BETA-GLUCURONIDASE AND INTERLEUKIN-1-BETA IN CREVICULAR FLUID

Treatment with the tetracycline HCL-containing (Actisite(R)) fiber has been shown to improve clinical measures of periodontitis, as well as reduce the number of sites infected with putative periodontal pathogen s. In this study, we examined the effect of the tetracycline fiber on biochemical mediators of the host's inflammatory response in gingival crevicular fluid (GCF). The total amount of the lysosomal enzyme beta- glucuronidase (beta G), considered a marker of primary granule release from polymorphonuclear leukocytes and interleukin-1 beta, a cytokine with important proinflammatory effects, were examined in GCF. Patients with localized recurrent periodontitis were followed over a 16 week p eriod. Treated teeth (Tx), teeth adjacent to treated teeth (ADJ) and c ontrol teeth (Cx) were studied. Following fiber therapy, the Tx teeth displayed statistically significant reductions in mean probing depth, depth of the deepest site and bleeding on probing over the 16 weeks of the trial. Significant reduction in the depth of the deepest site was also seen for the ADJ teeth over 16 weeks. Total beta G in GCF was re duced for the Tx teeth comparing baseline to 16 weeks, but no signific ant changes were observed for the ADJ or Cx teeth. Prior to treatment, total beta G for the Tx teeth was 211 +/- 49 U (mean+/-standard error ), versus 146 +/- 174 U for the ADJ teeth and 121 +/- 33 U for the Tx teeth. 16 weeks treatment, the mean values for these 3 categories of t eeth were comparable (Tx = 95 +/- 20 U, ADJ = 93 +/- 42 U and Cx = 103 +/- 29 U). For the Tx teeth, the maximum reduction in total PG follow ing therapy occurred at 6 weeks (65%). Total IL-1 beta was significant ly reduced for the Tx teeth at 3 and 6 weeks, but rebounded at 16 week s. In contrast to what was seen for PG, the maximum reduction in total IL-1 beta for the Tx teeth was observed at 3 weeks (68%). These data suggest that host mediators associated with increased risk for active disease are reduced following tetracycline fiber therapy. Future studi es will determine the relative importance of a reduced microbial chall enge versus a tetracycline-mediated direct modification of the host re sponse to account for the reduction in the host inflammatory response in GCF following tetracycline fiber therapy.