Abstract
Polymorphonuclear leukocytes (PMNs) take up and accumulate ciprofloxacin. This may allow them to enhance the delivery of this agent to the inflamed periodontium. Cross-sectional and longitudinal approaches were used to test the hypothesis. In the cross-sectional study, 7 periodontally healthy adults and 8 adults with untreated periodontitis were administered three doses of ciprofloxacin (500 mg bid). Gingival fluid (GF) and serum samples were obtained after 28 hours and analyzed by high-performance liquid chromatography (HPLC). In the longitudinal study, 8 adult periodontitis subjects were administered 500 mg ciprofloxacin bid for 8 days. After 28 hours, GF from 4 sites with 5 to 8 mm probing depths was sampled in each subject, serum samples were obtained, and 2 of the 4 sites were root planed. GF and serum were sampled again 7 days later (196 hours after the initial dose). The mean ciprofloxacin levels in the GF and serum of periodontally healthy subjects were 2.52 +/- 0.22 microg/ml and 0.47 +/- 0.05 microg/ml, respectively. In subjects with periodontitis, these levels were 2.69 +/- 0.44 microg/ml and 0.61 +/- 0.13 microg/ml, respectively. GF ciprofloxacin levels were significantly higher than corresponding serum levels in healthy and diseased subjects (P<0.01), but there were no significant differences in GF or serum levels between the 2 subject groups. Since GF flow was significantly higher at diseased sites, however, more ciprofloxacin was distributed to these sites than to healthy sites. In the longitudinal study, GF flow at 196 hours was 16% lower at root planed sites than at untreated control sites (P = 0.412). The minor decrease in this index of inflammation was accompanied by a small (9%), but statistically significant (P= 0.007), decrease in GF ciprofloxacin levels. GF ciprofloxacin levels decreased slightly at inflamed periodontal sites after root planing, but were significantly higher than serum levels even at healthy periodontal sites. Inflammation may enhance the distribution of ciprofloxacin to diseased sites, but it is not a major determinant of GF ciprofloxacin levels.
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