Background: Polymorphonuclear leukocytes (PMNs) take up and accumulate cipr
ofloxacin. This may allow them to enhance the delivery of this agent to the
inflamed periodontium.
Methods: Cross-sectional and longitudinal approaches were used to test the
hypothesis. In the cross-sectional study, 7 periodontally healthy adults an
d 8 adults with untreated periodontitis were administered three doses of ci
profloxacin (500 mg bid). Gingival fluid (GF) and serum samples were obtain
ed after 28 hours and analyzed by high-performance liquid chromatography (H
PLC). In the longitudinal study, 8 adult periodontitis subjects were admini
stered 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 w
ere obtained, and 2 of the 4 sites were root planed. GF and serum were samp
led again 7 days later (196 hours after the initial dose).
Results: The mean ciprofloxacin levels in the GF and serum of periodontally
healthy subjects were 2.52 +/- 0.22 mug/ml and 0.47 +/- 0.05 mug/ml, respe
ctively. In subjects with periodontitis, these levels were 2.69 +/- 0.44 mu
g/ml and 0.61 +/- 0.13 mug/ml, respectively. GF ciprofloxacin levels were s
ignificantly higher than corresponding serum levels in healthy and diseased
subjects (P <0.01), but there were no significant differences in GF or ser
um levels between the 2 subject groups. Since GF flow was significantly hig
her at diseased sites, however, more ciprofloxacin was distributed to these
sites than to healthy sites. In the longitudinal study, GF flow at 196 hou
rs 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 ci
profloxacin levels.
Conclusion: GF ciprofloxacin levels decreased slightly at inflamed periodon
tal sites after root planing, but were significantly higher than serum leve
ls even at healthy periodontal sites. Inflammation may enhance the distribu
tion of ciprofloxacin to diseased sites, but it is not a major determinant
of GF ciprofloxacin levels.