Antibacterial activity of povidone-iodine against an artificial biofilm of Porphyromonas gingivalis and Fusobacterium nucleatum.

OBJECTIVE: To investigate the antibacterial activity of povidone-iodine (PVP-I) on an artificial dual species biofilm of periodontal pathogens. DESIGN: Porphyromonas gingivalis or Fusobacterium nucleatum grown in broth culture was inoculated on polycarbonate membrane (PCM) tissue culture inserts. After incubation for 72 h, PVP-I solutions were applied to the biofilm for the time period ranging from 0.5 to 5 min. After addition of a deactivator, each PCM was removed and the biofilm on the PCM was serially diluted and plated on blood agar plates and cultured anaerobically for 7 days. Then viable bacteria were enumerated. RESULTS: In the dual species biofilm model, F. nucleatum showed an approximately 200-fold increase in viable counts when compared with mono-microbial biofilm. In dual species biofilm, PVP-I with concentration equal to or greater than 2% was required to significantly reduce P. gingivalis and F. nucleatum. When the contact time of PVP-I was increased to 1 min or greater, no difference in antibacterial activity of PVP-I was observed in any concentration. CONCLUSION: These results suggest that 30s application of 2% PVP-I would be effective in suppressing both P. gingivalis and F. nucleatum in dual-species biofilm, and this provides clinical implication for the control of subgingival biofilm.

Nicotine involved in periodontal disease through influence on cytokine levels.

Periodontal disease, for which smoking is a known risk factor, is infectious, and is associated with oral biofilm. Cytokines mediate and regulate immune and inflammatory responses. Lipopolysaccharide produced by periodontopathic bacteria plays a role in the progression of periodontitis. The effect of nicotine on cytokine production in mice was evaluated in this study. Nicotine (10 or 200 microg mouse(-1)) was administered intraperitoneally to 4-week-old female BALB/c mice, once a day, for 49 days. Control mice received injections of phosphate-buffered saline. Blood was collected from all mice and serum IL-6, IL-10, tumor necrosis factor (TNF)-alpha and IFN-gamma levels were measured by an enzyme-linked immunosorbent assay on the 42nd day. IL-6, IL-10 and IFN-gamma levels in the nicotine-treated mice were higher than those in the control mice. However, no differences were found in TNF-alpha levels between nicotine-treated and control mice. Lipopolysaccharide (20 microg mouse(-1)) purified from Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans) Y4 was administered intraperitoneally on the 49th day. A rapid increase in TNF-alpha was observed in the control mice at 2 h after administration of lipopolysaccharide. In contrast, no increase was noted in the nicotine-treated groups. Significantly higher levels of IFN-gamma were seen in the 200 microg nicotine-treated mice at 2 h after administration of lipopolysaccharide (P<0.05). The results showed that cytokine levels were influenced by nicotine in mice.