The aims of the present study were: (a) to determine the mechanism of action of taurolidine against bacterial species associated with periodontal disease, and (b) to evaluate the potential development of resistance against taurolidine as compared with minocycline. After visualizing the mode of action of taurolidine by transmission electron micrographs, the interaction with most important virulence factors (lipopolysaccharide (LPS), Porphyromonas gingivalis gingipains, Aggregatibacter actinomycetemcomitans leukotoxin), was analyzed. Then, 14 clinical isolates from subgingival biofilm samples were transferred on agar plates containing subinhibitory concentrations of taurolidine or minocycline up to 50 passages. Before and after each 10 passages, minimal inhibitory concentrations (MICs) were determined. Increasing MICs were screened for efflux mechanism. Taurolidine inhibited in a concentration-dependent manner the activities of LPS and of the arginine-specific gingipains; however, an effect on A. actinomycetemcomitans leukotoxin was not detected. One P. gingivalis strain developed a resistance against taurolidine, which was probably linked with efflux mechanisms. An increase of MIC values of minocycline occurred in five of the 14 included strains after exposure to subinhibitory concentrations of the antibiotic. The present results indicate that: (a) taurolidine interacts with LPS and gingipains, and (b) development of resistance seems to be a rare event when using taurolidine.

Background Taurolidine is thought to be an alternative antimicrobial in periodontal therapy. The purpose of this follow-up taurolidine study was to determine in more detail the mode of action of taurolidine against bacterial species being associated with periodontal disease. Further, a potential development of resistance against taurolidine in comparison with minocycline was to evaluate. Results Visualizing the mode of action of taurolidine to Porphyromonas gingivalis by scanning and transmission electron micrographs showed in part pores and release of constituents from the cell wall. The interaction of taurolidin with bacterial cell wall is also supported by the finding that taurolidine inhibited in a concentration-dependent manner the activities of LPS and of the P. gingivalis arginine-specific gingipains. However, an effect on A. actinomycetemcomitans leukotoxin was not found. When transferring 14 clinical isolates from subgingival biofilm samples (4 P. gingivalis, 2 A. actinomycetemcomitans, 2 Tannerella forsythia, 2 Fusobacterium nucleatum, 4 oral streptococci) on agar plates containing subinhibitory concentrations of taurolidine up to 50 passages, one P. gingivalis strain developed a resistance against taurolidine which was probably linked with efflux mechanisms. When antimicrobial pressure was removed, MIC reverted to baseline value. Testing development of resistance to minocycline in a similar way, an increase of MIC values occurred in five of the 14 included strains after exposure to subinhibitory concentrations of the antibiotic. Efflux might play a role in one A. actinomycetemcomitans strains, but obviously not in the other four strains. Removing antimicrobial pressure for a few passages did not revert the increased MIC values. Conclusion Taurolidine interacts with LPS and gingipains. Development of resistance seems to be a rare event when applying taurolidine. A potential development of resistance might be associated with efflux mechanisms.

Background Taurolidine is thought to be an alternative antimicrobial in periodontal therapy. The purpose of this follow-up taurolidine study was to determine in more detail the mode of action of taurolidine against bacterial species being associated with periodontal disease. Further, a potential development of resistance against taurolidine in comparison with minocycline was to evaluate. Results Visualizing the mode of action of taurolidine to Porphyromonas gingivalis by scanning and transmission electron micrographs showed in part pores and release of constituents from the cell wall. The interaction of taurolidin with bacterial cell wall is also supported by the finding that taurolidine inhibited in a concentration-dependent manner the activities of LPS and of the P. gingivalis arginine-specific gingipains. However, an effect on A. actinomycetemcomitans leukotoxin was not found. When transferring 14 clinical isolates from subgingival biofilm samples (4 P. gingivalis, 2 A. actinomycetemcomitans, 2 Tannerella forsythia, 2 Fusobacterium nucleatum, 4 oral streptococci) on agar plates containing subinhibitory concentrations of taurolidine up to 50 passages, one P. gingivalis strain developed a resistance against taurolidine which was probably linked with efflux mechanisms. When antimicrobial pressure was removed, MIC reverted to baseline value. Testing development of resistance to minocycline in a similar way, an increase of MIC values occurred in five of the 14 included strains after exposure to subinhibitory concentrations of the antibiotic. Efflux might play a role in one A. actinomycetemcomitans strains, but obviously not in the other four strains. Removing antimicrobial pressure for a few passages did not revert the increased MIC values. Conclusion Taurolidine interacts with LPS and gingipains. Development of resistance seems to be a rare event when applying taurolidine. A potential development of resistance might be associated with efflux mechanisms.