Objectives: The complexity of the periodontal microbiota resembles that of the gastro-intestinal tract, where infectious diseases are treatable via probiotics. In the oro-pharyngeal region, probiotic or replacement therapies have shown some benefit in the prevention of dental caries, otitis media, and pharyngitis but their effectiveness in the treatment of periodontitis is unknown. Therefore this study addressed the hypothesis that the application of selected beneficial bacteria as an adjunct to rootplaning would inhibit periodontopathogen recolonization of periodontal pockets.
Methods: Eight male beagle dogs with periodontal pockets were used in this split-mouth, double blind, randomized trial. At baseline, 4 teeth in each jaw were randomly assigned to receive: (1) rootplaning alone (Rp), (2) Rp + subgingival application of Streptococcus salivarius, (3) Rp + subgingival application of Streptococcus mitis (4) Rp + subgingival application of Streptococcus sanguinis. In the lower jaw, the application of these species was repeated at week 1, 2 and 4. At baseline and 2, 4, 6, 8 and 12 weeks later, subgingival plaque samples were taken and analyzed via bacterial culturing and checkerboard DNA-DNA hybridization.
Results: Although clear reductions in total anaerobic bacteria, black pigmented bacteria, Porphyromonas gingivalis and Prevotella intermedia were present 2 weeks after rootplaning, a fast recolonization of these pathogens took place. However, subgingival application of the streptococci inhibited or retarded this recolonization depending on the species applied. S. salivarius had the most pronounced inhibitory effect. Repeated applications were more effective than a single application. Checkerboard DNA-DNA hybridization analysis showed a shift towards a more host compatible microbiota at week 12 but only for those treatments in which beneficial bacteria were applied.
Conclusion: Within his limits, this study confirmed the hypothesis that the subgingival application of beneficial species can prolong the beneficial microbial shift towards a less pathogenic microbiota. (Supported by NIH grant DE015360 (MQ))