title: Reduction of periodontal pathogens adhesion by antagonistic strains.
abstract: BACKGROUND
  Periodontitis results from a shift in the subgingival microflora into a more pathogenic direction with Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans considered as periodontopathogens. In many cases, treatment procures only a temporary shift towards a less pathogenic microflora. An alternative treatment could be the deliberate colonization of pockets with antagonistic microorganisms to control the adhesion of periodontopathogens. The aim of this study was to identify bacterial strains that reduce adhesion of periodontopathogens to surfaces.
  
  
  METHODS
  Streptococcus sanguinis, Streptococcus crista, Streptococcus salivarius, Streptococcus mitis, Actinomyces naeslundii, and Haemophilus parainfluenzae were evaluated as potential antagonists against P. gingivalis ATCC 33277, P. intermedia ATCC 49046, and A. actinomycetemcomitans ATCC 43718 as periodontopathogens. Adhesion of periodontopathogens to the bottom plate of a parallel plate flow chamber was studied in the absence (control) and the presence of pre-adhering antagonistic strains up to a surface coverage of 5%.
  
  
  RESULTS
  The largest reduction caused by antagonistic strains was observed for P. gingivalis. All antagonistic strains except S. crista ATCC 49999 inhibited the adhesion of P. gingivalis by at least 1.6 cells per adhering antagonist, with the largest significant reduction observed for A. naeslundii ATCC 51655 (3.8 cells per adhering antagonist). Adhering antagonists had a minimal effect on the adhesion of A. actinomycetemcomitans ATCC 43718. Intermediate but significant reductions were perceived for P. intermedia, most notably caused by S. mitis BMS.
  
  
  CONCLUSIONS
  The adhesion of P. gingivalis was inhibited best by antagonistic strains, while S. mitis BMS appeared to be the most successful antagonist.
authors.affiliation: Department of Biomedical Engineering, University Medical Center Groningen, and University of Groningen, Groningen, The Netherlands. c.g.van.hoogmoed@med.umcg.nl
authors.forename: C G
authors.initials: CG
authors.lastname: Van Hoogmoed
authors.forename: G I
authors.initials: GI
authors.lastname: Geertsema-Doornbusch
authors.forename: W
authors.initials: W
authors.lastname: Teughels
authors.forename: M
authors.initials: M
authors.lastname: Quirynen
authors.forename: H J
authors.initials: HJ
authors.lastname: Busscher
authors.forename: H C
authors.initials: HC
authors.lastname: Van der Mei
mesh_terms: D000190:Actinomyces / Q000502:physiology; D016976:Aggregatibacter actinomycetemcomitans / Q000502:physiology*; D000898:Antibiosis / Q000502:physiology*; D001422:Bacterial Adhesion / Q000502:physiology*; D001431:Bacteriological Techniques; D015169:Colony Count, Microbial; D044135:Haemophilus parainfluenzae / Q000502:physiology; D006801:Humans; D010518:Periodontitis / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000502:physiology*; D018713:Prevotella intermedia / Q000502:physiology*; D013291:Streptococcus / Q000145:classification / Q000502:physiology; D034361:Streptococcus mitis / Q000502:physiology; D013298:Streptococcus sanguis / Q000502:physiology