title: Collagen-binding streptococcal surface proteins influence the susceptibility of biofilm cells to endodontic antimicrobial solutions.
abstract: BACKGROUND
  Previous studies have indicated that the antimicrobial efficacy of endodontic irrigants may be diminished in the presence of patient tissues and fluids. With Streptococcus gordonii as a model microorganism, we used a genetic approach to investigate the hypothesis that bacterial surface proteins with collagen-binding abilities may function to protect biofilm cells from antiseptics commonly used in root canal treatment.
  
  
  METHODS
  S. gordonii strain DL1 or isogenic mutant strains with deletions of genes encoding collagen-binding surface proteins were grown in microtiter plates to form 8-hour biofilms. Planktonic cells were aspirated, and the remaining biofilm cells were buffer-washed and then incubated with either pH-adjusted buffer or potentially protective solutions of type I collagen, serum, or saliva. Biofilms were rewashed, pulsed with sodium hypochlorite, chlorhexidine digluconate, or BioPure MTAD, and then rewashed. Fresh medium was added, and survivor cell growth was monitored for 24 hours.
  
  
  RESULTS
  Buffer-treated biofilm cells of all 3 strains were similarly killed by sodium hypochlorite, chlorhexidine digluconate, and MTAD. Collagen, serum, and saliva significantly protected strain DL1 from all 3 antiseptics compared with buffer-treated cells (P ≤ .0004). However, preincubation with collagen, serum, or saliva left both mutant strain biofilms significantly more susceptible to all 3 antiseptics than were respectively treated strain DL1 biofilms (P ≤ .005).
  
  
  CONCLUSIONS
  Interactions of S. gordonii surface proteins with collagen or similar components in serum and saliva may play roles in protecting biofilm cells from endodontic antiseptics. Elucidating molecular mechanisms underlying bacterial resistance to antimicrobials may facilitate the development of more effective treatments.
authors: Department of Periodontics and Endodontics, School of Dental Medicine, University at Buffalo, Buffalo, New York 14214, USA.
authors: Timothy L
authors: TL
authors: Violante
authors: Elaine M
authors: EM
authors: Haase
authors: M Margaret
authors: MM
authors: Vickerman
mesh_terms: D000891:Anti-Infective Agents, Local / Q000494:pharmacology*; D001425:Bacterial Outer Membrane Proteins / Q000378:metabolism*; D018441:Biofilms / Q000187:drug effects*; D002710:Chlorhexidine / Q000494:pharmacology; D019343:Citric Acid / Q000494:pharmacology; D024042:Collagen Type I / Q000378:metabolism*; D015169:Colony Count, Microbial; D004318:Doxycycline / Q000494:pharmacology; D004352:Drug Resistance, Microbial / Q000502:physiology*; D006801:Humans; D011136:Polysorbates / Q000494:pharmacology; D011485:Protein Binding; D012388:Root Canal Irrigants / Q000494:pharmacology*; D012463:Saliva; D012973:Sodium Hypochlorite / Q000494:pharmacology; D054773:Streptococcus gordonii / Q000737:chemistry / Q000187:drug effects / Q000502:physiology
chemical_list: D000891:Anti-Infective Agents, Local; D001425:Bacterial Outer Membrane Proteins; D024042:Collagen Type I; C475043:MTAD (intracanal irrigant); D011136:Polysorbates; D012388:Root Canal Irrigants; D019343:Citric Acid; D012973:Sodium Hypochlorite; D004318:Doxycycline; D002710:Chlorhexidine