D-amino acids reduce Enterococcus faecalis biofilms in vitro and in the presence of antimicrobials used for root canal treatment.
Enterococcus faecalis is the most frequent species present in post-treatment disease and plays a significant role in persistent periapical infections following root canal treatment. Its ability to persist in stressful environments is inter alia, due to its ability to form biofilms. The presence of certain D-amino acids (DAAs) has previously been shown to reduce formation of Bacillus subtilis biofilms. The aims of this investigation were to determine if DAAs disrupt biofilms in early and late growth stages for clinical E. faecalis strains and to test their efficacy in disrupting E. faecalis biofilms grown in sub-minimum inhibitory concentrations of commonly used endodontic biocides. From thirty-seven E. faecalis strains, the ten "best" biofilm producers were used to test the ability of a mixture containing D-leucine, D-methionine, D-tyrosine and D-tryptophan to reduce biofilm growth over a period of 24, 72 and 144 hours and when compared to their cognate L-Amino Acids (LAAs). We have previously shown that sub-MIC levels of tetracycline and sodium hypochlorite promotes biofilm growth in clinical strains of E. faecalis. DAAs were therefore tested for their effectiveness to reduce biofilm growth in the presence of sub-minimal concentrations of sodium hypochlorite (NaOCl-0.031%) and Odontocide™ (0.25% w/v), and in the presence of Odontopaste™ (0.25% w/v). DAAs significantly reduced biofilm formation for all strains tested in vitro, while DAAs significantly reduced biofilm formation compared to LAAs. The inhibitory effect of DAAs on biofilm formation was concentration dependent. DAAs were also shown to be effective in reducing E. faecalis biofilms in the presence of Odontopaste™ and sub-MIC levels of NaOCl and Odontocide™. The results suggest that the inclusion of DAAs into current endodontic procedures may reduce E. faecalis biofilms.
Microbiology laboratory, The School of Dentistry, The University of Adelaide, Adelaide, South Australia, Australia.
Peter S
http://orcid.org/0000-0001-7554-9717
PS
Zilm
Microbiology laboratory, The School of Dentistry, The University of Adelaide, Adelaide, South Australia, Australia.
Victor
V
Butnejski
Microbiology laboratory, The School of Dentistry, The University of Adelaide, Adelaide, South Australia, Australia.
Giampiero
G
Rossi-Fedele
Australian Centre for Antimicrobial Resistance Ecology, Research Centre for Infectious Disease, School of Biological Science, The University of Adelaide, Adelaide, South Australia, Australia.
Stephen P
SP
Kidd
School of Public Health, The University of Adelaide, Adelaide, South Australia, Australia.
Suzanne
S
Edwards
School of Engineering, University of South Australia, Adelaide, South Australia, Australia.
Krasimir
K
Vasilev
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D018441:Biofilms / Q000254:growth & development*; D003786:Dental Pulp Cavity / Q000382:microbiology; D013293:Enterococcus faecalis / Q000254:growth & development*; D006801:Humans; D007930:Leucine / Q000494:pharmacology*; D008715:Methionine / Q000494:pharmacology*; D008826:Microbial Sensitivity Tests; D050296:Microbial Viability / Q000187:drug effects; D012388:Root Canal Irrigants / Q000494:pharmacology*; D012390:Root Canal Therapy / Q000009:adverse effects; D012973:Sodium Hypochlorite / Q000494:pharmacology; D014364:Tryptophan / Q000494:pharmacology*; D014443:Tyrosine / Q000494:pharmacology*
D000900:Anti-Bacterial Agents; D012388:Root Canal Irrigants; D014443:Tyrosine; D014364:Tryptophan; D008715:Methionine; D012973:Sodium Hypochlorite; D007930:Leucine