Fluoride, triclosan and organic weak acids as modulators of the arginine deiminase system in biofilms and suspension cells of oral streptococci.
BACKGROUND
The arginine deiminase system (ADS) of oral bacteria is a major generator of alkali (ammonia) in dental plaque and is considered to have anticaries effects. However, many of the antimicrobial agents used in oral care products may reduce alkali production by the ADS. The objective of our work was to assess the sensitivity of the ADS of oral streptococci to commonly used antimicrobials, fluoride, triclosan and organic weak acids.


METHODS
Streptococcus sanguinis NCTC 10904 and Streptococcus ratti FA-1 were grown in suspension cultures and mono-organism biofilms. ADS activity at pH values of 4, 5 and 6 was assessed, and the actions of the agents was determined in terms of reduced production of alkali from arginine, inhibition of ADS enzymes and changes in uptake of arginine.


RESULTS
ADS activity was not greatly affected by pH changes between 4 and 6 and was greater per unit of biomass for cell suspensions than for biofilms. NaF was a poor inhibitor, while triclosan was highly effective with a 50% inhibitory dose for the two organisms between 0.03 and 0.05 and between 0.10 and 0.15 mm-h for suspension cells and biofilms, respectively. The weak acid indomethacin was nearly as potent at pH 4.0 as triclosan, while capric and lauric acids were less potent, especially for biofilms. The methyl ester of lauric acid was slightly stimulatory. The major targets for the inhibitors appeared to be transport systems for arginine uptake, although carbamate kinase was a secondary target.


CONCLUSIONS
Triclosan, indomethacin, caprate and laurate can reduce ADS activity in dental plaque.
Barboza-Silva
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Department of Microbiology and Immunology and Center for Oral Biology, University of Rochester Medical Center, Rochester, NY, USA. ebarboza_silva@yahoo.com.br
Castro
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Marquis
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D000891:Anti-Infective Agents, Local / Q000494:pharmacology*; D001120:Arginine / Q000378:metabolism; D018441:Biofilms / Q000187:drug effects; D001692:Biological Transport / Q000187:drug effects; D002327:Cariostatic Agents / Q000494:pharmacology; D003652:Decanoic Acids / Q000494:pharmacology; D003773:Dental Plaque / Q000201:enzymology / Q000382:microbiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006867:Hydrolases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology*; D007848:Laurates / Q000494:pharmacology; D007850:Lauric Acids / Q000494:pharmacology; D017851:Phosphotransferases (Carboxyl Group Acceptor) / Q000037:antagonists & inhibitors; D012969:Sodium Fluoride / Q000494:pharmacology; D013291:Streptococcus / Q000187:drug effects* / Q000201:enzymology*; D014260:Triclosan / Q000494:pharmacology*
D000891:Anti-Infective Agents, Local; D002327:Cariostatic Agents; D003652:Decanoic Acids; D007848:Laurates; D007850:Lauric Acids; C030358:lauric acid; C031071:decanoic acid; D014260:Triclosan; C089549:lauric acid methyl ester; D012969:Sodium Fluoride; D001120:Arginine; D017851:Phosphotransferases (Carboxyl Group Acceptor); C019288:carbamate kinase; D006867:Hydrolases; C019723:arginine deiminase; D007213:Indomethacin