title: Inhibition of Streptococcus mutans biofilm accumulation and polysaccharide production by apigenin and tt-farnesol.
abstract: OBJECTIVE
  Apigenin is a potent inhibitor of glucosyltransferases and tt-farnesol affects the membrane integrity of Streptococcus mutans. We investigated the influence of apigenin and tt-farnesol, alone and in combination, on the accumulation, polysaccharide composition and viability of S. mutans UA159 biofilms.
  
  
  METHODS
  Initially, biofilms were grown for 54 h; then, the early-formed biofilms were treated for 1 min twice daily with one of the following: (i). 1.33 mM tt-farnesol; (ii). 1.33 mM apigenin; (iii). apigenin + tt-farnesol (1.33 mM each); (iv). vehicle control (20% ethanol with 0.75% dimethyl sulphoxide); (v). 0.12% chlorhexidine (1.33 mM); or (vi). physiological saline (145 mM NaCl). The procedure was repeated at biofilm ages of 78 and 102 h, and biofilms were harvested at 126 h. The dry weight, protein concentration, number of cfu, and polysaccharide composition per biofilm were determined.
  
  
  RESULTS
  The dry weights of the biofilms treated with the test agents were significantly less (30-50%) than those treated with vehicle control (P < 0.05). Biofilms treated with the test agents also resulted in lower amounts of extracellular alkali-soluble glucans, intracellular iodophilic polysaccharides and, to a lesser extent, fructans. The fructosyltransferase activity was affected only by apigenin and apigenin + tt-farnesol. The recoverable viable counts of S. mutans were slightly lower (0.5 to 1 log10 decrease in cfu/biofilm) after apigenin and tt-farnesol treatments compared with the vehicle control. Chlorhexidine displayed potent bactericidal activity, and virtually halted the further accumulation of early-formed (54 h old) biofilms.
  
  
  CONCLUSIONS
  Apigenin and tt-farnesol affected the accumulation and polysaccharide content of S. mutans biofilms without major impact on the bacterial viability.
authors.affiliation: Eastman Department of Dentistry, University of Rochester Medical Center, Rochester, NY 14642, USA. Hyun_Koo@urmc.rochester.edu
authors.forename: H
authors.initials: H
authors.lastname: Koo
authors.forename: M F
authors.initials: MF
authors.lastname: Hayacibara
authors.forename: B D
authors.initials: BD
authors.lastname: Schobel
authors.forename: J A
authors.initials: JA
authors.lastname: Cury
authors.forename: P L
authors.initials: PL
authors.lastname: Rosalen
authors.forename: Y K
authors.initials: YK
authors.lastname: Park
authors.forename: A M
authors.initials: AM
authors.lastname: Vacca-Smith
authors.forename: W H
authors.initials: WH
authors.lastname: Bowen
mesh_terms: D000891:Anti-Infective Agents, Local / Q000494:pharmacology; D047310:Apigenin; D018441:Biofilms / Q000187:drug effects* / Q000254:growth & development; D002710:Chlorhexidine / Q000494:pharmacology; D015169:Colony Count, Microbial; D005204:Farnesol / Q000494:pharmacology*; D005419:Flavonoids / Q000494:pharmacology*; D005964:Glucosyltransferases / Q000378:metabolism; D006801:Humans; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis*; D013295:Streptococcus mutans / Q000187:drug effects* / Q000254:growth & development
chemical_list: D000891:Anti-Infective Agents, Local; D005419:Flavonoids; D011135:Polysaccharides, Bacterial; D005204:Farnesol; D047310:Apigenin; D005964:Glucosyltransferases; D002710:Chlorhexidine