Sensitivity of Candida albicans biofilm cells grown on denture acrylic to antifungal proteins and chlorhexidine.
OBJECTIVE
Candida albicans cells form biofilms on polymeric surfaces of dentures and other prostheses introduced into the oral cavity. Many biofilm microorganisms exhibit resistance to antimicrobial agents; C. albicans cells may also develop resistance to naturally occurring antifungal peptides in human saliva including histatins (Hsts) and defensins (hBDs). Therefore, we evaluated Hst 5 activity on C. albicans biofilm cells compared to planktonic cells and measured whether surface treatment of denture acrylic with Hst 5, hBD-3, or chlorhexidine gluconate could inhibit in vitro biofilm development.


METHODS
Acrylic disks were preconditioned with 500 microl saliva for 30 min, and inoculated with C. albicans cells (10(6)cells/ml) for 1h, at 37 degrees C. Non-adherent cells were removed by washing and disks and were incubated in YPD growth medium for 24, 48, and 72 h at 37 degrees C. Candidacidal assays were performed on 48-h-biofilms and on planktonically grown cells using Hst 5 (15.5, 31.25, and 62 microM). Cell adhesion was compared on disks pre-coated with 0.12% chlorhexidine gluconate, 50 microM Hst 5, or 0.6 microM hBD-3 after 24, 48, and 72 h growth.


RESULTS
No significant difference was observed in sensitivity to Hst 5 of biofilm cells compared to planktonic cells (p>0.05). Pre-coating disks with hBD-3 did not inhibit biofilm development; however, Hst 5 significantly inhibited biofilm development at 72 h, while 0.12% chlorhexidine significantly inhibited biofilm development at all time intervals (p<0.05).


CONCLUSIONS
C. albicans biofilm cells grown on denture acrylic are sensitive to killing by Hst 5. Surface coating acrylic with chlorhexidine or Hst 5 effectively inhibits biofilm growth and has potential therapeutic application.
Pusateri
Christopher R
CR
Department of Restorative Dentistry, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY 14214, USA.
Monaco
Edward A
EA
Edgerton
Mira
M
D000180:Acrylic Resins / Q000737:chemistry*; D000891:Anti-Infective Agents, Local / Q000494:pharmacology*; D000935:Antifungal Agents / Q000494:pharmacology*; D018441:Biofilms / Q000187:drug effects* / Q000254:growth & development; D002176:Candida albicans / Q000187:drug effects* / Q000254:growth & development; D002448:Cell Adhesion / Q000187:drug effects; D002710:Chlorhexidine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015169:Colony Count, Microbial; D003764:Dental Materials / Q000737:chemistry*; D003819:Denture Bases / Q000382:microbiology*; D054808:Histatins / Q000494:pharmacology; D006801:Humans; D008422:Materials Testing; D019904:Polymethyl Methacrylate / Q000737:chemistry; D012463:Saliva / Q000502:physiology; D013499:Surface Properties; D013696:Temperature; D013997:Time Factors; D023083:beta-Defensins / Q000494:pharmacology
D000180:Acrylic Resins; D000891:Anti-Infective Agents, Local; D000935:Antifungal Agents; C422950:DEFB103A protein, human; D003764:Dental Materials; C068075:HTN3 protein, human; D054808:Histatins; D023083:beta-Defensins; C040291:Lucitone; D019904:Polymethyl Methacrylate; C010882:chlorhexidine gluconate; D002710:Chlorhexidine