The effect of ethylenediamine-tetraacetic acid on Candida albicans.
AuthorsSen BH, et al. Show all Journal
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000 Nov;90(5):651-5.
Department of Restorative Dentistry and Endodontology, Ege University, Izmir, Turkey. firstname.lastname@example.org
OBJECTIVES: The aim of this study was to evaluate the antifungal effect of ethylenediamine-tetraacetic acid (EDTA) on Candida albicans, comparing it with that of various disinfectants and common antifungal agents.
STUDY DESIGN: Two clinical oral isolates and 1 standard strain of C albicans were included in this study. Main contents of the test solutions were sodium hypochlorite, EDTA, chlorhexidine, hexetidine, benzalkonium chloride, povidone-iodine, nystatin, and ketoconazole. The agar diffusion method was used to determine the antifungal effects of the solutions. Zones of inhibition were recorded and the results were analyzed statistically by using a 2-way analysis of variance.
RESULTS: EDTA demonstrated the highest antifungal activity in comparison with routine antifungal drugs and all other solutions (P <.0001). Oral cavity isolate was more resistant to the test solutions (P <.0001).
CONCLUSION: The selection of irrigating and disinfecting solution in root canals of patients with a particularly high incidence of oral candidiasis gains extreme importance. EDTA may be strongly recommended during endodontic therapy of these patients.
Inhibition on Candida albicans biofilm formation using divalent cation chelators (EDTA)
Gordon Ramage, Brian L. Wickes, José L. López-Ribot
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Candida albicans can readily form biofilms on both inanimate and biological surfaces. In this study we investigated a means of inhibiting biofilm formation using EDTA (Ethylenediaminetetra-acetic acid), a divalent cation chelating agent, which has been shown to affect C. albicans filamentation. Candida albicans biofilms were formed in 96-well microtitre plates. Cells were allowed to adhere for 1, 2, and 4 h at 37°C, washed in PBS, and then treated with different concentrations of EDTA (0, 2.5, 25, and 250 mM). EDTA was also added to the standardized suspension prior to adding to the microtiter plate and to a preformed 24 h biofilm. All plates were then incubated at 37°C for an additional 24 h to allow for biofilm formation. The extent and characteristics of biofilm formation were then microscopically assessed and with a semi-quantitative colorimetric technique based on the use of an XTT-reduction assay. Northern blot analysis of the hyphal wall protein (HWP1) expression was also monitored in planktonic and biofilm cells treated with EDTA. Microscopic analysis and colorimetric readings revealed that filamentation and biofilm formation were inhibited by EDTA in a concentration dependant manner. However, preformed biofilms were minimally affected by EDTA (maximum of 31% reduction at 250 mM). The HWP1 gene expression was reduced in EDTA-treated planktonic and biofilm samples. These results indicate that EDTA inhibits C. albicans biofilm formation are most likely through its inhibitory effect on filamentation and indicates the potential therapeutic effects of EDTA. This compound may serve a non-toxic means of preventing biofilm formation on infections with a C. albicans biofilm etiology.