Silver Diamine Fluoride and Potassium Iodide Disruption of In Vitro Streptococcus mutans Biofilm.

Purpose: The purpose of this study was to investigate the inhibitory in vitro effects of silver diamine fluoride (SDF) with and without a saturated solution of potassium iodide (SSKI) on established Streptococcus mutans biofilm.Methods: Fifty µl of an overnight S. mutans culture (106 CFU per mL) in Tryptic Soy Broth (TSB) and three ml of fresh TSB supplemented with one percent sucrose (TSBS) were incubated for 24 hours to establish an S. mutans biofilm in six-well tissue culture plates. Four treatments (SDF, SSKI, SDF plus SSKI, and untreated control) were used to disrupt the biofilm. The biofilm groups were each treated with reagent and washed; the biofilm was collected, diluted, and spiral-plated onto blood agar plates; and an automated counting machine was used to determine the bacterial colony forming units (CFU).Results: The control had significantly more CFU than the SSKI, SDF, and SDF plus SSKI groups (P<.0001). The SSKI group had significantly more CFU than the SDF and SDF plus SSKI groups (P<.0001). The SDF group had significantly fewer CFU than the SDF plus SSKI group (P=.02). The reduction from the control was more than seven-fold for SDF, four-fold for SDF plus SSKI, and two-fold for SSKI.Conclusions: SDF alone, SDF plus SSKI, and SSKI disrupted an established S. mutans biofilm. SDF alone had the greatest overall disruption.

Inactivation of the antibacterial activity of iodine potassium iodide and chlorhexidine digluconate against Enterococcus faecalis by dentin, dentin matrix, type-I collagen, and heat-killed microbial whole cells.

The antibacterial activity of chlorhexidine digluconate and iodine potassium iodide on Enterococcus faecalis A197A was tested in the presence of dentin, dentin matrix, dentin pretreated by EDTA and citric acid, collagen, and heat-killed cells of Enterococcus faecalis and Candida albicans. Medications were preincubated for 1 h with each of the potential inhibitors and tested for their antibacterial activity against E. faecalis, strain A197A. Surviving bacteria were sampled after 1 and 24 h of incubation. Dentin matrix and heat-killed microbial cells were the most effective inhibitors of chlorhexidine, whereas dentin pretreated by citric acid or EDTA showed only slight inhibition. Dentin and skin collagen showed some inhibition at 1 h but not after 24 h. Iodine potassium iodide was effectively inhibited by dentin, dentin matrix, and heat-killed microbial cells. Skin collagen and dentin pretreated by EDTA or by citric acid showed little or no inhibitory effect on iodine potassium iodide. Different components of dentin are responsible for the divergent patterns of inhibition of the antibacterial activity of chlorhexidine digluconate and iodine potassium iodide. Chemical treatment of dentin before applying the medication into the root canal may alter the antibacterial effect of the medication.

Inactivation of root canal medicaments by dentine, hydroxylapatite and bovine serum albumin.

AIM: This study examined and compared the inhibition of the antibacterial effect of saturated calcium hydroxide solution, chlorhexidine acetate and iodine potassium iodide by dentine, hydroxylapatite and bovine serum albumin. METHODOLOGY: Enterococcus faecalis strain A197A prepared to a suspension of 3 x 10(8) cells per ml in 0.5% peptone water was used. Fifty microL of saturated calcium hydroxide solution, 0.05% chlorhexidine acetate or 0.2/0.4% iodine potassium iodide were incubated at 37 degrees C with 28 mg dentine powder (DP), hydroxylapatite (HA) or bovine serum albumin (BSA) in 50 microL water for 1 h before adding 50 microL of the bacterial suspension. Samples for bacterial culturing were taken from the suspension 1 and 24 h after adding the bacteria. In further experiments, the amount of dentine was stepwise reduced from 28 mg 150 microL-1 to 2.8 mg 150 microL-1. RESULTS: Calcium hydroxide was totally inactivated by the presence of 28 mg of DP, HA or BSA. Chlorhexidine (0.05%) was strongly inhibited by BSA and slowed down by dentine. However, HA had little or no inhibitory effect on chlorhexidine. The antibacterial effect of 0.2/0.4% iodine potassium iodide on E. faecalis was totally inhibited by dentine (28 mg), but was practically unaffected by HA or BSA. A stepwise reduction of dentine from 28 mg 150 microL-1 to 2.8 mg 150 microL-1 was followed by a similar reduction of the inhibition of the antibacterial activity of chlorhexidine. Iodine potassium iodide was not inhibited at all with dentine amounts less than 28 mg. However, the effect of saturated calcium hydroxide solution was totally eliminated by dentine, in all four concentrations. CONCLUSION: Inhibition by dentine of the antibacterial activity of calcium hydroxide, chlorhexidine and iodine potassium iodide occurs by different mechanisms. Different components of dentine may be responsible for the inhibition of these three medicaments. Calcium hydroxide was particularly sensitive to inhibition by both inorganic and organic compounds.

Inactivation of local root canal medicaments by dentine: an in vitro study.

AIMS: The aim of the study was to investigate the inactivation by dentine of the antibacterial activity of various commonly used local root canal medicaments. METHODOLOGY: The medicaments tested were saturated calcium hydroxide solution, 1% sodium hypochlorite, 0.5% and 0.05% chlorhexidine acetate, and 2/4% and 0.2/0.4% iodine potassium iodide. Dentine was sterilized by autoclaving and crushed into powder with a particle size of 0.2-20 microns. Aliquots of dentine suspension were incubated with the medicaments in sealed test tubes at 37 degrees C for 24 h or 1 h before adding the bacteria. In some experiments bacteria were added simultaneously with dentine powder and the medicament. Enterococcus faecalis A197A was used as a test organism. Samples for bacterial culturing were taken from the suspensions at 5 min, 1 h and 24 h after adding the bacteria. RESULTS: Dentine powder had an inhibitory effect on all medicaments tested. The effect was dependent on the concentration of the medicament as well as on the length of the time the medicament was preincubated with dentine powder before adding the bacteria. The effect of calcium hydroxide on E. faecalis was totally abolished by the presence of dentine powder. Similarly, 0.2/0.4% iodine potassium iodide lost its effect after preincubation for 1 h with dentine before adding the bacteria. The effect of 0.05% chlorhexidine and 1% sodium hypochlorite on E. faecalis was reduced but not totally eliminated by the presence of dentine. No inhibition could be measured when full strength solutions of chlorhexidine and iodine potassium iodide were used in killing E. faecalis. CONCLUSIONS: The dentine powder model appears to be an efficient tool for the study of interactions between local endodontic medicaments, dentine, and microbes.