The hypothesis that Enterococcus faecalis resists common intracanal medications by forming biofilms was tested. E. faecalis colonization of 46 extracted, medicated roots was observed with scanning electron microscopy (SEM) and scanning confocal laser microscopy. SEM detected colonization of root canals medicated with calcium hydroxide points and the positive control within 2 days. SEM detected biofilms in canals medicated with calcium hydroxide paste in an average of 77 days. Scanning confocal laser microscopy analysis of two calcium hydroxide paste medicated roots showed viable colonies forming in a root canal infected for 86 days, whereas in a canal infected for 160 days, a mushroom-shape typical of a biofilm was observed.Analysis by sodium dodecyl sulfate polyacrylamide gel electrophoresis showed no differences between the protein profiles of bacteria in freefloating (planktonic) and inoculum cultures. Analysis of biofilm bacteria was inconclusive.These observations support potential E. faecalis biofilm formation in vivo in medicated root canals.The most common reasons for failures in conservative root canal therapy are related to problems in instrumentation. However, occasionally, bacteria resistant to conservative therapy may also be involved (1). "Bacteria-associated endodontic failures together with pulp-periapical infections refractory to conventional treatment represent the unresolved bacteriological problems in endodontics" (2). Numerous studies have shown that persistent endodontic infections are often caused by Enterococcus faecalis (1, 3).Virulence factors of E. faecalis, such as hemolysin, gelatinase, and enterococcal aggregation substance (EAS) play an important role in the bacterium's pathogenesis (4). However, the mechanism through which E. faecalis persists in the root canal is not well understood. E. faecalis seems to be highly resistant to the medications used during treatment and is one of the few organisms that has been shown to resist the antibacterial effect of calcium hydroxide (5, 6). There is little research to explain why E. faecalis is resistant to root canal therapy. It is easily destroyed when grown in vitro, but it becomes resistant when present in the environment of the root canal system (7). Therefore, E. faecalis must undergo some type of change while in the root canal system, possibly activating some virulence factor that makes it more resistant. Alternatively, it may form a biofilm.Biofilms, also known as plaque, are complex communities of bacteria embedded in a polysaccharide matrix (8). Suspended, i.e. planktonic, bacteria that are either leaving or joining the biofilm surround the biofilm. The growth conditions vary between biofilm and planktonic environments. For this reason, proteins expressed by biofilm bacteria may differ from those expressed by their planktonic counter parts, and both the biofilm bacteria and the planktonic bacteria may differ from bacteria maintained in the laboratory.The purpose of this study was to test the hypothesis that E. faecalis forms a biofi...
Enterococcus faecalis is a pathogen that persists in medicated root canals. Here, we tested the hypothesis that the E. faecalis proteases, serine protease and gelatinase, and the collagen-binding protein (Ace) contribute to adhesion to the root canal. Scanning electron microscopy was used to examine dentin binding by four E. faecalis strains: OG1RF, the wild type, and three mutant derivatives of OG1RF, TX5128, TX5243 and TX5256 deficient in serine protease and gelatinase, serine protease, and Ace, respectively. For each strain, 20 root halves were exposed to 3 x 10(9) to 5 x 10(9) cells/ml for 6 h, and 50 fields per root half were examined for adherent bacteria. Statistical analysis revealed that adherence of OG1RF was significantly greater than the mutant strains (P < 0.001), while significant differences were not detected between the protease mutants. The data indicate that serine protease and Ace aid E. faecalis binding to dentin, while the role of gelatinase is uncertain.
The aim of this study is to evaluate the effectiveness over application time of different formulations of a novel endodontic irrigant (QMix™ 2in1) composed of a polyaminocarboxylic acid chelating agent, a bisbiguanide antimicrobial agent, a surfactant and deionized water to remove the root canal smear layer and expose patent dentinal tubules compared to a standard solution of 17% EDTA. Eighty human tooth roots from extracted, single-rooted teeth were instrumented (size 40.06) using 0.2 mL of sodium hypochlorite (6.15%) between each file size with a 3 mL water rinse after final instrumentation. Eight groups of 10 roots were irrigated with 3 mL of different formulations of QMix: QMix A, QMix B, and QMix C, or 17% EDTA for 60 and 90 s, respectively, then rinsed with 5 mL of sterile water. The roots were irrigated using a standard irrigation syringe and a 30 ga side-vent needle with an apical-coronal motion to within 1 mm of the working length. The coronal, middle and apical thirds of one canal surface of each root was evaluated at 1000× using scanning electron microscopy. The presence of smear layer was scored using a 5-point scale. Data were analyzed with the Kruskal-Wallis rank sums test, the Steel-Dwass, all-pairs comparison test, and the Steel method (with control) test. Irrigant type was highly significant (p < 0.007). Combined 60 and 90 s exposure data indicated QMix A (p = 0.014) and QMix C (p = 0.028) were superior to EDTA. While at the 90 s exposure time, smear layer removal by solutions QMix A (p = 0.043), QMix B (p = 0.018), and QMix C (p = 0.011) was superior to EDTA. All irrigants removed smear layer more effectively at the coronal and middle levels compared to the apical level (p < 0.001). Analysis showed all three QMix formulations were superior to EDTA in smear layer removal and exposure of dentinal tubules in the root canal system in single-rooted teeth.
An in vitro study was conducted to determine the susceptibility of the yeast Candida albicans to various intracanal irrigants and medications. The minimum inhibitory concentration (MIC) of sodium hypochlorite, hydrogen peroxide, chlorhexidine digluconate, and aqueous calcium hydroxide that is required to kill a standardized inoculum of C. albicans was determined. Growth of the yeast was measured by optical density. Sodium hypochlorite, hydrogen peroxide, and chlorhexidine digluconate were effective anticandidal agents with MICs of <10 microgram/ml, 234 microgram/ml, and <0.63 microgram/ml, respectively. Aqueous calcium hydroxide had no activity. A standardized inoculum of C. albicans cells was also placed in direct contact with either calcium hydroxide paste or camphorated para-monochlorophenol (CPMC), and candidal growth was assessed by colony counts on Sabouraud's dextrose agar. Calcium hydroxide paste and CPMC, when maintained in direct contact with C. albicans, were effective antifungal agents.
Contamination of the root canal system by persistent, enteric bacteria via leakage through interim restorations has been well documented. This in vitro study evaluated the ability of interappointment medications to prevent contamination of the root canal system by Enterococcus faecalis. Coronally unsealed, medicated tooth roots fixed in a closed system were contaminated daily with a standardized, aerobic, broth culture of E. faecalis. Four medications were evaluated (n = 15): group A, calcium hydroxide/methylcellulose paste; group B, camphorated parachlorophenol/calcium hydroxide paste; group C, 1% chlorhexidine/methylcellulose gel; and group D, calcium hydroxide points. The mean number of days to contamination as indicated by turbidity in the closed system was the following: group A, 37; group B, 46; group C, 16; group D, 5; and a positive control (no medication), 3. A one-way analysis of variance with a Scheffe post hoc test (p = 0.05) detected significant differences in effectiveness with A and B superior to C and D, and C superior to D.
Because of its excellent osteogenic potential, autogenous bone is the preferred grafting material for dental procedures; however, bone collected in osseous coagulum traps is subject to contamination by oral bacteria. This study assessed bacterial contamination of osseous coagulum and tested treatments for reducing contamination. Fifty bone samples from patients undergoing implant osteotomy procedures were collected in osseous coagulum traps, divided into groups of 10, and rinsed with normal saline, 0.12% chlorhexidine, or 50 mg/mL tetracycline. Twenty control samples received no treatment. The bone samples were plated in triplicate on selective and differential media to assay aerobic and anaerobic bacteria and potential bacterial pathogens, including staphylococci, streptococci, enterics, and black-pigmented bacteria (BPB). Inoculations were performed with an Autoplate 4000, and plates were incubated at 37 degrees C either aerobically or in a Coy anaerobic chamber. Bacteria were isolated from all samples. In control samples, the mean colony-forming units (cfu) per milliliter of suspended osseous coagulum was 6.5 x 10(4) +/- 9.6 x 10(4) in aerobic cultures and 4.8 x 10(4) +/- 6.9 x 10(4) in anaerobic cultures. Viridans streptococci were isolated from 46 samples, with a mean of 2.9 x 10(4) +/- 4.1 x 10(4) cfu/mL. Enterics were in 16 samples with cfu ranging from 200 cfu/mL to 3.4 x 10(4) cfu/mL. Mannitol nonfermenting staphylococci were found in one sample at 106 cfu/mL. BPB were not isolated. A Mann-Whitney U test with significance set at P = .05 determined that the only statistically significant reductions in bacterial numbers occurred in tetracycline-treated samples of anaerobic bacteria (5-fold decrease, P = .02) and aerobic bacteria (6-fold decrease, P = .01). Tetracycline treatments effected a 7-fold decrease in streptococci, but the difference was not significant (P = .07). These data indicate significant bacterial contamination of bone collected in osseous coagulum traps and justify further research into methods for eliminating that contamination.
Atherogenic ω-6 lipids are physiological ligands of peroxisome proliferator-activated receptors (PPARs) and elicit pro- and antiatherogenic responses in vascular cells. The objective of this study was to investigate if ω-6 lipids modulated the early growth response-1 (Egr-1)/PPAR crosstalk thereby altering vascular function. Rat aortic smooth muscle cells (RASMCs) were exposed to ω-6 lipids, linoleic acid (LA), or its oxidized form, 13-HPODE (OxLA) in the presence or absence of a PPARα antagonist (MK886) or PPARγ antagonist (GW9662) or PPAR-specific siRNA. Our results demonstrate that ω-6 lipids, induced Egr-1 and monocyte chemotactic protein-1 (MCP-1) mRNA and protein levels at the acute phase (1–4 hrs) when PPARα was downregulated and at subacute phase (4–12 hrs) by modulating PPARγ, thus resulting in altered monocyte adhesion to RASMCs. We provide novel insights into the mechanism of action of ω-6 lipids on Egr-1/PPAR interactions in vascular cells and their potential in altering vascular function.
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