Enterococcus faecalis -An Endodontic Challenge

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E.gallinarum. E.faecalis ferments mannitol, sucrose, sorbitol and aesculin and grows on tellurite bood agar producing black colonies. E.faecalis posses a group D carbohydrate cell wall antigen called Lancefield antigen, which is an intracellular glycerol teichoic acid associated with the cytoplasmic membrane. The cell wall contains a large amount of peptidoglycan and teichoic acid. Peptidoglycan, a cross linked peptide sugar helps it to counteract osmotic pressure of the cytoplasm and provides cell wall strength and shape. It has a polysaccharide backbone of alternating Nacetyl glucosamine and N-acetylmuramic acids. Virulence and survival factors of E.faecalis E.faecalis possesses certain virulence factors including lytic enzymes, Aggregation substance (AS), pheromones and lipoteichoic acid. 4 Aggregation Substance. AS is a 37 KDa surface- localized protein, a plasmid- encoded adhesin. The adhesin mediates cell-cell contact which facilitates the plasmid exchange between recipient and donor strains. AS plays a role in the dissemination of plasmid –encoded virulence factors, protects against polymorphonuclear leukocyte or macrophage mediated killing and enhance the virulence by activating the quorum –sensing mode of cytolysin regulation. Surface protein esp. It is a large chromosome encoded surface protein which has multiple repeat motifs.A study by Toledo-Arana et al demonstrated that in the presence of the surface protein esp, hydrophobicity,biofilm formation and adherence to biotic surfaces were increased. Collagen -binding protein (Ace): It helps E.faecalis bind to collagen in dentin. Gelatinase and serine protease. E.faecalis secretes proteases like gelatinase and serine protease.Their secretion is autoregulated through the fsr system.Gelatinase is a non plasmid-encoded metalloendopeptidase.Gelatinase contributes to bone resorption and degradation of dentin organic matrix,thus playing an important role in pathogenesis of periapical inflammation.Serine protease cleaves peptide bonds and was shown to contribute to the binding of E.faecalis to dentin. Cytolysin: It is a plasmid encoded toxin that is produced by beta-hemolytic E.faecalis isolates .Cytolysin lyses erythrocytes, polymorphonuclear neutrophils and macrophages,kills bacterial cells and may lead to reduced phagocytosis. Lipoteichoic acid (LTA):Lipoteichoic acid can be regarded as a molecule contributing to the virulence of E.faecalis through the facilitation of aggregate formation and plasmid transfer.LTA of E.faecalis was reported to be doubled in quantity during the viable but non culturable (VBNC) state suggesting a role for LTA during this period. 5 Hyaluronidase (spreading factor) is considered to facilitate the spread of bacteria as well as their toxins through host tissues. The presence of microorganisms including E.faecalis in periapical lesions may also be related to the activity of a degrading bacterial enzyme such as hyaluronidase. Extracellular superoxide: It is associated with enterococcal virulence, and it has been shown that its production is significantly higher in invasive strains than in commensal isolates. Pheromones:Pheromones from E.faecalis are chemotactic for human neutrophils and triggers superoxide production. Antibiotic resistance and other virulence traits, such as cytolysin production can be disseminated among strains of E.faecalis via sex pheromone system. E.faecalis is a persister due to its ability to survive under harsh environmental conditions. It grows in high salt concentrations, wide temperature range and tolerates a broad pH range and starves until an adequate nutritional supply becomes available. Studies have shown that it might be serum delivered fluid from the periapical tissues which sustain the microbial flora. E.faecalis can enter the viable but non culturable (VBNC) state, a survival mechanism adopted by a group of bacteria when exposed to environmental stress and resuccitate upon returning to favourable conditions. It is small 36
enough to invade the dentinal tubules and lives in the dentinal tubules.Collagen binding protein help it to bind to the dentin. E.faecalis has the ability to establish mono-infections in medicated root canals. The organism has the ability to acquire, accumulate and share extrachromosomal elements, encoding virulence traits, which help to colonize, compete with other bacteria, resist host defense mechanisms and produce pathological changes directly through the production of toxins or indirectly through the induction of inflammation. E.faecalis has the advantage of forming biofilms. Hence it has a certain degree of protection and homeostasis. Biofilms grow in a nutrient -deprived ecosystem as it concentrates trace elements and nutrients by physical trapping and electrostatic interaction. The bacterial cells residing in a biofilm communicate, exchange genetic materials and acquire new traits. This communication takes place by quorum sensing. E.faecalis resists intra canal medicaments like calcium hydroxide by maintaining pH homeostasis. E.faecalis as an endodontic biofilm. E.faecalis forms intracanal biofilms,periapical biofilms and biomaterial centered infection. Invitro experiments have revealed distinct stages of the development of E.faecalis biofilm on root canal dentin. In stage 1, E.faecalis cells adhered and formed microcolonies on the root canal dentin surface. In stage 2, they induced bacterial mediated dissolution of the mineral fraction from dentine substrate. This localized increase in calcium and phosphate ions promotes mineralization (or calcification) of the E.faecalis biofilm in stage 3. The mature biofilm structure formed after 6 weeks of incubation and showed signs of mineralization. The mineralized E.faecalis biofilm showed a carbonated –apatite structure as compared to natural dentin which had carbonated-florapatite structure. Dentin degradation occurred in a nutrient deprived state and has been observed to be a consequence of the interaction of bacteria and their metabolic products on dentine. E.faecalis biofilm has been observed in root canal obturating materials (biomaterial centered infection). Disinfectants and E.faecalis Studies have shown that 3% to full strength sodium hypochlorite (NaOCl) is effective for all presentations of E.faecalis including its existence as a biofilm. However, many of the studies about the antibacterial effect of NaOCl against root canal bacteria are in vitro studies, in either “neutral” test tube conditions, in root canals of extracted teeth, or in dentine blocks infected with a pure culture of one organism at a time. EDTA (Ethylene diamine tetraacetic acid) when used along with NaOCl is effective in removing the inorganic portion of the dentin. Smear layer removal provides access of irrigants to the dentinal tubules. 0.1% sodium benzoate solution added to 10% citric acid solution will increase the chances of killing E.faecalis. A 2-min rinse of 2% chlorhexidine liquid can be used to remove E.faecalis from the superficial layers of dentinal tubules up to 100 µm. 2% chlorhexidine gel is effective at completely eliminating E.faecalis from dentinal tubules for 15 days. Maria Teresa et al observed in their studies that it was not possible to eradicate E.faecalis biofilms using chlorhexidine alone. 6 They found that the alternating use of chlorhexidine and cetrimide (0.1% and 0.05%) killed 100% of E.faecalis biofilm cultures. Cetrimide when used destructures the EPS (Extra polymeric substance) matrix. There after, chlorhexidine was able to react more directly on E.faecalis, possibly exerting its bactericidal potential to a greater degree. Orstavik D and Haapasalo M concluded from their study that 2% / 4% Iodine, potassium iodide (IKI) appeared as a more potent irrigant than sodium hypochlorite and chlorhexidine. 37
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Enterococcus faecalis -An Endodontic Challenge

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