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Endodontic microbiology

This document provides an overview of endodontic microbiology. It begins with an introduction to how microorganisms cause pulp and periradicular infections. It then discusses the mechanisms of microbial pathogenicity and virulence factors. It describes the microbial ecology of the root canal ecosystem and how the environment changes over time. It outlines the various routes of root canal infection and the typical microbes involved in primary, secondary, and persistent intraradicular infections. It also discusses extraradicular infections. The document covers biofilm formation and bacterial interactions. It concludes with discussing treatment measures and references.

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Endodontic Microbiology  ANJALI SAVITA  MDS I  DEPT OF CONSERVATIVE AND ENDODONTICS
Contents  Introduction  Mechanisms of Microbial Pathogenicity  Microbial Ecology and the Root Canal Ecosystem  Routes of canal infection  Endodontic microbiota  Types of endodontic infections  Biofilm and bacterial interaction  Bacterial treatment measures  Conclusion  References
INTRODUCTION Microorganisms cause virtually all pathoses of the pulp and the periradicular tissues. To effectively treat endodontic infections, clinicians must recognize the cause and effect of microbial invasion on the dental pulp space and the surrounding periradicular tissues.
Mechanisms of Microbial Pathogenicity and Virulence Factors Pathogenicity Virulence Virulence factors
Bacterial virulence factors
Microbial Ecology And Root Canal Ecosystem In the very initial phases of the pulpal infectious process: facultative bacteria predominate. After a few days or weeks, oxygen is depleted loss of blood circulation in the necrotic pulp. Growth of obligate anaerobic bacteria. The root canal infection is a dynamic process, and different bacterial species apparently dominate at different stages. Sundqvist & Figdor 2003, Sundqvist 1994
Necrotic pulp cavity becomes reservoir for microbes Disintegrated tissue and fluids becomes nutrients for microorganism Nutrients are polypeptide and amino acids Nutrient supply + Bacterial interactions + low 𝑶 𝟐 tension determine the type of predominant bacteria. Growth of anaerobes provides environment for metabolization of peptides and amino acids
Some species produce metabolic bi-products which is essential for growth of other species Antagonist relationship may occur among bacteria Some biproducts (e.g. Ammonia) can either be nutrient or toxin. Bacteriocins( antibiotic like substances) inhibit growth of other bacteria Chemo mechanical RC preparation help to disrupt and destroy microbial ecosystem and perfect obturation eliminates the pulp cavity as reservoir.
NUTRIENT SUPPLY TO MICROBES
ROUTES OF ROOT CANAL INFECTION Sundqvist 1994 Siqueira & Janeiro 2002
Correlation With Pathoses And Treatment Endodontic infections are polymicrobial Periradicular tissues posses Excellent collateral circulation Lymphatic drainage. Vast amount of undifferentiated cells. Periradicular pathoses develop in response of Microorganisms Microbial biproducts Inflammatory mediators Instrument trauma Chemicals
Endodontic Microbiota More than 700 species of bacteria are recognized as normal inhabitants of oral cavity. Root canal microflora is dominated by Anaerobic bacteria. Streptococci Staphylococci Corynebacterium Yeast Gram +ve(75%) Spirochetes Neisseriae Bacteroides Fusobacterium, Pseudomonas. Gram –ve(24%)
Anaerobic Actinomyces Eubacterium Propionibacterium Peptostreptococci Facultative Enterococcus Streptococci lactobacillus
Anaerobic Treponema Porphyromonas Prevotella Fusobacterium Tannerella Facultative Neisseria Capnocytophaga lactobacilllus
Types Of Endodontic Infections Intraradicular Infections Extraradicular Infection
Primary Intrardicular Infection Primary infection is caused by microorganisms that initially invade and colonize the necrotic tissue. Primary infections are characterized by a mixed consortium composed of 10-30 species per canal. The number of bacterial cells in an infected canals varies from 103-108 per root canal Siqueira et al 2005 Sakamoto et al 2007 Vianna et al 2006
Bacteria Involved In Primary Intraradicular Infection Gram Negative Gram Positive Prevotella Porphyromonas Tanerella Fusobacterium Dialister Campylobactor Treponema Actinomyces Peptostreptococcus Eubacterium Filifactor Microaerophillic streptococci
Saccharolytic; Prevotella P. Intermedia P. Nigrescense P. Tannerae P. Denticola P. multissachari- vorax Asaccharolytic; Porphyromonas P.endodontalis P.gingivalis BACTEROIDS They seem to play important role in etiology of both acute and chronic apical periodontitis. Black pigmented bacteria, Gram +Ve Siqueira et al 2001 Sundqvist et al 1989 Dougherty et al 1998
Recently findings from molecular studies have also suggested that some anaerobic species commonly found in primary infection Tenerella Forsythia Pseudoramibactor Alactolyticus Filibactor Acolis Dialister pnuemosintes Siqueira et al 2004,2005
In majority of bacteriological studies on periapical lesions, it has been observed that Porphyromonas and Prevotella had a higher prevalence in periradicular lesions associated with pain, purulent abscess and teeth refractory to conventional root canal treatment. Kiryu et al. 1994 Trowbridge & Stevens 1992 Bogen &Slots 1999 Yamasaki et al. 1998
Gram negative obligate nonmotile anaerobic bacteria. Most common in symptomatic infection and abscess or exacerbation lesion than asymptomatic infection. 5 subspecies of F. Nucleatum have been found which are different in genetic data but no study found that which subspecies have more virulence factor. Different type of subspecies are found in the same root canals. Fusobacterium Nucleatum Moraes et al 2002 Siqueira et al 2005
Spirochete Although spirochetes have been frequently observed in samples by microscopy, they had never been identified to the species level. The application of molecular diagnosis to identification of spiral bacteria has been overlooked the culture techniques. They can be classified in 2 group; Saccharolytic and Asaccharolytic. T. Denticola, T. Sokranskii have been detected in both symptomatic and asymptomatic lesion. Dewhirst et al 2000 Baumgartner et al 2007 Rocas et al 2003
Secondary Intraradicular Infections If microorganisms are allowed to remain at the time of filling , there is increased risk of adverse outcome of the endodontic treatment Sjogren et al 1997 Waltimo et al 2005
Bacteria Involved In Secondary Intraradicular Infection Pseudomonas aeruginosa. Staphylococcus sp. Escherichia coli. Candida sp.
Persistant Intraradicular Infection Infections caused by microorganisms that resisted the intracanal antimicrobial procedures. Fungi and Gram positive facultative bacteria, particularly Enterococcus faecalis, are predominant in such cases.
E. Faecalis Non spore forming, fermentative Facultative anaerobic, Gram positive coccus. This species has been found in low prevalence value in case of primary infection and more relate in asymptomatic cases than symptomatic cases. Rocas et al 2005
E. feacalis has been found in root filled teeth evincing persistent apical periodontitis in prevalence values ranging from 30-90% of the cases. This species can be inhibited by other members of mixed bacterial consortium commonly present in primary infection. Sedgley et al 2006
Virulence factors of E. Faecalis But its still not confirmed which factor play an important role in pathogenesis. Kayaoglu et al 2004 Lytic enzymes Cytolysin Gelatinase Hyaluronidase Pheromones Lipoteichoic acid Adhesion molecules
Why E. feacalis can survive in root filled teeth? Studies have revealed that E. feacalis has ability to penetrate far into dentinal tubules that can escape from intracanal instrumentation and irrigants. Haapasalo et al 1989 Siqueira et al 1996
E.feacalis has been shown to be able to form biofilms in root canals and this ability can be important for bacterial resistance and persistence in the instrumented canals. Distel et al 2002 The ability to resist high pH value seems to be related to functional proton pump to acidfy. So, is resistant to calcium hydroxide. Evans et al 2002
E.feacalis can enter a VBNC state which can survive in adverse environmental condition, including starvation. They has the ability to survive in environments in scarcity of nutrients and to flourish when the nutrient source is reestablished and has a capacity to recover in root canal treated teeth for 12 months without nutrients. Figdor et al 2003 Sedgley et al 2005
Prevalence of E. Faecalis in samples from root canal treated teeth with apical periodontitis. Data from Culture (Yellow bars) and data from Molecular (Blue bars) studies
Fungi It is also possible that yeasts from oral cavity gain access to root canal as contaminant during endodontic procedures. Siren et al 1997 Siqueria & Sen et al 1997 They can overgrow after inefficient intracanal antimicrobial procedures, which can cause imbalance in microbiota. Siqueira et al 2004 E. faecalis and yeast, mainly C. albicans, has been repeatedly identified as the species most commonly recovered from root canals undergoing retreatment, in cases of failed endodontic therapy and canals with persistent infections.
Dentino phillic microorganism due to its ability to colonize and invade to dentin by their hyphae. Resist to some intracanal medication such as calcium hydroxide. Release hydrolytic enzyme and can form monoinfection biofilm in root canals. Waltimo et al 1999 Matusow et al 1981
Ashraf et al 1997 Najzar & Fleger et al CA in the root canal system of teeth with periapical lesions was more noticeable and statistically significant compared to the teeth without periapical lesions 55% of root canals contain Candida cell. Presence of fungi in root canals more than expected and the knowledge of persistent periapical infections may advocate the use of antifungal agents in modern endodontic therapy.
Prevalence of microorganism detected in root canal treated teeth with post treatment disease. Data is from taxon-specific PCR assay
Extraradicular infections Extra radicular infections are characterized by, microbial invasion & proliferation in the inflamed peri radicular tissue as a result of intra radicular infections. The development of periradicular lesions creates a barrier with in the body to prevent further spread of microorganisms. Bone tissue is resorbed and substituted by a granulation tissue containing defense elements, such as cells (phagocytes) and molecules (antibodies and complement molecules).
A dense wall composed of polymorphonuclear leucocytes, or less frequently an epithelial plug, is usually present at the apical foramen, blocking the egress of microorganisms into the periradicular tissues. Very few endodontopathogens can advance through such barriers. However, microbial products can diffuse through these defence barriers and are able to induce or perpetuate periradicular pathosis Vigil et al.1997 In recent years there is resurgence of the idea of extraradicular microbes in apical periodontitis lesions with implied, controversial suggestion that extraradicular infection is the cause of many failed endodontic treatment.
Extraradicular infection can be independent of Intraradicular infection. Case of apical actinomyces in which non surgical endodontics, calcium hydroxide, systemic erythromycin, and finally, a regimen of systemic metronidazole failed to resolve the draining fistula associated with a maxillary lateral incisor. but following periapical surgery, the lesion resolved. Haapasalo et al. 1987
16 periapical granuloma that were collected “during normal periapical curettage, apecectomy, or retrograde filling”. It was seen that most of the organism cultured were Veillonella species, Streptococcus milleri, Streptococcus sanguis, Actinomycetes naeslundii, Propionibacterium acnes and Bacteroides species Iwu & Wallace 1990
Those extra radicular infections which are caused by intra radicular bacteria are treated easily by RCT. Eg: Sinus Tract If the extra radicular infection which are caused by outer side are treated only by Endodontic Surgery. Eg: Actinomycosis Cohen & Burns 2002
Remnants of Dental pulp Calculus Caries on tooth crown Leakage of rubber dam Contamination of instrument Irrigation solution Intracanal medicaments SOURCE OF MICROBES DURING TREATMENT
Loss or leakage of restorative material Tooth fracture SOUCE OF MICROBES DURING APPOINTMENTS
Loss or leakage of restorative material Tooth fracture Secondary caries Delay in placement of permanent filling or crown prosthesis. SOUCE OF MICROBES AFTER ROOT CANAL TREATMENT
Biofilm And Bacterial Interaction Sessile multicellular microbial community characterized by cells that are firmly attached to a surface and embedded in a self produced matrix of extracellular polymeric substances. AAE, 2004 Defined as community of microcolonies of microorganisms in an aqueous solution that is surrounded by a matrix made of glycocalyx, which also attaches the bacterial cell to a solid substratum. Grossman, 13 edition  Definition
According to kishen There are four distinct stages in development of biofilm  Formation of a conditioning layer  Planktonic bacterial cell attachment  Detachment (seeding dispersal)  Bacterial growth and biofilm expansion.
Autopoiesis Ability to self organize. Homeostasis Ability to resist environmental disturbances. Synergy More effective in association with fellow microorganisms. Communality Response to environmental challenges as combined unit. Caldwell et al The biofilm has following attributes that makes it resistance to clinical
Communications between bacterial cells residing in a biofilm is attained through signaling molecules by a process called as Quorum sensing Quorum sensing is mediated by low molecular weight molecules- autoinducers Qs leads to Exchange of genetic materials between species Antibiotic resistance  Nutrient breakdown Xenobiotic metabolism Coordinated behaviour of biofilm
Endodontic biofilms are therapeutically significant as they are one of the basic survival methods for bacteria during starvation.  Endodontic biofilms help bacteria to survive because Ability to protect bacteria from environment Ability to entrap nutrients for the growth of microbial constituent. Offer a safe environment to exchange of genetic material Provide inherent resistance to antimicrobial agents (irrigants & ICM) Caldwell et al
Classification Of Endodontic Biofilm Intracanal microbial biofilm Formed on radicular dentin in an endodontically infected tooth Various distinct types of bacteria can develop these biofilms, but E. faecalis is responsible for one of the most therapy resistant and prevalent endodontic biofilms Extraradicular microbial biofilm Root surface biofilms Formed on the cemental surfaces around root apex of an endodontically infected tooth Eg: F. Nucleatum Periapical microbial biofilm Isolated biofilms independent of internal or external surface of the root canal Actinomyces and P. propionicum have shown to form periapical lesion resistant to endodontic therapy.
Bacterial Treatment Measure Infection control All patients should be treated as if they have transmissible disease. Disinfect tooth surface & rubber dam with Chlorhexidine or NaOCL. Use physical barriers like - Face shield - Rubber dam - Mask - Gloves & Gowns
Removal of source of irritation helps in healing of periradicular lesion. Source of irritation is generally the reservoir of infection (pulp cavity). Achieved by thorough debridement of root canals. RC debridement is the achieved by proper instrumentation with use of canal irrigants
Irrigants Flush out debris Dissolve organic remnants Antimicrobial lubricants Irrigants  Saline  Sodium hypochlorite(NaOCl)  CHX  Hydrogen peroxide (𝐻2 𝑂2)  Citric acid  EDTA Sonic and ultrasonic devices can improve irrigant effect Spratt et al 2001
ICM Penetrate dentinal tubules Induces calcific barrier Antimicrobial Eliminates pain ICM  Formocresol  PCP &CPC  Glutaraldehyde  Cresatin  Thymol The current IC Medicament of choice is Ca (OH)2
DRAINAGE Key to manage an abscess and cellulitis Achieved through the canal and incision Reduces discomfort, toxins, pressure Incision of indurated swelling releases Blood Serous fluid Bacteria & biproducts Inflammatory mediators Drainage removes these irritants & improves local circulation.
Adjunctive Antibiotic therapy Antibiotics are not a substitute for local treatment. The majority of endodontic cases can be treated without antibiotics. Pain & swelling of endodontic origin are managed by debridement & drainage Do not require antibiotics Without systemic sign & symptoms Symptomatic pulpitis Apical periodontitis Draining sinus tract Localized swelling Fouad et al.1996 Henry et al. 2001 Keenan et al. 2006 Cope et al. 2014
Prophylactic Antibiotics for Medically Compromised Patients Distant infection are high in case of transient bacteremia. Bacteremia puts medically compromised patients at a great risk. Procedures that may produce bleeding induce bacteremia. Procedures induces bleeding Rubber dam Local injections Surgical procedures Over-instrumentation ExtirpationPrior to surgical procedures gum & mucosa should be disinfected with: Chlorhexidine or iodine-glycerin
Medically compromised patients at great risk of bacteremia include: Rheumatic & congenital disease Prosthetic cardiac valves. Valvular prolapse& regurgitation Previous infective endocarditis Systemic pulmonary shunts Arterio-venous shunts Uncontrolled diabetes. Immunosuppressed & immunologically deficient cases Medically compromised patients at risk of bacteremia must receive a regimen of antibiotics that follows the recommendations of American Heart Association (AHA)
Antibiotics Antibiotics are prescribed in conjunction with endodontic procedures. Therefore antibiotics without endodontic procedures not effective. Antibiotic are prescribed when Systemic involvement Persistent infection Spreading infection Fever 38°c Malaise Trismus Diffuse swelling Cellulitis Signs & symptoms of systemic Involvement & spread infection Alone or in combination Antibiotics should be continued for 2 to 3 days after disappearance of signs & symptoms.
Selection of an Antibiotic Regimen Penicillin remains the antibiotic of choice. However, penicillin is allergic to approx. 10% of humans. Adequate blood level of penicillin must be maintained. Inexpensive Antibiotics + proper endo procedure results in significant improvement within 48 hours. Effective against many facultative & strict anaerobes. Has low toxicity Initial oral dose of 1000mg followed by 500 mg/6hours. Penicillin
Alternative choice for patients allergic to penicillin Ineffective against most anaerobes & serious infections. GI upset on ingestion of milk while yogurt gives relief. Transient deafness Available as Erywell, Althrocin. Effective against facultative bacteria. Has low toxicity Dose 1000mg followed by 500mg/6 hours. Erythromycin
Alternative choice for patients allergic to penicillin Greater antibacterial spectrum. Less GI upset Available as Clariwell, Klacid, Amicalri, Claribid Macrolide Semisynthetic derivative of erythromycin Has low toxicity Dose 500 mg/8-12 hours Clarithromycin
Not recommended for penicillin allergic patients. broad spectrum but does not include anaerobes. long use pseudomembranous colitis. Available as Climycin, Dalacin C, Myocin Cefaclor(2nd generation) effective against anaerobes. Clindamycin effective gm +ve & -ve bacteria. Facultative & strict anaerobes. Dose 150 to 300 mg/6 hours. Cephalosporin
Ineffective against aerobes Metronidazole with Penicillin or other antibiotic is effective in endo infection Available as Flawell, Flagyl Effective against anaerobes Dose 250 to 500 mg/ 6 hours. Metronidazole
There is international concern about the overuse of antibiotics and the emergence of antibiotic -resistant bacterial strains Dentists prescribe approximately 10% of antibiotics dispensed in primary care, it is important not to underestimate the potential contribution of the dental profession to the development of antibiotic resistant bacteria In the UK, it has been reported that 40% of dentists prescribed antibiotics at least three times each week, and 15% prescribed antibiotics on a daily basis Pallasch et al. 2000 Cope et al. 2014 Lewis 2008
Furthermore, one Cochrane systematic review has found no evidence to support the use of antibiotics for pain relief in irreversible pulpitis Agnihotry et al. 2016 Thus, two systematic reviews concluded that infection must be systemic or the patient must be febrile or immunocompromised to justify the need for antibiotics. For these reasons, prescription of antibiotics by dentists should be limited Matthews et al. 2003 Mohammadi 2009 Rodr íguez -Núñez et al. 2009
Antibiotic sensitivity of the bacteria found within the oral cavity is gradually decreasing, and a growing number of resistant strains are being detected , in particular Porphyromonas spp. and Prevotella spp .However, the phenomenon has also been reported for alpha haemolytic streptococci (“Streptococcus viridans”) and for drugs such as macrolides, penicillin and clindamycin. Bresco -Salinas et al. 2006 Aracil et al. 2001 Groppo et al. 2004 Inappropriate use of antibiotics not only drives antibiotic resistance and misuses resources; it also increases the risk of potentially fatal anaphylactic reactions and exposes people to unnecessary side effects Gonzales et al. 2001 Costelloe et al. 2010, Cope et al. 2014
Culturing Required when empirical use of antibiotics is not effective Rubber dam isolation. Disinfection with NaOCl or other disinfectant. Access opening with sterile instruments Microbial sampling with sterile paper points or aspiration.
Aspiration is done with 16 to 20 gauge needle. In dry canals place a drop of a sterile solution before sampling Submucosal swellings should be sampled by aspiration before incision Samples are immediately placed in the media. Antimicrobial irrigating solutions should not be used before sampling.
Conclusion Microbes seeking to establish in the root canal must leave the nutritionally rich and diverse environment of the oral cavity, breach enamel, invade dentine, overwhelm the immune response of the pulp and settle in the remaining necrotic tissue within the root canal.  During that time they have to compete in a limited space with other microbes for the available nutrition. The bacterial community profiles in treated cases vary from individual to individual, indicating that distinct bacterial combinations can play a role in treatment failure.
References  Kenneth M. Hargreaves, Stephen Cohen. Cohen’s Pathways of the Pulp. 10th edition. Elsevier, Mosby.2011  Ingle, Bakland, Baumgartner. Ingle’s Endodontics 6. BC Decker. 2008  Sabeti M, Slots J: Herpesviral-bacterial coinfection in periapical pathosis. J Endod 30:69, 2004  Siqueira JF, Jr, Rôças IN: Polymerase chain reaction-based analysis of microorganisms associated with failed endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 97:85, 2004.  Sakamoto M, Siqueira JF, Jr, Rôças IN, Benno Y: Molecular analysis of the root canal microbiota associated with endodontic treatment failures. Oral Microbiol Immunol 23:275–281, 2008.
 Zoletti GO, Siqueira JF, Jr, Santos KR: Identification of Enterococcus faecalis in root-filled teeth with or without periradicular lesions by culture-dependent and –independent approaches. J Endod 32:722, 2006.  Rôças IN, Hulsmann M, Siqueira JF, Jr: Microorganisms in root canal- treated teeth from a German population. J Endod 34:926, 2008.  Rôças IN, Siqueira JF, Jr, Aboim MC, Rosado AS: Denaturing gradient gel electrophoresis analysis of bacterial communities associated with failed endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 98:741, 2004.  Kaufman B, Spangberg L, Barry J, Fouad AF: Enterococcus spp. in endodontically treated teeth with and without periradicular lesions. J Endod 31:851, 2005.  Aruna Kanaparthy, Rosaiah Kanaparthy:Biofilms-The Unforgiving Film in Dentistry (Clinical Endodontic Biofilms) . Dentistry 2012, 2:7  Adalberto R. Vieira, Jose F. Siqueira, Domenico Ricucci. Dentinal Tubule Infection as the Cause of Recurrent Disease and Late Endodontic Treatment Failure: A Case Report. JOE — Volume 38, Number 2, February 2012
Abou-Rass M, Bogen G(1998) Microorganisms in closed periapical lesions. International Endodontic Journal, 1 :39-47 Baumgartner JC, Falkler WA(1991) Bacteria in the apical 5 mm of infected root canals. Journal of Endodontics, 17:380–383. Bogen G, Slots J(1999) Black-pigmented anaerobic rods in closed periapical lesions. International Endodontic Journal, 3:204-10. Cohen S, Burns RC (2002) Pathways of the pulp, ed 8. Harcourt Asia Co., India,: 457-500. Cruse WP, Bellizzi R (1980) A historic review of endodontics, 1689–1963, part 1. Jornal of Endodontics, 6: 495–499.
 Dymock, D; Weightman, A J; Scully, C; Wade, W G (1996) Molecular analysis of microflora associated with dentoalveolar abscesses. Journal of Clinical Microbiology, 34 : 537-542  Goumas PD, Naxakis SS, Papavasiliou DA, Moschovakis ED, Tsintsos SJ, Skoutelis A (1997) Periapical abscesses: causal bacteria and antibiotic sensitivity. : Journal of Chemotherapy, 6:415-9.  G. Sundqvist & David Figdor (2003) Life as an endodontic pathogen, Ecological differences between the untreated and root-filled root canals. Endodontic Topics, 6: 3–28.  Haapasalo M, Ranta K, Ranta H (1987) Mixed anaerobic periapical infection with sinus tract. Endodontics & dental traumatology, 3; 83-5.  HedmanWJ (1951) An investigation into residual periapical infection after pulp therapy. Oral Surgery Oral Medicine Oral Pathology, 4 : 1173-9.
 Henderson B, Wilson M (1998) Commensal communism and the oral cavity. Journal of Dental Research, 77 : 1674–1683.  Hirshberg A, Tsesis I, Metzger Z, Kaplan I, Aviv T. Israel (2003) Periapical actinomycosis: A clinicopathologic study. Oral Surgery Oral Medicine Oral Pathology Oral Radiology Endodontics, 95:614-20.  Iwu C, Wallace T (1990) The microbiology of periapical granuloma. Oral Surgery Oral Medicine Oral Pathology, 69: 502-5.  Jansen H-J, van der Hoeven JS (1997) Protein degradation by Prevotella intermedia and Actinomyces meyeri supports the growth of non-proteincleaving oral bacteria in serum. Journal of Clinical Periodontology, 24: 346– 353.  Jansen H-J, van der Hoeven JS, Walji S, Goertz JH, Bakkeren JA (1996) The importance of immunoglobulin breakdown supporting the growth of bacteria in oral abscesses. Journal of Clinical Periodontology, 23: 717–723.  Kiryu T, Hoshino E, Iwaku M (1994) Bacteria invading periapical cementum. Bacteria invading periapical cementum. Journal of Endodontics,4:169-72

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Endodontic microbiology

  • 1.
    Endodontic Microbiology  ANJALI SAVITA MDS I  DEPT OF CONSERVATIVE AND ENDODONTICS
  • 2.
    Contents  Introduction  Mechanismsof Microbial Pathogenicity  Microbial Ecology and the Root Canal Ecosystem  Routes of canal infection  Endodontic microbiota  Types of endodontic infections  Biofilm and bacterial interaction  Bacterial treatment measures  Conclusion  References
  • 3.
    INTRODUCTION Microorganisms cause virtuallyall pathoses of the pulp and the periradicular tissues. To effectively treat endodontic infections, clinicians must recognize the cause and effect of microbial invasion on the dental pulp space and the surrounding periradicular tissues.
  • 4.
    Mechanisms of MicrobialPathogenicity and Virulence Factors Pathogenicity Virulence Virulence factors
  • 6.
  • 7.
    Microbial Ecology AndRoot Canal Ecosystem In the very initial phases of the pulpal infectious process: facultative bacteria predominate. After a few days or weeks, oxygen is depleted loss of blood circulation in the necrotic pulp. Growth of obligate anaerobic bacteria. The root canal infection is a dynamic process, and different bacterial species apparently dominate at different stages. Sundqvist & Figdor 2003, Sundqvist 1994
  • 8.
    Necrotic pulp cavitybecomes reservoir for microbes Disintegrated tissue and fluids becomes nutrients for microorganism Nutrients are polypeptide and amino acids Nutrient supply + Bacterial interactions + low 𝑶 𝟐 tension determine the type of predominant bacteria. Growth of anaerobes provides environment for metabolization of peptides and amino acids
  • 9.
    Some species producemetabolic bi-products which is essential for growth of other species Antagonist relationship may occur among bacteria Some biproducts (e.g. Ammonia) can either be nutrient or toxin. Bacteriocins( antibiotic like substances) inhibit growth of other bacteria Chemo mechanical RC preparation help to disrupt and destroy microbial ecosystem and perfect obturation eliminates the pulp cavity as reservoir.
  • 10.
  • 11.
    ROUTES OF ROOTCANAL INFECTION Sundqvist 1994 Siqueira & Janeiro 2002
  • 12.
    Correlation With PathosesAnd Treatment Endodontic infections are polymicrobial Periradicular tissues posses Excellent collateral circulation Lymphatic drainage. Vast amount of undifferentiated cells. Periradicular pathoses develop in response of Microorganisms Microbial biproducts Inflammatory mediators Instrument trauma Chemicals
  • 13.
    Endodontic Microbiota More than700 species of bacteria are recognized as normal inhabitants of oral cavity. Root canal microflora is dominated by Anaerobic bacteria. Streptococci Staphylococci Corynebacterium Yeast Gram +ve(75%) Spirochetes Neisseriae Bacteroides Fusobacterium, Pseudomonas. Gram –ve(24%)
  • 14.
  • 15.
  • 16.
    Types Of EndodonticInfections Intraradicular Infections Extraradicular Infection
  • 17.
    Primary Intrardicular Infection Primaryinfection is caused by microorganisms that initially invade and colonize the necrotic tissue. Primary infections are characterized by a mixed consortium composed of 10-30 species per canal. The number of bacterial cells in an infected canals varies from 103-108 per root canal Siqueira et al 2005 Sakamoto et al 2007 Vianna et al 2006
  • 18.
    Bacteria Involved InPrimary Intraradicular Infection Gram Negative Gram Positive Prevotella Porphyromonas Tanerella Fusobacterium Dialister Campylobactor Treponema Actinomyces Peptostreptococcus Eubacterium Filifactor Microaerophillic streptococci
  • 19.
    Saccharolytic; Prevotella P. Intermedia P. Nigrescense P.Tannerae P. Denticola P. multissachari- vorax Asaccharolytic; Porphyromonas P.endodontalis P.gingivalis BACTEROIDS They seem to play important role in etiology of both acute and chronic apical periodontitis. Black pigmented bacteria, Gram +Ve Siqueira et al 2001 Sundqvist et al 1989 Dougherty et al 1998
  • 20.
    Recently findings frommolecular studies have also suggested that some anaerobic species commonly found in primary infection Tenerella Forsythia Pseudoramibactor Alactolyticus Filibactor Acolis Dialister pnuemosintes Siqueira et al 2004,2005
  • 21.
    In majority ofbacteriological studies on periapical lesions, it has been observed that Porphyromonas and Prevotella had a higher prevalence in periradicular lesions associated with pain, purulent abscess and teeth refractory to conventional root canal treatment. Kiryu et al. 1994 Trowbridge & Stevens 1992 Bogen &Slots 1999 Yamasaki et al. 1998
  • 22.
    Gram negative obligatenonmotile anaerobic bacteria. Most common in symptomatic infection and abscess or exacerbation lesion than asymptomatic infection. 5 subspecies of F. Nucleatum have been found which are different in genetic data but no study found that which subspecies have more virulence factor. Different type of subspecies are found in the same root canals. Fusobacterium Nucleatum Moraes et al 2002 Siqueira et al 2005
  • 23.
    Spirochete Although spirochetes havebeen frequently observed in samples by microscopy, they had never been identified to the species level. The application of molecular diagnosis to identification of spiral bacteria has been overlooked the culture techniques. They can be classified in 2 group; Saccharolytic and Asaccharolytic. T. Denticola, T. Sokranskii have been detected in both symptomatic and asymptomatic lesion. Dewhirst et al 2000 Baumgartner et al 2007 Rocas et al 2003
  • 24.
    Secondary Intraradicular Infections Ifmicroorganisms are allowed to remain at the time of filling , there is increased risk of adverse outcome of the endodontic treatment Sjogren et al 1997 Waltimo et al 2005
  • 25.
    Bacteria Involved InSecondary Intraradicular Infection Pseudomonas aeruginosa. Staphylococcus sp. Escherichia coli. Candida sp.
  • 26.
    Persistant Intraradicular Infection Infectionscaused by microorganisms that resisted the intracanal antimicrobial procedures. Fungi and Gram positive facultative bacteria, particularly Enterococcus faecalis, are predominant in such cases.
  • 27.
    E. Faecalis Non sporeforming, fermentative Facultative anaerobic, Gram positive coccus. This species has been found in low prevalence value in case of primary infection and more relate in asymptomatic cases than symptomatic cases. Rocas et al 2005
  • 28.
    E. feacalis hasbeen found in root filled teeth evincing persistent apical periodontitis in prevalence values ranging from 30-90% of the cases. This species can be inhibited by other members of mixed bacterial consortium commonly present in primary infection. Sedgley et al 2006
  • 29.
    Virulence factors ofE. Faecalis But its still not confirmed which factor play an important role in pathogenesis. Kayaoglu et al 2004 Lytic enzymes Cytolysin Gelatinase Hyaluronidase Pheromones Lipoteichoic acid Adhesion molecules
  • 30.
    Why E. feacaliscan survive in root filled teeth? Studies have revealed that E. feacalis has ability to penetrate far into dentinal tubules that can escape from intracanal instrumentation and irrigants. Haapasalo et al 1989 Siqueira et al 1996
  • 31.
    E.feacalis has beenshown to be able to form biofilms in root canals and this ability can be important for bacterial resistance and persistence in the instrumented canals. Distel et al 2002 The ability to resist high pH value seems to be related to functional proton pump to acidfy. So, is resistant to calcium hydroxide. Evans et al 2002
  • 32.
    E.feacalis can entera VBNC state which can survive in adverse environmental condition, including starvation. They has the ability to survive in environments in scarcity of nutrients and to flourish when the nutrient source is reestablished and has a capacity to recover in root canal treated teeth for 12 months without nutrients. Figdor et al 2003 Sedgley et al 2005
  • 33.
    Prevalence of E.Faecalis in samples from root canal treated teeth with apical periodontitis. Data from Culture (Yellow bars) and data from Molecular (Blue bars) studies
  • 34.
    Fungi It is alsopossible that yeasts from oral cavity gain access to root canal as contaminant during endodontic procedures. Siren et al 1997 Siqueria & Sen et al 1997 They can overgrow after inefficient intracanal antimicrobial procedures, which can cause imbalance in microbiota. Siqueira et al 2004 E. faecalis and yeast, mainly C. albicans, has been repeatedly identified as the species most commonly recovered from root canals undergoing retreatment, in cases of failed endodontic therapy and canals with persistent infections.
  • 36.
    Dentino phillic microorganism due toits ability to colonize and invade to dentin by their hyphae. Resist to some intracanal medication such as calcium hydroxide. Release hydrolytic enzyme and can form monoinfection biofilm in root canals. Waltimo et al 1999 Matusow et al 1981
  • 37.
    Ashraf et al1997 Najzar & Fleger et al CA in the root canal system of teeth with periapical lesions was more noticeable and statistically significant compared to the teeth without periapical lesions 55% of root canals contain Candida cell. Presence of fungi in root canals more than expected and the knowledge of persistent periapical infections may advocate the use of antifungal agents in modern endodontic therapy.
  • 38.
    Prevalence of microorganismdetected in root canal treated teeth with post treatment disease. Data is from taxon-specific PCR assay
  • 39.
    Extraradicular infections Extra radicularinfections are characterized by, microbial invasion & proliferation in the inflamed peri radicular tissue as a result of intra radicular infections. The development of periradicular lesions creates a barrier with in the body to prevent further spread of microorganisms. Bone tissue is resorbed and substituted by a granulation tissue containing defense elements, such as cells (phagocytes) and molecules (antibodies and complement molecules).
  • 40.
    A dense wallcomposed of polymorphonuclear leucocytes, or less frequently an epithelial plug, is usually present at the apical foramen, blocking the egress of microorganisms into the periradicular tissues. Very few endodontopathogens can advance through such barriers. However, microbial products can diffuse through these defence barriers and are able to induce or perpetuate periradicular pathosis Vigil et al.1997 In recent years there is resurgence of the idea of extraradicular microbes in apical periodontitis lesions with implied, controversial suggestion that extraradicular infection is the cause of many failed endodontic treatment.
  • 41.
    Extraradicular infection canbe independent of Intraradicular infection. Case of apical actinomyces in which non surgical endodontics, calcium hydroxide, systemic erythromycin, and finally, a regimen of systemic metronidazole failed to resolve the draining fistula associated with a maxillary lateral incisor. but following periapical surgery, the lesion resolved. Haapasalo et al. 1987
  • 42.
    16 periapical granulomathat were collected “during normal periapical curettage, apecectomy, or retrograde filling”. It was seen that most of the organism cultured were Veillonella species, Streptococcus milleri, Streptococcus sanguis, Actinomycetes naeslundii, Propionibacterium acnes and Bacteroides species Iwu & Wallace 1990
  • 43.
    Those extra radicularinfections which are caused by intra radicular bacteria are treated easily by RCT. Eg: Sinus Tract If the extra radicular infection which are caused by outer side are treated only by Endodontic Surgery. Eg: Actinomycosis Cohen & Burns 2002
  • 44.
    Remnants of Dental pulp Calculus Carieson tooth crown Leakage of rubber dam Contamination of instrument Irrigation solution Intracanal medicaments SOURCE OF MICROBES DURING TREATMENT
  • 45.
    Loss or leakageof restorative material Tooth fracture SOUCE OF MICROBES DURING APPOINTMENTS
  • 46.
    Loss or leakageof restorative material Tooth fracture Secondary caries Delay in placement of permanent filling or crown prosthesis. SOUCE OF MICROBES AFTER ROOT CANAL TREATMENT
  • 47.
    Biofilm And BacterialInteraction Sessile multicellular microbial community characterized by cells that are firmly attached to a surface and embedded in a self produced matrix of extracellular polymeric substances. AAE, 2004 Defined as community of microcolonies of microorganisms in an aqueous solution that is surrounded by a matrix made of glycocalyx, which also attaches the bacterial cell to a solid substratum. Grossman, 13 edition  Definition
  • 48.
    According to kishen Thereare four distinct stages in development of biofilm  Formation of a conditioning layer  Planktonic bacterial cell attachment  Detachment (seeding dispersal)  Bacterial growth and biofilm expansion.
  • 51.
    Autopoiesis Ability to self organize. Homeostasis Abilityto resist environmental disturbances. Synergy More effective in association with fellow microorganisms. Communality Response to environmental challenges as combined unit. Caldwell et al The biofilm has following attributes that makes it resistance to clinical
  • 52.
    Communications between bacterialcells residing in a biofilm is attained through signaling molecules by a process called as Quorum sensing Quorum sensing is mediated by low molecular weight molecules- autoinducers Qs leads to Exchange of genetic materials between species Antibiotic resistance  Nutrient breakdown Xenobiotic metabolism Coordinated behaviour of biofilm
  • 53.
    Endodontic biofilms aretherapeutically significant as they are one of the basic survival methods for bacteria during starvation.  Endodontic biofilms help bacteria to survive because Ability to protect bacteria from environment Ability to entrap nutrients for the growth of microbial constituent. Offer a safe environment to exchange of genetic material Provide inherent resistance to antimicrobial agents (irrigants & ICM) Caldwell et al
  • 54.
    Classification Of EndodonticBiofilm Intracanal microbial biofilm Formed on radicular dentin in an endodontically infected tooth Various distinct types of bacteria can develop these biofilms, but E. faecalis is responsible for one of the most therapy resistant and prevalent endodontic biofilms Extraradicular microbial biofilm Root surface biofilms Formed on the cemental surfaces around root apex of an endodontically infected tooth Eg: F. Nucleatum Periapical microbial biofilm Isolated biofilms independent of internal or external surface of the root canal Actinomyces and P. propionicum have shown to form periapical lesion resistant to endodontic therapy.
  • 55.
    Bacterial Treatment Measure Infectioncontrol All patients should be treated as if they have transmissible disease. Disinfect tooth surface & rubber dam with Chlorhexidine or NaOCL. Use physical barriers like - Face shield - Rubber dam - Mask - Gloves & Gowns
  • 56.
    Removal of sourceof irritation helps in healing of periradicular lesion. Source of irritation is generally the reservoir of infection (pulp cavity). Achieved by thorough debridement of root canals. RC debridement is the achieved by proper instrumentation with use of canal irrigants
  • 57.
    Irrigants Flush out debris Dissolve organic remnants Antimicrobial lubricants Irrigants  Saline Sodium hypochlorite(NaOCl)  CHX  Hydrogen peroxide (𝐻2 𝑂2)  Citric acid  EDTA Sonic and ultrasonic devices can improve irrigant effect Spratt et al 2001
  • 58.
    ICM Penetrate dentinal tubules Induces calcific barrier Antimicrobial Eliminates pain ICM  Formocresol  PCP&CPC  Glutaraldehyde  Cresatin  Thymol The current IC Medicament of choice is Ca (OH)2
  • 59.
    DRAINAGE Key to managean abscess and cellulitis Achieved through the canal and incision Reduces discomfort, toxins, pressure Incision of indurated swelling releases Blood Serous fluid Bacteria & biproducts Inflammatory mediators Drainage removes these irritants & improves local circulation.
  • 60.
    Adjunctive Antibiotic therapy Antibioticsare not a substitute for local treatment. The majority of endodontic cases can be treated without antibiotics. Pain & swelling of endodontic origin are managed by debridement & drainage Do not require antibiotics Without systemic sign & symptoms Symptomatic pulpitis Apical periodontitis Draining sinus tract Localized swelling Fouad et al.1996 Henry et al. 2001 Keenan et al. 2006 Cope et al. 2014
  • 61.
    Prophylactic Antibiotics forMedically Compromised Patients Distant infection are high in case of transient bacteremia. Bacteremia puts medically compromised patients at a great risk. Procedures that may produce bleeding induce bacteremia. Procedures induces bleeding Rubber dam Local injections Surgical procedures Over-instrumentation ExtirpationPrior to surgical procedures gum & mucosa should be disinfected with: Chlorhexidine or iodine-glycerin
  • 62.
    Medically compromised patientsat great risk of bacteremia include: Rheumatic & congenital disease Prosthetic cardiac valves. Valvular prolapse& regurgitation Previous infective endocarditis Systemic pulmonary shunts Arterio-venous shunts Uncontrolled diabetes. Immunosuppressed & immunologically deficient cases Medically compromised patients at risk of bacteremia must receive a regimen of antibiotics that follows the recommendations of American Heart Association (AHA)
  • 63.
    Antibiotics Antibiotics are prescribedin conjunction with endodontic procedures. Therefore antibiotics without endodontic procedures not effective. Antibiotic are prescribed when Systemic involvement Persistent infection Spreading infection Fever 38°c Malaise Trismus Diffuse swelling Cellulitis Signs & symptoms of systemic Involvement & spread infection Alone or in combination Antibiotics should be continued for 2 to 3 days after disappearance of signs & symptoms.
  • 64.
    Selection of anAntibiotic Regimen Penicillin remains the antibiotic of choice. However, penicillin is allergic to approx. 10% of humans. Adequate blood level of penicillin must be maintained. Inexpensive Antibiotics + proper endo procedure results in significant improvement within 48 hours. Effective against many facultative & strict anaerobes. Has low toxicity Initial oral dose of 1000mg followed by 500 mg/6hours. Penicillin
  • 65.
    Alternative choice forpatients allergic to penicillin Ineffective against most anaerobes & serious infections. GI upset on ingestion of milk while yogurt gives relief. Transient deafness Available as Erywell, Althrocin. Effective against facultative bacteria. Has low toxicity Dose 1000mg followed by 500mg/6 hours. Erythromycin
  • 66.
    Alternative choice forpatients allergic to penicillin Greater antibacterial spectrum. Less GI upset Available as Clariwell, Klacid, Amicalri, Claribid Macrolide Semisynthetic derivative of erythromycin Has low toxicity Dose 500 mg/8-12 hours Clarithromycin
  • 67.
    Not recommended forpenicillin allergic patients. broad spectrum but does not include anaerobes. long use pseudomembranous colitis. Available as Climycin, Dalacin C, Myocin Cefaclor(2nd generation) effective against anaerobes. Clindamycin effective gm +ve & -ve bacteria. Facultative & strict anaerobes. Dose 150 to 300 mg/6 hours. Cephalosporin
  • 68.
    Ineffective against aerobes Metronidazolewith Penicillin or other antibiotic is effective in endo infection Available as Flawell, Flagyl Effective against anaerobes Dose 250 to 500 mg/ 6 hours. Metronidazole
  • 70.
    There is internationalconcern about the overuse of antibiotics and the emergence of antibiotic -resistant bacterial strains Dentists prescribe approximately 10% of antibiotics dispensed in primary care, it is important not to underestimate the potential contribution of the dental profession to the development of antibiotic resistant bacteria In the UK, it has been reported that 40% of dentists prescribed antibiotics at least three times each week, and 15% prescribed antibiotics on a daily basis Pallasch et al. 2000 Cope et al. 2014 Lewis 2008
  • 71.
    Furthermore, one Cochranesystematic review has found no evidence to support the use of antibiotics for pain relief in irreversible pulpitis Agnihotry et al. 2016 Thus, two systematic reviews concluded that infection must be systemic or the patient must be febrile or immunocompromised to justify the need for antibiotics. For these reasons, prescription of antibiotics by dentists should be limited Matthews et al. 2003 Mohammadi 2009 Rodr íguez -Núñez et al. 2009
  • 72.
    Antibiotic sensitivity ofthe bacteria found within the oral cavity is gradually decreasing, and a growing number of resistant strains are being detected , in particular Porphyromonas spp. and Prevotella spp .However, the phenomenon has also been reported for alpha haemolytic streptococci (“Streptococcus viridans”) and for drugs such as macrolides, penicillin and clindamycin. Bresco -Salinas et al. 2006 Aracil et al. 2001 Groppo et al. 2004 Inappropriate use of antibiotics not only drives antibiotic resistance and misuses resources; it also increases the risk of potentially fatal anaphylactic reactions and exposes people to unnecessary side effects Gonzales et al. 2001 Costelloe et al. 2010, Cope et al. 2014
  • 73.
    Culturing Required when empiricaluse of antibiotics is not effective Rubber dam isolation. Disinfection with NaOCl or other disinfectant. Access opening with sterile instruments Microbial sampling with sterile paper points or aspiration.
  • 74.
    Aspiration is donewith 16 to 20 gauge needle. In dry canals place a drop of a sterile solution before sampling Submucosal swellings should be sampled by aspiration before incision Samples are immediately placed in the media. Antimicrobial irrigating solutions should not be used before sampling.
  • 75.
    Conclusion Microbes seeking toestablish in the root canal must leave the nutritionally rich and diverse environment of the oral cavity, breach enamel, invade dentine, overwhelm the immune response of the pulp and settle in the remaining necrotic tissue within the root canal.  During that time they have to compete in a limited space with other microbes for the available nutrition. The bacterial community profiles in treated cases vary from individual to individual, indicating that distinct bacterial combinations can play a role in treatment failure.
  • 76.
    References  Kenneth M.Hargreaves, Stephen Cohen. Cohen’s Pathways of the Pulp. 10th edition. Elsevier, Mosby.2011  Ingle, Bakland, Baumgartner. Ingle’s Endodontics 6. BC Decker. 2008  Sabeti M, Slots J: Herpesviral-bacterial coinfection in periapical pathosis. J Endod 30:69, 2004  Siqueira JF, Jr, Rôças IN: Polymerase chain reaction-based analysis of microorganisms associated with failed endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 97:85, 2004.  Sakamoto M, Siqueira JF, Jr, Rôças IN, Benno Y: Molecular analysis of the root canal microbiota associated with endodontic treatment failures. Oral Microbiol Immunol 23:275–281, 2008.
  • 77.
     Zoletti GO,Siqueira JF, Jr, Santos KR: Identification of Enterococcus faecalis in root-filled teeth with or without periradicular lesions by culture-dependent and –independent approaches. J Endod 32:722, 2006.  Rôças IN, Hulsmann M, Siqueira JF, Jr: Microorganisms in root canal- treated teeth from a German population. J Endod 34:926, 2008.  Rôças IN, Siqueira JF, Jr, Aboim MC, Rosado AS: Denaturing gradient gel electrophoresis analysis of bacterial communities associated with failed endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 98:741, 2004.  Kaufman B, Spangberg L, Barry J, Fouad AF: Enterococcus spp. in endodontically treated teeth with and without periradicular lesions. J Endod 31:851, 2005.  Aruna Kanaparthy, Rosaiah Kanaparthy:Biofilms-The Unforgiving Film in Dentistry (Clinical Endodontic Biofilms) . Dentistry 2012, 2:7  Adalberto R. Vieira, Jose F. Siqueira, Domenico Ricucci. Dentinal Tubule Infection as the Cause of Recurrent Disease and Late Endodontic Treatment Failure: A Case Report. JOE — Volume 38, Number 2, February 2012
  • 78.
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