Endo. Microbiology
Endo. Microbiology
Endo. Microbiology
96]
Endodontic microbiology
L Lakshmi Narayanan, Vaishnavi C
Department of Conservative Dentistry & Endodontics, SRM Kattankulathur Dental College & Hospital, SRM University, Chennai, India
Abstract
Root canal therapy has been practiced ever since 1928 and the success rate has tremendously increased over the years
owing to various advancements in the field. One main reason is the complete understanding of the microbiology involved
in the endodontic pathology. This has helped us to modify the conventional treatment plans and effectively combat the
microorganisms. Now, studies are aiming to explore the characteristics of the “most” resistant organism and the methods
to eliminate them. This article gives an insight of the microbiology involved in endodontic pathology and discusses its
role in our treatment procedure. Information from original reviews listed in PubMed, published from 1995 to 2010, has
been mainly included in this review.
Keywords: Bacterial infections; biofilms; dental pulp microbiology; Enterococcus faecalis; gram positive bacteria; periapical
periodontitis/microbiology.
Faulty restoration: Studies have proven that salivary anaerobic Gram negative coccobacilli which have been
contamination from the occlusal aspect can reach the consistently detected in endodontic infections.
periapical area in less than 6 weeks in canals obturated with • Dialister pneumosintes and
guttapercha and sealer.[5] If the temporary seal is broken • Dialister invisus.
or if the tooth structure fractures before final restoration, 4) Fusobacterium is also a common member of endodontic
or if the final restoration is inadequate, bacteria may gain microbiota.
access to the periapical tissue and result in infection. • Fusobacterium nucleatum
• Fusobacterium periodonticum
Extent: Microorganisms might reach the principal and/or 5) Spirochetes are highly motile, spiral-shaped, Gram
lateral canals migrating from an infected tooth to a healthy negative bacteria with periplasmic flagella. All oral
pulp as a consequence of the contiguousness of the tissues, spirochetes fall into the genus Treponema.[9] Prevalent
thereby spreading the infection to an adjacent tooth. species are
• Treponema denticola
CORRELATION OF MICROBES TO • Treponema sacranskii
INFECTION • Treponema parvum
• Treponema maltophilum and
Almost 700 bacterial species can be found in the oral
• Treponema lecithinolyticum.
cavity, with any particular individual harboring 100–200 of
6) Gram positive anaerobic rods have also been found in
these species.[6] Once the root canal is infected coronally,
endodontic microbiota like
infection progresses apically until bacterial products or
• Pseudoramibacter alactolyticus
bacteria themselves are in a position to stimulate the
periapical tissues, thereby leading to apical periodontitis. • Filifactor alocis
Endodontic infections have a polymicrobial nature, with • Actinomyces spp.
obligate anaerobic bacteria conspicuously dominating • Propionibacterium propionicum
the microbiota in primary infections. There are various • Olsenella spp.
microorganisms related to intra-radicular and extraradicular • Slackia exigua
infections and organisms involved in persistent infection. • Mogibacterium timidum and
They are discussed below. • Eubacterium spp.
7) Gram positive cocci that are present in endodontic
Intraradicular infections infection:
The endodontic pathogens that cause the primary • Parvimonas micra (previously called Peptostreptococcus
intraradicular infections are the following. micros or Micromonas micros)
• Streptococcus spp. which include
1) Black pigmented Gram negative anaerobic rods include
Streptococcus anginosus
species formerly known as Bacteroides melaninogenicus.
Streptococcus mitisi
These bacteria have been reclassified into two
genera: (a) saccharolytic species – Prevotella and (b) Streptococcus sanguinis
asaccharolytic species – Porphyromonas.[7] • Enterococcus faecalis.
Prevotella species detected in endodontic infections Other bacterial spp. which are present in low to
moderate values include
include
• Campylobacter spp. which are Gram negative
• Prevotella intermedia
anaerobic rods; common species are
• Prevotella nigrescens
Campylobacter rectus and
• Prevotella tannerae
Campylobacter gracilis.
• Prevotella multissacharivorax
• Catonella morbic which is a saccharolytic obligate
• Prevotella baroniae and
anaerobic Gram negative rod
• Prevotella denticola.
• Veillonella parvula
Porphyromonas species detected in endodontic
infections include • Eikenella corrodens
• Porphyromonas endodontalis and • Granulicatella adiacens
• Porphyromonas gingivalis. • Neisseria mucosa
2) Tannerella forsythia (previously called Bacteroides forsythus • Centipeda periodontii
or Tannerella forsythenis) was the first periodontal • Gemella morbillorum
pathogen to be detected in endodontic infection.[8] • Capnocytophaga gingivalis
3) Dialister species are asaccharolytic obligately • Corynebacterium matruchotii
The presence of viruses in the root canal has been reported Sometimes, yeasts, commonly C. albicans, are also found in
only for non-inflamed vital pulps of patients infected small amounts.
with human immunodeficiency virus and herpes viruses
where living cells are found in abundance.[12,13] Among E. faecalis and yeast, mainly C. albicans, has been repeatedly
the Herpes spp., the human cytomegalovirus and Epstein– identified as the species most commonly recovered
Barr virus may be implicated in the pathogenesis of apical from root canals undergoing retreatment, in cases of
periodontitis. failed endodontic therapy and canals with persistent
infections.[18,19] E. faecalis are gram positive cocci and
Extraradicular infections facultative anaerobes. They are normal intestinal organisms
Intraradicular microorganisms usually constrain themselves and may inhabit the oral cavity and gingival sulcus. When
in the root canal due to the defense barrier. In specific this bacterium is present in small numbers, it is easily
circumstances, microorganisms can overcome this defense eliminated; but if it is in large numbers, it is difficult to
barrier and establish an extraradicular infection. This may eradicate. E. faecalis has many distinct features which
lead to development of acute apical abscess with purulent make it an exceptional survivor in the root canal. These
inflammation in periapical tissue. The extraradicular microorganisms can perform the following.
infections are dependent on or independent of an • Live and persist in poor nutrient environment
intraradicular infection. The dominant microorganisms • Survive in the presence of several medications
present are anaerobic bacteria[14-17] like (e.g., calcium hydroxide) and irrigants (e.g., sodium
• Actinomyces spp. hypochlorite)
The human commensal microbiota populates the mucosal LTA: LTA is a cell wall component of Gram positive bacteria,
surface of the oral cavity, gastrointestinal tract, urogenital composed of echoic acid and lipid.[31] LTA shares many of its
tract and surface of the skin. This commensal microbiota, pathogenic properties with LPS.[32] LTA is released as a result
which has coevolved with its host, has acquired the means of cell lysis and binds to target cells, which then interacts
of surviving and tolerating host defense mechanisms.[20,21] with circulating antibodies and activates complement
However, when the host is compromised, or if invading cascade and cause damage.
microorganisms are sufficiently pathogenic, disease can
develop. Pathogenicity refers to the ability of an organism Fimbriae: Fimbriae are long, filamentous macromolecules
to cause disease in another organism. These organisms found on the surface of many Gram negative bacteria. The
are known as pathogens which include bacteria, fungi, thin hair-like projections are made of protein subunits
viruses, protozoa and parasites. These pathogens are (they are distinct from flagella). Fimbriae are involved
capable of adhering, colonizing, surviving, propagating, at in attachment to surfaces and interactions with other
the same time evading host defense mechanisms such as bacteria.[33]
neutrophils, complement and antibodies. In addition, they
can cause tissue destruction directly or indirectly.[22] Direct Capsules: A capsule is a well-organized layer outside the cell
tissue damage can be induced by enzymes, exotoxins wall of the bacteria, generally composed of polysaccharides
and metabolites. Indirect tissue damage can be induced and other materials. Capsules serve to facilitate protection
from a host immune reaction capable of causing tissue of the bacterial cell against desiccation, phagocytosis,
destruction that is stimulated by bacterial components bacterial viruses and hydrophobic toxic materials such as
which include lipopolysaccharide (LPS), peptidoglycan detergents. Bacteria and fungi utilize capsule formation
(PG), lipoteichoic acid (LTA), fimbriae, outer membrane to inhibit complement activation and resist ingestion by
proteins, capsular components and extracellular vesicles. phagocytes.
The degree of pathogenicity or disease producing ability
of a microorganism is known as virulence. Several Extracellular vesicles: Extracellular vesicles are produced
physicochemical factors in the root canal have the potential by Gram negative bacteria and allow the release of
to influence the pathogenicity of bacteria, which include their products into the extracellular environment. The
the degree of anaerobiosis, pH level, the availability of contents include proteins and lipids that are involved in
exogenous and endogenous nutrients, as well as the a diverse array of activities including hemagglutination,
surfaces available for adherence like dentin. In infected hemolysis, bacterial adhesion and proteolytic activities.[34]
root-filled teeth, any medicament remnants and root filling Extracellular vesicles are a means by which bacteria interact
material are additional factors to influence pathogenicity. with prokaryotic and eukaryotic cells and can modulate
interactions between neighboring bacteria.[35,36]
Virulence factors
Many microorganisms found in endodontic infections are Exotoxins: Exotoxins are toxins released by a living cell,
commensals in the oral cavity, which have gained entry which can trigger excessive and aberrant activation
into the pulp tissue of the root canal typically via the of T cells.[37] Bacterial toxins can also target other
caries process. Identification and characteristics of specific microorganisms, e.g., bacteriocins, proteinaceous toxins
virulence factors that might play a role in endodontic produced by bacteria are bacteriostatic or bacteriocidal to
infections are discussed here. other bacteria.[38]
LPS: This is also known as endotoxin.[23] LPS is an integral Extracellular proteins: Many of these extracellular proteins
part of cell wall of Gram negative bacteria. When are enzymes which are produced by bacteria. These
released, LPS has numerous biologic effects including the enzymes are released during bacterial cell lysis which
contributes to spread of infection, including proteases that via leakage. It is difficult to differentiate between the
neutralize immunoglobulins and complement components.[39] microorganisms remaining from primary infections and
Enzymes like hyaluronate lyase, chondroitin sulphatase, new microorganisms contributing to the secondary
beta glucuronidase, DNase and acid phosphatase contribute infection. The remaining microorganisms from primary
to tissue disintegration. infection should have maintained the viability throughout
the treatment procedure. This might occur as a result of an
Short-chain fatty acids: These are major by-products of inability of chemomechanical instrumentation and because
fermentation process performed by obligate anaerobes, of inaccessible locations of bacteria in isthmuses, accessory
and include butyric acid and propionic acid. These acids canal and apical regions of canals.[49]
stimulate the inflammatory response and inflammatory
cytokine release which contribute to infection process.[40,41] Success of non-surgical endodontic treatment is limited by
the heterogeneity of patients and difficulty in maintaining
Polyamines: Polyamines are small, polycationic molecules standardized clinical conditions. Thus, a thorough
like putrescine, cadaverine, spermidine and spermine knowledge and understanding of these persistent
which contribute to clinical symptoms like pain (including endodontic microbes helps us to decide on surgical
percussion pain) and formation of sinus tract.[42] These treatment or retreatment.
polyamines act by modulating a variety of ion channels.[43]
BACTERIAL BIOFILMS
Superoxide anions: Superoxide anions are biologically
toxic and highly reactive free radicals. These are produced Biofilm is a mode of microbial growth where dynamic
by few bacterial species and also by the cells of immune communities of interacting sessile cells are irreversibly
system. They cause lysis of erythrocytes[44] and are involved attached to a solid substratum, as well as to each other,
in interspecies interaction. and are embedded in a self-made matrix of extracellular
polymeric substances.[50] The microorganisms living in a
However, diverse arrays of virulence factors are available community must have the following four basic criteria:[51]
to modulate the participation of microorganisms in host– 1. possess the abilities to self-organize (autopoiesis),
microbe interactions. An absolute cause and relationship 2. resist environmental perturbations (homeostasis),
occurs between the virulence factors and clinical signs and 3. be more effective in association than in isolation
symptoms in root canal infections. Apart from these, there (synergy) and
are additional mechanisms by which the microorganisms 4. respond to environmental changes as a unit rather
might modulate the infection process, which include the than single individuals (communality).
ability of some intracellular bacteria to inactivate the killing
mechanisms of phagocytic cells and thereby avoid being killed Development of biofilm
by macrophages and neutrophils.[45] In addition, some bacteria Bacteria can form biofilms on any surface that is bathed in
can genetically vary their surface antigens, thus causing a nutrient-containing fluid. The three major components
difficulty for the immune system to target these organisms.[46] involved in biofilm formation are bacterial cells, a solid
A thorough understanding of these virulence factors helps to surface and a fluid medium.
identify the therapeutic targets in endodontic infections.
Biofilm formation occurs in three stages given below.
IMPORTANCE OF UNDERSTANDING
MICROBIOLOGY FOR THE SUCCESS Stage 1: Adsorption of inorganic and organic molecules
OF NON-SURGICAL AND SURGICAL to the solid surface occurs, leading to the formation of
ENDODONTIC TREATMENT conditioning layer.
The presence of microorganisms in the dental pulp is Stage 2: Adhesion of microbial cells to the conditioned layer:
directly associated with the development of periapical There are many factors that affect the bacterial attachment
disease. Chemomechanical preparation of the infected root like pH, temperature, surface energy of the substrate,
canal using antimicrobial agents, followed by obturation nutritional availability, time of contact of bacteria, bacterial
and coronal restoration, provides a favorable outcome. cell surface charge and surface hydrophobicity. The bacteria
However, failure of root canal treatment sometimes occurs substrate interaction occurs in three phases:
due to persistent or secondary intraradicular infection.[47,48] • Phase 1: Transport of microbe to substrate surface
which is mediated by fimbriae, pili, flagella and
Microorganisms found in failed endodontically treated extracellular polysaccharides (glycocalyx).
teeth have either remained in the root canal from previous • Phase 2: Initial non-specific microbial–substrate
treatment or have entered during or after treatment adherence which occurs due to combination of
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Source of Support: Nil, Conflict of Interest: None declared.
sequence analyses of the bacteriocin 21 determinant encoded on the