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.

1. Endodontic
Microbiology
 ANJALI SAVITA
 MDS I
 DEPT OF CONSERVATIVE AND ENDODONTICS

2. 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

3. 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.

4. Mechanisms of Microbial Pathogenicity and
Virulence Factors
Pathogenicity
Virulence
Virulence factors

6. Bacterial virulence factors

7. 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

8. 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

9. 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.

10. NUTRIENT SUPPLY TO MICROBES

11. ROUTES OF ROOT CANAL INFECTION
Sundqvist 1994
Siqueira & Janeiro 2002

12. 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

13. 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%)

14. Anaerobic
Actinomyces
Eubacterium
Propionibacterium
Peptostreptococci
Facultative
Enterococcus
Streptococci
lactobacillus

15. Anaerobic
Treponema
Porphyromonas
Prevotella
Fusobacterium
Tannerella
Facultative
Neisseria
Capnocytophaga
lactobacilllus

16. Types Of Endodontic Infections
Intraradicular
Infections
Extraradicular
Infection

17. 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

18. Bacteria Involved In Primary 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 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

21. 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

22. 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

23. 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

24. 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

25. Bacteria Involved In Secondary
Intraradicular Infection
Pseudomonas
aeruginosa.
Staphylococcus
sp.
Escherichia
coli.
Candida sp.

26. 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.

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

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 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.

36. 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

37. 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.

38. Prevalence of microorganism detected in root canal treated teeth with post treatment disease.
Data is from taxon-specific PCR assay

39. 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).

40. 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.

41. 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

42. 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

43. 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

44. 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

45. Loss or leakage of
restorative material
Tooth fracture
SOUCE OF
MICROBES
DURING
APPOINTMENTS

46. 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

47. 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

48. 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.

51. 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

52. 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

53. 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

54. 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.

55. 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

56. 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

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 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.

60. 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

61. 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

62. 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)

63. 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.

64. 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

65. 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

66. 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

67. 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

68. 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

70. 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

71. 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

72. 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

73. 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.

74. 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.

75. 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.

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. 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.

79.  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.

80.  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