The document discusses the oral microflora, including the different oral habitats that microorganisms inhabit, such as the teeth, oral mucosa, tongue, and saliva. It describes the various microorganisms commonly found in the oral cavity, including streptococci, actinomyces, and candida albicans. It also defines several terms related to oral microflora and their ecology.

1. ORAL
MICROFLORA
Shilpa Arora
PG 1st Year
Department of Public
Health Dentistry 1

2. Contents
• Introduction
• Terminologies
• Oral Habitats
• Acquisition Of Oral Flora
• Host Microbe Relationship
• Growth And Its Measurement
• Factors Determining Bacterial Distribution
• Normal Oral Microflora
• Microflora Of Dental Plaque 2

3. • Microbiology of dental caries
• Microbiology of endodontics
• Microbiology of periodontal disease
• Applied aspect
• References
3

4. Introduction
• A “microbe” or “microscopic
organism” is a living thing
that is too small to be seen
with naked eye. We need to
use a microscope to see
them.
• Human beings like other
animals, harbor a wide array
of microorganisms both on
and in their bodies. 4

5. • The human body is continuously inhabited by many
different micro-organisms mostly bacteria, some
fungi and other micro-organisms, which under normal
circumstances in a healthy individual, are harmless,
and may even be beneficial. These micro-organisms
are termed, the normal micro flora.
• Oral micro flora : - Micro-organisms inhabiting the
oral cavity.
• All the micro-organisms which establish a more or
less permanent residence at oral surfaces in man, in
one or more of oral habitats, are referred to as normal
micro flora of human mouth. 5

6. • The mouth presents a series of different microhabitats,
each of which may be colonised by different micro-
organisms i.e. there are several different oral habitats,
where micro-organisms can grow.
• Each habitat contains its characteristic population with
many different microbial species. Bacteria are the most
predominant type of microorganisms present in human oral
cavity.
• More than 30 genera of bacteria have been detected in
human mouth. 25 of which are regular members of the oral
flora.
6

7. • These belong to both aerobic and anaerobic groups of
bacteria. Bacteria present in the oral cavity are both gram
positive and gram negative.
• On average 750 million microorganisms are present in each
ml of saliva.
• Natural microflora in the oral cavity become established
during childhood and then change throughout the life under
the influence of various environmental and behavioural
factors.
7

8. • It has been estimated that the human body is made up
of over 1014 cells of which only around 10% are
mammalian. The remainder are the micro-organisms
that comprise the resident micro flora of the host.
• Microorganisms in mouth were first described by
Anton von Leeuwenhoek in 1683.
8

9. Koch postulates
• Are four criteria designed to
establish a causal
relationship between a
causative microbe and a
disease.
Koch's postulates are:
• The microorganism must be
found in abundance in all
organisms suffering from the
disease, but should not be
found in healthy organisms. 9

10. • The microorganism must be isolated from a diseased
organism and grown in pure culture.
• The cultured microorganism should cause disease when
introduced into a healthy organism.
• The microorganism must be re-isolated from the
inoculated, diseased experimental host and identified as
being identical to the original specific causative agent.
10

11. There is a revised versions of Koch’s postulates: Fredricks
and Relman have suggested the following set of Koch’s
postulates for the 21st century:
• A nucleic acid sequence belonging to a putative pathogen
should be present in most cases of an infectious disease.
Microbial nucleic acids should be found preferentially in
those organs or gross anatomic sites known to be diseased,
and not in those organs that lack pathology.
• Fewer, or no, copies of pathogen-associated nucleic acid
sequences should occur in hosts or tissues without disease.
11

12. • With resolution of disease, the copy number of pathogen-
associated nucleic acid sequences should decrease or
become undetectable. With clinical relapse, the opposite
should occur.
• The nature of the microorganism inferred from the
available sequence should be consistent with the known
biological characteristics of that group of organisms.
12

13. • Tissue-sequence should be sought at the cellular level:
efforts should be made to demonstrate specific in situ
hybridization of microbial sequence to areas of tissue
pathology and to visible microorganisms or to areas where
microorganisms are presumed to be located.
• These sequence-based forms of evidence for microbial
causation should be reproducible.
13

14. Terminologies
Habitat: The site where a microorganism grows.
Ecology: Study of relationship between organisms and
their environment.
Ecological niche: The functional position of an organism
in its environment, comprising the living space, periods of
time during which it is active there and resources it obtains
there.
14

15. Aerobes: These organisms require oxygen for aerobic
cellular respiration to obtain energy.
Obligate aerobe: Is an organism that can survive and grow
only in an oxygenated environment.
Facultative anaerobes: Can use oxygen, but also have
anaerobic methods of energy production.
15

16. Capnophiles: Are which thrive in the presence of high
concentrations of carbon dioxide.
Oligotroph: An organism that can live in an environment
that offers very low levels of nutrients.
Microaerophiles: Organisms that may use oxygen, but
only at low concentrations
16

17. Indigenous Flora (Resident): It comprises those
indigenous species that are almost always present in high
numbers, greater than 1 per cent of the total viable count.
Supplemental Flora: The supplemental flora are those
bacterial species that are nearly always present, but in low
numbers, less than 1 per cent of total viable count
17

18. • Transient Flora: Comprise organisms "just passing
through" a host. At any given time a particular species
may or may not be represented in the flora.
• Pathogens: Microorganisms that have the potential to
cause disease.
• Opportunistic Pathogens: Micro-organisms that cause
disease only under exceptional circumstances .
18

19. True Pathogens: Micro-organisms that are consistently
associated with a particular disease.
Autochthonous: Species found characteristically in a
particular habitat.
Allochthonous: Organisms which originate from
elsewhere and are generally unable to colonize
successfully unless the ecosystem is severely disturbed.
19

20. Symbiosis: When both the host and the bacteria benefit
from their inter-relationship, it is termed symbiotic.
Antibiosis: It is the opposite of a symbiotic relationship.
Instead of helping each other, the bacteria and the host are
antagonistic to each other.
20

21. ORAL HABITATS
The major oral habitats are:-
NON TOOTH HABITATS
- Oral mucosa (lips
Cheeks, palate)
- Dorsum of tongue
- Saliva and tonsillar areas
- Appliances
21

22. • TOOTH HABITATS
- Sub gingival areas
- Root surfaces
- Pits and fissures
- Smooth surfaces
22

23. Oral mucosal habitats :
• Oral mucosa harbors organisms that can overcome
abrasive forces of food, tongue and teeth for
retention. Due to the washing effects of saliva, these
organisms should be able to reproduce in great
numbers to ensure survival by reattachment.
Lips
- Staphylococcus albus and micro-cocci
predominate
- large no. of Streptococci
(S. salivarius, S. mitis) 23

24. • Cheeks
- Predominant bacterium is Streptococcus mitor
with sanguis and salivarius .
- Yeasts may be isolated from carriers.
24

25. • Palate
-Streptococcal flora
resembling cheek
-Others like lactobacilli are
common
-Yeasts and lactobacilli in
denture wearers because of
protected environment.
25

26. • Tongue:
-Dorsal surface of the tongue is
ideal for retention of
microorganisms due to the presence
of surface papilla
-Predominant organisms-
Streptococcus salivarius, mitior,
haemophilus, small no. of Candida
albicans
26

27. Saliva:
• A wide variety of microbes as
most of the microbes which get
detached from the tissue / tooth
surface will appear in saliva.
• All species of streptococcus
especially Streptococcus oralis
and Streptococcus salivarius
are found in the saliva.
27

28. • Appliances : Dentures worn
in mouth for a considerable
period will become colonized
with microorganisms and may
alter the oral flora.
• Candida albicans can be found
in large numbers in the fitting
surfaces of acrylic dentures
while yeasts and lactobacilli in
particular, multiply on any
mucosal surface protected from
flow of saliva. 28

29. • Clasps and other parts of appliance that cause
stagnation will promote the build up of dental plaque
and hence lead to accumulation of various bacteria
and their products.
29

30. • The tooth surface:
It is unique as it
is not protected by surface
shedding mechanisms, which
occur in other tissues. It is
stable and gets covered by
pellicle, which is ideal for
streptococcal attachment.
Tooth habitats favorable for
harboring pathogenic plaque
include:
30

31. • Pits and Fissures:
• Provides excellent shelters for
organisms especially
Streptococcus sanguis and other
streptococci.
• Streptococcus mutans can also
be isolated at these sites even in
the absence of caries.
• Obligate anaerobes and gram –ve
species are infrequently isolated
or are absent.
31

32. • Smooth surface: The proximal area
immediately gingival to the contact area is
protected physically and is relatively free
from the effects of mastication, tongue
movements or salivary flushing. The
composition of the microflora varies and
is complex but is predominantly
Actinomyces and Streptococci.
• Tooth topography (such as a rough
surface due to defective/ poor
restoration), the size and shape of gingival
papilla (apically migrated papilla) and
oral hygiene can predispose the tooth to
caries or periodontal disease. 32

33. • Root surface:
• The proximal root surface near
the CEJ is usually unaffected by
flossing due to roughness. This
favors formation of mature,
isolated cariogenic plaque.
• Mainly, gram -ve obligate
anaerobes and Actinomyces are
present here.
33

34. • Sub-gingival areas: The initial
occupants of the sub- gingival
area are an extension of the
community from the adjacent
tooth surface.
• Metabolites released from the
plaque induce a strong
inflammatory response in the
sulcus leading to vascular
changes and release of Ig, PMNL
etc. This leads to a variation in
the local environment by removal
of some species and introduction
of newer ones. 34

35. • Thus, progressive changes from the cocci in the supra-
gingival plaque to filamentous bacteria and spirochetes in
the sub-gingival plaque is seen.
• Pathogenic Bacteroid melaninogenicus can exploit this
habitat and cause destruction of the gingival epithelium.
35

36. • Why the normal bacterial flora are located at
particular anatomical sites.
The normal flora exhibit a tissue preference or
predilection for colonization. This is referred to as
tissue tropism.
• One explanation for tissue tropism is that the host
provides an essential growth factor needed by the
bacterium. To explain why bacteria are not at an
alternative site, the host inherently provides an
inhospitable environment for the bacterium by the
production of such substances as stomach acids, bile
salts and lysozyme 36

37. Many of the normal flora are able to specifically
colonize a particular tissue or surface using their own
surface components like capsules, fimbriae, cell wall
components, as specific ligands for attachment to
specific receptors located at the colonization site.
37

38. Some of the indigenous
bacteria are able to
construct bacterial
biofilms on a tissue
surface, or they are able
to colonize a biofilm
built by another
bacterial species.
• Many biofilms are a
mixture of microbes,
although one member is
responsible for
maintaining the biofilm
and may predominate. 38

39. ACQUISITION OF ORAL FLORA
• The presence of nutrients, epithelial debris, and secretions
makes the mouth a favorable habitat for a great variety of
bacteria.
• The mouth presents a succession of different ecological
situations with age, and this corresponds with changes in the
composition of the normal flora.
39

40. • The process begins with the colonization of habitat by
pioneer microbial populations.
• In oral cavity of newborns, Streptococci are the pioneer
organisms.
• They fill the niche of the new environment and modify
the habitat and new population develops.
• When no additional niche is available for new
population, a stable assemblage of bacterial population is
achieved called as climax community.
40

41. At birth:
• The mouth of full term foetus is usually sterile, transient
flora from the birth canal may be acquired.
• Mouth then rapidly acquires organisms from mother and
from the environment.
• It consists of several Streptococcal and Staphylococcal
species with Lactobacilli, Neisseria and Yeasts.
• Streptococcus salivarius is the most common and forms
the pioneer community with Staphylococcus albus.
41

42. Infancy & Early Childhood
• The infant comes into contact with an ever-increasing
range of microorganisms and some become established as
part of commensal flora.
• The eruption of deciduous teeth provides a new
attachment surface and turns Streptococcus sanguis and
mutans as regular inhabitants of oral cavity.
• Anaerobes are few in number due to absence of deep
gingival crevice.
• Actinomyces , Lactobacilli are found regularly.
42

43. Adolescence
• The greatest number of organisms in mouth occur when
permanent teeth erupt.
• These teeth have deep fissures, larger inter proximal spaces
and deeper gingival crevice, allowing a great increase in
anaerobes.
Adulthood
• Its chief characteristic is its complexity of oral flora.
• There is an increase in Bacteroides and Spirochetes with
maturity of dental plaque.
43

44. • As the teeth are lost the available sites for
microbial colonisation decreases and
several species diminish
disproportionately in numbers.
• Edentulous persons harbour few
Spirochetes or Bacteroides but carriage
of Yeast increases.
• S.sanguis & mutans disappear.
44

45. • Microbes utilize the environment provided by the host to
gain their primary requirements which are nutrients, or, in
the case of viruses, nuclear synthetic machinery. The
results of this interaction, in terms of damage to the host,
vary and form the basis for broad categorization of host-
microbe symbiotic associations:
• Commensalism - Microbe derives benefit, host derives
neither benefit nor harm
• Mutualism - Microbe and host derive benefit from
association, which may be essential
• Parasitism - One benefits at the expense of the other
Host-Microbe Relationships
45

46. 46

47. • Organisms that inhabit the oral cavity-- The oral cavity is a
complex environment that contains both aerobic and
anaerobic conditions. It is hard to classify oral bacteria as
commensals because many species can aid in the formation
of plaque and dental carries, cause periodontal disease, or
become potential pathogens as they invade other body
tissue. Some also present mutualistic benefits such as
vitamin synthesis and the suppression of no indigenous
potential pathogens.
• Species of Streptococcus, Neisseria, Lactobacillus, and
Staphylococcus make up just a few of the many bacteria
present in the oral cavity. 47

48. • A healthy mouth is one of the best examples of a host
supporting enormous numbers of microorganisms with
no deleterious effect.
• Alterations in the balance between host and microbes can
result in pathogenesis: may be caused by alterations in
host defense or by changes in the micro flora (for
example, after antibiotic therapy).
48

49. • Growth of a biological system or of a living
organism, or part of one, may be defined as an
increase in mass or size (in any direction)
accompanied by the synthesis of macromolecules,
leading to the production of a newly organized
structure.
49

50. Measurement of Growth
• Growth may be estimated as an increase in the
number of bacteria, cell mass, or any cellular
constituent.
• When measuring populations counting methods can
be divided into two broad groups: total counts,
including both living and dead bacteria, and viable
counts in which only cells able to grow in the
conditions provided are counted.
• Both types of procedures are used commonly to
enumerate and evaluate oral bacteria.
50

51. Factors determining bacterial distribution
 Physicochemical factors
- Temperature
- Oxygen tension
- Hydrogen ion concentration
 Host factors
 Nutrient sources 51

52. Environmental Factors Influencing Growth
• Microorganisms in their natural environments and in the
laboratory are subjected to a wide variety of environmental
influences, which combine to determine whether growth
can occur and the rate at which it can occur.
• Organisms which are best adapted to the environment will
grow best and will consequently be selected from a mixed
population.
• For example, as organisms in subgingival plaque grow and
the periodontal pocket deepens, conditions become
increasingly anaerobic so the bacteria which come to
predominate in periodontal pockets do not require oxygen
for metabolism.
52

53. • Temperature: Temperature primarily affects the enzymes
of a microorganism: a rise in temperature increases enzyme
activity and allows a faster growth rate, until key enzymes
are denatured.
• The temperatures at which these events occur vary widely
amongst microbes, which all have characteristic
maximum, minimum and optimum temperatures for
growth.
• Organisms which inhabit the human body as commensals
and/or pathogens are mesophiles, and grow most rapidly
within the range 20 degree celsius to 45 degree celsius,
with growth optimum between 35 degree celsius and 40
degree celsius.
53

54. • pH: Most bacteria have an optimum pH for growth in the
range 6.5 - 7.5 with limits somewhere between 5 and 9.
• Acidophilic bacteria can grow at a low pH, and such
organisms are very important in oral microbiology as the
causative agents of caries: Lactobacilli and Mutans
Streptococci produce acid as end products of metabolism of
dietary sugars, and are able to survive and grow in the
acidic conditions created.
• The organisms found in periodontal disease are usually not
aciduric as they tend to rely for growth on protein/peptide
breakdown and this produces slightly alkaline end products.
54

55. • Oxygen: Bacteria vary widely in their requirements for
oxygen, ranging from obligate aerobes through facultative
anaerobes and micro-aerophiles to obligate anaerobes.
• Because oxygen and its derivatives are toxic and can
lethally damage certain cellular components, aerobic and
facultative organisms have evolved protective enzyme
systems which eliminate superoxide radicals. Hydrogen
peroxide can be removed by catalase and peroxidase
enzymes.
• In general, anaerobes lack protective mechanisms
55

56. • Aerobic bacteria use oxygen as the terminal electron
acceptor in respiration, and obligate aerobes have an
absolute requirement for oxygen to grow.
• Microaerophilic (eg. Campylobacter sp.) organisms require
a low concentration of oxygen for growth, and are sensitive
to atmospheric concentrations.
• Facultative anaerobes, such as Streptococci and Neisseria,
use oxygen but also grow in its absence although growth is
usually slower without oxygen.
56

57. • An obligate anaerobic organism is one whose energy
generating and synthetic pathways do not require
molecular oxygen, and which demonstrates a high degree
of adverse sensitivity to oxygen.
• Because of their extreme sensitivity, obligate anaerobes
must be cultivated in the absence of atmospheric oxygen
and a low redox potential must be maintained in the growth
medium.
• These cultivation techniques, and anaerobic sampling
methods, are essential when examining samples from, for
example, periodontal pockets or abscesses which contain
high numbers of obligate anaerobic bacteria 57

58. Metabolism of Oral Microorganisms
• Oral microorganisms derive nutrients from saliva and
gingival crevicular fluid.
• Carbohydrate metabolism is of attention because of its role
in caries production. End products of such fermentation in
the mouth are varied e.g., Streptococcus mutans produces
only lactic acid from sugars, some lactobacilli produce
lactic acid and ethanol, whereas yeasts convert glucose to
ethanol and CO2.
58

59. • The substrates used are also varied and many of the
anaerobes seen in the mouth are able to utilize amino acids
as substrates for fermentation; therefore, periodontal
organisms are predominantly proteolytic.
59

60. • Diet as a nutrient source
– Three factors influences the effectiveness of the diet as a
microbial nutrient sources.
– These are the 1) Chemical composition of the diet 2) The
physical consistency of its components 3) The frequency
of its ingestion.
– The macromolecular nutrients such as starches, proteins
and lipids are normally not available to the oral flora
because their transit time through the oral cavity is too
short for them to be degraded to useable nutrients.
60

61. - If physical consistency of the food that contain them
permits retention such as fibrous food between the teeth or
sticky foods in fissures pits and contact points then some
utilization of starches and proteins could occur.
- Carbohydrates such as sucrose and lactose are readily
metabolized by the oral flora.
- It is this bioavailability of these simple sugars that make
them cariogenic.
61

62. • In dental decay the consistency of the diet and the
frequency of ingestion may be more important than
diet composition.
• Both consistency and frequency influence the length
of time that food remains in contact with the plaque
and thus is available for bacterial use.
• When snacks are taken between meals they augment
the time of nutrient availability.
62

63. • The consistency of food also influences the plaque flora.
Liquid foods such as fruit juices and tonics are usually
swallowed quickly and for this reason they are not readily
available to oral flora.
• Thus for those subjects who eat between meals, sugar
could be detected in their saliva during most of the day.
Some microbial fermentation was ongoing in the plaque
the most of the day.
• The pH at plaque enamel interface probably was below pH
5.5. This is the critical pH for enamel demineralization.
63

64. • Saliva as a nutrient source
- Saliva is homeostatic fluid that buffers the plaque,
provide nutrients to flora. It contains about 1% solids,
which include glycoproteins, inorganic salts, amino acids,
glucose.
• Gingival crevicular fluid
- Gingival crevice contain serum transudate that contains
tissue and serum proteins as well as free amino acid,
vitamins, glucose.
64

65. • Shed cells
- The epithelial surfaces of oral cavity shed their surface
cells.
- These cells can be lysed by the hypotonicity of saliva
and their contents are then available for microbial nutrients.
• Bacteria
- The bacteria themselves can provide nutrients for each
other. Lactic acid producing bacteria such as Streptococcus
and lactate utilizing species such as Veillonella alkalescens.
65

66. • Definition :
Collectively describes various microbial types
frequently found by culture or microscopy on skin, mucous
membrane or body cavities in normal healthy individuals.
• Criteria :
 Frequently encountered in typical human anatomic
regions.
 As often in absence of disease as in it’s presence .
 Primary habitat – Human species .
NORMAL ORAL MICROBIAL FLORA
66

67. Types :
INDIGENOUS FLORA – Almost always present.
Eg: Streptococci, Actinomyces and Neisseria.
SUPPLEMENTAL FLORA – Nearly always present
( Most potential dental
pathogens )
Eg: Lactobacilli, S. mutans, P. gingivalis
TRANSIENT FLORA – Organisms “just passing through” a
host.
Eg: Coliforms
67

68. • Significance :
 Provide protection and contribute to general immunity of
host
 Provide a barrier to colonization ( eg: bacterial
interference for E. coli )
 Aids in nutrition of host – Vit K , B12 etc. produced by
microorganisms.
 May cause opportunistic infections ( candida )
68

69. Oral
Microflora
Bacteria Virus Fungi ProtozoaMycoplasma Spirochaetes
69

70. Bacteria
Cocci
Gram
positive
Gram
negative
Bacilli
Gram
positive
Gram
nagative
70

71. Oral flora
• Bacteria:
• Gram +ve bacteria
• Cocci : Of all the
bacteria present in the
oral cavity Streptococci
constitute the single
largest group.
• Others include :-
GRAM POSITIVE
COCCI
-S. oralis
- S. sanguis
-S. mutans
-S. mitior
-S. salivarius
-S. milleri
-S.faecalis
-Peptostreptococcus
-Peptococci
(anaerobic) 71

72. • Bacilli: Lactobacilli are widely
present and frequently found in
the oral cavity. 27 recognized
species of lactobacilli are known
with important ones being
• L. acidophilus
• L. salivarius
• L. casei
• Others include:-
GRAM POSITIVE
BACILLI
- L. Acidophillus
- L. casei
- L. Rhamnosus
- L. fermentum
- Actinomyces israelii
- A. naeslundii
- A. viscosus
- Eubacterium
saburreum
- clostridium 72

73. • Gram -ve bacteria:
• Cocci: Veillonella are
the most numerous ,
accounting for 10% of
cultivable salivary and
tongue flora. Neisseria
are also seen.
• (Bacteroid species and
F. nucleatum are most
commonly occurring
bacilli in gingival
sulcus area)
GRAM
NEGATIVE
COCCI
- Veillonella
alcalescens
- Neisseria
subflava
-N. Mucosa
- N.sicca
GRAM
NEGATIVE
BACILLI
- Haemophilus
- Actinobacillus
- Eikenella
- Capnocytophaga
- Campylobacter
- Bacteroides
-Porphyromonas
- Prevotella
- Fusobacterium
- Leptotrichae
73

74. Treponemes:
• Spirochetes such as :-
T.vincenti are common inhabitants
of gingival crevices and are often
associated with periodontitis
SPIROCHAETES :
- Treponema
denticola
- T.macrodentium
- T. scoliodontum
- T. vincentii
- Borrelia buccale
- B. vincentii 74

75. Mycoplasma: These pleomorphic organisms are
regularly seen in plaque, calculus, periodontal pockets
etc.
• M. salivarium is the most predominant species
75
MYCOPLASMA – M. orale
M. salivarium
M.pneumonione

76. • Fungi: Candida albicans is the most
common fungus isolated from the oral
cavity & is detected in high numbers
in gingival flora, periodontal abscess,
infected root canals etc.
Other fungi isolated are
• Pencillium
• Aspergillus
• Hemispora
•
FUNGI –
- Candida albicans
- C . Glabrata
- C . tropicalis
76

77. • Protozoa: Are present in
periodontal diseases
77
PROTOZOA –
- Entamoeba
gingivalis
- Trichomonas
tenax

78. • Virus:
• EBV
• Mumps virus
• Measles
• Influenza virus
( can be observed during the active stage of the
disease)
78

79. • Supply of certain nutrients.
• Aid in food digestion and protection.
• Oral bacteria like intestinal flora produce certain vitamins
and cofactors which are needed by humans. These include
vitamin K, biotin and riboflavin.
• Production of digestive enzymes such as amylase, lipase
and protease .
Benefits of oral flora
79

80. • In the presence of resident flora it is difficult for exogenous
organisms to establish themselves and produce disease.
Growth of organisms such as C. diptheriae, S. pyogens,
Staph. aureus has shown to be inhibited in vitro by S.
mitior.
• Helps in maturation of host immune system.
80

81. Microflora of Dental Plaque
81

82. • According to WHO : Plaque is highly specific and
selective but structurally variable clinical entity
characterized by sequential colonization of microorganisms
on the surface of teeth, restoration and other parts of the oral
cavity. It is made up of mucins, desquamative epithelial
cells and microorganisms embedded in an extracellular
matrix. 82

83. CLASSIFICATION
i. Based On Location
a) Supragingival
Coronal
Marginal
b) Subgingival
Tooth associated
Epithelial
associated.
ii. Based on time
- Early plaque
- Mature or late plaque 83

84. 84

85. Composition of dental plaque
Bacteria + Intercellular matrix = Dental plaque
• Bacteria -- 70 to 80 per cent of total material.
• Mycoplasma, fungi, protozoa and viruses
• Intercellular matrix:
• Organic components Inorganic components
85
• Carbohydrates:
Levan
Glucan
Galactose
• Glycoproteins
Calcium
Phosphorus
Magnesium
Potassium
Sodium

86. • Host cells- Epithelial cells, macrophages & leucocytes
86

87. Microbial specificity of periodontal disease
“Non Specific Plaque Hypothesis”
Walter Loesche, 1976
“Specific Plaque Hypothesis”
Walter Loesche , 1976
87

88. • This hypothesis proposes that collective groups of different
bacteria have the total complement of virulence factors
required for periodontal tissue destruction and that some
bacteria can substitute for others absent from the pathogenic
consortium.
• This hypothesis implies that plaque will cause disease
irrespective of its composition, and it is supported by the
clinical findings of numerous bacterial species in diseased
periodontal pockets.
88
The Non-specific Plaque Hypothesis

89. • It states that only certain plaque is pathogenic, and its
pathogenicity depends on the presence of or increases
in specific microorganisms.
• Newman et al (1976) and Slots (1976) demonstrated
that the microbial composition of subgingival plaque
taken from diseased sites differed substantially from
the samples taken from healthy sites in subjects with
localized juvenile periodontitis (LJP).
89
The specific plaque hypothesis

90. • Tanner et al. (1979) and Slots (1977) demonstrated
that the microbes recovered from lesion sites from
subjects with adult periodontitis differed from the
microbes from healthy sites in the same subjects and
also from lesion sites in LJP subjects.
90

91. Ecological plaque hypothesis
• In the 1990s, marsh and coworker developed the
ecologic plaque hypothesis as an attempt to unify the
existing theories on the role of dental plaque in oral
disease.
• According to the ecologic plaque hypothesis, disease
is the result of an imbalance in the total microflora
due to ecological stress, resulting in an enrichment of
some oral pathogens or disease related micro-
organisms.
91

92. • The health associated dental plaque microflora is
consider to be relatively stable over time or in a state of
dental equilibrium.
• The host control subgingival plaque to some extent by
tempered immune response and low levels of GCF flow.
• Host response may be brought about by the excessive
accumulation of dental plaque or by plaque independent
host factors (eg: the onset of an immune disorder,
changes in hormonal balance such as pregnancy or
environmental factors eg, smoking, diet) 92

93. • Change in the host status such as inflammation , tissue
degradation and/or high GCF flow, may lead to a shift in
the microbial population in plaque.
• The Ecological plaque hypothesis is entirely consistent
with observation that disease associated organisms are
minor components of the oral microflora in health, these
organisms are kept in check by interspecies competition
during microbial homeostasis
93

94. • Disease is caused by the overgrowth of specific elements of
dental plaque when the local microenvironment changes,
but it is not necessity the same species in each case.
• Eliminating the disease-inducing stimulus whether it is
microbial, host or environmental will help to restore
microbial homeostasis.
94

95. • Ecologic plaque hypothesis in relation to periodontal
disease : gingivitis & periodontitis
• Accumulation of plaque causes inflammation of
adjacent tissues (gingivitis) & other environmental
changes that forms the growth of gram-ve anaerobes &
proteolytic species including periodontal pathogens.
• The increased proportion of such species results in
destruction of periodontal tissues (i.e. periodontitis).
95

96. 96

97. • Stage 1: Acquired pellicle formation:
Involves the adsorption of salivary proteins to apatite
surfaces via electrostatic ionic interactions
• Stage 2: Transport and Adherence of pioneering
organisms:
Transition between pellicle to plaque is rapid. The first
constituents are cocci with small numbers of epithelial cells
and PMNL’s which initially adhere via
electrostatic interactions (reversible). A little later specific
interactions between adhesins on microbial surface and
receptors in the pellicle result in irreversible adhesions. 97

98. • S. mutans and S. Sanguis produce glycans in the
presence of sucrose which aids in adherence to pellicle
and also promotes adherence to other micro organisms
• Within 8-10 hours, about 10,000 cells/ mm2 are
deposited. An extra-cellular matrix develops consisting
of polysaccharides and salivary organisms multiply with
time.
98

99. • Stage 3: Co-Aggregation (Within 1-3 days):
The metabolic products of
the pioneering organisms alter the immediate
environment such as creating conditions with a low
redox potential suitable for anaerobes.
Other organisms become incorporated into the
plaque with a resulting gradual increase in microbial
complexity, biomass and thickness.
99

100. • Stage 4: Multiplication:
The proliferation of the attached
micro-organisms and further aggregation produces a
confluent growth and a biofilm.
• Stage 5: Seeding:
Detachment of cells from this bio film
into the saliva results in colonization of fresh sites.
100

101. • Listgarten in 1976 has described highly specific
interspecies microbial interactions:
– “Corncob” formations
– “Test tube Brush”/Bristle Brush formations 101

102. 102
Corn cob formation
• Corncob formations have been
observed between rod-shaped
bacterial cells (e.g. Bacterionema,
C.matruchotii or F.Nucleatum) that
form the inner core of the structure
and coccal cells (e.g. Streptococci
or P. gingivalis) that attach along
the surface of the rod-shaped cell.
• “Corn cob” formations were
occasionally seen as a feature of
plaque present on teeth associated
with gingivitis.

103. 103
Test tube Brush”/Bristle Brush formations
• This consists of one or
several filaments aligned
perpendicular to the central
filament.
• “Bristle-brush” formations
are commonly seen in the
subgingival plaque of teeth
associated with periodontitis.

104. SUPRAGINGIVAL
PLAQUE
SUBGINGIVAL
PLAQUE
MATRIX 50% Matrix Little or no matrix
FLORA Mostly gm +ve flora, cocci &
short rods
Mostly gm-ve rods &
spirochetes
MOTILE BACTERIA Few Common
ANAEROBIC/
AEROBIC
Aerobic unless thick Highly anaerobic
METABOLISM Predominantly carbohydrate Predominantly proteins
SPECIES
DIVERSITY
Little initially, increasing with
time
Great
104

105. SELECTED BACTERIAL SPECIES FOUND IN DENTAL
PLAQUE
Facultative Anaerobic
Gram-Positive Streptococcus mutans
Streptococcus sanguis
Actinomyces viscosus
Gram-negative Actinobacillus
actinomycetemcomitan
s
Capnocytophypa
species
Eikenella corrodens
Porphyromonas gingivalis
Fusobacterium nucleatum
Prevotella intermedia
Bacteroides forsythus
Campylobacter rectus
Spirochetes Treponema denticola
(Other Treponema species)105

106. 106

107. 107

108. • Factors which determine the ultimate composition and
pathogenicity of plaque
• Bacterial factors
– Extra-cellular products: eg. glucans produced by S.
mutans are sticky and help in co- aggregation
– Bacterial interactions: are important for bacteria that
cannot attach directly to the tooth. Eg. Vellionella which
of incapable of direct attachment accumulates on
A.viscosus.
108

109. • Host factors:
• Oral cleansing mechanism such as salivary flow,
movements of tongue and cheek control the plaque
formation rate.
• Saliva influences
–The plaque pH by its buffering action and acid
neutralization.
–Inhibition of adherence by coating the surface
receptors
–Inhibition of adherence via promotion of bacterial
agglutination
109

110. • Immune response: Main sources of immune
components in oral cavity are:
– IgA and antibodies in saliva which compete with
bacterial adherence and influences their metabolism,
growth and accumulation.
– Crevicular fluid which contains antibodies, leukocytes,
complement factors etc.
110

111. Microbiology of Dental Caries
111

112. • Over the years, there has been a debate whether one or
more specific bacteria are principally involved in the
initiation of caries or if this disease is caused by a non –
specific mixture of bacteria.
• Given the variations found in the microbial composition,
it seems unlikely that the initiation and progression of all
carious lesions are associated with identical or even
similar plaques.
• However, there is evidence that some bacteria – S.
mutans, Lactobacilli and Actinomyces are more
important than others.
112

113. • S. mutans: The feature that supports its role as cariogenic
organisms are its:
- Rapid generation time
- Acidogenic nature
- Production of extra cellular polysaccharides from
sucrose which aids on adherence and acts as a nutrient
- Isolated in high numbers in caries active mouth in
incipient lesions
- Capacity to attain critical pH for enamel
demineralization more rapidly than other plaque bacteria.
113

114. • Once caries initiates, the local environment alters and
other bacteria arrive and take up the process of
progression of the caries eg Lactobacilli.
114

115. • Lactobacilli for many years was believed to be the
causative agent of dental caries as
- High numbers were obtained in most enamel
caries
- Production of caries in germ-free rats
- Able to synthesis extra cellular and intra cellular
polysaccharides form glucose.
- Produce lactic acid at pH < 5
115

116. • Although these properties seemed valuable to a cariogenic
organism, it was also seen that their affinity for the tooth
surface and their number prior to development of caries
was low.
• They were, in fact, absent from incipient lesions while
present is significant numbers in developed caries.
• Thus, they were categorized as secondary invaders which
caused progression of caries due to their acidogenic and
aciduric properties.
116

117. • Other Cariogenic micro organisms:
• Actinomyces species: A.viscosus & some other Gram +ve
bacilli are involved in the initiation of lesions on root
surface.
• Role played by a large number of other bacteria isolated
from caries such as Arachnia, Eubacterium, Rothia etc are
not yet clearly known.
• Veillonella: Is a species which is supposed to be
antagonistic to the caries process. Its protective role is
contributed to its ability to decrease the acidity within the
plaque. 117

118. Difference between Cariogenic & Non
Cariogenic plaque
Cariogenic plaque Non-Cariogenic plaque
Plaque served from carious area
is called cariogenic plaque.
If plaque obtained from sound
enamel surface of same teeth.
The rate of sucrose consumption
high in cariogenic plaque
Rate of sucrose consumption is
lesser in non cariogenic plaque.
Rate of Lactic acid formation is
high
Rate of lactic acid formation is
less
118

119. Bacteria in cariogenic plaque
synthesis more intracellular
glycogen, amylopectin by
polysaccharides
Bacteria in non cariogenic
plaque synthesis less
intracellular glycogen as
compared to cariogenic plaque
Cariogenic plaque formed
approximately twice as much
extracellular polysaccharide
from sucrose.
Non Cariogenic plaque formed
less than cariogenic plaque.
Cariogenic plaque contains
higher level of S. mutans.
Non cariogenic plaque contains
higher proportion of S. sanguis
and Actinomyces.
119

120. • Pit and fissure caries: Smooth surface caries:
120
Streptococcus sanguis
Other Streptococci
Lactobacilli sp
Actinomyces sp
Streptococcus mutans
Streptococcus Salivarius

121. Root surface caries: Deep dentinal caries:
121
Actinomyces viscosus
Actinomyces naeslundii
Other filamentous rods
Streptococcus mutans
Streptococcus sanguis
Streptococcus salivarius
Lactobacillus sp
Actinomyces naeslundii
Actinomyces viscosus
Other filamentous rods
Streptococcus mutans

122. Microbiology of Endodontics
122

123. • A large number of bacteria and some fungi can cause
infection in the dental pulp as well as periapical tissues.
• Dental pulp is a unique formative organ with limited
capacity to withstand bacterial, mechanical and chemical
attack. When bacteria enter the pulp it is unusual for the
host defenses to completely eliminate them. Healing is
uncommon and necrosis results
• With pulpal degeneration, antigens collect within the root
canal system and move to the periapical tissues and
further inflammatory responses lead to formation of
abscess, granulomas or cysts.
123

124. • Sources of infection:
- Infected carious lesion / iatrogenic exposure
- via periodontal tissues through exposed dentinal tubules,
lateral accessory canals or apical foramen.
- By the lymphatic / hematogeneous route i.e anachoresis
(localization of transient bacteria in the blood into an inflamed
area, such as a traumatized / inflamed pulp.)
- Traumatic displacement / fracture can also become a route
for microbial ingress to the pulp.
• Once the disease sets in, these tissues can act as source for
spreading infection to various organs of body through blood
resulting in septicemia. 124

125. • Disease occurring secondary to endodontic treatment
include
- Infective endocarditis
- Cavernous sinus thrombosis
- Bacterial myocarditis
- Cerebral abscess
- Various lesions result as sequelae to pulp necrosis
such as granulomas, abscesses, actinomycosis, cellulites,
osteomylitis etc.
125

126. Microflora of traumatized
but intact teeth with necrotic
pulps
Mainly and predominantly
consists of B.melaninogenicus
in association with other
anaerobic bacteria.
Microflora of acute infections
of endodontic origin
Bacteroides in association
with
P. endodontalis, gingivalis and
Prevotella intermedius.
126

127. ]
Microflora of endodontic
‘flare-up’ infections
Obligate Anaerobes Such As
Veillonella
Capnocytophaga
Eiknella
Bacteroides
Fusobacterium
Treponema.
Microflora on refractory
endodontic cases are
E. faecalis
Candida albicans
Actinomyces israelii
127

128. Microflora of infected and
untreated necrotic pulp
Root canal flora of teeth with
clinically intact crowns but
having necrotic pulps and
diseased periapices is dominated
(>90% ) by the obligate
anaerobes.
Fusobacterium
Porphyromonas
Prevotella
Eubacterium
Peptostreptococcus
Endodontic flora in previously root
filled teeth
Actinomyces
Enterococcus, propionibacterium
128

129. Microbiology of Periodontal Diseases
129

130. Plaque induced Gingivitis- Harold Loe, 1965
Gram positive
S. intermedia
S. Sanguis
S.Mitis
S.oralis
A.Viscosus
A. Naesleundii
P. gingivalis
Gram negative
F. Nucleatum
P. intermedia,
Capnocytophaga
Haemophilus
Campylobacter
species.
Pregnancy
induced gingivitis
P. intermedia
130

131. Chronic Periodontitis
Spirochetes
P. gingivalis
A. actinomycetocomitans
Treponema Eubacterium
F. Nucleatum
C. Rectus
P. Intermedia
E. corrodens
131

132. • Recent studies have documented an association between
chronic periodontitis and viral microorganisms of the
herpes virus group, most probably Epstein Barr Virus I
(EBV-I) and human cytomegalovirus (HCMV).
• Further, the presence of subgingival EBV-I and HCMV are
associated with high levels of putative bacterial pathogens,
including P. Gingivalis. T. Forsythia, P. Intermedia and T.
Denticola.
• These data support the hypothesis that viral infection may
contribute to periodontal pathogenesis, but the potential
role of viral agents remain to be determined.
132

133. • Localized Aggressive Periodontitis –
Socransky, 1977
A.
actinomycetemcomitans
P. gingivalis
F. Nucleatum
Virus- EB virus
(EBV-I)
Human cytomegalo
virus (HCMV) 133

134. • Necrotizing ulcerative gingivitis
P. intermedia
Spirochetes (B.vincenti)
Fusobacterium
• Abscesses of Periodontium
F.nucleatum
P. intermedia
P. gingivalis
134

135. • Refractory periodontitis:
B. forsythus
F. nucleatum
P. gingivalis
E. corrodens
C. rectus
135

136. Applied aspect
The Window of Infectivity
• In 1993, Page Caufield and Colleagues presented a paper with
evidence to support a discrete “window of infectivity” for MS
colonization.
• As the teeth erupt into the oral cavity, they provide a virgin
habitat which enables MS to colonize the oral cavity avoiding
competition with other indigenous bacteria.
• Thus, in window period in deciduous teeth, the MS is
established by 7-31 months of age.
• Krass et al (1967), Edrman et al (1975) reported that at two to
six years of age, the child is less susceptible to acquiring MS.
136

137. The window occurs
• 38 of 46 infants acquired MS at median of 26 months
• 25% by 19months
• 75% by 31months
137

138. The “Window” end
• Window appears to close after all primary teeth erupt
• Once a stable plaque or biofilm covers the tooth
surface, MS is less likely to be established
• Children ages 2-6 have been shown to be less
susceptible to MS infection
138

139. 2nd Window of Infectivity
• A 2nd window is speculated at approximately 6 years
of age when 1st molars are erupting.
• It is present in permanent dentition between 6-12
years of age.
• Straetemans (1998) found that about 75% of children
uninfected at age 5 became infected by age 11
139

140. • The timing of immunization should precede the
“window of infectivity”.
• i.e. the period during which children usually become
infected with Mutans Streptococci which extends
from 19 to 31 months of age.( median age of 26
months).
140

141. References
• Ananthanarayan R, Paniker CKJ, Textbook of
Microbiology, 7th ed. Orient Longman Publications
• Newman MG, Takei HH, Carranza FA, Clinical
Periodontology, 9th ed. W B Saunders Company
Philadelphia.2000.
• Fejerskov O, Kidd E, Dental Caries The Disease and
its Clinical Management, 2ne ed. Blackwelll
Munksgaard. Singapore.2008.
141

142. 142