1. PRESENTED BY
ASHISH KARODE
MDS STUDENT

2. Histopathology of Dental CariesHistopathology of Dental Caries

3.  HISTOLOGY : Study of microscopic anatomy
of cells and tissues of plants and animals.
 HISTOPATHOLOGY: Microscopic
examination of tissues in order to study the
manifestations of disease.
 DENTAL CARIES: Microbial disease of
calcified tissues of teeth characterised by
demineralisation of inorganic portion and
destruction of organic portion.

4. Dental Caries
It is a microbial disease of the calcified tissues of the teeth,
characterized by demineralization of the inorganic portion
and destruction of the organic substance of the tooth.
Many researches/investigations for more than a hundred years have
been done, still, many aspects of the etiology of this disease is
obscure and efforts at prevention are only partly successful.

5. ► Dental caries or tooth decay is one of the most common of all
disorders, second only to common cold.
► Dental caries has afflicted more humans longer than any other
disease. It was first appeared about 1400 BC years ago. From
that time to the present, dental caries affected almost all
human populations, at all socioeconomic levels, and at all ages.
► Some isolated populations like Eskimos, some African natives,
and inhabitants of rural India are “immune” to dental caries
because they are not exposed to western food habits.

6.  The word ‘caries’ is derived from the Latin word ‘rot’.
It is the most prevalent disease affecting the human race,
 Practically spread all over the world,
 Affects both sexes and all races, all socio-economic strata
and people of all ages,
 Starts soon after teeth erupt into the oral cavity

7. Dental CariesDental Caries
Enamel CariesEnamel Caries Dentin CariesDentin Caries Cementum CariesCementum Caries
(Root caries)(Root caries)
Smooth surface cariesSmooth surface caries Pit and fissure cariesPit and fissure caries

8.  SMOOTH SURFACE CARIES
PIT AND FISSURE CARIES

9.  OF ENAMEL: Hard translucent tissue covering
the anatomical crowns.
 COMPOSITION: Inorganic matter 96%
Organic matter 0.2-0.8%
Water 1.2-4%
 STRUCTURE: Hydroxyappatite crystals laid in
form of rods, Striae of Retzius, rod sheath etc.

10.  OF DENTIN: Semi transparent calcified connective
tissue penetrated by small canals containing
protoplasmic processes belonging to cell which remain
outside the tissue in pulp cavity.
 COMPOSITION: Inorganic matter 61-73%
Organic matter 20.2-22.8%
Water 10.8-15.4%
 STRUCTURE: Hydroxyapatite crystals laid in form of
dentinal tubules, dentin matrix and Tomes fibres etc.

11.  DENTINO ENAMEL JUNCTION:
 Has more interprismatic substance, crossing
and branching of dentinal tubules, enamel
spindles and enamel lamellae.

12.  OF CEMENTUM: Bone like tissue arranged in
layers present around the anatomical root
 COMPOSITION: Inorganic matter 65-70%
Organic matter 35-40%
 STRUCTURE: Acellular cementum and cellular
cementum.

13.  Causative Factors
• Presence of caries pathogens (MS, LB)
• Frequent or prolonged exposure to
fermentable carbohydrates
 Potentiating Factors
• Low fluoride exposure level
• Inadequate salivary flow

14. Causes of dental caries
• Pre-microbiology era
– Dental caries is the death (decay) of a
tissue
• Microbiology period era
– Dental caries is a microbe related disease

15. The first microbes
observed
• Anton Van Leeuwenhoek
(1632-1723) developed
the microscope and was
the first to discover oral
bacterial flora: “I didn’t
clean my teeth for three
days and then took the
material that had lodged
in small amounts on the
gums above my front
teeth…. I found a few
living animalcules..”

16. Re-isolation of “Mutans streptococci”:
 • Streptococcus mutans (human) (same
species Clark isolated in England in 1924)
 • Streptococcus sobrinus (human)
 • Streptococcus rattus (rats)
 • Streptococcus cricetus
 • Streptococcus ferus
 • Streptococcus macacae
 • Streptococcus downeii

17. 1. Acid production (acidogenicity)
• Lower the pH to below 5.5, the critical pH. Drives
the dissolution of calcium phosphate (hydroxyapatite)
of the tooth enamel
• Inhibit the growth of beneficial bacteria, promote the
growth of aciduric bacteria.
• Further lower the pH, promote progression of the
carious lesion

18. • Allows the cariogenic bacteria to thrive under acidic
conditions while other beneficial bacteria are
inhibited. This results in dominance of the plaque
by cariogenic bacteria
2. Acid tolerance (aciduricity)
3. Glucan formation
• Glucan mediated biofilms are more resistant to
mechanical removal
• Bacteria in these biofilms are more resistant to
antimicrobial treatments
Allows the cariogenic bacteria to stick onto the teeth
and form a biofilm

19.  Ecological niche: Human oral cavity
 “Intentionally designed … to be a cariogenic
organism” (Coykendall 1976)
 Carciogenic properties
 Ability to produce acid
(acidogenicity)
 Ability to withstand acid
conditions (aciduricity), at
the expense of benign flora
 Ability to adhere to teeth

22. Both pathogenic and commensal (nonharmful) bacteria exist in a
natural plaque.
At sound site, the pathogenic bacteria may exist in low numbers
to cause any clinical effect, or they may exist in higher numbers,
but the acid produced is neutralized by the action of other
bacteria.
Disease is a result of a shift in the balance of the residence micro
flora driven by a change in the local environment (frequent
sugar intake etc).

23. Plaque on the surface
of the tooth
(enamel)

24.  Lesion Initiation
• MS present in low numbers in plaque (carrier state)
• Frequent sugar supply gives MS competitive advantage
 • ECP helps adhere them firmly to tooth surface
 • Metabolism of sugar to acid by products lowers pH
 • Few organisms can survive in low pH (aciduric)
 • MS proportions increase
 • This lowers the pH further and decreases the number of
competing organisms
 • Once the pH low enough (critical pH, 5.0-5.5) tooth
mineral begins dissolving
 • Mineral loss follows down the grain of the enamel rods

25.  • Saliva dilutes & buffers acid & contains concentrated
calcium & phosphate ions
 • When sugar present, net demineralization rapidly
occurs
 • Between sugar episodes, remineralization slowly occurs
 • If remin periods exceed demin periods, subsurface
lesion will mineralize & arrest
 • If demin periods exceed remin periods, cavitation will
occur
 • Demin periods exceed remin periods when sugar Intake is
increased in intensity

28. The surface of a tooth i. e. covered by plaque,
which consists mainly of bacteria. Plaque is often
found close to the gum, in between teeth, in
fissures and at other "hidden" sites.
Demineralization:
When sugar and other fermentable
carbohydrates reaches the bacteria, they form
acids which start to dissolve the enamel - an
early caries lesion occurs due to loss of Calcium
and Phosphates
Remineralization:
When sugar consumption has ceased, saliva
can wash away sugars and buffer the acids.
Calcium and Phosphates can again enter the
tooth. The process is strongly facilitated by
fluorides
A CAVITY occurs if the Demineralization "wins" over the Remineralization over time

29. The first indication of tooth decay are
white spots on the enamel caused by the
loss of calcium.
If the demineralization process
outruns the natural remineralisation
process, the lesion grows and a cavity
is formed.
The bacteria may invade the pulp of
the tooth,
causing a consistent tooth pain,
especially during the night.
The bacteria may also
produce an abscess,
and eventually the tooth
may be extracted by the
dentist.

30. SLOWLY PROGRESSING LESIONS GO
THROUGH MORE DEMIN/REMIN CYCLES
LEADING TO DARK SHALLOW LESIONS
RAPIDLY PROGRESSING LESIONS GO
THROUGH FEWER DEMIN/REMIN CYCLES
LEADING TO LIGHTER-COLORED, MORE
AGGRESSIVE LESIONS

31. 1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been stopped.
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.

33. ENAMEL CARIES
The early lesion is a white spot which appears
on the surface of the enamel. Caries spreads in
zones which are as follows.
 Translucent zone
 Dark zone
 Body of the lesion
 Surface zone

34. The zones seen before complete disintegration of enamel are:
Zone 1: Translucent zone,
-lies at the advancing front of the lesion,
-slightly more porous than sound enamel,
-it is not always present
Zone 2: Dark zone,
-this zone is usually present and referred
to as positive zone
-formed due to demineralization.
Zone 3: Body of the lesion,
-found between the surface and the dark zone,
-it is the area of greatest demineralization,
Zone 4: Surface zone,
-relatively unaffected area,
-greater resistance probably due to greater degree of mineralization and
greater F concentration.

36. Pit And Fissure Caries:
-lesion begins beneath plaque, with decalcification of enamel
-pit and fissures are often deep, with food stagnation,
-enamel in the bottom of pit or fissure is very thin, so early dentin involvement
frequently occurs.
-here the caries follows the direction of the enamel rods.
-It is triangular in shape with the apex facing the surface of tooth and the
base towards the DEJ.
-when reaches DEJ, greater number of dentinal tubules are involved.
-it produces greater cavitation than the smooth surface caries and there is
more undermining of enamel.

41. Smooth surface Caries:
The earliest manifestation of incipient caries (early caries) of enamel is usually
seen beneath dental plaque as areas of decalcification (white spots).
The first change seen histologically is the loss of inter-rod substance of
enamel with increased prominence of the rods.
-this is followed by the loss of mucopolysaccharides in the organic substance.
-presence of transverse striations of the enamel rods,
- accentuated incremental lines of Retzius
as it goes deeper, the caries forms a triangular pattern or cone shaped lesion
with the apex towards DEJ and base towards the tooth surface.
Finally, there is loss of enamel structure, which gets roughened due to
demineralization, and disintegration of enamel prisms.

42. intact surface layer
incremental growth lines
striae of Retzius

44. Early lesion with intact
enamel
5-10% mineral loss, zone
of intact enamel
Lesion body 60%
or more mineral loss
translucent zone – 5-10%
mineral loss
normal enamel

50. The events of the dentinal caries are as follows:
 Defense reaction of the pulpodentinal complex
1. Seclerosis
2. Reactionary dentine formation
3. Sealing of the dead tracts
 Carious destruction
1. Demineralization
2. proteolysis

51. ARIES OF DENTIN
gins with the natural spread of the caries process along the DEJ and rapid
olvement of the dentinal tubules. The dentinal tubules act as tracts leading to
e pulp (path for micro-organisms).
rly Dentinal Changes:
itial penetration of the dentin by caries dentinal sclerosis,
alcification of dentinal tubules and sealing off from further penetration by
icro-organisms,
ore prominent in slow chronic caries.
Dentinal
sclerosis

53. Carious
lesion
Dentin reaction
to caries

54. Behind the transparent sclerotic zone, decalcification of dentin appears.
In the earliest stages, when only few tubules are involved, microorganisms may
be found penetrating the tubules Pioneer Bacteria.

55. This initial decalcification
involves the walls allowing
them to distend as the
tubules are packed with
microorganisms. Each tubule
is seen to be packed with pure
forms of bacteria, eg., one
tubule packed with coccal
forms the other tubule with
bacilli.

56. As the microorganisms proceed further they are distanced from the
carbohydrates substrate that was needed for the initiation of the caries.
Thus the high protein content of dentin must favour the growth of the
microorganisms.
Therefore proteolytic organisms might appear to predominate in the
deeper caries of dentin while acidophilic forms are more prominent in
early caries.

57. Advanced Dentinal Changes ;
-decalcification of walls, confluence of the dentinal tubules,
-tiny “liquefaction foci”, described by Miller are formed by the focal coalescing
and breakdown of dentinal tubules. These are ovoid areas of destruction parallel
to the course of the tubules which filled with necrotic debris and increase in size
by expanding.
The adjacent tubules are distorted and their course is bent due to this
expansion.

60. The destruction of dentin by decalcification and then proteolysis occurs in
numerous focal areas- leading to a necrotic mass of dentin of a leathery
consistency.
-clefts present in the carious dentin that extends at right angles to the
dentinal tubules, accounts for the peeling off of dentin in layers while
excavating.

62. Shape of the lesion is triangular with the
apex towards the pulp and the base
towards the enamel.
Zone 1; Zone of Fatty Degeneration of
Tome’s Fibers,(next to pulp)
-due to degeneration of the
odontoblastic process. This occurs
before sclerotic dentin is formed and
makes the tubules impermeable.
Zone 2; Zone of dentinal sclerosis,
-deposition of Ca salts in the tubules.
Zone 3; Zone of decalcification of dentin
Zone 4; Zone of bacterial invasion
Zone 5; Zone of decomposed dentin due to
acids and enzymes.

63. Root Caries
Root caries as defined by HAZEN, is a soft, progressive lesion
that is found anywhere on the root surface that has lost its
connective tissue attachment and is exposed to the environment.
-the root surface must be exposed to the oral environment before
caries can develop here.
-Plaque and micro-organisms are essential for the cause and
progression of the lesion, mostly Actinomyces,

64. -micro-organisms invade the cementum either along the Sharpey’s
fibers or between the bundles of fibers.
-spread laterally, since cementum is formed in concentric layers.
-after decalcification of cementum, destruction of matrix occurs
similar to dentin with ultimate softening and destruction of this
tissue.
-invasion of micro-organisms into the dentinal tubules, finally
leading to pulp involvement.
-the rate is slower due to fewer dentinal tubules than crown area

66.  Dark brown pigmented carious lesion , insensitive
to painful stimuli in which caries progression is
halted.

67.  ZONE 1: Surface layer- Brown in colour and of
leathery consistency.
 ZONE 2: Pigmented zone- Hard, dark brown in
colour, forming main bulk with presence of
coalesced bacteria bodies
 ZONE 3: Sclerotic layer-Hard, white zone
having highly calcified tubules with absence of
bacteria.

68.  Caries occuring beneath or around the existing
restoration.
 Histologically can occur as:
1. Outer lesion 20%
2. Wall lesion 11.9%
3. Both leisions 60% cases

70.  IN ENAMEL: A triangular outer lesion is seen which
continues with the dentinal lesion along the dentinal
wall. Both lesions are walled by dark zone.
 IN DENTIN: Appearance can be-
1. Superficial demineralization of cavity walls
2. Subsurface demineralization without visible changes of
wall surface
3. Subsurface demineralization with increased
mineralization of surface layer
4. Alternating zones of demineralization and
remineralization.

73. Dental caries is the result of the metabolic activities of bacteria in
microbial communities on teeth termed dental biofilms (often
referred to as dental plaque)
Hence, the presence of microbial communities on the
tooth surface is a prerequisite for caries lesions to
develop
Although there are different opinions as to how and which
microorganisms produce carious lesions, it is agreed that caries
cannot occur without microorganisms
73

74. The prevalence of dental caries (i.e., the
percentage of persons with >1 decayed, missing,
or filled teeth) in permanent teeth increases with
age, from 26% among persons aged 5--11 years to
67% among persons aged 12--17 years and 94%
for dentate adults (with >1 natural teeth) aged
>18 years.

76.  Complex ecology of the oral cavity.
 300 – 400 species are indigenous oral flora.
 History:
 Miller (1880): Little knowledge about bacteria.
 Clarke (1924): First who associate bacteria with dental caries
oFirst to isolate MS from human dental caries
oFirst to produce caries in extracted teeth.
 Orland (1955): Used animals to induce dental caries using
MS.

77.  1924: Clark recovered Gram-positive cells
 1960: Fitzgerald & Keyes found caries-
conducive streptococci to be Streptococcus
mutans

78.  What is virulence?
The ability of a bacterium to cause infection.
 Virulence factors: Two types:
 Those that promote bacterial colonization and
invasion of the host tissue
 Those that cause damage of the host tissue.

79.  The bacterium should be found in people with
the disease
 The bacterium should be isolated from the
lesions of infected person
 Pure culture, inoculated into a susceptible
individuals or animals should produce the
disease
 Same bacterium should be re-isolated from
intentionally infected animals or humans.

80.  Virulence is within the bacterium and is
independent of the host
 Isolation and growth of bacterium is necessary:
Yet, some pathogens not yet cultured
 Nos. 2 & 4: assume that all members of the
same species are virulent
 No. 3: Ethics with human subjects, Yet some
pathogens from humans can not cause the
same effect in animals.

81. BACTERIA
VIRUS
FUNGI
PROTOZOA
MYCOPLASMA
81
Natural microflora exists in harmonious
relationship with the host

82. Bacteria
Gram positive
cocci
Gram positive
Rods and
filaments
Gram negative
cocci
Gram negative
rods
1. Streptococc
us
2. Enterococc
us
1. Actinomyces
2. Eubacterium
3. Lactobacillu
s
4. Propionibact
erium
1. Neisseria
2. Veillonella
1. Haemophilus
2. Eikenella
3. Capnocytopha
ga
4. Actinobacillus
5. Porphyromona
s
6. fusobacterium82

83. 83
Fungi
Candida
Viruses
CMV
Coxsackie
A2,4,5,6,8,9,10 and 16
Hepatitis
HIV
Protozoa
Trichomonas tenax
Entamoeba gingivalis
Mycoplasma
M. salivarius
M. pneumoniae
M. hominis

84.  An organism must be acidogenic
 An organism must be aciduric
 An organism must exhibit tropism for teeth
 An organism must utilize refined sugar
(sucrose)
(Newburn, 1983)

86. Enamel
Pit & fissure
Dentin, Root

87. 87

88. 88

89. • Mutans Streptococci
• S. mutans
• S. sobrinus
• Viridans Streptococci
• S. mitis
• S. salivarius
• S. sanguinis

90. 90
Pit and fissure caries-
 most common carious lesions found in humans
 Fissures provide mechanical retention for the
bacteria. S mutans, S salivarius, S sanguis, L
acidophilus, L casei, A viscous, A nalsundii,
Actinomyces israelii develop fissure lesions

91. Smooth surface caries-
 A limited number of organisms have proved
able to colonize smooth surfaces in large
enough numbers to cause decay in test animals.
 Streptococcus mutans is very significant in this
respect.
91

92. Root caries-
 In rodents, gram – positive filamentous rods, including
actinomyces species have been associated with this type of
lesion
 Strains of Nocardia and S. sanguis may also cause root caries
 In cross-sectional studies of plaque overlying carious root
surfaces, mutans streptococci, alone or in combination with
lactobacilli, have been isolated more frequently or in higher
proportions than on sound root surfaces
(Billings et al., 1985; Brown et al., 1986; Fure et al., 1987; Keltjens et al., 1987;
Bowden et al., 1990; van Houte et al., 1990)
92

93. Deep dentinal caries-
 Because the environment in deep dentinal
lesions is different from that at other
locations the flora here is also different
 The predominant microbe- lactobacillus
93

94.  Secondary caries resembles Pit & Fissure caries
 3 associated microbes-
 S. mutans
 Lactobacillus
 Actinomyces viscous
 The presence in significant nos. of these bacterias in
dentin of Secondary caries indicates their role in
formation & development of Secondary carious lesions
(Gonzalez- Cabezas; 1999).
 Definite relationship between S. mutans & Secondary
caries
(Fontana et al;1996)
94

95.  Irrespective of the age of plaque and the diet, the
predominant organisms are gram-(+)ve cocci of the
genus streptococcus which form about 50% of the
total CFU recovered from young plaque
 These streptococci have been divided into various
groups based on their colonial morphology and
physiological characteristics
 Oral streptococci are isolated on Mitis-Salivaris
Agar, a selective medium that permits isolation from
mixed flora 95

96.  In 1924 Clarke isolated a streptococcus that
predominated in many human carious lesions
 He named them streptococcus mutans because
of its varying morphology
 Characteristics of S. mutans include
 Nonmotile
 Catalase negative
 Gram positive
 Cocci in short or medium chains.
 Opaque, cushion shaped colony on Mitis–
Salivarius bacitracin Agar
 Colony surface resembles frosted glass 96

97.  Adherence to teeth
 Extracellular polysaccharide synthesis
( glucan )
 Intracellular polysaccharide synthesis
 Acidogenicity
 Aciduricity

98.  TYPES: (Coykendall, 1989)
 S. anginosus : important in purulent infections
 S. bovis : found in patients with colon cancer
 S. mitis : similar to sanguis but doesn’t ferment any
sugar
 S. mutans : seven species (9 species – recent data)
 S. salivarius : in saliva, rare in infections
 S. sanguis : causes endocarditis
 S. vestbularis : new species from oral cavity.

99. Species Serotype Arg Raf Mel H2O2 Aero Baci Source
S mutans c, e, f - + + - + - Human
S rattus b + + + - + - Rats
S cricetus a - + + - - + Rats
S sobrinus d, g - - - + + - Human
S ferus c - - - - - + Rats
S macacae c - + - - - + Monkey
S downei h - - - - - + Monkey

100.  S orisus d pigs
 S orisus dentisuis p
 k

101.  Three factors:
 Ability to adhere to other bacteria and tooth surface
 Ability to rapidly metabolize nutrients (CHO)
 Ability to tolerate acidic environment.

102.  Saliva:
 Lysozyme
 IgA: (IgA protease), (IgA deficiency)
 Bacterial proteins:
 Ag I/II family: Adhere to saliva proteins
 Adhesin
 Fimbrial adhesion: Adhere to saliva pellicle
 glucan binding (GBP)

103. Pellicle glycoprotein
PBP*
(Adapted from Slots & Taubman,
1992)
*PBP: Pellicle Binding Protein
Initial Attachment
S. mutans

104. +
Sucrose Glucose Fructose
GTF-S** GTF-I*
(Adapted from Slots & Taubman,
1992)
*Insoluble form (α-1,3-linked) “Mutan” – polymerized by GtfB
**Soluble form (α-1,6-linked) “Dextran” – polymerized by GtfD
GtfC responsible for a mixture of α-1,3 & α-1,6
GTF Binding Glucans
Glucans

105. (Adapted from Slots &
Taubman, 1992)
Pellicle Glycoprotein
Glucan
Binding
Protein
Glucans
Aggregation
S. mutansS. mutans
S. mutans

106.  Through cell membrane, extrusion of protons:
 Membrane ATPase hydrolyze ATP molecules
 Hydrolysis of one ATP, results in extrusion of three
protons
 This results in elevation of cytoplasmic pH.
 When pH decreases, ATPase activity increases 4-
folds.

107.  Based on ability of S. mutans to synthesize
insoluble glucan.
 S. mutans have 3 genes:
 gtfB encodes GTF-I enzyme: insoluble glucan
 gtfC encodes GTF-SI enzyme: insoluble glucan
 gtfD encodes GTF-S enzyme: soluble glucan

108. Strain Gtase Adherence%
MT8148 I,SI/S 72.8 ± 2.6
B29 /SI/S 16.3 ± 1.0
B29 I/SI/S 46.9 ± 5.9
B58 I/ /S 9.6 ± 1.0
B58 I/SI/S 69.9 ± 1.8
B32 / /S 1.4 ± 0.4
(Fujiwara et al., 1996)

109.  Sterile mouth at birth
 S. sanguis and S. mutans colonize teeth
 Number of bacteria increases in the presence
of:
 Sucrose
 Caries
 Teeth

110. ACQUISITION OF S. mutans
Birth 5 Year
First Tooth 19 33
6.8 +/- 1.4 mo.
26
MS
N=38
Caufield et al., J Dent Res. 72:37-45, 1993.

111.  Important facts:
 Difficult to change S. mutans strain(s)
 High number of S.mutans strains and isolates.
 One (or more) strain (isolates) is/are present in the
mouth.

112. GENETIC VARIATIONS
OF S.mutans

113. Lactobacilli are -
 Gram (+)ve
 Non-spore forming
 Rods
 Grow best under microaerophilic conditions.
 Represents about 1% of the oral flora.
 Favorite habitat of lactobacilli is in the dentin
of deep carious lesions.
 Relatively low affinity for tooth surface.
113

114.  Preferentially colonize the dorsum of the
tongue
 Does NOT play a major part in initiation,
but important in progression
 With established low pH the number of
lactobacilli increases and the number of S.
mutans decreases
 Contribute to the demineralization of the
teeth once lesions are established
114

115. 115
 It is a gram positive, non motile, non spore
forming organism occurring as rods and
filaments. It is a good plaque former
 All speciesof actinomycesferment glucose,
producing mostly lactic acid, lesser amountsof
acetic and succinic acid, and tracesof formic acid.
 Most interest hascentered on A viscosusand A
naeslundii becauseof their ability to induceroot

116. 116
All speciesof actinomycesferment
glucose, producing mostly lactic acid,
lesser amountsof acetic and succinic
acid, and tracesof formic acid

117.  Anaerobic bacteria
 Taxonomically distant from streptococci but
have very similar sugar metabolism and can
produce lactic acid.
 Although well-known as gut inhabitants, it is
only quite recently that their occurrence in the
mouth and possible association with caries has
been recognized
 This change in viewpoint is because
 introduction of molecular detection methods
 the development of a selective medium using
mupiromycin to suppress growth of other bacteria 117

118. S.Mutans has the central role in etiology
of dental caries
If We understand the dental caries microbiology well, we
will be able to treat patients differently
It is of paramount value that the term “dental caries” not be
equated with “cavities” by dentists. The lesion is not the
disease, but the effect of the disease. The disease does not
occur without infection by cariogenic bacteria
To prevent, detect, and manage caries throughout life one
must not be restrictively focused on the end result of the
disease, cavities 118

119. Thank you