Dental Caries- Dr.Archana Mukunda

1. DENTAL CARIES
DR Archana Mukunda
Reader
Dept of Oral Pathology
Royal Dental College

2. • Human tooth is unique made of both mineralized
and soft tissue
• Enamel- hardest non vital tissue
• Dentin- hardest vital tissue
• Pulp- specialized connective tissue which contains
odontoblasts which form dentin throughout life

3. • Each tooth is composed of unique regional diversity
of anatomy, chemistry, sensory physiology, and
mineral and organic components that constantly
change throughout life
• Loss of tooth structure can be due to
a. Microbial- Dental caries
b. Non-microbial- attrition, abrasion, erosion

4. • The word CARIES was derived from the Latin word meaning
DECAY or ROT.
• a disease of modern civilization, prehistoric man rarely
suffered from Dental caries.
• The rate of caries remained low through
the Prehistoric era
• Periodic increases in caries prevalence occurred when Sugar
cane became more accessible to the Western world.

5. Definition
• Dental caries is an irreversible microbial disease
of the calcified tissues of the teeth,characterised
by demineralisation of the inorganic portion and
destruction of the organic substance of the
tooth,which often leads to cavitation.

6. Factors affecting caries prevalence
• Age: more in children
• Race: Less in blacks & more in whites
• Familial: Higher in mono zygotic twins
than dizygotic twins
• Sex:
More in permanent teeth of females
More in deciduous teeth of males

7. Etiology-the early theories
• Most disease was attributed to the presence of
unseen demons in the body or to an insult that
was caused against a particular god magic or
witch craft -Ruffer
• Legend of worms stated that dental caries
occurred from worms like any other disease

8. Etiology-the early theories
• Humoral theory: balance between 4 humour a)
blood, (b) phlegm, chemically. (c) black bile, and (d)
yellow bile determines mental & physical health and
imbalance causes disease.
• Vital theory: Hippocrates (460–357 BC) suggested
that caries originated from tooth itself due to normal
predisposition of tooth to filth accumulation and
hence corroding action by the same

9. Etiology-the early theories
• Aristotle (384–322 BC) observed a relationship of
eating sweets with dental caries ; soft & sweet figs
cause damage to teeth
• Chemical theory: Parmly (1820) caries is caused by
external factor & not internal. Robertson in 1935
showed that acid formation by fermentation of food
caused caries

10. Etiology-the early theories
• Parasitic theory: Erdl in 1843 was the 1st to related
micro organism and caries who showed
filamenetous organisms from membrane on tooth
Ficnus in 1847 called the tooth related micro
organism as denticolae

11. Newer theories
• Miller’s chemicoparasitic or the acidogenic
theory
• Proteolytic theory
• Proteolysis-chelation theory
• Sucrose chelation theory

12. W.D Miller’s chemicoparasitic or the
acidogenic theory-1882
• Caries is caused by acids produced by variety of
microorganisms of the mouth
• It is a chemoparasitic process consisting of two stages-
decalcification of enamel and dentin(preliminary stage)
and decalcification of the softened residue(subsequent
stage)
• Acids resulting in primary decalcificaion is produced by
the fermentation of starches and sugar from the
retaining centers of teeth

13. W.D Miller’s chemicoparasitic or the
acidogenic theory-1882
• Caries is caused by acids produced by
microorganisms of the mouth.
• DC is a chemoparasitic process consisting of two
stages- decalcification of enamel and
dentin(preliminary stage) and decalcification of the
softened residue(subsequent stage)
• Acids resulting in primary decalcificaion is produced
by the fermentation of starches and sugar from the
retaining centers of teeth.

14. W.D Miller’s chemicoparasitic or the
acidogenic theory-1882
• Caries is caused by acids produced by
microorganisms of the mouth.
• DC is a chemoparasitic process consisting of two
stages- decalcification of enamel and
dentin(preliminary stage) and decalcification of the
softened residue(subsequent stage)
• Acids resulting in primary decalcificaion is produced
by the fermentation of starches and sugar from the
retaining centers of teeth.

15. Keyes triad
Host
Substrate
Parasite

17. Role of Micro organisms
• Enamel caries- streptococcous mutans,
sanguis, mitis, salivarius, sobrinus
• Dentinal caries- Lactobacillus acidophillus
• Root caries- Actinomyces viscosus,
maeslundii, israelli, odontolyticus

18. Role of Carbohydrates
• Refined diet containing fermentable carbohydrates
• Dietary carbohydrate is involved and not salivary
carbohydrate
• Cariogenicity depends on
Frequency of ingestion
physical form
chemical composition
route of administration
presence of other food constituents

19. BACTERIA+SUGARS+TEETH ORGANIC
ACIDS CARIES

20. Role of Acids
• Bacteria degrades carbohydrate to form acids
• Lactic acid is the chiefly formed acids
• Other acids formed in small amounts are butyric
acid, succinic acid, propionic acid, ethanol, acetic
acid etc
• Homofermentative- which form 90% or more lactic
acid eg streptococci & lactobacillus
• Heterofermentative- form mixture of acids

21. • Accumulation of acid is greater by S mutans than
other strains
• Actinomyces are gram + rods
anaerobic conditions is homolactic
in Co2 presence is heterolactic

22. Streptococcus mutans : Gram + cocci arranged as
chains, isolated by Clark in 1924
• Are actively involved in caries initiation
• are highly localized on the surfaces of the teeth and
their abundance in the plaque is highest over initial
lesions
• their level of colonization within the plaque is
increased by sucrose consumption
• They do not colonize in mouth prior to the
eruption of teeth and after disappearance of teeth

23. • they synthesize insoluble macro-molecules from
sucrose that advance their attachment to the teeth
• Sucrose transport inside the cell is associated with
direct phosphorylation by glycolytic pathway
glucose – Glucans
Sucorse
Fructose- Fructans
Fructosyl transferase
Glycosyl transferase

24. • Glucans ( mutans & dextrans)- is insoluble,
extracellular adhesive fibrillar polymer moe
resistant to enzymatic attack, which helps in
accumulation of S mutans
• Fructans- Soluble , serves as a reservoir of
fermentable sugars for oral bacteria
• They form highly negatively charged lipotechoic
acid an extra cellular polymer contributing to
adhesiveness

25. • They store intracellular glycogen called
amylopectin
• Both intracellular & extracellular polysaccahrides
act as reservior prolonging glycolysis beyond meal
time
• They contain enzyme invertase which is activated
by inorganic phosphate to degrade sucrose into
glucose & fructose

26. • They form insoluble polysaccharides, more
aciduric, homo fermentative than other oral
streptococci
• Lactobacilli are gram + rods, anaerobic
• grows best at low pH; are aciophillic & aciduric
• S mutans provide favorable acid enviornment for
growth of lactobacilli
• L casei & L acidophilus are homofermentators
• L fermentum & L brevis are heteroferementators

27. • They are mainly responsible for caries progression
as they cannot adhere to the tooth surface
• Found more in deep dentinal caries

28. Lactobacilli
Streptococci

29. Role of dental plaque
• Tooth surface cannot shed like oral epithelium
• Pellicle- salivary glycoprotein adsorbed onto tooth
surface ; acts as double sided adhesive tape
• Plaque – pellicle + bacteria
• Dental plaque or microcosm = mucin,
desquamated epi cells, micro organism
• Tenacious thin film accumulated on surfaces not
constantly cleansed for 24-48hrs

30. • Bacteria & teeth have negatively charged surfaces
but are attracted by Vander waals forces which is
weak
• The polymers present on the surface of the bacteria
help in attaching the bacteria to the tooth surface
by ionic, hydro phobic or hydrogen bonds
• Techoic acid present in the cell wall may form
bridges with calcium ions onto pellicle surface

31. • Bacteria have specific receptors called adhesins
which bind to specific receptors on pellicle
• Adhesins which bind to sugar are called lectins
• Hydroxyapatite crystal in tooth = saliva is seen in
equillibrium
• In neutral pH, HA crystals dissolve to release
calcium, phosphate and hydroxyl ions the saliva is
supersaturated with calcium, phosphate and
hydroxyl ions which is deposited back onto tooth

32. • In acidic pH saliva is under saturated with
phosphate ions so HA crystals are dissolved from
tooth to re saturate saliva
• The ‘critical pH’ is the pH at which a solution is
just saturated with respect to a particular mineral.
For the HA crystal, it is approximately 5.5–6,
below which the enamel disintegrates.
• Critical pH for FA is 4.5

33. Streptococcus sobrinus produces a virulence-
associated immunomodulatory protein (VIP)
called enolase which suppresses the host-specific
immune response
It differs from S mutans
> requires sucrose for attachment and growth
in plaque
> lacks adhesins required for sucrose
independent attachment ; hence can grow on
smooth surface

34. Draw backs of theory
• Unable to explain specific site predilection
• Initiation of smooth surface caries
• Concept of dental plaque was later added in 1897
by William’s
• Does not explain why some population is caries
free
• The occurrence of arrested caries

35. PROTEOLYTIC THEORY
• The evidence given by the acidogenic theory was
considerable but it was not conclusive, and
alternative explanation was given in the form of
proteolytic theory by Gottlieb and Gottlieb 1944.
• Workers like “Heider, Bodecker (1878)and Abbott
(1879) contributed considerably to this theory

36. • Protelytic enzymes produced by the bacteria
destroy the organic matrix of enamel thereby
loosening the apatite crystal
• Hypocalcified structures in enamel like enamel
lamelle and enamel rods as thought to be path ways
for the advancing microorganisms

37. • It has been established that enamel contains 0.56 % of
organic matter of which 0.18% is keratin and 0.17 % is
a soluble protein
• Microorganisms invade the enamel lamelle and the
acid produced by the bacteria's causes damage to the
organic pathways in advance
• Yellowish pigment produced by the proteolytic
bacteria’s was only possible in the presence of dietary
carbohydrates.

38. Draw backs of the theory
• It couldn’t provide sufficient evidences to support the
claim that the initial attack on enamel is proteolytic
• It is not possible to produce caries in vitro using
proteolytic agents
• Proteolytic enzymes produced in plaque are capable of
producing periodontal disease
• However , this theory is still helpful in explaining the
progression of a more advanced carious lesion.

39. PROTEOLYSIS CHELATION THEORY
• Some of the minor flaws of the acidogenic and the
proteolytic theory were addressed in the
proteolysis chelation theory
• This theory was put forward by Schatz 1955 and
his co-workers

40. CHELATION
It is a process in which there is complexing of the
metal ions to form complex substance through
coordinate covalent bond which results in:
poorly dissociated /or
weakly ionized compound

41. • Hemoglobin in which 4 pyrrole nuclei are linked
to iron by a similar bond
• Chelation is independent of the pH of the medium.
• keratinolytic microorganisms attack enamel
resulting in the breakdown of the protein chiefly
keratin and results in the formation of soluble
chelates which decalcify enamel even at neutral pH
• Mucopolysaccarides may also act as secondary
chelators

42. Sucrose chelation theory
• Was proposed by Lura in 1967
• High content of sucrose in the oral cavity results in
formation of complex substance like calcium
saccharate by the action of phosphorylating
enzymes by bacteria
• These substances causes release of calcium and
phosphorous from enamel

43. Autoimmune theory
• Proposed by Burch and Jackson 1970
• Genes partly inherited and partly mutated
determine whether a site on tooth is at high risk or
low risk
• Odontoblasts may be the target in caries, which
may change the resistance of enamel to acid attack
• rejected theory based on epidemiology

44. Sulfatase theory
• Proposed by Pincus et al in 1950
• Bacteria in plaque producing sulfatase enzyme
hydrolyse mucotin sulfate of enamel and
chondrotin sulfate of dentin
• This results in formation of sulfuric acid which
decalcifies
• The amount of mucotin sulfate in enamel is very
less and not available for degradation

46. Caries susceptibility incidence of the
teeth
•Upper and lower 6s  95%
•Upper and lower 7s  75%
•Upper 5s  45%
•Upper 4s and lower 5s  35%
•Upper 1s and 2s  30%
•Upper 3s and lower 4s  10%
•Lower 1s ,2s and s  3%

47. CLINICAL FEATURES
• Chalky white spot on surface of tooth; indicates
area of demineralization (350-500µ); reversible
• The lesion may become brown as demineralization
progresses and turns into a cavity; irreversible
• The affected part of tooth is soft to touch
• Once caries reaches DEJ symptoms such as
sensitivity or pain can be felt
• Some times caries can be arrested and appear
brown and shiny

49. CLINICAL CLASSIFICATION OF CARIES
Based on anatomical site
-pit and fissure caries
-smooth surface caries
-linear enamel caries
-cervical caries
-root caries
Based on rapidity of caries progression
-acute dental caries
-chronic dental caries

50. Based on age
-infancy/nursing bottle caries
-adolescent caries
Based on whether it is new or recurrent
-primary/virgin caries
-secondary/recurrent caries

51. Pit and Fissure caries
• Occlusal surfaces of molars and premolars
• Buccal and lingual surfaces of molars, lingual
surface of maxillary incisors
• Among children, pit and fissure caries represent
90% of all dental caries
• As the decay progresses, caries in enamel nearest
the surface of the tooth spreads gradually deeper
• Once the caries reaches the dentin at the DEJ, the
decay quickly spreads laterally

52. • Within the dentin, the decay follows a triangle
pattern that points to the tooth's pulp
• This pattern of decay is typically described as two
triangles (one triangle in enamel, and another in
dentin) with their bases conjoined to each other at
the DEJ. This base-to-base pattern is typical of pit
and fissure caries, unlike smooth-surface caries
(where base and apex of the two triangles join).

55. Smooth surface caries
• Proximal caries, also called interproximal caries,
form on the smooth surfaces between adjacent
teeth below contact area
• May occur on gingival 3rd of buccal & lingual
surfaces of any other smooth tooth surface

57. NURSING BOTTLE CARIES
• Baby Bottle syndrome, bottle mouth syndrome,
nursing caries, bottle caries, infant caries, early
childhood caries etc
• Occurs as a result of inappropriate feeding of
children
• A form of rampant caries affecting the deciduous
dentition

59. Etiology
• Prolonged use of nursing bottle containing juice,
milk, milk formula, or any other liquid sweetened
with fermentable carbohydrates.
• Prolonged breast feeding, sugar or honey
sweetened pacifiers
• The stagnation of fluid in the neck of anterior teeth
leads to fermentation of the carbohydrate which
produces acid causing caries

60. • Causes wide spread destruction of deciduous
teeth, usually the maxillary incisors followed by 1st
molar then cuspid
• Caries does not affect the mandibular teeth as they
are covered by tongue

61. ROOT CARIES
• Root caries is defined by Hazen as a
soft, progressive lesion that is found
anywhere on the root surface that has
lost connective tissue attachment and is
exposed to the oral environment
• Earlier referred to as cemental caries
• Predominant in the elderly
• usually occur when the root surfaces
have been exposed due to gingival
recession

63. • When the gingiva is healthy, root caries is
unlikely to develop because the root surfaces are
not as accessible to bacterial plaque. The root
surface is more vulnerable to the
demineralization process than enamel because
cementum begins to demineralize at 6.7 pH,
which is higher than enamel's critical pH
• Regardless, it is easier to arrest the progression of
root caries than enamel caries because roots have
a greater reuptake of fluoride than enamel.

64. • Root caries is most likely to be found on facial
surfaces, then interproximal surfaces, then
lingual surfaces. Mandibular molars are the
most common location to find root caries,
followed by mandibular premolars, maxillary
anteriors, maxillary posteriors, and mandibular
anteriors.

65. Rampant caries
• Rampant caries signifies advanced or severe
decay on multiple surfaces of many teeth
• Rampant caries may be seen in individuals with
xerostomia, poor oral hygiene, stimulant use
(due to drug-induced dry mouth), and/or large
sugar intake.

66. • If rampant caries is a result of previous radiation
to the head and neck, it may be described as
radiation-induced caries
• Problems can also be caused by the self
destruction of roots and whole tooth resorption
when new teeth erupt or later from unknown
causes

68. Radiation caries
• Form of rampant caries occuring in patients
undergoing radiation therapy of head & neck
• Xerostomia , increase in viscosity & low pH of
saliva
• Causes brown or black discoloration of crown or
disintegrating the crown as irregularly shaped
discolored stump or complete amputation of neck
of tooth

69. Acute caries
• Runs a rapid clinical course & results in early
pulp involvement
• Seen in children & young adults- as dentinal
tubules are open & show no sclerosis
• The caries is so rapid that there is little or no
time for reparative dentin deposition

70. • The initial entry is small & rapid spread at DEJ ,
large involvement of dentin with large internal
excavation
• Lesions are light yellow in color
• Is usually associated with pain

71. Chronic caries
• That form of caries which progresses slowly and
tends to involve pulp much later than acute
caries
• The entrance to the lesion is almost invariably
larger than that of acute caries
• Common in adults; appears dark brown in color
• Allows sufficient time for both dentinal sclerosis
and secondary dentin deposition

72. Arrested caries- describes as a lesion
which becomes static without further
progression

73. • Affects both dentitions
• Occurs in large open cavities with lack of food
retention and in which the superficially softened
and decalcified dentin is gradually burnished until
it takes on a brown stained, polished, appearance
and is hard
• This is called eburnation of dentin

74. • Sclerosis of dentinal tubules and secondary dentin
formation occurs
• Another form seen on proximal surfaces of teeth in
which adjacent teeth have been extracted,
revealing a brown stained area at or just below
contact point

75. Recurrent caries
• Recurrent caries, also described as secondary,
are caries that appears at a location with a
previous history of caries. This is frequently
found on the margins of fillings and other dental
restorations.

76. Histopathology of dental caries

77. • As the enamel loses minerals, and dental caries
progresses, the enamel develop several distinct
zones, visible under a light microscope. From
the deepest layer of the enamel to the enamel
surface, the identified areas are the:
• Zone 1-translucent zone
• Zone 2-dark zone
• Zone 3-body of the lesion
• Zone 4-surface zone

80. TRANSLUCENT ZONE
Zone of Initial demineralization
• More porous than the normal enamel; pore
volume is 1%
• These pores are larger than the normal enamel.
• Chemical analysis show that there is a fall in the
magnesium and carbonate content as compared to
the normal enamel
• Zone may not always present

81. • In this zone , pores or voids form along the enamel
prism(rod) boundaries (due to easy H+ ion
penetration)
• It appears structureless when perfused with
quinolone solution (having refractive index
comparable to that of enamel) and seen with
polarized light (hence translucent)

82. Dark zone
• Called as positive zone
• This zone contains 2-4% by volume pores
• Does not transmit polarized light
• Smaller air filled pores make the region opaque as
quinoline cannot enter into smaller pores

83. • The smaller size of the pores may form a sieve like
structure preventing escape of minerals helping in
remineralization

84. Body of the Lesion
• This zone has pore volume of 5% periphery -25%
center
• It contains appetite crystals larger than the normal
enamel
• more of an effort for the remineralization but by the
further attack there is further dissolution of the
mineral
• Thus this is the zone of maximum demineralization

85. Surface zone
• This is about 40 micrometer thick
• Relatively unaffected by caries
• Pore volume less than 5%
• Radiopaque
• Hypermineralized

86. Smooth surface caries

87. Smooth surface caries
Early macroscopic changes
- An area of decalcification
- White spot
- Brown spot
Early microscopic changes
- Accentuation of Striae of Retzius
- Accentuation of perikymata

88. Pit & Fissure caries

89. Zones of dentinal caries
• Zone 1- zone of fatty degeneration of Tome’s fibres
• Zone 2- zone of dentinal sclerosis characterised by
deposition of calcium salts in dentinal tubules
• Zone 3- zone of decalcification of dentin,a narrow
zone ,preceding bacterial invasion
• Zone 4- zone of bacterial invasion of decalcified
but intact dentin
• Zone 5- zone of decomposed dentin

90. Zone 1: zone of fatty degeneration of Tomes’ fiber
• the most advancing front of dentinal caries
• characterized by the presence of a layer of fat
globules ; hence stains red with the stain, sudan red
• significance: 1) fat layer leads to impermiability of
the dentinal tubules (DT) – trying to prevent
further invasion of carious lesion
2) favors sclerosis of dentin in zone 2.

91. Zone 2: zone of dentinal sclerosis
• layer of sclerotic dentin which appears white in
transmitted light
• calcification of DT as a reaction of vital pulp and
vital dentin to carious invasion , so as to prevent
further penetration of microorganisms
• formation of this zone is minimal in rapidly
progressing caries, and prominent in slow caries

92. Zone 3: zone of decalcification of dentin
• this zone lies above the zone of sclerotic dentin
• initial decalcification of only the walls of the DT
• presence of PIONEER BACTERIA- first of the
microorganisms penetrating DT before there is any
clinical evidence of caries
• Bacteria present in individual DT are in pure form
(i.e. either completely cocci or completely bacilli;
not in mixed form)

93. Zone 4: zone of microbial invasion
• Is a layer above zone 3
• Characterized by the presence of microorganisms
• in early stage of caries- acidogenic microorganisms
• in deeper layer- proteolytic microorganisms replace
acidogenic bacteria
• supports the hypothesis that initiation (by acidogenic
bacteria) and progression ( by proteolytic
microorganisms ) are 2 distinct processes in caries
development

94. • During initiation phase- in the early stage when
caries is not deep , acidogenic bacteria predominant
which utilizes carbohydrate for their metabolism
• Later in progression phase – as the caries goes
deeper , less and less of carbohydrate substrate
available , hence acidogenic bacteria are replaced
by proteolytic microorganisms which uses dentinal
protein for their metabolism

95. Zone 5: zone of decomposed dentin
• Most superficial zone of early dentinal caries
• no recognizable structure in decomposed dentin
• collagen and minerals seem to be absent
• great number bacteria dispersed in this
decomposed granular matter
• Diameter of dentinal tubules increases as it is
packed with bacteria

96. • Focal coalescence & breakdown of few dentinal
tubules form tiny liquefactive foci – a ovoid area
of destruction parallel to dentinal tubules filled
with necrotic debri
• This produces compression & distortion of DT &
their course in bent around liquefactive focus
• Numerous focal areas coalesce & give leathery
consistency to necrotic mass of dentin

97. • Transverse clefts are seen in this necrotic dentin
extending at right angles to dentinal tubules
• Occurs due to extension of carious process along
lateral branches of tubules
• These clefts are seen parallel to the contour lines of
dentin
• This allows peeling away dentin in layers with a
hand instrument

98. Thickening of
dentinal
tubules

99. Liquefactive foci

101. Transverse cleft

103. ROLE OF FLUORIDES
IN DENTAL CARIES

104. • Fluoride is the ionic form of the element fluorine, the
13th most abundant element in the earth's crust
• Fluoride is negatively charged and combines with
positive ions (e.g., calcium or sodium) to form stable
compounds (e.g., calcium fluoride or sodium fluoride)
• In humans, fluoride is mainly associated with
calcified tissues (i.e., bones and teeth) because of its
high affinity for calcium

105. • Fluoride reduces the incidence of dental caries and
slows or reverses the progression of existing lesions
• Fluoride concentrated in plaque and saliva inhibits the
demineralization of sound enamel and enhances the
remineralization (i.e., recovery) of demineralized
enamel
• As acids are produced by bacteria fluoride is released
from plaque which takes up calcium and phosphate
released by demineralization

106. • Fluoride is taken up more readily in demineralized
enamel than sound enamel
Functions of fluoride
• concentrates in dental plaque and inhibits cariogenic
bacteria from utilizing the carbohydrate to produce
acid
• Also reduces adhesive polysaccharides produced by
bacteria
• Fluorapatite crystals are more resistant to acid attack
crtical pH is 4.5

107. • Fluoride can be supplemented as water, salt, milk
fluoridation & topical appilication
• Fluoride works primarily via topical mechanisms
which include
a. Inhibits demineralization at the crystal surfaces in the
tooth
b. Enhances remineralization at the crystal surfaces
inhibition of bacterial enzymes

109. AIDS FOR CARIES
DETECTION

110. Caries Diagnosis
• The primary aim of effective diagnosis and
treatment planning is early detection of incipient
caries and interception of carious process before
significant amount of tooth destruction occurs.
Various diagnosis methods are available to detect
caries activity at early stages:-
• Identification of subsurface demineralization
(inspection, radiography and dye uptake methods)
• Bacterial testing
• Assessment of environmental conditions such as
pH, salivary flow and salivary buffering.

111. • Visual- good in detecting lesions but does not give
good results for non cavitated caries
• Visual & Tactile- probe or explorer is used along
with visual- may lack preventive
• X- rays- is a vital tool to detect occult proximal
caries and depth of the lesion

112. Explorer
Dental floss
Radiographs

113. Fiber-optic transillumination test (FOTI)-
• This device is based on the principle of light
scattering
• Light is scattered more in a carious tissue than in a
non-carious tissue, it is observed as a dark shadow
against a light background
• 1st used for detection of anterior proximal lesions
now used for posterior proximal lesions

114. Transillumination
Digital imaging

115. Digital imaging fiber-optic transillumination
(DIFOTI)
• The device works on the same principle of light scattering,
but the human eyes are replaced by CCD intraoral camera
to capture the image and instantly project in the monitor
• Laser/Light-induced fluorescence Diagnodent - sound
enamel & dentin and carious lesion have auto fluorescence
due to presence of chromophores ; The difference in the
fluorescing capacity of the sound tooth and the carious
lesion can be recorded or observed

116. Digital Substraction
radiography
Diagnodent

117. • Electrical caries meter (ECM)- The electrical
conductivity of a normal tooth is less compared to
a demineralized lesion; as electrical conductivity
increases after porous enamel is filled with ionic
fluid
• Caries detecting dyes- uses protein dye acid red
Which stains the organic matrix of less mineralized
dentin & differentiates between infected & non
infected dentin

118. Caries detecting
dyes

119. CARIES
VACCINE

120. • Caries vaccine is a vaccine used to prevent & protect
tooth against caries
• S mutans is the main etiological agent hence vaccine
are developed against it
• S mutans cell surface contains adhesins, GTFs, and
glucan binding proteins (GBP). These substances are
used as antigens for vaccine preparation
•

121. • Antibodies against these antigens block adherence of S
mutans onto HA crystal
• antibodies formed are S-IgA Antibodies in saliva (secretory
immune system) or IgG or IgM (systemic immunity)
• In GCF its mainly S-IgA

122. • Antibody with specificity for S. mutans adhesins
interferes with bacterial adherence  prevent dental
caries
• Antibody directed to GTF: interferes with activity of
the enzyme and thus plaque formation
• Antibodies against GBP prevents ability of mutans
strep to bind to glucans
• Antibodes against dextranase prevents convertion of
glucans into glucose for glycolysis

123. • Caries vaccines can be given by
1. mucosal route like oral, intranasal, tonsillar,
minor salivary glands, rectal routes
2. adjuvants
cholera toxin subunits
monophosphoryl lipid A
3. recombinant vaccines
cloned antigens
recombinant vector

124. • The antigen stimulate the immune system thereby
producing antiobodies S Ig A

125. Problems with caries vaccine
• Not known how to generate long-term IgA
response to antigens
▫ Studies of rodents and humans show periods of
elevated IgA levels for weeks/months (would require
frequent “booster” innoculations)
 Argument that even delayed infection of S. mutans
would be beneficial since newly erupted teeth are more
susceptible to cariogenic attack than teeth that had
more time to mature (calcification)

126. Caries control measures
•Chemical
•Mechanical
•Nutritional

127. Chemical
1)Substances that alter tooth surface structure
• Fluorides-topical,water
fluoridation,tablets,drops,dentifrices,mouthwashes
• Bisbiguanides-chlorhexidine
• Silver nitrate.zinc chloride,potassium ferrocyanide

128. 2)Substances which interferes with carbohydrates
metabolism through enzymatic alteration
• Vitamin K
• Sarcoside
3)Substances which interfere with bacterial growth
and metabolism
• Urea and ammonium compounds
• Chlorophyll
• Nitrofurans
• Penicillins
• Other antibiotics

129. Nutritional
restriction of refined carbohydrates

130. Mechanical
• Dental prophylaxis
• Tooth brushing
• Dental flossing
• Detergent foods
• Chewing gums
• Pit and fissure sealants

132. Treatment
• The goal of treatment is to preserve tooth structures
and prevent further destruction of the tooth.
• Dental restoration Restorative materials include
dental amalgam, composite resin, porcelain, and
gold .
• When the decay is too extensive, there may not be
enough tooth structure remaining to allow a
restorative material to be placed within the tooth.
Thus, a crown may be needed. This restoration
appears similar to a cap and is fitted over the
remainder of the natural crown of the tooth. Crowns
are often made of gold, porcelain, or porcelain fused
to metal.

133. • In certain cases, endodontic therapy may be
necessary for the restoration of a tooth.
Endodontic therapy, also known as a "root canal",
is recommended if the pulp in a tooth dies from
infection by decay-causing bacteria or from
trauma. During a root canal, the pulp of the
tooth, including the nerve and vascular tissues, is
removed along with decayed portions of the
tooth. The canals are instrumented with
endodontic files to clean and shape them, and
they are then usually filled with a rubber-like
material called gutta percha. The tooth is filled
and a crown can be placed. Upon completion of a
root canal, the tooth is now non-vital, as it is
devoid of any living tissue.

134. • An extraction can also serve as treatment for dental
caries. The removal of the decayed tooth is
performed if the tooth is too far destroyed from the
decay process to effectively restore the tooth.
Extractions are sometimes considered if the tooth
lacks an opposing tooth or will probably cause
further problems in the future, as may be the case
for wisdom teeth.Extractions may also be preferred
by patients unable or unwilling to undergo the
expense or difficulties in restoring the tooth.

136. Caries activity and susceptibility
• Caries activity refers to the increment of active
lesions new or recurrent over a stated period of
time.
• Caries susceptibility refers to the inherent
tendency of the host and target tissues,the tooth
to be afflicted by the caries process.

138. Caries activity tests Caries susceptibility
tests
• Lactobacillus
colony test
• Colorimetric
Snyder test
• Swab test
• Salivary
streptococcus
mutans level test
• Enamel solubility
test
• Salivary reductase
test

139. T
H
A
N
K
Y
O
U