Dental Caries

PRESENTED BY:
RAM KUMAR ADHIKARI
B.D.S. 4th BATCH (3rd YEAR)
KDCTH

CONTENTS
 Introduction of dental caries.
 Pre disposing factors of dental caries.
 Different types of dental caries.
 Diagnosis of dental caries.
 Prevention of dental caries.

INTRODUCTION OF DENTAL CARIES
• 'Caries' is Latin for 'rot' or ‘decay’.
• Dental caries means rotten or decayed teeth.
• Caries is the noun which names the disease.
• Carious is the adjective, not 'a caries’, 'a carious
area' or 'an area of caries'.
• Benjamin Franklin stated that “ hot things, sharp
things, sweet things, cold things, all rot the teeth
and make them look like old things”.

HISTORICAL BACKGROUND
• Dental caries is considered as a ‘disease of modern
civilization’.
• Prehistoric man rarely suffered from tooth
destruction.
• Pre Neolithic periods(12,000 BC ) anthropological
studies revealed that dolicocephalic skulls did not
exhibit dental caries.

HISTORICAL BACKGROUND (contd.)
• Neolithic periods(12,000 to 3000 BC) skulls
from brachycephalic man showed carious
teeth.
• Caries in prehistoric man(3000 to 750 BC).
• Pithecanthropus- earliest known ancestors,
there was no evidence of dental caries.
• Evidence of caries was found in skulls of
prehistoric race who lived in central Europe
about 15,000 yrs ago.

DEFINITION
• According to WHO- Dental caries is a microbial
multifactorial disease of calcified tissue of teeth,
characterized by demineralization of the inorganic
portion and destruction of organic content.
MICROBIOLOGY
1. Bacteria involved :
• Streptococci e.g. mutans, sobrinus
• Lactobacilli e.g. acidophilus
2. Possibly associated bacteria :
• Steptococci e.g. mitis
• Actinomyces e.g. viscosus

CARIOGENIC PROPERTIES OF
MICROORGANISM
• They are able to produce acid rapidly from fermentable
carbohydrates (acidogenic).
• They thrive under acid conditions (aciduric).
• Produce extracellular and intracellular polysaccharides
which contribute to the plaque matrix; intracellular
polysaccharides can be used for energy production and
converted to acid when sugars are not available

VARIOUS FACTORS INFLUENCING THE
PROGRESSION OF CARIES
• Bacteria in dental plaque
• Substrate such as a fermentable carbohydrate
(dietary sugars)
• A susceptible tooth surface
• Time

ROLE OF PLAQUE
• Plaque is an adhesive layer which deposits on the surface
of the tooth and has colonies of bacteria.
• It prevents the escape of acid into the saliva.
• It protects acid from buffering action of saliva due to its
diffusion limiting properties.
• In 2weeks the plaque is mature but there are considerable
site-to-site variations in its composition. Each site can be
considered as unique and these local variations may explain
why lesions progress in some sites but not others in the
same mouth.

ROLE OF PLAQUE (contd.)
In the upper picture, a disclosing agent reveals the plaque,
while in the lower picture the plaque has been removed.
White spot lesions are visible on the canines, but not on other
tooth surfaces, although plaque is present.

ROLE OF CARBOHYDRATE
• Caries prevalence is low in populations adhering to a
primitive way of living and a diet of local products
with little sugar.
• A drastic increase in caries is invariably seen when
these population “improve "their standard of living
and adopt a modern “civilized "diet with high sugar
content.
• A strong correlation between caries development
and sugar consumption.
• Refined carbohydrates are more caries producing
than crude carbohydrates.
• Bacteria +Sugars +Teeth → Organic acids → Caries

ROLE OF CARBOHYDRATE (contd.)
More
availability of
substrate for
bacteria
More chances
of CARIES
Diffusion in
plaque due to
low molecular
weight
Acid formation
•Aspartic acid
•Butyric acid
•Glutamic acid
Demineralization
of teeth
CARBOHYDRATE
Synthesis of polysaccharide
•Glucan from glucose
•Levan from fructose
•Dextran from sucrose
Holding the plaque
over the tooth
surface
CARIES

• The carbohydrate rapidly diffuse in the plaque
and fermented to form acids there. So, pH at the
surface of tooth falls below critical level causing
rapid demineralization of enamel.
• The plaque remains acidic for some time, taking
30–60 min to return to its normal pH in the
region of 7.
• The curve drawn for pH during carbohydrate diet
is termed as Stephan’s curve.

The shaded area represents the risk of carious attack to
the tooth surface: this area is larger in a patient with
extensive caries.
Stephan’s curve.

A SUSCEPTIBLE TOOTH SURFACE
• Surface enamel is more resistant to caries than subsurface
enamel.
• Surface enamel has high mineral content as fluoride, zinc,
lead and iron.
• Hypoplastic enamel, deep narrow occlusal fissures, buccal
or lingual pits predispose tooth to develop caries.
Enamel hypoplasia Occlusal pits and fissures

A SUSCEPTIBLE TOOTH SURFACE
(contd.)
• Attrition at occlusal surface causes lesser chance of
caries.
• Rotated, malaligned, out of positioned, teeth are
difficult to clean and favour the development of caries.
• Under normal conditions, the tooth is continually
bathed in saliva. It is capable of remineralizing the early
carious lesion because it is supersaturated with Ca and P.
• When salivary buffering capacity has been lost, a low Ph
environment is encouraged and persists for longer
duration causing demineralization of enamel.

TIME
1. It is evident that the mere existence of the
three factors operating together does not
result in instantaneous mineral loss.
2. Therefore a fourth circle is often added to
stress the time dimension taken for dental
caries to develop.

Microorganisms
Host
&
tooth
Substrate
Time
Caries
The four circle diagrammatically represent
the parameters involved in the carious
process. All four factors must be acting
concurrently (overlapping of the circles) for
caries to occur.

OTHER FACTORS
• Age
• Sex
• Geography
• Race
• Economics status
• Nutrition
• Health status

Schematic illustration of the determinants of the caries process.
Those that act at the tooth surface level are found in the inner
circle, while the more distant determinants are found in the outer
circle. (Adapted from Fejerskov and manii, 1990)

THEORIES OF CARIES
FORMATION
• Early theories:
The legend of the worm
• Endogenous theories:
Humoral theories
Vital theories
• Exogenous theories:
Chemical (acid) theory
Parasitic (septic) theory
Chemicoparasitic (acidogenic)
theory
Proteolytic theory
Proteolysis chelation theory
Sucrose chelation theory
• Other theories:
Sulfatase theory
Autoimmune theory

THEORIES OF CARIES FORMATION(contd.)
There is no universally accepted opinion of the etiology of
dental caries. Various theories have been proposed from
time to time to study the caries formation.
EARLY THEORIES OF CARIES ETIOLOGY
The legend of the worm theory:-
• Earliest reference of tooth decay and toothache came
from the ancient Sumerian text known as ‘the legend of
the worm’.
• In Japanese the word for dental caries is ‘mush – ha
(mushi – room; ha – tooth), meaning hollow tooth.
• The same terminology is employed by the Chinese; the
word for hollow tooth is ‘chung Choo’.

The legend of the worm (contd.)
• The early history of India, Egypt and the writing
of Homer and popular lore also make reference
to the worm as the cause of toothache.
• Remedy for toothache –mix beer, plant known as
Salkilbir and oil together and put it on the tooth.
• Fumigation devices continued to be used in
England late 19th century.
• An interesting therapeutic method applied by the
Chinese about 2700 BC for the treatment of
various disease including dental tissues was
acupuncture.

ENDOGENOUS THEORIES
A. Humoral Theory:
Greek physicians advanced the humoral theory of
disease.
The ancient Greeks considered that a persons physical
and mental constitution was determined by the relative
proportions of the four elemental fluids of the body
which correspond to the four humors,
• Blood Sanguine
• Phlegm Phlegmatic
• Black bile Melancholic
• Yellow bile Choleric
Hippocrates, ‘the father of medicine’, while favoring the
concept of humoral pathology also referred to the
accumulated debris around teeth and to their corroding
action. He also stated that stagnation of juices in the
teeth was the cause of toothache.

ENDOGENOUS THEORIES (contd.)
B. Vital Theory:
A vital theory of tooth decay was advanced
towards the end of the 18th century, which
postulated that tooth decay originated, like
bone gangrene form within the tooth itself.

EXOGENOUS THEORIES
A. Chemical (Acid) theory:
• In the 17th and 18th centuries paralleling new
insights into chemistry, there emerged the concept
that teeth are destroyed by acids formed in the
oral cavity.
• Robertson proposed that dental decay was caused
by acid formed by fermentation of food particles
around teeth.
• Since fermentation was at this considered to be a
strictly non- vital process, the possibility that
microorganisms were involved was not, as yet
recognized.

EXOGENOUS THEORIES (contd.)
B. Parasitic or Septic Theory
In 1843 – filamentous parasites are removed
from carious cavities.
Dental caries was thought to develop as a
result of the infiltration and decomposition of
the enamel cuticle, the inter prismatic
substance of enamel and finally dentin.

C. Miller’s Chemicoparasitic Theory
(Acidogenic theory)-1884
Theory states that caries is caused by acids produced
by microorganisms of the mouth.
Miller was student of Koch and his extensive studies
of the oral micro flora and its relationships to caries
were greatly influenced by Koch and other scientists
of the day. Form Koch he learned to isolate, stain
and identify bacteria.

Miller’s Chemicoparasitic Theory (Acidogenic
theory) -contd.
• At this time, Pasteur had discovered that the process of
conversion of sucrose to lactic acid is mediated by micro
organisms.
• This enabled Miller to assign to oral microorganisms the
rule of acid formation and thus assigned a chemical role
to flora which is the basis of his Chemicoparasitic theory
of dental caries.
• He published the results of his studies in 1882. He
formulated the hypotheisis in which he stated: Dental
decay is a chemico parasitic process consisting of two
stages, entitled text “Die Mikroorganismen der
Mundhohle”.

Miller’s Chemicoparasitic Theory (Acidogenic
theory) -contd.
•The decalcification of enamel results in its total
destruction. Decalcification of dentin, as a
preliminary stage, followed by dissolution of
the softened residue.
•The acid which affects this primary
decalcification is derived from the fermentation
of starches and sugar lodged in the retaining
centers of the teeth.

D.The Proteolytic Theory-1956
• Mature enamel is more highly mineralized tissue. The human
tooth contains about 1.5% to 2% organic material, of which
0.3% to 0.4% is protein i.e. glycoprotein.
• According to the PROTEOLYTIC THEORY, the organic component
is most vulnerable and is attacked by hydrolytic enzymes of
microorganisms. This precedes the loss of the inorganic phase.
• Gottlieb (1944) stated that the initial action was due to
proteolytic enzymes which attacks the lamellae, rod sheaths,
tufts and walls of the dentinal tubules.
• He suggested that a coccus, probably Staphylococcus aureus,
causative organisms of dental caries.

The Proteolytic Theory (contd.)
• According to Gottlieb, acid alone produces chalky
enamel but i.e. not true caries. His ideas were based on
the observations of histological specimens and the
similarity between carious enamel and enamel whose
organic components were stained with silver nitrate.
• There has been no bacteriological confirmation between
staphylococcus pyogenes and caries.
• Gottlieb stated that yellow pigmentation was
characteristic of caries and is due to pigment produced
by proteolytic organisms.

The Proteolytic Theory (contd.)
Conclusion
• It is not an universally accepted theory as
there is no satisfactory evidence to support
that the initial attack on enamel is proteolytic.
• Caries can occur in the absence of proteolytic
organism.
• Proteolysis may occur in the advanced carious
lesion but not in initiation of caries.

E. Proteolysis Chelation Theory
• Originated by Schatz & Martin
• This theory considers dental caries to be a simultaneous
microbial degradation of the organic components of enamel by
proteolysis and the dissolution of the minerals of the tooth by
the process known as chelation.
• The breakdown products of the organic components of enamel
(keratin, citrates, mucopolysaccharide, lipids) may have
chelating properties and can dissolve the minerals in enamel.
• Chelates is a complex compound of ion(ca) and two or more
groups.
• The proteolysis-chelation theory states that inorganic and
organic portions of enamel are attacked simultaneously and it
occur independent of pH of the medium.

Proteolysis Chelation Theory (contd.)
This theory is also not universally accepted as it
cannot explain the following facts:
Increased caries incidence with increased
sugar intake.
Increased caries activity with increased
lactobacillus count.
Decreased caries incidence following topical
or systemic administration of fluoride.

E. Sucrose Chelation Theory
• Proposed by Eggers-Lura (1967)
• Theory suggests that sucrose itself cause
dissolution of enamel by forming unionized
calcium saccharates.

OTHER THEORIES
A.Auto-immunity theory
In this theory, it is suggested that
'forbidden clones' of lymphocytes attack
target cells (odontoblast) rendering the
tooth vulnerable to caries attack.

Distribution of dental caries according to tooth
surface:-
Occlusal > Interproximal >Buccal
Caries Susceptibility
Individual teeth
According to Brekhus(1931)
Teeth %
Upper and lower 1st molar 95%
Upper and lower 2nd molar 75%
Upper 2nd bicuspids 45%
Upper 1st bicuspids 35%
Lower 2nd bicuspids 35%
Upper central and lateral incisors 30%
Upper canine and lower 1st
premolar
10%
Lower anterior teeth 3%

CLINICAL RISK ASSIGNMENT FOR CARIES
A patient is at high risk for the development of new cavitated
lesions if:
1. High mutans streptococci (MS) counts are found.
Bacteriologic testing MS should be done if:
 The patient has one or more medical health history risk factors.
 The patient has undergone antimicrobial therapy
 The patient presents with new incipient lesion
 The patient is undergoing orthodontic care
 The patient’s treatment plan calls for extensive restorative dental
work
2. Any two of the following factors are present:
– Two or more active carious lesions
– Large number of restorations
– Poor dietary habits
– Low salivary flow

CLASSIFICATION OF DENTAL CARIES
1.CLINICAL CLASSIFICATION
• According to the stage of lesion progression:
1. Non cavitated lesion
2. Cavity
• According to the severity of the disease:
1. Acute caries (active)
2. Chronic caries (slowly progression)
3. Stabilized caries (arrested)
• According to clinical manifestation:
1. White spot lesion macula caroisa
2. Superficial caries caries superficialis
3. Medium caries caries media
4. Deep caries caries profunda
5. Secondary caries caries secundaria

CLASSIFICATION OF DENTAL CARIES (contd.)
2. ANATOMICAL
According to anatomical depth of the defect:
1. Enamel caries
2. Dentin caries
3. Cementum caries
According to location of the lesion:
1. Coronal caries
2. Occlusal surfaces
3. Smooth surfaces
4. Approximal surfaces
5. Root caries
According to intensively of caries within the dentition:
1. Single lesion
2. Multiple lesions
3. Systemic destruction

According to the stage of lesion progression
1.Non cavitated lesion
Initial form of caries development in which there is
whitish discoloration of the surface of the tooth
occur and there is no cavity developed.
1.CLINICAL MANIFESTATION
A white spot lesion at the entrance
to the fissure on a molar.

2. Cavitated lesion
The progression of white spotty lesion leads to the
formation of the cavitated lesion which may be
minimally or maximally extended from the tooth
surface to inward direction (towards pulp).

According to the severity of the disease:
1. Acute caries (active)
• It is a form of dental caries which runs a rapid clinical
course.
• It is usually occurs in children and younger individual
having larger dentinal tubules without sclerosis which
facilitate faster spread of caries.
• The opening of the lesion is usually naarrow which
prevents entry of salivary buffer to neutralize acid
formed by fermentation.
• Pain is usually present in acute caries with pulp
involvement.

RAMPANT CARIES
• It is acute fulminating type of caries that involves
multiple teeth in multiple surfaces.
• This caries involves those teeth surfaces that are
considered immune to caries
• A caries increment of ten or more new carious
lesions over a period of about one year is
characteristic of rampant caries.
• This occurs in about 4-8 years for deciduous teeth
but in 11-19 years for permanent teeth.
Rampant caries in adult Rampant caries in 10 year adult boy

NURSING BOTTLE CARIES (Baby bottle syndrome)
• It is a form of rampant caries affecting the deciduous
dentition, most commonly the four anterior.
• It occurs due to prolonged use of nursing bottle containing
milk or sweetened juice, breastfeeding or sweetened
pacifiers as an aid for sleeping after one year of age.
• Caries rapidly develops, so after some time only root
stumps remain in mouth at the place of carious teeth.
• Mandibular anterior teeth are protected by tongue and
continuously cleansed with saliva, so usually not affected.

2.Chronic caries (slowly progression)
• It is a slow progressing dental caries usually affecting
adult patients.
• The opening of the cavity is wide, causing less
retention of plaque and more entry of salivary buffer.
• As the process is slow, there is sclerosis of dentine
and formation of reparative dentine to protect the
pulp.
• The carious dentine is stained deep brown.
• Pulp involvement is a late feature and pain is usually
not evident in chronic dental caries.

3. Stabilized caries (arrested)
• Carious lesion, whose progression is ceased due to
cleansing action of toothbrush, mastication and saliva,
because of the wide opening of the lesion.
• Affected dentine is burnished and becomes brown,
hard and polished (termed as eburtion of dentine)
An arrested carious
lesion in the lower first
premolar. The lesion was
well into dentine, but
the tissue was hard and
shiny.

According to clinical manifestation:
1. White spot lesion macula caroisa
• The earliest visible sign of enamel caries is
the ‘white spot lesion’.
• The active lesion is matt and feels rough if a
sharp probe is gently drawn across it.

2. Superficial caries (Caries of superficialis)
• At a superficial caries the area of destruction of enamel
is determined without violation of enamel – dentine
connection and without changes in a dentine.
• There is destruction of enamel – dentine connection at
progress of process, and there is the next stage of
carious process.

3. Middle caries (Caries of media)
A middle caries is characterized three areas which
appear at research of cut of tooth in a light
microscope:
1st – to disintegration and demineralization;
2nd – transparent and to the intact dentine;
3d – reparative dentine and changes in pulp of tooth.

4.Deep caries (Caries of profunda)
• At research of cut of tooth with a deep carious cavity in a
light microscope appear, as well as at a middle caries, three
areas:
• 1st – to disintegration and demineralization;
• 2nd – transparent and to the intact dentine;
• 3d – reparative dentine and changes in pulp of tooth.
• It should be noted that at a deep caries more expressed
changes appear in pulp of tooth, than at the middle depth of
cavity both in hard fabrics of tooth and in pulp of tooth.
• In a vascular-nervous bunch changes have likeness with
sharp inflammation, up to complete disintegration of axial
cylinders of nervous fibres.

5. Secondary caries caries secundaria
• Secondary caries occurs at the junction of a restoration
and the tooth and may progress under the restoration.
• It is often termed recurrent caries.
• This condition usually indicates that micro leakage is
present, along with other conducive to caries

2. ANATOMICAL
According to anatomical depth of the defect:
1. Enamel caries
• Four zones can be identified.
• The lesion has a conical shape with apex facing the dentine.
1. Translucent zone
2. Dark zone
3. Body of the lesion
4. Surface zone
1. Translucent zone
2. Dark zone
3. Body of the lesion
4. Surface zone

Enamel caries (contd.)
Surface (a) appears to be intact. Body of lesion (b) shows enhancement of
striae of Retzius. Dark zone (c) surrounds body of lesion while translucent zone
(d) is evident over entire advancing front of lesion.

a. Translucent Zone
• The deepest zone is the translucent zone and represents the
advancing front of the enamel lesion.
• The name refers to its structure less appearance when perfused
with quinoline solution and examined with polarized light.
• In this zone, the pores or voids form along the enamel prism
(rod) boundaries, presumably because of the ease of hydrogen
ion penetration during the carious process.
• When these boundary area voids are filled with quinoline
solution, which has the same refractive index as enamel, the
features of the area disappear.
• The pore volume of the translucent zone of enamel caries is 1%,
10 times greater than normal enamel.

b. Dark Zone
• The next deepest zone is known as the dark zone because it
does not transmit polarized light.
• This light blockage is caused by the presence of many tiny
pores too small to absorb quinoline.
• These smaller air- or vapor-filled pores make the region
opaque.
• The total pore volume is 2% to 4%.
• There is some speculation that the dark zone is not really a
stage in the sequence of the breakdown of enamel; rather,
the dark zone may be formed by deposition of ions into an
area previously only containing large pores.

Dark Zone(contd.)
• It must be remembered that caries is an episodic
disease with alternating phases of demineralization
and remineralization.
• There is also a loss of crystalline structure in the dark
zone, suggestive of the process of demineralization
and remineralization.
• The size of the dark zone is probably an indication of
the amount of remineralization that has recently
occurred.

c.Body of the Lesion
• The body of the lesion is the largest portion of the
incipient lesion while in a demineralizing phase.
• It has the largest pore volume, varying from 5% at
the periphery to 25% at the center.
• The striae of Retzius are well marked in the body
of the lesion, indicating preferential mineral
dissolution along these areas of relatively higher
porosity.

Body of lesion (contd.)
• The first penetration of caries enters the enamel
surface via the striae of Retzius. The interprismatic
areas and these cross-striations provide access to
the rod (prism) cores, which are then preferentially
attacked.
• Bacteria may be present in this zone if the pore
size is large enough to permit their entry.
• Studies using transmission electron microscopy
(TEM) and scanning electron microscopy (SEM)
demonstrate the presence of bacteria invading
between the enamel rods (prisms) in the body
zone.

d.Surface Zone
• The surface zone is relatively unaffected by the caries attack.
• It has a lower pore volume than the body of the lesion (less than
5%) and a radiopacity comparable to unaffected adjacent
enamel.
• The surface of normal enamel is hypermineralize by contact
with saliva and has a greater concentration of fluoride ion than
the immediately subjacent enamel.
• It has been hypothesized that hypermineralization and
increased fluoride content of the superficial enamel are
responsible for the relative immunity of the enamel surface.
• However, removal of the hypermineralized surface by polishing
fails to prevent the reformation of a typical, well-mineralized
surface over the carious lesion.

Surface Zone (contd.)
• Thus, the intact surface over incipient caries is a
phenomenon of the caries demineralization process
rather than any special characteristics of the superficial
enamel.
• Nevertheless, the importance of the intact surface cannot
be overemphasized, because it serves as a barrier to
bacterial invasion.
• As the enamel lesion progresses, conical-shaped defects in
the surface zone can be seen by SEM.
• These are probably the first sites where bacteria can gain
entry into a carious lesion.
• Arresting the caries process at this stage results in a hard
surface that may at times be rough, though cleanable

According to anatomical depth of the defect
2. Dentin caries
 In cross section dentin caries is V shaped with base at dentino-
enamel junction and apex toward pulp.
 Five different zones have been described in carious dentin. The
zones are most clearly distinguished in slowly advancing
lesions.
 In rapidly progressing caries, the difference between the zones
becomes less distinct.
Different zones in dentinal caries are:
1. Normal dentin
2. Subtransparent dentin
3. Transparent dentin
4. Turbid dentin
5. Infected dentin

Dentin caries (contd.)
Zones of Dentinal Caries.
5
4
3
2
1
Observing from the pulpal side at the
advancing edge of carious lesion following
different zones can be seen.
ZONE 1
Zone of fatty degeneration of Tomes’
fibers
ZONE 2
Zone of dentinal sclerosis/Subtransparent
dentin
ZONE 3
Zone of decalcification/Transparent
dentin
ZONE 4
Zone of bacterial invasion/Turbid dentin
ZONE 5
Zone of decomposed dentin/Infected
dentine

Zones of Dentinal Caries.
Caries advancement in dentin proceeds through three
changes:
a. weak organic acids demineralize the dentin;
b. the organic material of the dentin, particularly
collagen, degenerates and dissolves; and
c. the loss of structural integrity is followed by invasion
of bacteria.

Zone 1: Normal Dentin.
•The deepest area is normal dentin, which has
tubules with odontoblastic processes that are
smooth, and no crystals are in the lumens.
•The inter tubular dentin is normal.
•No bacteria are in the tubules.
•Stimulation of the dentin (e.g.by osmotic gradient
[from applied sucrose or salt], a bur, a dragging
instrument, or desiccation from heat or air)-
produces a sharp pain.

Zone 2: Subtransparent Dentin/ Zone of
sclerosis
• Zone of demineralization of the intertubular
dentin and initial formation of very fine
crystals of calcium salt in the tubule lumen.
• Damage to the odontoblastic process is
evident however no bacteria are found in the
zone.
• Stimulation of the dentin produces pain, and
the dentin is capable of remineralization.

Zone 3: Transparent Dentin/ Zone of Decalcification
without Bacterial Invasion
• Zone of carious dentin that is softer than normal dentin and
shows further loss of mineral from the inter-tubular dentin
and many large crystals in the lumen of the dentinal
tubules.
• Stimulation of this region produces pain.
• No bacteria are present.
• The collagen cross-linking remains intact in this zone.
• The intact collagen can serve as a template for
remineralization of the intertubular dentin.
• This region remains capable of self-repair if the pulp is vital.

Zone 4: Turbid Dentin/ Zone of Decalcification
with Bacterial Invasion
Zone of bacterial invasion and is marked by widening
and distortion of the dentinal tubules, which are filled
with bacteria.
There is very little mineral present and the collagen in
this zone is irreversibly denatured.
The dentin in this zone will not self-repair.
This zone cannot be remineralized and must be
removed before restoration.

Decalcified section of carious dentine
showing dentinal tubules penetrated
by deeply staining bacteria. In places
the tubules appear to have been
pushed apart by aggregations of
bacteria called liquefaction foci.

Decalcified section of carious
dentine showing tubules
penetrated by bacteria. The
tissue appears to have split at
right angles to the tubules
along the incremental lines of
growth. These splits are called
transverse clefts.

Zone 5: Infected Dentin.
• The outermost zone
• Infected dentin consists of decomposed dentin.
• There is no recognizable structure to the dentin
and collagen and mineral seem to be absent.
• Great numbers of bacteria are dispersed in this
granular material.
• Removal of infected dentin is essential to sound,
successful restorative procedures as well as
prevention of spreading the infection.

INFECTED AND AFFECTED DENTINE
INFECTED DENTINE AFFECTED DENTINE
Infected dentin has bacteria present Affected dentin has no bacteria
Collagen is irreversibly denatured. Collagen is reversibly denatured
Not remineralizable and must be removed Remineralizable, and should be preserved
Zones 4 (turbid zone) and 5 (infected
dentine)
Zones 2 (subtransparent dentin) and 3
(transparent dentin)
In chronic (slow) caries, infected dentin usually is discolored & because the bacterial front is
close to the discoloration front, it is advisable in caries removal to remove all discolored dentin
unless judged to be within 0.5 mm of the pulp.
In acute (rapid) caries the discoloration is very slight & the bacterial front is well behind the
discoloration front, some discolored dentin may be left, although any "clinically remarkable“
discoloration should be removed.

GV Black Classified Carious Lesions into 6 types
based on their location:
• Class I
• Class II
• Class III
• Class IV
• Class V
• Class VI
Classification of Dental Caries (contd.)

Class I Caries
All pit-and-fissure caries are
Class I, and they are assigned to
three groups, as follows.
Caries on the occlusal surface
of premolars and molars
Caries on Occlusal Two Thirds
of the Facial and Lingual
Surfaces of Molars.
Caries on the lingual surface of
maxillary incisors
GV Black Classification of Dental Caries (contd.)

Class II Caries
Caries on the proximal surfaces of posterior
teeth are Class II.

Class III Caries
Caries on the proximal surfaces of anterior
teeth that do not involve the incisal angle are
Class III

Class IV Caries
Caries on the proximal surfaces of anterior teeth
that do involve the incisal edge are Class IV.

Class V Caries
Caries on the gingival third of the facial or lingual
surfaces of all teeth (except pit and fissure lesions)
are Class V.

Class VI Caries
Restorations on the incisal edge of anterior teeth
or the occlusal cusp heights of posterior teeth are
Class VI.

WHO classification
The shape and the depth of the carious lesion can
be scored on a 4 point scale:
D1-Clinically detectable enamel lesions with intact
(non-cavitated) surfaces.
D2-Clinically detectable cavities limited to enamel.
D3-Clinically detectable lesions in dentin (with
and without cavitation of dentin).
D4–Lesions into the pulp.
Classification of Dental Caries (contd.)

Professor Nigel Pitts. The ‘iceberg of dental caries’. Diagnostic
thresholds used in epidemiology and practice. In epidemiological surveys
the iceberg ‘floats’ at the D3 threshold (cavity in dentine). Most lesions
arrestable by preventive care are hidden below the water. If patients who
only present with D1 and D2 lesions are described as ‘caries-free’ by
epidemiologists.

Caries Diagnosis
Diagnosis:
The use of scientific or clinical methods to establish the cause
and nature of person’s illness or injury and the subsequent
functional impairment caused by the pathology.- Tabers
Cyclopedic dictionary
Objective:
1. To identify patients with lesions that require surgical
(restorative) treatment.
2. To identify patients with lesions that require non-
surgical (preventive) treatment.
3. To identify patients who are at high risk for developing
carious lesions.

Diagnosis is important for three reasons:
• It forms the basis for a treatment decision. Active lesions require
some form of active management whereas arrested lesions do
not.
• Informing the patient. The patient is central to the management
of the carious process. It is the patient who will control the
process, not the professional. The dentist’s role is to inform the
patient whether any action is required.
• Advising health service planners. Epidemiological surveys inform
the politicians who commission them of the state of health and
disease of the population. These surveys should assist them to
direct money appropriately.
Caries Diagnosis
WHY IS DIAGNOSIS IMPORTANT?

Diagnostic Methods
1. Identification of subsurface demineralization
(inspection, radiography, dye uptake methods).
2. Bacterial testing.
3. Assessing environmental conditions (pH,
salivary flow, salivary buffering).
Caries Diagnosis (contd.)

A patient is at high risk for the development of new cavitated
lesions if:
1. High mutans streptococci (MS) counts are found.
Bacteriologic testing MS should be done if:
 The patient has one or more medical health history risk factors.
 The patient has undergone antimicrobial therapy
 The patient presents with new incipient lesion
 The patient is undergoing orthodontic care
 The patient’s treatment plan calls for extensive restorative dental
work
2. Any two of the following factors are present:
– Two or more active carious lesions
– Large number of restorations
– Poor dietary habits
– Low salivary flow
CLINICAL RISK ASSIGNMENT FOR CARIES

Assessment Tools:
1- Patient History.
2- Clinical Examination.
3- Nutritional Analysis.
4- Salivary Analysis.
5- Radiographic Assessment.

Assessment Tools
1- Patient History
– Caries Risk Indicators
Factors High Risk Characteristics
Age less than 18, older than 65
Socioeconomic lower Status
Medications Reduced Salivation
Fluoride History Lack of Fluoride during tooth
development
Dietary Habits high intake of carbohydrate, tobacco and
alcohol
Genetic Predisposition Family of history of disease
General Health Debilitation and decreased ability to self-
care

Assessment Tools
1- Patient History
– Caries Risk Indicators
A past history of caries
experience is the best
predictor of future caries
activity

Assessment Tools
2- Clinical Examination:
 Salivary function.
 Plaque accumulation.
 Inflammation of soft tissues.
 Poor oral hygiene.
 Cavitated lesions .
 Existing restorations.
Risk of Caries
Development

Assessment Tools
3- Nutritional Analysis
Frequent exposure to sucrose increases the
likelihood of plaque development by the
more cariogenic MS organisms.

Assessment Tools
4- Salivary Analysis:
Secretion Rate:
High level of salivary flow:
cariostatic effect
Xerostomia or dry mouth:
favorable environment
for caries development

Assessment Tools
4- Salivary Analysis
 Secretion Rate.
 Buffering Capacity.
 Number of MS and Lactobacilli:
High S.mutans count high risk
Low S.mutans count low risk

Assessment Tools
4- Salivary Analysis
Patient Check-Up kit from GC

Assessment Tools
5- Radiographic Assessment
• Although radiographs may show caries that is not visible
clinically.
• The minimal depth of a detectable lesion on a radiograph is
about 500 lam.
• Although radiographs tend to underestimate the histologic
extent of a carious lesion, approximately 60% of teeth with
radiographic proximal lesions in the outer half of dentin
are likely to be noncavitated.
• Thus, many lesions evident radiographically are not
cavitated and should be remineralized rather than restored.

Medical History Factors Associated With Increased Caries Risk

Caries Diagnosis for Pits and Fissures
1-U.S. Public Health Service criteria USPHS :
1. Softening at the base of the P&F.
2. Opacity surrounding the P&F.
3. Softening of enamel that may be flaked
away.
2- Technical Tools.

 Cavitation at the base of a pit or fissure sometimes can
be detected tactilely as softness or by binding of the
explorer tip.
 However, mechanical binding of an explorer in the pits
or fissures may be due to noncarious causes, such as
the shape of the fissure, sharpness of the explorer, or
force of application.
 Thus, explorer tip binding is not by itself a sufficient
indication to make a caries diagnosis.

The use of sharp
dental explorer
noncavitated incipient lesions
could become cavitated
Cavitated means that extensive enamel demineralization has lead to destruction
of the walls of the pit or fissure and bacterial invasion has occurred.
Demineralization of the underlying dentin is usually extensive by the time the
cavitation has occurred.

Pits & Fissure Caries Treatment Decision Making
Noncavitated (caries-free):
• No radiolucency below occlusal enamel
• Deep grooves may be present
• Superficial staining may be present in grooves
• Mechanical binding of explorer may occur
Cavitated (diseased):
• Chalkiness of enamel on walls and base of pit or fissure
• Softening at the base of a pit or fissure
• Brown-gray discoloration under enamel adjacent to pit or fissure
• Radiolucency below occlusal enamel

The following feature indicate that the caries may be arrested:
 White or brown spot lesions with shiny surface
If a cavitated lesion exists in a pit or fissure, it must be restored. If the pit or fissure is not
cavitated but at risk, then it should be sealed. The pits and fissures of molar teeth in children
should be sealed routinely as soon as possible after eruption. Pits and fissures in adults
should be sealed if the adult is found to have multiple active lesions or found to be at high
risk.

Caries Diagnosis for Smooth Surfaces
• Bitewing radiographs are the most typical method for
evaluation of the proximal smooth surfaces for evidence of
demineralization because these areas usually are not readily
assessed visually or tactilely.
• An early lesion is detectable radiographically as a localized
decrease in the density of the enamel immediately below
the proximal contact, resulting in a radiolucent area on the
radiograph.
• Proximal radiolucencies detectable on bite-wing radiographs
should be examined clinically because many are not
associated with cavitation of the surface and are not
conclusive evidence for restorative treatment.

Proximal Caries Treatment Decision Making
Non cavitated:
• Surface intact; use of an explorer to judge surface must be done with
caution because excessive force can cause penetration of intact surface over
demineralized enamel
• Opacity of proximal enamel may be present
• Radiolucency may be present
• Marginal ridge is not discolored
• Opaque area may be seen in enamel by translumination
Cavitated:
• Surface broken, detectable visually or tactilely; temporary mechanical
separation of the teeth may aid diagnosis
• Marginal ridge may be discolored
• Opaque area in dentin on translumination
• Radiolucency is present

The following indicate that the lesion is arrested:
Cavitated lesion, often dark
brown, with hard dentin at their
bases, the lesions are not plaque
covered and are often remote
from gingival margin.
Shiny white or brown lesion,
often well exposed due to
recession, the lesion are not
plaque covered.

Tactile examination (careful!)
• A sharp, curved probe (Briault) can be used gently to try to
determine whether an approximal lesion is cavitated, but if
this instrument or a scaler is used in a heavy-handed manner,
it can actually cause cavitation.
Caries Diagnosis for Smooth Surfaces- Approximal
surfaces

Bitewing radiographs
• The bitewing radiograph is of paramount importance in the diagnosis of
the approximal carious lesion, although it should be remembered that
the technique is relatively insensitive as it is not able to detect early
subsurface demineralization.
• In this technique the central beam of X-rays is positioned to pass at
right angles to the long axis of the tooth, and tangentially through the
contact area.
• The film is positioned in a film holder on the lingual side of the
posterior teeth.
• The patient then closes the teeth together on the film holder.
• A beam-aiming device on the holder guides the position of the tube.
• This directs the beam at right angles to the film and the contact areas of
the teeth.

A bitewing radiograph is being taken. The film is held lingually by a film holder and the
patient closes together on a part of this holder. A beam-aiming device helps the operator
position the tube so that the beam is directed at right angles to the film.

Diagrammatic representations of caries on bitewing radiographs.
Appearances graded
0–2 are unlikely to be
cavitated, while grade
4 will almost certainly
be cavitated. The
problem comes with
grade 3 which may or
may not be cavitated

Transmitted light
• Transmitted light can also be of considerable assistance in the
diagnosis of approximal caries.
• This technique consists of shining light through the contact point.
• A carious lesion has a lowered index of light transmission and
therefore appears as a dark shadow that follows the outline of the
decay through the dentine.
A mirror view of the palatal aspect of
the upper anterior teeth. Lesions are
visible mesially and distally on the
upper right central incisor.

FIBEROPTIC TRANSILLUMINATION:
• Carious lesion have lowered index of light transmission, when teeth
are examined with the fiberoptic light source, caries appears as a dark
shadow
• After drying the tooth, a fiberoptic probe can be placed in the buccal
or lingual embrassures directly beneath the contact area between two
adjacent teeth.
• If caries is present , dark shadow is seen beneath the marginal ridge
Advantage
 Non invasive
 No radiation hazard
 No permanent record
Fiberoptic Transillumination is used in the area where there is Difficulty
in placing probe

FIBEROPTIC TRANSILLUMINATION
Proximal
Caries
Use of a fibreoptic light in the diagnosis of approximal caries

Digital Imaging Fiber-Optic Transillumination (DIFOTI)
The DIFOTI (Electro-Optical Sciences Inc.) uses white light, a CCD camera, and
computer-controlled image acquisition and analysis to detect caries

Tooth separation
• One further technique to assist with the diagnosis of approximal
caries is the use of tooth separation.
• A small round elastic is forced between the contact points using a
special pair of applicating forceps.
• After a few days the teeth are separated. The dentist can now feel,
very gently, with a probe to detect whether a cavity is present.
• Alternatively, a little elastomer impression material can be injected
between the teeth.
• After a few minutes the set material can be removed with a probe
and the impression examined to see whether there is a cavity.

Tooth separation
(a) Orthodontic separator is placed between the canine and first premolar. (b)
Separation achieved 48 hours later. Note it is not possible to see the distal
surface of the canine clearly. (c) Taking an elastomer impression of the contact
area. (d) Elastomer impression of the contact area showing no cavitation on the
distal aspect of the canine; a restoration is not needed.

Caries Diagnosis for Root Surfaces
Active lesions are close to gingival margin and plaque covered.
Soft and leathery in consistency.
Visual
white – yellow – light brown – dark brown.
Tactile
Soft (easily penetrated) – hard.
Rate of progression
Slow (due to remineralization &exposure to saliva and fluoride).
Rapid (due to rapid progression in dentin).
Arrested lesions are:
Often some distance from gingival
margin and not covered with plaque.
As hard as surrounding root surface.

Detection with chemical dyes
•Dyes are a diagnostic aid for detecting caries in questionable
areas (i.e., for locating soft dentin that is presumably
infected).
•Fusayama introduced a technique in 1972 that used a basic
fuchsin red stain to aid in differentiating layers of carious
dentin.
•Because of potential carcinogenicity, basic fuchsin was
replaced by another dye, acid red 52, which showed equal
effectiveness.
•Studies show dye stains are about 85% effective in detecting
all caries in a tooth.
•Clinical removal of caries without the aid of a dye is 70%
effective

Detection with chemical dyes
A, Prepared tooth before adding
caries indicator.
B, The tooth is treated with a 1%
acid red 52 solution for 10
seconds.
C, After rinsing with water for 10
seconds, some tooth structure
shows discoloration. The stain
indicates decalcified dentin. If the
stained tooth structure is soft and
appears carious, it should be
removed.
D, After removal of soft, carious
tooth structure, some harder, less
stained tooth remains, giving a
pink appearance to some areas of
this tooth. This healthy, stained
tooth structure should not be
removed.

Caries Activity Tests:
Salivary Bacteria.
Plaque Index.
Diet.
Salivary Analysis.

Goal
• To reduce the number of cariogenic
bacteria.
• To limit tooth demineralization.
Caries Prevention

Preventive methods include
• Limiting pathogen growth and metabolism.
• Increasing the resistance of the tooth surface
to demineralization
Caries Prevention

A. General Health.
B. Fluoride Exposure.
C. Immunization.
D. Salivary Function.
E. Antimicrobial Agents.
F. Diet.
G. Oral Hygiene.
H. Xylitol Gums.
I. Pit and Fissure Sealants.
J. Restorations.
Caries Prevention

A. General Health
Declining health...
Decreased patient’s immunologic system...
Increased risk for caries...
Need for increased preventive measures.
Caries Prevention
Patients should be examined for:

B. Fluoride Exposure
Fluoride in trace amounts increases the resistance
of tooth structure to demineralization
1- Fluoride ions enhances the precipitation of
fluoroapatite from Ca and PO4 ions into the
tooth structure, which is more acid resistant
2- Allows the remineralization of incipient non
cavitated lesions
3- Fluoride has an antimicrobial acitivity
Caries Prevention

B. Fluoride Exposure
Caries Prevention
Route Method of Delivery Conc.
Systemic Public Water Supply 1 ppm More than 10ppm...fluorosis
Topical
(self-application)
Low dose / High frequency rinses
(0.05% NaF daily)
225 ppm Individual patients at home
High dose / Low frequency rinses
(0.2% NaF weekly)
900 ppm Supervised rinses in public
schools
Fluoridated Dentifrices (daily) 1000 ppm
Topical
(professional
application)
Acidulated phosphate fluoride
gel (annually or semiannually)
12,3000 ppm Most effective and least
objectionable
Sodium Fluoride sol. (2%) 20,000 ppm
Stannous Fluoride sol.(8%) 80,000 ppm Bitter metallic taste,
staining
Fluoride Varnish Higher uptake, but lower
dosage

C. Immunization
?
Potential Side Effects
Safety
Cost
Caries Prevention

D. Salivary Functioning
Role of Saliva:
- Washing away food.
- Buffering capacity.
- Lubricant.
- Remineralization.
- Antimicrobial.
Caries Prevention

Role of Saliva:
- Washing away food.
- Buffering capacity.
- Lubricant.
- Remineralization.
- Antimicrobial.
Caries Prevention
Salivary stimulants
•Gums
•Paraffin waxes
•Saliva subsitutes
(Sialgen)
D. Salivary Functioning

E. Antimicrobial Agents
Caries Prevention
Agent Mechanism of
Action
Persistence in the
Mouth
Side Effects
Chlorohexidine Antiseptic; prevents
bacterial adherence
long Bitter taste, stains teeth
and tongue brown,
mucosal irritation

F. Diet
Dietary Sucrose
Increase MS colonization in plaque
Increase caries potential of plaque
Prolonged decline in pH
Caries Prevention

Dietary Counselling
 To identify the sources of sucroses and acidic
foodstuffs
 To reduce the frequency of
their ingestion
Caries Prevention
F. Diet

G. Oral Hygiene
Plaque Free Surfaces: Do Not Decay
Caries Prevention
Mechanical Plaque Removal Topical Antibiotics
Does not engender the risk of
infection with opportunistic
organisms
Long term use predisposes the
patient to infection with
antibiotic resistant pathogens
(Candida Albicans)

G. Oral Hygiene
Plaque Free Surfaces: Do Not Decay
Caries Prevention
Flossing
Brushing
Rinsing

H. Xylitol Gums
 Natural sugar obtained from birch trees
 MS cannot ferment xylitol
 Xylitol reduces the MS by altering their
metabolic pathways
Caries Prevention

I. Pit & Fissure Sealants
A preventive method for P & F caries
1- Mechanical filling of the P & F with resin
2- MS cannot reach P & F
3- Easier cleaning of P & F during mastication and
brushing
Caries Prevention

Advantages
1. Prevent caries in newly erupted teeth
2. Arrest incipient caries
3. Prevent bacterial growth in sealed fissures
4. Prevent infection of
other sites
Caries Prevention

Caries Treatment
In the Past
Drill and Fill Approach
In the Present
Early Detection and Remineralization
In the Future?

Refrences
Sturduvant’s Art And Science Of Operative Dentistry,
Fifth Edition Chap. 3; Pg: 102- 130
Essential Of Dental Caries, Third Edition , Oxford
University Press
Fundamental of Operative Dentistry, Second Edition,
Quintessence publishing co.
Tooth-Colored Restoratives Principles and Techniques,
Ninth edition, BC Decker Inc
Clinical Text on Oral Pathology, Ruchir Tripathi

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