CARIOLOGY

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 CONTENTS
INTRODUCTION
DEFINITION
HISTORY
EPIDEMOLOGY
ETIOLOGY OF DENTAL CARIESEARLY
THEORIES & CURRENT CONCEPTS
FACOTRS INFLUENCING ETIOLOGY
PATHOPHYSIOLOGY OF CARIES

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 CLASSIFICATION OF CARIES
HISTOPATHOLOGY OF CARIES
CARIES DIAGNOSIS
CARIES PREVENTION
CARIES TREATMENT
CONCLUSION
BIBLIOGRAPHY.

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 For there never yet
philosopher that could endure
the toothache patiently

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 INTRODUCTION
TEETH ARE TOOLS that have evolved to
ensure survival of species.
Caries is a biosocial disease rooted in the
technology and economy of our society.
Dental caries is unique not only in terms of
pathological mechanism ; other aspects, social
and economic , are also worthy of note.
While it is true that diseases of the teeth and
their supporting tissues do not normally kill
humans they certainly affect the persons
efficiency and they can , if neglected, provoke
serious conditions elsewhere in the body. Their
contribution to the general fund of human
misery is legendary . 5
 DEFINITION
Localized post eruptive, pathological process of
external origin involving softening of the hard tissue
and proceeding to the formation of a cavity (WHO) .
Is an infectious microbiological disease of teeth that
results in localized dissolution and destruction of
calcified tissues (STRUDEVANT) .
Microbial disease of the calcified tissues of the teeth
characterized by demineralization of the inorganic
portion and destruction of organic substance of the
teeth (SHAFER) .
It is fundamentally a microbiological disease which
affects the calcified tissues of the teeth, beginning
first with localized dissolution of the inorganic
structures by acids of bacterial origin leading to
disintegration of organic matrix (ERNEST NEWBURN)
.
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 HISTORY
5000 B.C LEGEND OF WORM: Ancient sumerian text- clay
tablet found in euphrates valley in lower
meepotomian areas.
2700 B.C Chinese used acupuncture as a treatment for
various diseases including dental diseases.
1819 L.S.PARMLEY- caries began on the enamel surface
and speculated that a chemical agent was
involved.

1867 Leber and Rotenstein reported microorganisms

and activity of acid producing bacteria
1871,1873, Clark,Tomes,Magiot-Bacteria was essential for
1878 caries.

1881 Underwood and Milles caries was due to

bacteria, affecting organic and inorganic
elements
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1915 Baumgarner acids produced by bacteria were
capable of destroying the inorganic portion

1915 Glies & klinger- found high no. of microorganisms

in persons with caries.

1924 Clarke isolated streptococcus mutants from

carious lesions

1927 Jay and Voorhees found the presence of

L.acidopilus was potent for development of caries

1944,194 Gottleib & Gottleib, Diamond& Applebaum caries

6 is essentially a proteolytic process

1951 Manley and Hardwick pointed out that acidogenic

and proteolytic theories need not be separate

1952 Finn stated that lower 1st molar was most

frequently affected
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 EPIDEMOLOGY:

Decline in caries prevalence in developed

countries.
Increasing prevalence of caries in less developed
countries.
Most common epidemiologic measure of caries is
evaluation of measure of permanent teeth that are
diseased, missing or filled (DMF).

Geographical differences:
More remote areas of world with less access to
refined foods shows decreased incidence of caries.
Caries often rightly called Disease of the civilization
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 Family differences:
More caries rate seen in siblings of individuals with
high caries rates & less incidence seen in siblings of
caries immune individuals.
Children of high caries incident parents shows
higher caries incidence.
Attributed mainly to genetic factors such as tooth
morphology, salivary flow rate and also to dietary
habits and oral hygiene habits of the family.

Race:
Blacks , chainese & east indians have considerably
less caries than american whites.
The english are known to have appalingly poor
teeth & a higher caries incidence compared to
italians & russians.
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 Gender:
Girls show high caries incidence than boys of
same age till early teens.
Attributed to earlier eruption of teeth in girls
because of early growth spurt.
Significant as teeth are maximally susceptible
to caries immediately after eruption.

AGE:
Even at age six around 20% of the children
have caries incidence in their permanent
dentition.
Most frequently involved is the first permanent
molar (six yr molar)
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 Socioeconomic & behavioral
factors
Socioeconomic factors are the major
determinants of oral health of both
children and adults worldwide
It determines the following factors
1)Social class
2)Income
3)Education
4)Knowledge
5)Attitude
6)Behavior
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 CARIES SUSEPTIBILITY IN
PERMANENT DENTITION:
Sites ranked in decreasing order of
occurrence
1)Fissure of the molars
2)Mesial & distal surface of first molars.
3)Mesial surface of second molars & distal
surface of second premolars.
4)Mesial & distal surface of maxillary first
premolars
5)Distal surface of canines & Mesial surface
of mandibular first premolars
6)Approximal surface of maxillary incisors. 13

 Etiology of dental caries:
THEORIES OF DENTAL CARIES
Worm theory
Humor theory
Vital theory
Chemical theory
Parasitic / Septic theory
Acidogenic theory
Proteolytic theory
Proteolytic chelation theory
Sucrose chelation theory
Autoimmune theory

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 According to an ancient Sumerian text,
Worm
toothache was caused by a worm that
drank the blood of the teeth and fed on
theory:
the roots of the jaws.
This legend of the worm was discovered
on one of many clay tablets excavated
near Euphrates Valley of the lower
Mesopotamian area and estimated to
date from about 5000 BC."
Guy de Cahuliac (1300-1368), the
greatest surgeon of' the Middle Ages,
believed that worms caused dental
decay. As a cure he advocated
fumigation with seeds of leek, onion, and
hyoscyamine -used as a hypnotic,
sedative, and smooth muscle relaxant.
Antony van Leeuwenhoek (1700), the
father of modern microscopy, wrote a
letter to the Royal Society of London
describing little worms "taken out of a
corrupt tooth" and said that they caused
the pain in toothache. 15
 Humor theory
The ancient Greeks considered that a person's
physical and mental constitution was determined by
the relative proportions of the 4 elemental fluids of
the body- blood, phlegm, black bile, and yellow bile
which correspond to the 4 humors-sanguine,
phlegmatic, melancholic, and choleric. All diseases,
including caries, could be explained by an
imbalance of' these humors.

Hippocrates, suggested that both local and

systemic factors were related to the cause of caries.

Aristotle, noticed that soft, sweet figs adhered to

the teeth, putrified. and produced damage.
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 Vital theory
This theory regarded dental caries as originating
within the tooth itself, analogous to bone
gangrene.
This theory ,proposed at the end of 18th century
remain dominant until the middle of 19th century.
A clinically well- known type of caries is
characterized by extensive penetration into the
dentin, and even into the pulp , but with barely
detectable catch in the fissure.

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 Chemical theory:
Parmly(1819) rebelled against vital theory
and proposed that an unidentified chemical
agent caused caries.

Robertson(1835) and Regnart(1938)-carried

out experiments with different dilutions of
inorganic acids (sulfuric and nitric) found
that they corroded enamel and dentin.

Robertson proposed dental decay was

caused by acid formed by fermentation of
food particles around the teeth.
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 Parasitic/septic theory:
In 1843 Erdl described filamentous parasites in
the surface membrane (plaque) of teeth.
Later Ficinus, a physician observed filamentous
microorganisms, which he called Denticolae, in
material taken from carious cavities.He implied
that these bacteria caused decomposition of
enamel and then the dentin.
Niether Erdl nor Ficinus explained how these
organisms destroyed tooth structure.
Leber & Rottenstein- dental caries commenced
purely as a chemical process but living
organisms continued the disintegration of
enamel & dentin.
Underwood & Miles(1880) SEPTIC THEORY
Acid capable of causing decalcification was
produced by bacteria feeding on the organic
fibrils of dentin.
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 CHEMICO-PARASITIC [ACIDOGENIC] THEORY

Also known as "Miller's chemicoparasitic

theory" as it was first postulated by
Willoughby. D. Miller in the year 1889 .
It proposes that "acids formed due to the
fermentation of dietary carbohydrates by
oral bacteria leads to progressive
decalcification of the tooth structures with
subsequent disintegration of the organic
matrix".
Therefore acidogenic theory states that the
process of dental caries involves two
stages:
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 According to
Miller, there are Dietary

four important carbohydrates

factors, which
can influence the
process of tooth
destruction in
the process of acids Tooth decay
Dental
plaque
dental caries and
these factors are
as follows:

Micro
organisms
.

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 Limitations:
This theory was unable to explain the predilection of
specific sites on a tooth to dental caries . The initiation
of caries on smooth surfaces was not accounted for by
this theory.
Miller believed that dental caries was caused by
multiple species of bacteria .This is understandable
since many bacterial species possess glycolytic
abilities. While current evidence for a specific bacterial
infection in dental caries is tantalizing, the concept is
not disputable.
This theory does not explain why some populations
are caries free.
The phenomenon of arrested caries is not explained
by this theory.

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 Proteolytic theory:
States that organic or protein elements of the
tooth are initial pathways of invasion by
microorganisms.
Enamel lamellae were considered as pathways for
microorganisms in the progress of dental caries.
Acc to Gottlieb & Gottlieb; Diamond & Applebaum
Caries is essentially a Proteolytic process; the
microorganisms invade the organic pathways &
destroy them in their advance. Acid formation
accompanied proteolysis.
The concept of the proteolytic theory was further
extended by Pincus in 1949 and he proposed that
the "sulfatase enzyme" liberated by gram-negative
bacilli, hydrolyze the sulfated mucosubstances of
enamel matrix and therefore liberate sulfuric acid,
glutamic acid and aspartic acid, etc. which
dissolve the mineral portion of the enamel as well.
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 limitations
No satisfactory evidence to claim that
the initial attack on enamel is
proteolytic.
Gnotobiotic studies: caries can occur in
the absence of proteolytic organisms.
To date no one has under physiological
conditions successfully demonstrated
significant loss of enamel tissue
through proteolytic activity.
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Proteolysis chelation theory:
This theory proposed by Schatez et al (1955)
implies a simultaneous microbial degradation
of the organic components (proteolysis) and
the dissolution of the minerals of the tooth by
the process of chelation.
The word chelate is derived from the Greek
word chelas meaning claw, and refers to
compounds that are able to bind metallic ions
as calcium, Iron, copper, zinc and other
metals by the secondary valence bonds. The
resulting chelates are non ionic and usually
soluble.
According to the proteolytic chelation theory
dental caries results from initial bacterial and
enzymatic proteolytic action on the organic
matter of enamel without preliminary
demineralization.
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 Such action, the theory suggests produces an
initial caries and a release of variety of complexing
agents such as amino acids, polyphosphates and
organic acids. The complexing agents then
dissolve the crystalline apatite.
Limitations:
Less than one percent of mature enamel is organic
in nature and the suggestion that this material
upon degradation can give rise to a significant
concentration of chelator sufficient to dissolve
upto 96% mineral matter has no experimental
support.
Also there is no substantial experimental evidence
that the initial carious lesion stems from a break
down of organic matter that is due to proteolytic
action.
While proteolysis chelation is an important
biological phenomenon, its primary role in the
etiology of the dental caries has not been
corroborated.
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 Sucrose chelation theory:
Egglers-Lura(1967) proposed sucrose itself & not
the acid derived from it can cause dissolution of
enamel by forming an ionized calcium
saccharate.
The theory states that calcium saccharates &
calciium complexing intermediates require
organic phosphate which is subsequently
removed from the enamel by phosphorylating
enzymes.
Limitations
The concentration of sulfated polysaccharides in
enamel is very small and not readily accessible as
a substrate for enzymatic degradation.
This is a highly unlikely hypothesis for the
degradation of tooth enamel.

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 Autoimmume theory:
The autoimmune theory of dental caries
suggests that few odontoblast cells at
some specific site within the pulp of few
specific teeth are damaged by the
autoimmune mechanisms. For this reason
the defense capacity and integrity of the
overlying enamel or dentin in those
specific areas are compromised, and they
can be the potential site, for caries
development in future.
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Current concepts of
etiology:

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 Keyes 1960
Traditional Cariogenic
concept bacteria
(dental plaque)

Host factors: Diet:

Tooth Fermentable
Saliva carbohydrate

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Factors influencing caries
etiology:
Microbial flora
Dental plaque
Diet
Tooth
Saliva

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DIRTY MOUTH

100,000,000,000,000 bacteria/ mouth

> 700/ bacterial species.! 32
 Microorganisms:
TYPE OF MICROORGANISM HUMAN DISEASE
CARIES
PIT & S.Mutans Very significant
FISSURE S.Sanguis Uncertain
Lactobacillus Very significant
species By chance
Actinomyces
species
SMOOTH S.mutans Very significant
SURFACE S.salivarus By chance
ROOT A.Viscosus Very significant
SURFACE A.Naeslundii Very significant
S.Mutans Significant
S.Sanguis By chance
DEEP Lactobacilli Very significant
DENTINAL species Very significant
CARIES A.Naeslundii Very significant 33

Other filamentous
Virulence Factors of S. mutans
Specific adherence to tooth surface
using antigen I/II adhesin and GTF

Production of extracellular
polysaccharides (dextran)

Accumulation of intracellular
amylopectin-like polysaccharides
(carbon/energy reserve).
Lactic acid production from sugar
metabolism

High tolerance for acid

IgA proteases
inactivate secretory IgA by detaching
the Fc region of the immunoglobulin 34
 Lactobacillus:
Lactobacilli are Gram +ve, non spore
forming rods that generally grow best
under microaerophillic conditions.
The earlier notion that lactobacilli are the
main etiologic factor(Bunting et al 1925) in
causing dental caries has been discarded.
The population is influenced by dietary
carbohydrate content and intake
frequency.
They represent around 1% of oral flora.
They have low affinity for tooth surface
and are mainly seen in deep dentinal
lesions. 35

 L.casei and L.fermentum are the most
common oral species.
Other oral species include L.acidophilus,

L.salivarius(saliva),
L.brevis,
L.buchneri.
The heavier growth of lactobacilli at
active carious lesions do not imply their
causative role in caries
development.Though they can be
considered as secondary contributors.
Lactobacilli are both acidogenic &
aciduric & could therby multiply in low
ph of plaque & carious lesions.

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Oral Actinomyces:
Gram positive filamentous anerobes
Facultative -A.naeslundii
Anerobic- A.israelii
A.visosus
A.odonotyticus

Actinomyces sps. Is found

significantly in dental plaque & in
increasing proportions on decayed
rooth surfaces.
A.naeslundii predominates in young
children whereas A.viscosus in
teenagers and adults.

Viellonella:
Gram-ve cocci found predominantly
in plaque.
Anticariogenic property. 37
 Evidence of role of bacteria in
dental caries
Studies in animals and humans give following
conclusions
1.Teeth free from bacterial infection do not
develop caries.
2.Antibiotics are effective in reducing caries in
animals and humans.
3.Oral bacteria can demineralize enamel invitro
and produce lesions similar to naturally
occurring caries.
4.Specific bacteria can be isolated & identified
from plaque from various carious lesions
Classical germ-free studies
of Orland et al
1954 38

 Dental plaque
A soft translucent,
and tenaciously
adherent material
accumulating on
the surface of the
teeth.

There are 2
hypothesis
concerning the
pathogenicity of
plaque :
1)Non Specific
plaque hypothesis
2)Specific plaque
hypothesis
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Nonspecific plaque
hypothesis:
In the past, and as an extension of millers
chemico parasitic theory, the total plaque
was viewed as a pathogenic structure
which had to be eliminated or reduced if
caries was to be prevented.
If all plaques were similar in their potential
to induce caries, the main difference
between health and disease states might
be expected in the quantitative aspects of
plaque accumulation.
This possibility carries with it the
implication that mechanical debridement
should be the dominant method of disease
control(loesche-1982).
Further specific anti microbial agents
should be limited in their efficacy since the
accumulation or activity of the old plaque
requires suppression.
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 Specific plaque hypothesis:
It is based on the observation that plaque
is not always associated with disease.
Plaques can be identified as pathogenic
only when they are associated with
clinical disease.
As only few microorganisms are capable
of caries production treatment based on
this hypothesis is aimed at elimination of
the specific pathogenic organisms but not
total plaque elimination.

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 Demonstrated for first time in histologic
preparations by Williams (1897).
It is composed of 80% water & 20% solids.
Bacteria & salivary proteins comprise 50% of
the dry weight of plaque.
It also contains carbohydrates(polymers of
glucans, fructans & heterosaccharides) &
lipids 25% of the dry weight.
Inorganic components- 5-10% of the dry
weight.
The accumulation of plaque on the teeth is a
highly organized and ordered sequence of
events.
Adherent bacteria have special receptors for
adhesion to the tooth surface and also
produce a sticky matrix that allows them to
cohere to each other. 42
Formation of dental plaque:

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 Properties of Cariogenic
Plaque:
The rate of sucrose consumption was
noticeably higher in cariogenic plaques.
The rate of lactic acid formation was
considerably higher in cariogenic plaques.
Bacteria in cariogenic plaques synthesized
more intracellular glycogen-amylopectin-
type polysaccharides.
Upto 20% of sucrose consumed within 15
minutes was converted into intracellular
polysaccharides by cariogenic plaque.
Cariogenic plaques formed approximately
twice as much extra cellular
polysaccharides from sucrose as did
noncariogenic plaques.
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 Cariogenic plaques contained higher levels
of streptococcus mutans than
noncariogenic plaques.-Noncariogenic
plaques harboured higher levels of
S.sanguis and Actinomyces than cariogenic
plaques.

Noncariogenic plaques had significantly

higher proportion of dextranase producing
organisms.

Noncariogenic plaques had higher levels of

veilonella and contained slightly lower
concentration of lactic acids and slightly
higher conc of acetic and propionic acids.
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 Tooth:
COMPOSITION:
Studies indicate that the surface enamel is
more resistant to caries than subsurface
enamel.
Surface enamel is more highly mineralized
lower in CO2 , dissloves at slower rate in
acids , contains less water and tends to
accumulate greater quntities of flouride zinc
lead & iron than the subsurface enamel.
These factors apparently contribure to
caries resistance & are partly responsible for
the slow disintegration of surface enamel
than the underlying enamel in initial carious
lesions.
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MORPHOLOGIC CHARECTERISTICS:
Deep narrow occlusal fissures, buccal or
lingual pits
Entrapment of food, bacteria, debris

Rapid carious development.

POSITION:
Malaligned, Out of poisition, Rotated teeth

Difficult to cleanse, favour accumulation of

food & debris

Dental Caries 47
 Saliva:
COMPOSITION:
1. Inorganic constituents:
Positive ions- Ca ,H+, Mg, K
Negative ions- carbondioxide, carbonate,Cl,
F,phosphate, thiocyanate.

2.Organic constituents:
Carbohydrate-Glucose
Lipids-cholesterol, lecithin
Nitrogen nonprotein- NH3,nitrites, urea
and aminoacids.
Nitrogen protein-globulin, mucin, total
proteins
Enzymes- carbohydrases (amylase, maltase),
proteases (trypsin), oxidases (catalase, oxidase)
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 Role of saliva:
1)Bacterial clearance
2)Direct antibacterial activity
3)Buffer
4)Remineralization

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pH OF SALIVA:
It is determined mainly by the bicarbonate
concentration.(85%) .
Phosphates and proteins in saliva constitute
the other buffer systems, but the
constitution of these in saliva are too low to
be of significance. So the pH will vary
according to the bicarbonate content.
The buffering capacity of saliva is a very
significant property affecting the carious
process.
The saliva pH increases with flow rate. It
may be slightly acidic as it is secreted at an
unstimulated flow rate but it may reach a
pH of 7.8
Other salivary components contributing to
the ability of saliva to neutralize the acidity
are ammonia, urea and statherin.
Sialin is an arginine peptide which is the
recently described pH rise factor present in
saliva which rapidly clears glucose from
plaque, increases base formation and
elevates pH in the plaque.

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 Concept of critical pH
pH at which any particular saliva ceases to
be saturated with calcium and phosphorus
ions is referred to as critical pH.
The critical pH value is 5.5
Below this value the inorganic constituents
dissolve .
With conc. of H+ ions, more phosphate
ions leave the solid apatite phase.
Above this pH the remineralization takes
place.

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QUANTITY OF SALIVA:
The normal secretion is 700 to 800 ml per
day. It may influence caries incidence. This is
especially evident in cases of salivary gland
aplasia and xerostomia in which salivary flow
may be entirely lacking with rampant dental
caries the typical result.

VISCOSITY OF SALIVA:
It depends on the mucin content.A high
caries incidence is associated with thick
mucinous saliva.
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 Factors affecting
mineralization:
Statherin : is an acid peptide
Contains high levels of proline, tyrosine and
phosphoserine.
They inhibit spontaneous precipitation of
calcium phosphate salts from supersaturated
saliva and prevents crystal growth favoring
remineralization .

Histatins : a group of histadine rich proteins.

They bind to hydroxyapatite and prevent
calcium phosphate precipitation from a
supersaturated saliva enhancing the stability of
hydroxyapatite
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 Proline-Rich proteins :acidic proline rich
protein.
Prevents the precipitation of calcium
phosphate from the supersaturated saliva.
A decrease in the proline rich proteins
resulted in sulcal and smooth surface caries.

Cystatins : they prevent the action of

potentially harmful protease on the soft
tissue of the oral cavity.
Protects the tooth structure by promoting
super saturation of saliva with calcium and
phosphate.

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Mucins : plays multiple roles
Salivary mucins are MG1 and MG2.

1. MG1 tightly binds to the tooth surface.

protects the tooth surface from the chemical
and physical attack including acid change.

2. MG2 can also bind but can be easily

displaced
By aggregation. it promotes clearance of oral
bacteria.
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Bacterial clearance:
Around 1 1.5 l of saliva is secreted by
various glands in a day which lubricates
the oral tissues, bathes the teeth and
plaque before being swallowed.
Flushing action is adequate to remove
virtually all of non adherent bacteria
Most effective during mastication or oral
stimulation.
Large volumes of saliva also dilute and
buffer the plaque acids
56
 ANTIBACTERIAL AGENTS IN SALIVA:

1)Lactoferrin : Iron binding protein

Prevents iron from being used
by the organism for metabolism.
Organisms susceptible: Aerobic
Facultative
anaerobic bacteria.

2)Lysozyme : has a direct antimicrobial

affect.
They bind to the bacterial cell
wall and Destabilizes the cell
wall allowing autolysis to take place.
57
3)Peroxidase : produced from the acinar cells
of the major salivary
glands.
The enzyme contains heme
and uses thiocyanate and
hydrogen peroxide produced by the oral
bacteria inhibiting glucose
metabolism in bacteria.
4) Salivary IgA: produced by the plasma cells
present in the salivary
glands.
They are multivalent antibodies.
They bind to bacterial surface and prevent
adherence.
58
 Remineralization:

Saliva is supersaturated with Ca 2+ and P

ions.
When local pH is high enough(>5.5),
demineralization process may be reversed
by remineralization of damaged tooth
structure.
This results in a dark, harder, pigmented
surface termed as arrested caries.
On dentinal surfaces, it is termed eburnated
dentin
59
 Pathophysiology of caries:
Caries development is not a single
event of lowered pH but caused by of
many episodes of long duration
demineralization (lowered pH).
The rate of caries progression
depends on the dynamic equilibrium
between factors promoting and
opposing demineralization.

60
61
Histopathology of caries:
Enamel caries:

62
Zones of dentinal caries:
1. Normal dentin
2. Subtransparent dentin
3. Transparent dentin
4. Turbid dentin
5. Infected dentin

63
 Caries diagnosis
In Greek Dia means thoroughly
Gignoska means to know

WHAT IS DIAGNOSIS ?
it is the art or act of identifying a
disease
Diagnosis : is a determination and
judgment
of variation from normal
..As utilization of scientific knowledge for
identifying a disease process and to
differentiate it from other disease 64

 Conventional Advanced Methods
1. Visual and tactile 1. Dental digital
examination radiography
mouth mirror & 2. Subtraction
probe radiography
tooth separation 3. Tuned aperture comp.
tomography
2. Radiographic method 4. Fiber optic
transillumination
IOPA
5. Digital fiber optic
bite wing
transillumination
3. Xeroradiography
6. Quantitative light
4. Dyes induced fluorescence
7. Laser fluorescence

8. Electrical conductance
measurement
65
9. Electric current

 Visual and tactile examination:

Conventional method for detection

Visual examination is aided by
compressed air
Tactile examination mirror and
probe

66
 Radiography:
Radiography has been gold standard
to detect the dental caries.
Primarily for the detection of lesions
on proximal surfaces of teeth that
are not clinically visible Occlusal
caries may also be detected
once it has progressed into dentin.

67
 Principle:
Radiographic diagnosis of caries the
mineral
content of enamel and dentin
decreases,
decrease in the attenuation of X-ray
beam as it passes through the teeth
area appears radiolucent on the
radiograph

68
 Conventional radiography:
Many techniques available,
two types of techniques are
popular and commonly practiced
IOPA
Bitewing
Bite wing radiography:
Used to detect proximal caries
Important to detect incipient
lesions at contact points.
Cervical margins of restoration
Alveolar crest height
Lamina dura
Size of pulp chambers
69
 Dyes:
Dye are used to visualize a
substance from its routine
background or if several
objects have similar
appearance colouring by dye is
to discriminate between them
for identification.
The observation of dye may
be:
Qualitative to observe the
colour or differentiate coloured
objects from non- coloured
ones.
Quantitative - Intensity of
colour is to be determined
In caries diagnosis qualitative
examination ie visual
appearance of dye is sufficient.
70
Reqirements of dyes.
Dyes for detection of caries in enamel
Procion
Calcein
Fluorescent dye studied invitro but
invivo
Brilliant blue enhance diagnostic
quality of during transillumination
Dyes for detection of caries in dentin:
2 layers of carious dentin

outer carious dentin inner

carious dentin
(Infected, unremineralizable)
(uninfected remineral.)

71
Caries detector:
Composition:
0.5% Basic Fuchsin + Propylene
Glycol.
technique using basic fuchsin
which aids in differentiating 2 layers
of carious dentin was introduced.
Dye was considered as
carcinogenic
Replaced by Acid Red 52 ( Acid
Rhodamine B) which functions almost
same as fuchsin when dissolved in 1%
solution of propylene glycol.
Disadvantage:
Level of infection in stained and
unstained dentin at the DEJ were
measured not all dye stainable
dentin was infected
72
Caries activity tests:
Caries activity : the increment of
active lesions (new or recurrent)
over a slated period of time.
Ideal requisites: (SYNDER)
MAXIMUM CORRELATION

RELIABILITY AND VALIDITY

SIMPLICITY

RAPID RESULTS

INEXPENSIVE
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NON-INVASIVE
Various caries activity tests:
LACTOBACILLUS COLONY COUNT
CALORIMETRIC SNYDER
THE SWAB TEST
S.MUTANS LEVEL IN SALIVA
DIP-SLIDE METHOD
SALIVARY BUFFER CAPACITY TEST
ENAMEL SOLUBILITY
SALIVARY REDUCTASE TEST
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 Bibliography:
1) Sturdevant's Art and Science of
Operative Dentistry-5th edition
2) Cariology Ernest Newbrun- 3rd edition
3) Essentials of Preventive and Community
dentistry- Soben Peter -2nd edition
4) A Textbook of Oral Pathology sixth
edition shafers
5) Principles of preventive & community
dentistry Soben Peter

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THANK YOU

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