Dental Caries

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DENTAL CARIES

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Transcript of Dental Caries

Page 1: Dental Caries

DENTAL

CARIES

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Contents

Introduction

Etiology of dental caries

Histopathology of dental caries

Diagnosis of dental caries

References

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Introduction

Dental caries continues to be a major problem

in dentistry and should receive significant

attention in everyday practice, not only from

the standpoint of restorative procedures but

also in terms of preventive measures designed

to reduce the problem.

Caries is on the decline in the industrial

countries but it is on the increase in the

developing countries due to increased sugar

consumption.

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

It is essential to understand that cavitation in teeth are signs of bacterial infection.

It has effected humans since prehistoric times, but the prevalence of this disease has increased greatly in modern times due to dietary changes.

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Dental caries 5

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Tooth is covered by plaque, which consists mainly of bacteria. Plaque is often found close to the gum, in between teeth, in fissures and at other "hidden" sites.

Demineralization: When sugar and other fermentable carbohydrates reaches the bacteria, they form acids which start to dissolve the enamel - an early caries lesion occurs due to loss of Calcium and Phosphates

Remineralization: When sugar consumption has ceased, saliva can wash away sugars and buffer the acids. Calcium and Phosphates can again enter the tooth. The process is strongly facilitated by fluorides

A CAVITY occurs if the Demineralization "wins" over the Remineralization over time 6

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

Progression of dental caries 7

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Acc. to WHO it is defined as a localized post

eruptive pathological process of external origin

involving softening of the hard tooth tissue and

proceedings to the formation of a cavity.

It can also be defined as localized chemical

dissolution of the tooth surface caused by

metabolic events taking place in the biofilm

(dental plaque) covering the affected area.

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It may develop at any tooth site where biofilm

develops and remains for a period of time.

Biofilm is a prerequisite for caries lesion to

occur. Biofilm is characterized by continued

microbial activity resulting in continued

metabolic events in the form of minute pH

fluctuation.

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EPIDEMIOLOGY

Dental caries may be considered a disease of

modern civilization , since prehistoric man rarely

suffered from this form of tooth destruction .

Anthropologic studies of VON LENHOSSEK

revealed that the Dolicocephalic skulls of men

from pre Neolithic periods (12000 BC) did not

exhibit dental caries but skulls from

Bracycephalic man of the Neolithic periods

(12000 to 3000 BC) contained carious teeth.

The cervical areas of teeth in older persons

were frequently affected .

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CARIES SUSCEPTIBILITY OF

INDIVIDUAL TEETH

BREKHUS (1931 ) studied a group of students at the university of Minnesota and reported the following caries susceptibility incidence of the teeth

Upper and lower first molar : 95 %

Upper and lower second molars : 75 %

Upper second bicuspids : 45%

Upper first bicuspid :35%

Lower second bicuspids : 35%

Upper central and lateral incisor : 30 %

Upper cuspids and lower first bicuspids : 10%

Lower central and lateral incisors : 3 %

Lower cuspids : 3%

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ETIOLOGY OF DENTAL

CARIES

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Etiology

Development of dental caries depends on :

1. Microflora: acidogenic bacteria that colonize

the tooth surface.

2. Host :quantity and quality of saliva , quality of

the tooth.

3. Diet : intake of fermentable carbohydrates,

especially sucrose ,but also starch.

4. Time : total exposure time to acids produced

by the bacteria of the dental plaque.

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Caries Tetralogy[Newbrun 1982]

Includes a fourth

factor, time to the

still existing

concept of Keyes,

depicting the

significance of

changes taking

place over a

period.

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Classification of dental caries

ACCORDING TO MORPHOLOGY

-Pit and fissure caries

-Smooth surface caries

ACCORDING TO CHRONICITY

-Acute dental caries

-Chronic dental caries

ACCORDING TO PROGRESSION

-Primary caries

-Secondary (Recurrent )caries

-Arrested caries

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ACCORDING TO SEVERITY AND PROGRESSION

-rampant caries

-nursing caries

-radiation caries

ACCORDING TO PART OF TOOTH STRUCTURE INVOLVED

-Enamel caries

-Dentinal caries

-Cemental caries

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PIT AND FISSURE CARIES

Pit and fissure with high steep walls and

narrow bases are prone to develop caries.

Retention of food debris and microorganisms.

Early caries appear brown or black, soft ‘catch’

of a fine explorer point.

Lateral spread of caries through a narrow

opening at the DEJ.

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SMOOTH SURFACE CARIES

Early appears as a faint white opacity of the enamel without loss of the continuity of the surface.

Preceded by the formation of a microbial or dental plaque.

As caries penetrates enamel,it assumes bluish white appearance.

Proximal caries begins just below contact point.

The typical cervical carious lesion is crescent shaped cavity with chalky area.

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ACUTE DENTAL CARIES

Rapid clinical course resulting in early pulp

involvement with pain.

Progress rapidly so less time for secondary

dentin depositionis present

E.g.Nursing bottle caries commonly affects 4

deciduous maxillary incisors. It is a type of

RAMPANT caries which primarily affects all

deciduous incisors.

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CHRONIC DENTAL CARIES

Progresses slowly and tends to involve pulp

much later.

Sufficient time for sclerosis of dentinal tubules

and secondary dentin deposition.

Carious dentin stains deep brown.

PAIN is not a common feature.

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RECURRENT CARIES

Caries occuring in immediate vicinity of a

restoration.

Usually due to inadequate extension of the

original restoration favoring retention of debris.

Poor adaptation of filling material to the cavity

which produces a leaky margin.

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ARRESTED CARIES

Static or stationary caries which do not show

any tendency for further progression.

Occurs exclusively in caries of occlusal

surfaces characterised by a large open cavity

which lack food retention.

EBURNATION OF DENTIN : gradual

burnishing of superficial softened and

decalcified dentin until it takes on a hard

brown stained, polished appearance.

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RAMPANT CARIES

It occurs as a sudden , rapid and almost

uncontrollable destruction of teeth , involving

surfaces of teeth that are ordinarily caries

free(proximal and cervical surfaces of anterior

teeth including the mandibular incisors get

affected)

A caries increment of 10 or more new lesions

over a period of about a year is characteristic

of rampant caries attack

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NURSING CARIES

It is a specific form of rampant decay of

primary teeth of infants and toddlers.

Affects maxillary primary incisors due to

prolonged nursing habit esp. when the child is

sleeping

Also named as baby bottle tooth decay or

early childhood caries

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RADIATION CARIES

Common complication of radiotherapy of oral

cancer lesions and radiation induced

xerostomia

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Hypothesis concerning the etiology

of caries

Two hypothesis:

Older one : promotes the universal presence

of potential pathogens in plaque and assumes

that all accumulation of plaque are pathogenic.

Latter one promotes that accumulation of

plaque could be regarded as normal in the

absence of disease.

Plaque is assumed pathogenic only when

signs of disease are present.

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The difference between two hypothesis was

identified and discussed by Loesche:

First one : non specific plaque hypothesis

Second one: specific plaque hypothesis

Problem with non-specific hypothesis was that

it requires a therapeutic goal that completely

eliminates plaque in all patients that requires a

continuous therapy directed to total plaque

elimination.

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Acc . to specific theory ,plaque can be

identified as pathologic only when they are

associated with clinical disease. So treatment

can be aimed at elimination of the specific

pathogenic organisms.

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Caries- latin word –rot or decay.

Its etiology is agreed to be a complex problem

complicated by many indirect factors that

obscure the direct causes.

Many theories have evolved through years of

investigation and observation attempting to

explain its etiology.

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The early theories

1. The legend of worms : the earliest reference is from the ancient sumerians known as legend of worms. This dates back around 5000 BC . The idea behind this was that caries was caused by worms and worms are the cause of toothache.

2. Endogenous theory: it was advocated by Greek physicians, who proposed that dental caries is produced by internal action of acids and corroding humors.They also proposed the Vital theory of tooth decay,which postulated that tooth decay originated from within the tooth itself.

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3. Chemical theory:Parmly in 1820 observed that dental decay affected externally and not internally. He proposed that unidentified chemical agent was responsible for caries.

4. Parasitic theory:Erdl in 1843 was first to relate microorganisms to caries as a positive agent. Ficnus in 1847 attributed dental caries to denticolae(decay related to microorganisms). But this was soon disseminated as it was proposed that dental caries commenced as a purely chemical process and bacteria were essential for caries as an exogenous source of the acids.

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Miller‟s chemico-parasitic theory OR

Acidogenic theory

Proposed by Willoughby D Miller in1882.

He stated that caries is caused by acids

produced by microorganisms of the mouth.

“Dental decay is a chemico-parasitic process

consisting of two stages , the de-calcification

of enamel , which results in its total

destruction and the de-calcification of dentin

as a preliminary stage,followed by dissolution

of the softened residue”

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The acid that affects the de-calcification is

derived from the fermentation of starches and

sugars lodged in the retaining centres of the

teeth.

He isolated numerous microorganisms, some

were acidogenic and others were proteolytic.

A no. of these bacteria were capable of

producing lactic acid.

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He proposed that caries was not caused by

any single organism but a variety of

microorganisms.

Essential factors in caries process:

1. Microorganisms

2. Carbohydrate substrate

3. Acid production

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This theory is the backbone of current

knowledge and understanding of the etiology

of dental caries.

Drawbacks : theory was unable to explain the

predilection of specific sites on a tooth to

caries and the initiation of smooth surfaces

was not accounted by this theory.

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The proteolytic theory

The previous theory was not wholly accepted.

Then this theory came into existence.

Proposed by Gottlieb and Gottlieb(1944).

This theory proposed that the organic

material(enamel lamellae and rod sheaths) or

protein elements are the initial pathway of

invasion by microorganisms.

They also admit that acid formation

accompanied the proteolysis.

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Pincus(1949) proposed that enamel proteins

are mucoproteins, yielding sulphuric acid upon

hydrolysis.

In support of this theory Gram negative bacilli

capable of producing sulfatase were also

isolated.

This acid dissolves the enamel, combining

with the calcium to form calcium sulphate.

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Drawbacks : no sulfatase has been

demonstrated at the site of carious lesion.

No such enzyme has also been demonstrated

in the oral cavity.

The proteolysis of organic matrix of dentin may

indeed occur after demineralization and there

is no satisfactory evidence to support the claim

that the initial attack on enamel is proteolytic.

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The proteolysis-chelation theory

Proposed by Schatz et al (1955).

Proposed a simultaneous microbial

degradation of the organic components

(proteolysis) and the dissolution of minerals of

the tooth by the process known as chelation.

Chelation is a process involving the

complexing of a metallic ion to a complex

substance through a coordinate covalent

bond(highly stable , poorly dissociated).

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This theory considered caries to be a bacterial

destruction of teeth where the initial attack is

essentially on the organic components of the

enamel. this breakdown product has chelating

property hence dissolves the minerals in

enamel (at a neutral or alkaline ph).

Thus this theory suggested that

demineralization of enamel could arise without

acid formation.

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Drawback : it was concluded that saliva and

plaque do not contain substances in sufficient

amount to chelate calcium in detectable

amounts from enamel.

Also chelation is unlikely to be involved in the

initiation of the lesion, it may play a minor role

in the established lesion.

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Sucrose chelation theory

Proposed by Egglers-Lura (1967).

He proposed that sucrose itself and not the

acid derived from it cause dissolution of

enamel by forming an ionized calcium

saccharates.

This theory stated that calcium saccharates

and calcium complexing intermediaries require

inorganic phosphate which is subsequentaly

removed from the enamel by phosphorylating

enzymes.

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Drawback : since saliva is an abundant source

of inorganic phosphates for bacterial

utilization, it is highly improbable that depletion

of phosphate in plaque by oral microbial

metabolism results in phosphate withdrawl

from enamel.

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Role of plaque in dental caries

Dental plaque is soft, translucent and

tenaciously adherent material accumulating on

the surface of teeth and not readily removed

by rinsing with water .

It is composed of bacteria and their by-

products.

Accumulation of plaque on teeth is highly

organized and ordered sequence of events

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It is estimated that 1mm³ of plaque weighing

about 1mg contains more than 200 million

bacteria.

A few specialized organisms (streptococci )

are able to adhere to oral surfaces like mucosa

and tooth surface.

These bacteria produce a sticky matrix that

allows them to coadhere to each other .

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Plaque growth

The initial bacteria are called pioneer bacteria

or colonizers. (mainly streptococcal strains).

These bacteria proliferate and spread laterally

to form a mat-like covering over the tooth

surfaces.

When the entire surface is covered ,growth of

colonies increases the thickness of plaque .

Further growth of bacteria produces a vertical

growth away from the tooth surface forming

vertical columns called palisades .

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These bacteria allow the adherence of other

organisms like filamentous bacteria,which are

unable to adhere directly to the tooth surface.

Proliferation of new invading bacteria produce

entangled masses of filaments forming

“corncob” like structure.

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Early stages of plaque

succession

After professional removal of all organic material and bacteria from the tooth surface , a new coating of organic material begins to accumulate immediately.

Within 2 hrs, a cell free , structureless organic film, the pellicle, covers the tooth surface.

Some of the proteins of pellicle are biologically active and have a significant impact on microorganisms attemptimg to colonize the tooth surface.

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The early stages of recolonization of the

cleaned tooth surface involves adhesion

between the pellicle and the pioneering

bacteria.

S. sangius , A. viscosus and

peptostreptococcus are the main pioneering

species capable of attaching to the pellicle

within 1 hr after tooth cleaning.

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The adhesion process is selective and

requires specific organism receptor capable of

binding to certain areas on the precipitated

salivary proteins of the pellicle.

The enzyme glucosyltransferase may be

crucial in the adherence of organisms to the

pellicle when sucrose is present as it

enhances the polymerization of the

extracellular matrix that helps in the formation

of tenaciously adherent colonies.

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Late stages

Late stages are mainly responsible for causing

caries.

In early stages there are primarily aerobic

communities lacking pathogenic potential.

As the plaque matures,more and more acid is

produced from metabolism mainly lactic acid.

This increased production of acid leads to

prolonged drop in pH , increasing the potential

for enamel demineraliztaion.

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Tooth habitat for pathogenic plaque

The tooth surface is stable and covered with

the pellicle and thus the ideal site for the

attachment of many oral streptococci.

If left undisturbed , plaque builds rapidly to

sufficient depth to produce anaerobic

environment.

Some favorable tooth habitats for plaque are:

Pit and fissures

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Smooth enamel surface immediately gingival

to the contact area and in the gingival 1/3 of

facial and lingual surface.

Root surface near the cervical line.

Subgingival areas.

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Pits and fissures

Highest prevalence of all dental caries.

Provide excellent shelter for organisms.

The relative proportion of organisms most

probably determine the cariogenic potential of

the pits and fissures.

The appearance of microorganisms in pits and

fissures is followed by caries 6-24 months

later.

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Sealing the pits and fissures just after tooth

eruption may be the most important event in

their resistance to caries.

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Smooth enamel surfaces

The proximal enamel surfaces gingival to the

contact area are the 2nd most susceptible area

to caries.

In very young patient,gingival papilla fills

completely the interproximal spaces under the

proximal contact.

So proximal caries are less likely to develop

where the favorable soft tissue architecture

exists.

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Conversely, apical migration of papilla creates

more habitats for surface colonizing bacteria.

The gingival aspect of the facial and lingual

smooth enamel surface is not rubbed by the

bolus of food and not properly cleaned by the

brush.

These surface areas are habitats for the

caries- producing mature plaque.

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Root surface

The proximal root surface , often is unaffected

by the action of oral hygiene procedures,

because of its concave anatomic surface.

This favors the formation of mature, caries

producing plaque and thus root caries lesion.

Also, the facial and lingual root surface when

exposed to the oral environment harbors

caries producing plaque.

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Role of microorganisms

To initiate carious lesion in enamel , the

organisms must also be able to colonize the

tooth surface.

The most important bacteria responsible for

carious lesion are- Strepococcus mutans.

The second bacteria closely related to caries

is Lactobacillus.

It was proposed that one or more organisms

are implicated in the initiation of caries

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While others distinctly different organisms may

influence the progression of disease.

Cariogenic bacteria:

S . mutans

S. salivarius

S. mitior

S.oralis

S.milleri

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S. sangius

Peptostreptococcus intermedius

Lactobacillus acidophillus

L . casei

A. viscosus

A. neaslundii

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Localization of bacteria related to

caries

Type of caries

1. Pit and fissure

2. Smooth surface

organisms

S. mutans (very significant)

Lactobacillus (very significant)

S . Sangius (uncertain)

Actinomyces (by chance)

S. mutans (very significant)

S. salivarius (by chance)

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3. Root surface

4. Deep dentinal

caries

A. viscosus (very significant)

A. naeslundii (very significant)

S. mutans (significant)

Lactobacilli sp. (very significant)

A. naeslundii (very significant)

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Role of acids

Carbohydrate degradation occurs through

enzymatic breakdown and the acid formed are

chiefly lactic acid although others such butyric

acid are also formed.

The mere presence of acid in the oral cavity is

of far less significance than the localization of

acids upon the tooth surface.

Generally , monosaccharides and disaccarides

result in the greatest fall in plaque pH.

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Anaerobic catabolism of carbohydrates called

fermentation predominates in plaque. After

breakdown one molecule of glucose breaks

down into two molecules of lactic acid.

Bacteria :

Homofermenters (streptococci, lactobacilli)

Heterofermenters

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Organisms which produce 90 % or more lactic

acid as the end product are called homo-

fermentative.

Organisms which produce a mixture of

metabolites including other organic acids such

as propionic , Butyric acid, Ethanol etc are

called hetero-fermentative.

The proportion of lactic acid and other organic

acid formed by plaque may be markedly

affected by growth conditions and the type of

bacteria present.

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Caries is a multifactorial disease in which there is interplay of four primary factors :

Host

Microbial flora

Substrate

Time

Thus, caries require a susceptible host, a cariogenic flora, and a suitable substrate that must be present for a sufficent time.

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Factors

A. Tooth

B. Saliva

Components

Composition

Morphologic characteristics

Position

Composition

pH

Quantity

Viscosity

Antibacterial factors

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C. Diet

D. Systemic conditions

Physical factors (quality

of diet)

Local factors

(carbohydrate content,

Vitamin

content,Fluoride

content)

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Tooth factors

Composition of teeth : the composition of teeth

undoubtedly influence the initiation and the

rate of progression of a carious lesion .

Composition of enamel : enamel is the hardest

calcified tissue in the body, because of its high

content of mineral salts and their crystalline

arrangement.

Enamel: inorganic=96%, organic=4%.

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Enamel attains a maximum thickness of

2.5mm on the cusps of the molars, thinning

down to almost a knife edge at the neck of the

tooth.

Acc. to Brudevold et al surface enamel is more

resistant to caries than subsurface enamel.

Surface enamel is more highly mineralized .

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Tends to accumulate greater quantities of fluoride, zinc , lead, iron etc than subsurface enamel.

Also initial carious lesions indicate that marked decalcification is observed in subsurface enamel while the outer surface is relatively intact.

The surface dissolves at a slower rate in acids, Contains less water and has more organic material than subsurface enamel.

These factors apparently contribute to caries resistance and are partly responsible for slower degradation of surface enamel than the underlying enamel in initial carious lesion

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Composition of dentin: dentin forms the bulk

and general form of the tooth.

Dentin : inorganic=65%

organic=35%

The dentinal tubules form a passage for

invading bacteria , resulting in rapid

penetration and spread of caries to the pulp.

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Composition of cementum: cementum is the

mineralized dental tissue, covering the

anatomic roots of human teeth.

Cementum : inorganic=45-50%

organic=50-55%

Cementum has the highest fluoride content of

all the mineralised tissues.

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Physical characteristics

Tooth size:it has been assumed that low caries

may have smaller teeth and the larger teeth

were found more caries susceptible and are

found in the oral cavity for a shorter time

period .

the effect of tooth size would be negligible in

comparison with the combined effects of other

factors.

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Morphologic characteristics

The morphologic characteristics of tooth have

been suggested as influencing the initiation of

dental caries.

Caries susceptibility in the permanent dentition

may be ranked in the following order :

1. Fissures of molars

2. Mesial and distal surface of first molars.

3. Mesial surface of 2nd molars and Distal

surface of 2nd premolars.

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4. Mesial and distal surfaces of the maxillary first

premolars.

5. Distal surfaces of the canines and mesial

surface of md. 1st premolar

6. Proximal surface of max. incisors.

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Fissures : the only morphologic feature which

conceivably might predispose to the

development of caries is the presence of deep,

narrow, occlusal fissures or buccal or lingual

pits.

Such fissures tend to trap food, bacteria and

debris, so caries may develop rapidly in these

areas.

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But as the attrition advances, the inclined

planes become flattened , providing less

opportunity for entrapment of food in the

fissures, and the predisposition towards the

caries diminishes.

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Surfaces: certain surfaces of teeth are more

prone to decay , whereas other surfaces rarely

show decay.

md. 1st molar: occlusal > buccal > mesial >

distal >lingual.

Max. 1st molar: occlusal >mesial>lingual>

buccal>distal.

Max. LI: lingual surfaces are more susceptible.

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All available evidences indicate that alteration

of the tooth structure by disturbances in

formation or in the calcification is of only

secondary importance in dental caries. The

rate of caries progression may be influenced ,

but caries initiation is affected only to a very

little extent.

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Morphology of CEJ

An exposed CEJ is a potential area of plaque

retention . So root caries tend to develop along

the CEJ.

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Exposure of root surfaces

In the young , healthy adult, root surfaces like

the CEJ are not exposed to the oral cavity.

Prevalence of exposed root surfaces is age-

related or from gingival recession associated

with periodontal disease.

Morphologically, the surface of intact

cementum and the CEJ are very rough ,

compared to the enamel surface. And the

rough surface is highly retentive to plaque .

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Position of tooth

Teeth which are malaligned, out of position ,

rotated or otherwise not normally situated may

be difficult to cleanse and tend to favor the

accumulation of food and debris.

This in susceptible persons would be sufficient

to cause caries in a tooth .

The position seems to be a minor factor in the

etiology of caries.

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Saliva and dental caries

Introduction :saliva is the primary means by

which the pt. exerts control over its oral flora.

Who made the 1st observation of the influence

of saliva on caries is hidden in the mists of

time, but around 1900 there were several case

reports on the deleterious effects of absence

of saliva.

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Functions of saliva

Saliva has manifold functions in protecting the

integrity of the oral cavity from food residue ,

debris and bacteria :

1. Saliva has some buffering effect against

strong acids and bases.

2. Saliva provides the ions needed to

remineralize the teeth.

3. Saliva has antibacterial, antifungal and

antiviral capacities.

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The principal properties of saliva that protects

the teeth against caries are:

1. Dilution and clearance of dietary sugars.

2. Neutralization and buffering of the acids in

plaque.

3. Supply of ions for remineralization.

4. Both endogenous and exogenous antiplaque

and antimicrobial factors.

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An important function of saliva is dilute and

eliminate substances. This is a physiological

process referred to as salivary clearance or

oral clearance.

After an intake of sugar, the salivary glands

will be stimulated by the taste or chewing to

increase the flow rates, resulting in swallow,

which eliminate some of the sugar from the

oral cavity which inturn helps in caries

prevention

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pH of saliva:

The pH at which saliva ceases to be saturated

with calcium and phosphate is referred to as

critical pH .

Critical pH= 5.5

The main determinants of critical pH are the

total calcium and phosphate conc. in saliva.

This value was determined by Schmidt-

Neilsen, 1946.

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At this pH no demineralization or

remineralization will take place.

Below this pH, demineralization occurs as

phosphate ion of apatite crystals get converted

to hydrogen phophates by increased hydrogen

ion.

Thus, solubility of tooth depends on the pH of

surrounding medium.

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In the pH range of 2-6 the solubility increases by a factor of 10 for each pH drop of one unit.

Stephan curve: he stated that inspite of saliva buffer capacity the plaque pH will drop immediately after the sugar intake to values below critical pH, whereafter it slowly returns to normal.

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Under resting conditions,pH of plaque is reasonably constant,6.9-7.2

Following exposure to sugars the pH drops very rapidly(in few minutes) to lowest level(5.5 to 5.2-critical pH) and at this pH,the tooth surface is at risk

During this critical period,the tooth mineral dissolves. Repeated fall of pH over a period of time leads o more and more mineral loss from the tooth surface,resulting in initiation of dental caries

Later slowly it returns to original value over a period of 30-60 minutes,approximately

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Quantity of saliva:

In patients with reduced quantity of

saliva(salivary gland aplasia or xerostomia) ,

the cleaning properties of saliva in the mouth

are impaired.

Which leads to low oral sugar clearance,

which increases caries risk.

the unstimulated flow rates has been found to

be diagnostically more important than the

stimulated one.

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Individuals with unstimulated flow rates <0.2

ml/min have an elevated demineralization rate

and a high risk of developing caries.

This low flow rates also favors acidic

environment, with an increase in cariogenic

microflora.

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Thus, a low saliva flow rate not only will

prolong clearance time and periods with low

plaque pH, but may also change the ecology

of mouth.

In such cases the rate of progression of caries

is also faster as compared to cases with

normal flow rates.

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Viscosity :

Occasional workers have reported that a high

caries incidence is associated with thick

mucinous saliva.

The viscosity of saliva is due largely to the

mucin content derived from submaxillary,

sublingualand accessory glands.

The significance of this factor is not clear.

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Role of diet

The role of diet and nutrition factor deserves special consideration because of the often observed differences in caries incidence of various population who subsist on dissimiliar diets.

A diet rich in fermentable carbohydrate is indisputably a very powerful risk factor for caries.

Following consumption , depending on the quality of salivary gland function , a certain amount of saliva is stimulated by particular characteristic of food, such as taste, intensity of mastication.

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Fermentable carbohydrates

1.Monosaccharides

Glucose

Fructose

2. Disaccharides

Sucrose

Maltose

Lactose

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3. Polysaccharides

Glucan

Fructan

Mutan

Starch

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Sucrose is regarded as the most important in

dental caries.

Sucrose is refined from sugar cane or beet

and is the most common dietary sugar .

The dietary sugar all diffuse rapidly into the

plaque and are fermented to lactic acid or can

be stored as intracellular polysaccharides by

the bacteria.

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This mechanism prolongs the fall in pH and

promotes a suitable environment for acidogenic

bacteria.

Sucrose is unique as it is the substrate for

production of extracellular polysaccharide

(fructans and glucan) and insoluble matrix

polysaccharide (mutans).

Thus , sucrose favors colonization by oral

microorganisms and increase the stickiness of

plaque, allowing it to adhere in larger quantities to

the teeth.

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Because of this effect on the quality of plaque ,

sucrose is considered to be somewhat more

cariogenic than other sugars.

Also other dietary disaccharides and

monosaccharides are regarded as risk factors.

All are rapidly fermented on plaque-covered

tooth surfaces.

Glucose, fructose, maltose give identical fall in

pH but for lactose fall in pH is smaller.

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In frequently consumed snack food such as

sweets and drinks less fermentable and non-

cariogenic sweeteners are increasingly being

used as substitute for potentially cariogenic

sugars.

These are : caloric or non-caloric sweeteners.

Caloric: sorbitol, xylitol, mannitol

Non-caloric : saccharin, cyclamate, aspartame

They cannot be fermented by acidogenic

bacteria.

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Physical properties of food and cariogenicity:

The Physical properties of food may be significant by affecting food retention, food clearance, solubility and oral hygiene.

Physical properties of food may improve the cleansing action and reduce retention of food with in the oral cavity and increase saliva flow

Physical nature of Diet:

Roughage food cleans the teeth from adherent debris during mastication.

Soft refined food tends to adhere to the teeth and are not removed because of general lack of roughage.

Mechanical cleansing by detergent foods may have some role in caries control.

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Carbohydrate content of diet

Most important factor in dental caries

Vitamin content of Diet

Vitamin A: Definite effect on developing teeth in animals. No effect on humans.

Vitamin D: Children suffering from Vit. D deficiency may exhibit slightly higher degree of caries experience.

Vitamin K: It may act as a anticaries agent by virtue of its enzyme inhibiting activity in carbohydrate degradation cycle.

Vitamin B complex: Vit. B6 acts as an anticaries agent by selectively altering the oral flora by promoting the growth of non cariogenic organisms which suppress the non cariogenic forms.

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Calcium and phosphorus dietary intake :

Disturbance in calcium and phosphorus

metabolism during the period of tooth

formation may result in severe enamel

hypoplasia and defects of the dentin.

Fluorine content of diet: Dietary fluoride is

relatively unimportant compared to fluoride in

drinking water because of its metabolic

unavailability.

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Dietary studies

Vipeholm study: (Gustafsson et al -1954):

This study was conducted in a mental

institution for 5 yrs in Vipeholm hospital.

The institutional diet provided was nutritious ,

with little sugar, and no provision for between

meal snacks.

The dental caries rate experienced was

relatively low.

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7 groups:

1. Control group

2. Sucrose group(300gm sucrose)

3. Bread group (345gm bread-50gm of sugar)

4. Chocolate group(65gm – daily-for last 2yrs)

5. Caramel group((22caramel-70gm sugar)

6. 8-toffee group (60gm sugar- for 3 yrs)

7. 24- toffee group(120 gm sugar-18 months)

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Conclusions

Increased caries risk-

1. Increase in sugar content.

2. if sugar consumed in a form that will be retained on tooth.

3. If sugar is consumed in between meals.

4. It varies widely in between individuals.

5. Upon withdrawl of the sugar rich foods, the increased caries activity rapidly disappears.

6. Clearance time of the sugar correlates closely with caries activity.

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This study showed that the physical form of

carbohydrates is much more imporatnt in

cariogenicity than the total amount of sugar

ingested.

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Hopewood house study (Sullivan- 1958):

The dental status of children between 3-14 yrs

of age at Hopewood house was studied for

10yrs.

All lived on a strictly institutional diet.

The absence of meat and a rigid restriction of

refined carbohydrate were the two principal

features.

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The meals were supplemented by vitamin

concentrates and an occasional serving of

nuts and a sweetening agent such as honey.

DMFT /child after 10 yrs -1.6

53% of the children were caries free.

Conclusion: the children‟s oral hygiene was

poor, calculus uncommon but gingivitis in 75%

of children.

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This showed that dental caries can be reduced

by diet control even in the presence of

unfavourable oral hygiene.

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Turku sugar study (Scheinin, Makinen -1975):

This study was done to test the effects of

chronic consumption of sucrose, fructose and

xylitol on dental caries.

3 groups:

1. Sucrose group-35 people

2. Fructose group-38 people

3. Xylitol group-52 people

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A dramatic reduction in the incidence of dental

caries was found after 2 yrs of xylitol

consumption.

Fructose was cariogenic as sucrose for the

first 12 months but became less so at the end

of 24 months.

It was also found that frequent between meal

chewing of a xylitol gum produced an

anticariogenic effect.

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Hereditary fructose intolerance (Froesch 1959):

It is caused by the remarkably reduced levels of hepatic, fructose -1-phosphate aldolase into two or three carbon fragments to be further metabolized.

Persons affected with this rare metabolic disorder have learned to avoid any food that contains fructose or sucrose, Because the ingestion of these foods causes symptoms of nausea, vomiting, malaise, tremor , excessive sweating , and even coma due to fructosemia.

Newburn 1969, found that caries prevalence was extremely low in persons with HFI.

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Systemic factors

Heredity :it has been linked with the dental

caries incidence in scientific literature for many

years.

In 1899, acc to GV Black when the family

remains in one locality , the children living

under the conditions similar to those of parents

in their childhood , the susceptibility to caries

will be very similar in the great majority of

cases.

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But there is still no such evidence that heredity

has a definite relation to dental caries

incidence.the possibility exists that if there is

such relation, it may be mediated through

inheritance of tooth form structure, which

predisposes to caries immunity or

susceptibility.

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Pregnancy and lactation: it is a common

clinical observation that a woman during the

later stages of pregnancy or shortly after birth

of the child will manifest a significant increase

in caries activity.

In nearly all cases it is revealed that the

woman has neglected her oral care.

So caries incidence is actually a local problem.

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Intake of medicine containing sucrose – fiber

supplements for constipation, cough mixtures

and antibiotics may affect caries risk

Psychiatric patients: carbohydrates favor

uptake of tryptophan to the brain and serotonin

production is enhanced. Thus its intake may

induce relaxation.

Also psychiatric drugs impair salivary gland

functioning.

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Occupation: in which frequent food sampling is

required, may be associated with increased

caries risk.Eg.Confectionary industry, bakery

workers.

Socio-economic status: higher caries

prevalence in children with low socio-

economic background.

This is due to lesser parental knowledge , their

lesser involvement in oral hygiene and lesser

involvement in topical and supplementary F

regimes.

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HISTOPATHOLOGY OF

DENTAL CARIES

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Caries of enamel

Smooth surface caries: The earliest manifestation of incipient enamel caries is the appearance of an area of decalcification, beneath the dental plaque, which resembles a smooth, chalky white area. There is loss of interprismatic substance, with increased prominence and roughening of the ends of the enamel rods.

It forms a cone shaped lesion with the Apex towards the DEJ and the base towards the surface of tooth. There is loss of continuity of the enamel surface and the surface feels rough to the point of an explorer.

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Pit and fissure caries:

Pit and fissures are often of such depth that food

stagnation with bacterial decomposition in the

base to be expected. The enamel in the bottom of

the Pit or fissure may be very thin, so that early

involvement frequently occurs.

When caries occurs it follows the direction of

enamel rods and forms a cone shaped lesion with

its apex at the outer surface and its base towards

the DEJ. Because of its shape it tends to produce

more undermining of enamel.

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Enamel Caries :

Zone 1-translucent Zone

Zone 2- Dark Zone

Zone 3- Body Of The Lesion

Zone 4- Surface Zone

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Four zones are clearly distinguishable.

Zone 1: The translucent Zone: Advancing front of the

enamel lesion. It is not always present.

Zone 2: Dark Zone: It is referred to as the positive

zone, because it is always present. It is formed as a

result of demineralization.

Zone 3: Body of the Lesion: It is the area of greatest

demineralization.

Zone 4: Surface Zone: Appears relatively unaffected.

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Caries of dentin

It begins with the natural spread of the process

along the DEJ and the rapid involvement of

great numbers of dentinal tubules. The initial

penetration of the dentin by caries may result

in dentinal sclerosis resulting in calcification of

dentinal tubules, that tends to seal them off

against further penetration by microorganisms.

It most commonly occurs in older adults.

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The destruction of dentin through a process of

decalcification followed by proteolysis, forming

necrotic mass of dentin of a leathery

consistency.

As the carious lesion progresses, various

zones of carious dentin may be distinguished

which tends to assume a triangular shape with

the apex towards the pulp and the base

towards the enamel.

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Dentin caries:

Zone 1: Zone of fatty degeneration of

Tomes fibres

Zone 2: Zone of Dentinal sclerosis

Zone 3: Zone of decalcification of dentin

Zone 4: Zone of bacterial invasion

Zone 5: Zone of decomposed dentin

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Following zones are seen:

Zone 1: Zone of fatty degeneration of Tomes

fibres.

Zone 2: Zone of Dentinal sclerosis-

characterized 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.

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Caries of cementum (Root

caries)

Dental plaque and microbial invasion are an essential part of the cause and progression of this lesion.

Microorganisms involved in root caries are filamentous rather than coccal. Microorganisms invade the cementum either along sharpey’s fibers or between bundles of fibers.

Lesion spreads laterally between the various layers.

As carious process continues there is invasion of microorganisms in to dentinal tubules, subsequent matrix destruction and finally pulp involvement.

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DIAGNOSIS OF DENTAL

CARIES

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Clinical inspection of the teeth at the chairside

does not allow the dentist to observe the

caries process itself. What dentists can do is to

examine the consequences of microbial

metabolic activity when looking for signs of

lesions that have formed as a result of it. This

is what caries diagnosis is about: detection of

signs and symptoms of caries

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Diagnosis is defined as the “art or act of

identifying a disease from its signs and

symptoms”(Merriam-Webster,2003)

The logic is that the course of the diseases

may be changed for the better if they are

detected and treated before they reach a stage

at which they elicit symptoms or require more

invasive intervention. Therefore, in dental

practice, diagnosis is closely linked with the

management options.

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The primary objective of caries diagnosis is to

identify those lesions that require surgical

(restorative) treatment , those that require

nonsurgical treatment , and those who are at

high risk for developing carious lesions.

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Why do we diagnose caries?

Diagnosis is important in:

Detecting and excluding disease

Assesing prognosis

Contributing to the decision making process

with regard to further diagnostic and

therapeutic management

Informing the patient

Monitoring the clinical course of the disease

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Diagnostic tests need to be valid and reliable.

Validity means that test should measure what it is intended to measure e.g. a white spot lesion with a matt surface indicates an active lesion which has not yet cavitated

Reliability or reproducibility means that the test can be repeated with the same result e.g. dentist would recognize the same white spot lesion with matt surface as an active lesion. There should be intra- as well as inter-examiner reproducibility

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Differential diagnosis

When performing a caries diagnosis it should

be appreciated that not all opaque lesions on

the tooth surface represent dental caries.

All opacities reflect a decreased mineral

content in the enamel, but may be caused by

different mechanisms,either during enamel

formation or posteruptively.

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Dental fluorosis has a symmetric distribution on homologous teeth & in mild cases,appears as fine white horizontal striae reflecting the perichymatal pattern of enamel.

When such white lines merge in the gingival part of the tooth,they are suggestive of inactive non-cavitated carious lesions(smooth on probing). Such lesion is arch,banana or kidney shaped, reflecting the retention of plaque along the curvature of the gingival margin

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Prerequisites for detection and

diagnosis

The diagnosis of caries require good lighting and dry,clean teeth

When teeth have been cleaned,each quadrant of mouth is isolated with cotton wool rolls to prevent saliva wetting the teeth once they have been cleaned

Thorough drying should be carried out by gentle blast of air from three-in-one syringe as white spot lesions are more obvious when the teeth are dry and saliva can obscure small cavities

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Methods of caries detection

Conventional techniques:

Visual observation

Tactile inspection

Radiography:

• Intra-oral periapical radiographs

• Bitewing radiographs

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Recent advances:

Dental digital

radiography

Caries-detector dyes

Fiber-optic

transillumination

Quantitative light-

induced fluorescence

Laser fluorescence

Ultrasound

Xeroradiography

Electroconductivity

measurements

Microbiologic methods

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Visual observation

It encompasses the use of criteria such as detection of white spot, discoloration & frank cavitations.

Careful examination of teeth under clean & dry condition using good illumination reveal:-

- brownish discoloration of pit and fissures

- opacity beneath pit & fissure or marginal ridge.

- frank cavitation of tooth surface.

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For practical purposes,begin with the upper

right molars and move tooth by tooth and

surface by surface to upper left molars,then

jump to the lower left molars and finish up with

the lower right molars. A consistent

examination pattern ensures that no teeth or

surfaces are missed

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Various aids-

Magnification loupes

Slides have been used to gather information

about caries. With the use of slides pictures of

posterior teeth tell us more about

discoloration, decalcification & translucencies

Use of separators in detection of proximal

caries

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Magnification loupe

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Loupes are comfortable to wear

Inexpensive

Freely available in various magnifications

E.g:

• 2.5 Flip Up Loupes

• 3.0x and 3.5x Galilean Flip-Up Optics

• 2.5 Custom TTL Loupes

• NEW Custom TTL Loupes on Safety Frame

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Tactile inspection

The teeth are examined by the aid of

dental mouth mirror and a sharp probe

The mouth mirror is used to displace the

cheeks and lips and to facilitate vision in

difficult to reach areas on the teeth

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Reflected light from the mouth mirror can be

applied to search for dark shadows,which may

be suggestive of dentinal lesions

Transmitted light from the operating lamp is

particularly helpful for examining the approximal

surfaces of anterior teeth

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An explorer is useful in caries diagnosis

as a tool to remove plaque and debris and

check the surface characteristics of

suspected carious lesions.

- curved explorer is used for examination of pit and fissures .

- inter proximal explorer is used to detect proximal caries.

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The surface texture of lesion is sensed through

minute vibrations of the instrument by the

supporting fingers when moving the tip of the

probe at an angle of 20-40 degrees across the

surface

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One should definitely abstain from poking

vigorously into the tissue,thereby running the

risk of causing irreversible damage to the

surface layer of an incipient lesion,which may

potentially accelerate localized lesion

progression

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Some researchers are concerned that probing

of suspected carious lesions may serve to

spread infective plaque(i.e. mutans

streptococci) to other teeth in the same

mouth,thereby facilitating carious lesion

development. However,this this concern has

not been confirmed as transferred

microorganisms would not survive unless their

new econiche favored their existence

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Tactile finding suggestive of caries are:- • „binding‟ or „catch‟ of explorer tip • Frank cavitation at the base of pit or fissure • Softness at base of pit or fissure • Opacity surrounding the pit or fissure

Feeling of „catch‟ may be due to non carious reasons also, this may depend on:

• shape of fissure

• sharpness of explorer

• force of application

• path of explorer placement

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Radiographs

Conventional , intra-oral periapical & bite wing radiographs are used to diagnose dental caries.

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Advantages:-

- non-invasive method

- disclose site inaccessible to other diagnostic methods.

- keeps a permanent record for maintaining progress or arrest of carious lesions.

Disadvantages:-

- only a 2-D image of 3-D object.

- doesn‟t reveal the earliest stages of caries development..

- radiolucency may be due to caries, wear, fracture, or due to cervical burn out.

- radiographic diagnosis is subjective , prone to observer bias.

- extent of caries as seen in the radiographs is usually lesser than actual defect.

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BITEWING RADIOGRAPH:

Role For detecting occlusal caries:-

• Initial enamel caries are difficult to detect on bitewing radiographs due to 3 D shape of occlusal surface.

• caries involving the buccal and lingual grooves on molars mimic occlusal lesions due to superimposition.

Role in detecting proximal caries:-

• Early proximal enamel lesions are seen as small radiolucent notch below contact area.

• Advanced proximal caries are seen as dark triangular area in proximal enamel with its base towards the external tooth surface.

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Diagrammatic representations of

caries on bitewing radiograph

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Uses:

Detecting incipient proximal caries.

Examining many teeth in one radiograph.

Checking cervical margins of restoration.

Noting the size of pulp chamber.

Monitoring the progress or arrest of caries.

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Fiberoptic transillumination

Diagnostic method by which visible light is transmitted through the tooth from an intense light source,e.g a fine probe with an exit diameter of 0.3-0.5 mm

Principle of it is that there is a different index of light transmission for decayed & sound tooth

Tooth which is decayed has a lower index of light transmission than the sound tooth structure

It is effective specially when used in anterior region.

It is used as an adjunct to visual and radiographic method

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If the transmitted light reveals a shadow when the tooth is observed from the occulusal surface this may be associated with the presence of a carious lesion

The narrow beam of light is of crucial importance when the technique is used in premolar and molar region

For optimal performance the probe should be brought in from the buccal or lingual aspect at an angle of about 45 degrees to the approximal surfaces pointing apically,while looking for dark shadows in the enamel or dentin

Shadows are best noticed when the office light is switched off

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Advantage:

Does not produce overlapping images as in

case of posterior crowding

Can be easily used in pregnant women when

radiation has to be avoided

Disadvantage :

FOTI fails to detect incipient proximal caries

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Digital fiberoptic Trans

illumination

Image captured by the camera are sent to a

computer for analysis , which produce digital

images that can be viewed.

Advantages:-

- instantaneous image projections

- image quality is easy to control

- can detect incipient & recurrent caries very

early

- non invasive

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Disadvantages :-

- doesn‟t measure the depth of lesion

- Difficult to distinguish between deep

fissure , stain and dental caries.

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Tooth separation

Neither radiographs nor FOTI can help to

identify the presence of a cavity on contacting

approximal surfaces. Therefore, tooth

separation has been introduced

Orthodontic elastic separators are applied for

2-3 days around the contact areas of surfaces

to be diagnosed,after which assess to

inspection and probing is improved

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This technique may create some

discomfort,especially in patients with

established dentitions.

It requires an extra visit

Therefore,at present this technique is not

recommended for routine use in general

practice

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Xeroradiography

Advance technique alternative method to

conventional radiography

In xero radiography image is recorded on

photo conductive selenium coated plate rather

than X ray film. Selenium coated plate is

charged & placed in to light tight cassette. This

photoreceptor is placed intra orally & exposed

to X ray beam causing selective discharge.

The amount of discharge is related to radiation

striking photoreceptor.

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During developing the selenium plate is

exposed to cloud of charged powder particle

called TONER , next the plate is dried to

remove the liquid vehicle of toner particles.

Processed image is transferred to opaque

elastic base with the help of clear adhesive

tape.

USES:

help to diagnose initial caries

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ADVANTAGES:-

-“Edge enhancement” can demarcate area of varying dentition specially at margins.

-Less radiation exposure.

-no wet processing.

-Both -ve & +ve prints are possible.

DISADVANTAGES:-

-Expensive

-Development process should be completed within 15 minutes

-Electric charge over the film may cause discomfort to the patient.

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Digital radiographic method

This method offer a more superior means of detecting caries than conventional radiographs.

Introduced in 1987

The application of computer technology to

radiography.

Has allowed image acquistation, manipulation,

storage, retrieval & transmission to remote sites

in digital format.

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Digital imaging sensor is used (CCD) instead

of radiographic film.

The signal from CCD is sent to computer

where it is digitized in 256 gray levels & is

viewed on screen with enhanced density &

contrast.

It is of two types:

• Direct digital radiography

• In-Direct digital radiography

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Direct digital radiography:

Image is acquired by detector that is sensitive to electro magnetic energy & data is converted into digitized form

It is of two types:

1: photo stimulable phosphor {PSP}

2: charged couple device sensor {CCD}

Other type:

-complementary metal oxide semiconductor {CMOS}

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PSP:

The interactions between X-ray photons & crystals of PSP excite the electrons of phosphor. Further on irradiation with ruby laser,trapped electrons are released causing emission of shorter wave length of light in blue region of spectrum. The intensity of emitted blue light is proportional to amount of X ray absorbed by phosphor which can be detected by photo multiplier tube. The output of tube is digitized to form image.

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CCD:

Consists of a chip of pure silicon. When CCD interacts with X ray, an electric charge is created. After exposure, electric charge is sequentially transferred to computer which is acquired as an image later.

USES of digital radiography:

1: Early detection of caries.

2: In endodontics, it helps to measure root canal length, working length & distance between apex and obturating material.

3: It also helps to assess bone loss.

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The software has been designed to assist in

locating and classifying proximal surface

caries in digital intraoral radiographs

The analysis is completed in seconds and an

enlarged image of the radiograph being

evaluated is displayed, along with the possible

decay area

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This helps to identify and calculate the

probability of enamel and dentin caries based

on a unique histological database.

We simply select the area of interest and the

software automatically outlines any consistent

alignment of radiolucent features directing our

attention to the area of interest for closer

examination.

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ADVANTAGES:-

- Reduce radiation dose.

- Instant image visualization

- No need for dark room

- No processing error

- Image can be magnified

- Contrast and density of image can be enhanced.

DISADVANTAGES:-

- Expensive

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Electric conductance

measurement

sound enamel is an insulator due to its high inorganic content . On the other hand , carious enamel has a measurable conductivity which increase with degree of demineralization.

Two devices were developed in 1980‟s

- vanguard electronic caries detector.

- caries meter

• Both instrument measures the electrical conductance between the tip of a probe placed in a fissure and connector attached to an area of high conductance.

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Low conductance of tooth is primarily caused

by enamel

Increased conductance & decreased

resistance are indicative of the presence of

hypo &/or demineralization

When a potential of less 1volt applied,

resistance of above 6,00,000 ohms indicates

caries free tooth. Resistance below 2,50,000

indicates caries.

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Factors affecing electronic resistance

measurement:

Porosity

Surface area

Thickness of tissues

Hydration of enamel

Temperature

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Advantages

-More accurate in diagnosis of early occlusal caries than visual method , radiographs or FOTI .

-Can monitor the progress of caries.

Disadvantages

-Hypomineralized area , enamel cracks can cause misleading reading.

-time consuming procedure

-Requires the use of sharp metal explorer which can cause traumatic defect in pits and fissures.

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Caries detecting dyes

Principle-

Increased porosity- through the development of capillary like micro voids- is earliest change in carious lesion

For detection of enamel caries • Calcien • Zyglozl-22

For detection of dentin caries • Fuschin • Acid red system • 9-aminoacridine

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Limitations:

Does not stain bacteria but organic collagen

matrix of less mineralized dentine

No differentiation between infected and

affected dentine possible

High risk of over treatment

Also stains healthy dentine with naturally high

collagen content: circumpulpal dentine

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Laser Fluorescence

Use of fluorescence for detection dates back

1929, when Benedict observed that normal

teeth fluoresce under UV illumination.

Aids in the detection of occlusal caries

The machine emits light at a wavelength of

655nm and this is transported through a fibre

bundle to the tip of a handpiece. The tip is

placed against the tooth surface & rotated

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The laser light will penetrate the tooth. Different fibers in the tip receive the reflected light and fluorescence from the lesion,thought to be produced from bacterial porphyrins

The received light is measured & its intensity is an indication of size and depth of carious lesion

The machine does not detect the mineral loss

Reproducibility has shown to be good but can be confused by staining and calculus,giving high reading when active caries is not present

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Monochromatic light is used at 350,410 &

530nm on carious & non carious teeth.

In carious teeth emission spectra shifts to

more than 540nm i.e. red range of EM

spectrum.

It has been recently found that when

illuminated with argon laser,carious tissue

appears as dark, fiery, and orange-red in color.

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Diagnodent:

Based on principle of fluorescence.

It uses a diode laser light source & a fiber optic

cable that transmits light to a hand held

probe.

Emitted fluorescence is collected at probe tip,

processed & presented on display as an

integer between -9 to99.

-9 indicates healthy teeth & increased

fluorescence indicates caries particularly value

above 20.

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The Diagnodent operates at a wavelength of 655 nm.

At this specific wavelength, clean healthy tooth structure exhibits little or no fluorescence, resulting in very low scale readings on the display.

However, carious tooth structure will exhibit fluorescence, proportionate to the degree of caries, resulting in elevated scale readings on the display of the Diagnodent.

An audio signal allows the operator to hear changes in the scale values. This enables the focus to be on the patient, not solely on the device.

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Limitations:

Cannot determine the depth of lesion.

Reading may alter due presence of food debris, plaque.

Not able to detect recurrent caries. Alloy restoration exhibits little or no fluorescence, while the composites, ceramics & cements emit their own fluorescence.

Reading changes at different angulations of probe tip.

Caries indicator dyes cannot be used simultaneously with diagnodent.

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Quantitative light fluorescence

This methodology began with observation in1978 by a scientist in Sweden that the use of a laser light of selected wavelength markedly enhances the visibility of early non carious lesions

QLF uses light with wavelengths around 405 nm to excite yellow fluorescence at wavelengths above 520 nm.

Its diagnostic capacity is based on the mechanism that the intensity of natural fluorescence of a tooth is decreased by scattering due to a caries lesion.

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Two-photon image of a carious tooth

Carious area shown in green

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The initial work was based around the use of

multiphoton microscopy to build up a three

dimensional image of the tooth.

This revolutionary technique enables the

dentist to see right into the tooth but is

complex to use and not suitable for general

dental practitioners.

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Ultrasonography

Involves use of sound waves for detection

With the use of this instrument, sonic velocity

& specific accoustic impedance can be

determined for dentin & enamel as well as for

soft tissue & bone.

In ultrasound frequency vibration is greater

than 20 Khz. which is more than audible

range{1500-20,000hz/sec}.

In sonography, sound waves are used in

frequency of 1-20Mhz.

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Scanners used for sonography generate electric impulse that are connected into ultra –high frequency sound waves by transducer{ device which convert electric energy into sound energy}

Transducer is a thin piezo electric crystals made up of great number of dipoles arranged in geometric pattern. Electric impulse generated by scanner causes dipole in crystals to re-align themselves with electric field & thus sudden change causes a series of vibrations that produce the sound waves that are transmitted into the tissues being examined.

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When ultra sonography beam passes

through or interacts with tissues of

different sound, energy causes

obstruction, reflection , refraction diffusion.

Sonic waves that reflected back towards

transducer cause change in the thickness

of piezoelectric crystal, which produces an

electric signal which is amplified and

displayed on monitor.

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Fluorogenic enzyme assay: it is a new method to count cells “in situ”, based on a fluorogenic enzyme assay that measures the activity of alkaline phosphatase. Increasing cell number has close correlation with alkaline phosphatase activity and this relationship did not change with time in culture. This method is able to estimate relative cell numbers over a range from about 104 to 105×105 for many cell types. The method is rapid and efficient, making it a useful method for studying streptococcus and lactobacillus activity in active root lesions.

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Lactobacillus colony count test : This test estimates the number acidogenic Lactobacillus bacteria in the patient’s saliva by counting the number of colonies appearing on the tomato peptone agar plates (pH 5.0).

Streptococcus mutans count test: This test measures the number of S.mutans colony forming units per volume of saliva from the root lesion. It is cultured on the Mitis Salivarius Agar (MSA), selective streptococcal medium.

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All the above mentioned methods may be used as an adjunct to visual inspection. However to be used in practice the methods must be better than clinical-visual and radiographic examination.

They must be convenient to use,not too expensive and must be reproducible

Only laser fluorescence(diagnodent) and digital radiography are currently used in practice and seem to be suitable techniques for detection of caries

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References

Fejerskov Ole, Kidd Edwina.Dental caries:the disease and its clinical management.2nd Ed.

Roberson TM.Sturdevant‟s Art & Science of Operative Dentistry.4th Ed.

Kidd Edwina. Essentials of dental caries

Shafer, Hine, Levy.Textbook of oral pathology.5th Ed.

Soben Peter. Preventive and Community Dentistry. 3rd Ed.

Nikiforuk Gordon. Understanding dental caries part1

Newbrun.Cariology

Hiremath SS. Textbook of preventive and community dentistry

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THANK YOU