Dental caries: etiology, pathogenesis, classification

BHAVYA
DEPARTMENT OF CONSERVATIVE DENTISTRY & ENDODONTICS
CONTENTS
1)INTRODUCTION
2)DEFINITION
3)EPIDEMIOLOGY
4)ETIOLOGICAL THEORIES
5)CAUSE AND EFFECT MODEL
6)PATHOGENESIS
7)CLASSIFICATION
8)HISTOPATHOLOGY
9)CONCLUSION
INTRODUCTION
Dental caries is as ancient as mankind & has the longest association with the dental profession.
The agonizing fact is that despite several efforts towards total eradication, this disease is still prevalent.
For Caries in Latin means, ‘rotten’.
r a nonprofessional, caries meant a hole in the tooth and for dental professionals, it meant destruction of tooth structure in the
form of cavitation.
Dental caries is a multifactorial infectious disease which has reached epidemic proportions in recent times.
In India, surveys done on school children revealed caries prevalence of approximately 58%.
DEFINITION
W D Miller 1890 - dental decay is a chemo parasitic process consisting of two stages: decalcification or softening of the
tissue and dissolution of soften residue.
G V Black 1910-Disintegrationof the tooth substancemolecule by molecule and was caused by the fermentation of foods
inside the mouth
Shafer (1980)-Dental caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by
demineralization of the inorganic tissues and destruction of the organic substance of the tooth.
Sturdevant(1993)-Dental caries is aninfectious microbial disease of the tooth that results inlocalized dissolution
anddestruction of calcified tissues.
Dental caries is a process that brings about the progressive demineralization of the inorganic component of the tooth,
accompanied by disintegrationof the organicportion. (Glossary of operative dentistry term, 1983).
WHO -Dental caries is defined as a localized post eruptive, pathological process of external origin,involving softeningof
hard tooth tissues, & proceeding into the formation of
EPIDEMIOLOGY
FACTORS AFFECTING CARIES PREVALENCE: -
RACE: -People living insame geographical area but belonging todifferent race have differing caries incidence.
-Generally, Chinese, Blacks, Indians have lesser caries incidence than the Caucasian whites.
FAMILIAL:-There appears to be heredity involved.
-Children of parents with low caries experience also show lesser caries incidence and vice versa.
AGE:-Dental caries is more prevalent in children up to12 years.
•Incidence decreases somewhat in younger & middle age group & increases again by the older age.
ETIOLOGICAL THEORIES OF DENTALCARIES
THE LEGEND OF WORM THEORY
According to this theory the cause of dental caries was thought to be invasion of worms into teeth.
ETIOLOGICAL THEORIES OF DENTALCARIES
HUMORAL THEORY
Corroding humors
◙Dental caries was produced by internal action of acids & corroding humors.

Hippocrates & couple of other authors favoredthis concept & also added that accumulated debris around the teeth helped in
corroding action.
They further stressed that stagnation of juices over tooth surfaces caused toothache.

VITAL THEORY
It was postulated in this theory that tooth decay originated from within the tooth itself.
The histological appearance of caries showing wider area beneath & smaller pinpoint area on the top of the toothfavors this
concept.
CHEMICAL THEORY
In the early 18th century, a new concept was emerged, that teeth were destroyed by acids formed in the oral cavity.
The exact nature of acids & the exact mechanism of their formation were not known.
Robertson (1835) proposed that acids cause dental decay, which was formed by fermentation of food particles.
PARASITIC THEORY
Erdl1843, described filamentous parasites in the membrane of tooth surfaces .
Dental caries was thought to develop as a result of infiltration & decomposition of enamel cuticle.

CHEMOPARASITIC/ ACIDOGENIC THEORY

This theory was proposed by W.D.Millerin 1889.
It elucidated a combined effort of the acids (chemo) and the oral microorganisms (parasite) in tooth decalcification.
According to this theory, the microorganisms in the oral cavity metabolize the dietary starch & produce organic acid that dissolves
tooth minerals.

W.D. Miller stated that “Dental decay is a chemico-parasitic processconsisting of two stages”-
1.Decalcification of enamel, which results in total destruction & decalcification of dentin.
2. Followed by dissolution of softened residue.
Acid derived from the fermentation of starches & sugar lodged in the retaining centres of the teeth.
Significance-Miller’s assigned an essential role to 3 factors in the caries process
1.The oral microorganism in acid production & proteolysis
2.The carbohydrate substrate.
3.The acid which causes dissolution of tooth minerals.

DRAWBACKS
Miller’s chemico parasitic theory was unable to explain the predilection of specific sites on a tooth to dental caries & initiation
of smooth surface caries was not accounted by this theory.

Miller’s theory doesn’t explain why some people are caries free & the phenomenon of arrested caries.

PROTEOLYTIC THEORY
Gottlieb 1944
organic or protein elements of tooth as initialpathway of invasionby microorganisms.
the initial action is due to proteolytic enzymes at slightly alkaline pH attacking the lamellae, rod sheaths, tufts & walls of
tubulesetc.
According to him staphylococciplay a vital role in initiatingproteolytic activity.

Later, Pincus(1949) proposed that the Nysmith'smembrane & enamel proteins are mucoproteins which were acted upon by
sulphataseenzyme of the bacilli yielding sulphuric acid.
CRITICS TO PROTEOLYTIC THEORY
Enamel is a highly structured tissue. Though enamel contains 2.0 to 3.5% organic matrix out of which 0.6% is protein, initiation of
caries with breakdown of this small percentage of protein is highly questionable.
Significant loss of enamel tissue through proteolytic activity has not been proved experimentally.
This theory lacks experimental support.
PROTEOLYSIS-CHELATION THEORY
Schatz et al.1955 proposed the theory of simultaneous microbial degradation of organiccomponents ( hence, proteolysis) &
dissolution of inorganic components of tooth by process called chelation.

The word “chelate” refers to compound that are able to bind metallic ions such as calcium, iron, copper, zinc etc. by valence bond.

This theory considers dental caries to be a bacterial destruction of organic component of enamel & the breakdown products of
these organic components to have chelating properties & thereby dissolve the minerals in the enamel even at the neutral/alkaline
ph.

A variety of complexing agents such as amino acids, amines & peptides etc. are the breakdown products of organic components of
enamel & dentin which can act as chelates.
DRAWBACK-
Since enamel contains very little of organic component, could its dissolution produce sufficient amount of chelates to disintegrate
the rest of inorganic enamel is doubtful.
Summing up all the refined observations made in the framework of Miller’s theory, we find that all of them point accusing fingers
at three major factors as causative factors in dental caries.

The Venn's diagram with three intersecting circles, two circles depict diet & dental plaque/ microbial factors and third circle
depicts the host.
Another circle was added, the time/frequency factor. It depicts the
duration of the intersection of the above factors. The longer the
intersection of the dietary sucrose & the cariogenic microbes in the
plaque, the more deleterious is the effect of acid on the dissolution of
tooth mineral
THE HOST FACTOR
COMPOSITION
1)The surface of enamel has more minerals & organic matter & less water.
2) Certain elements like F, Cl, Zn, Pb accumulate more on the surfaceenamel than the sub surface enamel.
3) surface enamel more resistant to caries than subsurface enamel.
4) With passage of time teeth become more resistant to caries because of decrease in permeability & increase in nitrogen &
fluoride content.

MORPHOLOGY

Deep pits & fissures make tooth susceptible to caries because of food impaction & bacterial stagnation.

POSITION
1) Irregularities in the arch form , CROWDING & OVERLAPPING also favor the development of caries.
2) Partially impacted third molars are more prone to caries.

SALIVA
COMPOSITION-
Caries prone individuals have low Ca & P levels.
The caries immune persons exhibit a greater Ammonia content in saliva which retards the plaque formation & neutralizes acid
formationto a certain extent.
pH OF SALIVA-
The pH at which any particular saliva to be saturated with calcium and phosphorus is referred to as the “CRITICAL pH”.
It varies according to Ca & P concentration, but it is usually about 5.5.
Below this value, the inorganic material of the tooth may dissolve.
ANTIBACTERIAL ACTIVITY-
Lysozyme an antibacterial agent present in saliva –can inhibit airborne & water borne micro-organism in oral cavity to some
extent, but its role in caries inhibition is doubtful.
Antibodies like IgA & IgG against specific bacteria have been reported in human saliva.
QUANTITY & VISCOSITY OF SALIVA
Human beings suffering from decreased flow of saliva or lack of salivary secretions usually increasedrate of dental caries.
Certain drugs influence salivary flow & in turn results in caries. Drugs which lead to xerostomia include anti-depressant,
antihistamines etc.
THE MICROFLORA
Streptococcus mutansplays a vital role in initiation of caries.
The main etiological micro-organisms in occlusal & pit &fissure caries is the Streptococcus mutans.
1.Ferments mannitol & sorbitol.
2.Are lactic acid formers which easily colonise on the tooth surface.
3.Are more aciduricthan other streptococci.
ENAMEL CARIES
Streptococcus mutans
DENTIN CARIES
Streptococcus mutans, lactobacillus species.
ROOT CARIES
Actinomycesspecies
THE SUBSTRATE ( DIET)
Diet is the third factor in initiation & progression of caries.
PHYSICAL NATURE OF DIET
Modern diet includes refined foods, soft drinks & eatables which lead to collection of debris predisposing to more caries. It has
been demonstrated that Mastication of food reduces the no. of micro-organisms.

CHEMICAL NATURE OF DIET

The carbohydrate content of diet has been almost universally accepted as one of the most important factors in dental
caries process.
Only refined carbohydrates are effective.
For caries production following factors are responsible :
-Type of carbohydrate e.g. monosaccharide's, disaccharides or polysaccharides.
-Frequencyof intake.
-Time of stagnation.
The principle carbohydrates available in human diets are starch, sucrose & some lactose with less glucose, fructose & maltose.
Sucroseis unique in that it can serve in formation of insoluble extracellular polysaccharides& thereby enhance plaque formation
& microbial aggregation on the tooth surface.
Another factor promoting caries is the consumption of snacks between meals. Frequent consumption of cooked starches, sweets,
etc.

VITAMIN CONTENT OF DIET: -

Of all vitamins, only VitD and VitK appear to have some role in the caries process.
VitDmay have an indirect effect on caries process. Its deficiency can cause enamel hypoplasia which can make the tooth more
susceptible to caries.
VitK has enzyme inhibiting action in carbohydrate degradation cycle. Can be utilized as an anticariogenicagent.

FLUORINE CONTENT: -
While topical and water fluoridation has been known to be effective in caries control, dietary fluorine may have no role as it is
unavailable metabolically.

SYSTEMIC FACTORS

HEREDITY: -
Racial tendency for high or low caries may be explained by heredity. However, local factors like change in dietary habits can
change this tendency.
Possible that caries tendency may be inherited through tooth form & structure.

PREGNANCY & LACTATION: -

Commonly observed that during pregnancy, women tend to neglect their oral health owing to all her attention being diverted to
that of care for the newborn.

PATHOGENESIS

ENAMEL PELLICLE + BACTERIA

PLAQUE FORMATION

PLAQUE BACTERIA + FERMENTABLE CARBOHYDRATE

( FOOD)
ACID PRODUCTION

ACID + ENAMEL

DEMINERALISATION AND DISSOLUTION OF INORGANIC AND ORGANIC STRUCTURES OF TOOTH

DENTAL CARIES

DENTAL BIOFILM
Dental plaqueis abiofilmor mass of bacteria that grows on surfaces within the mouth.
It is also known as DENTAL BIOFILM, MICROBIAL PLAQUE
In order to persist, oral micro-organisms have to attach to a surface & grow; otherwise they will be lost from habitat.
A biofilm is defined as the population or community of bacteria living in organized structures that are firmly attached to a
surface & enmeshed in a self produced matrix of extracellular polymeric substance.

DEVELOPMENT OF DENTAL BIOFILM

The development of dental biofilm can be divided in to several arbitrary stages :
1.Pellicle formation
2.Microbial colonization
3.Microbial succession
4.Mature biofilm

1.PELLICLE FORMATION
Micro-organisms do not colonize directly on the mineralized tooth surface.
The teeth are always covered by an acellular proteinaceous film;
known as pellicle that forms on the‘naked’ tooth surface within
minutes.

The major constituentsof the pellicle are salivary glycoproteins, phosphoproteins, lipids and, to a lesser extent, components from
the GCF.
The pellicle plays an important modifying role in caries and erosion because of its permeable-selective nature restricting
transport of ions in and out of the dental hard tissues. The presence of a pellicle inhibits subsurface demineralization of enamel.
Frequent mouth rinses with milk or cream increase the
thickness and electron density of the pelliclebut it is not clear whether such modification of the pellicle provides additional
protection against demineralization of the enamel.

2. MICROBIAL COLONIZATION
Microbial colonization of teeth requires that bacteria adhere to the surface.
Initially, bacteria are non-specifically associated with tooth surface under van der waal’s & electrostatic forces.
Later, these weak interactions become stronger owing to adhesins on the microbial cell surface.
Colonization occurs in 4-24 hrs after the pellicle formation.
The initial colonizers a highly selected part of the

oral microflora, mainly S. sanguinis, S. oralis and S. mitis.

3. MICROBIAL SUCCESSION
As the microbiota ages the most striking change is a shift
from a Streptococcus-dominated plaque to a plaque dominated by Actinomyces.
Thus, the initialestablishment of a streptococcal flora appears to be a necessary precursorfor the subsequent proliferation of
other organisms.
Such population shift are known as MICROBIAL SUCCESSION.
This shift will occur within 7 -9 days after microbial colonization.

4. MATURE BIOFILM
After about a week of undisturbed growth, the microflora develops into a climax communitythat harbors a broad range of
bacterial species.
The climax community is characterized by microbial homeostasis that tends to prevent colonization by invading species.
PLAQUE HYPOTHESIS

TO EXPLAIN THE ROLE OF DENTAL BIOFILM IN THE ETIOLOGY OF DENTAL CARIES…!!!

For many years, there were two main schools of thought on the role of plaque bacteriain the etiology of dental caries.
First, THE SPECIFIC PLAQUE HYPOTHESIS , which proposed that out of the diverse collection of organisms comprising
the resident plaque microflora, only a single or few no. of species were actively involved in disease.
This hypothesis focusedefforts on controlling disease by targeting preventive measures & treatment against a limited no.
of organisms, such as by vaccination or gene therapy or by antimicrobial treatment.
Second, THE NON-SPECIFIC PLAQUE HYPOTHESIS, which considered that disease is the outcome of the overall
activity of the total plaque microflora.
More recently an alternative hypothesis has been proposed , THE ECOLOGICAL PLAQUE HYPOTHESIS which reconciles
key elements of the earlier two hypothesis.
The ecological plaque hypothesis proposes that the organisms associated with disease may also be present at sound site, but at
too low level .
Disease is a result of a shift in the balance of the resident microflora driven by a change in local environmental conditions

Pathogenesis of dental caries is due to disturbances in two types of homeostasis / physiological equilibrium that exit in an
oral cavity.
1. Disruption of microbial homeostasisin the biofilm.
2. Disruption of mineral homeostasis between the tooth and the ‘oral fluid’.

DISTURBANCE IN MICROBIAL HOMEOSTASIS

The microbial colony in the tooth can sustain mild disturbances without much alteration in its structure and composition.
If the disturbance is severe and persistent, it results in the shift in the equilibrium.
One of the initial colonizers on the tooth surface is the Streptococcus species, predominantly, S. oralis, S. sanguis, and S. mitiswith
S. mutanscomprising only 1% of the colonizing population.
Flora in the biofilm can metabolize fermentable simple sugars in the diet through complex biochemical pathways to produce
various organic acidsas the byproducts, resulting in enamel dissolution.
However, oral fluids buffer the acidic interface within 30–60 minutes with bicarbonates and phosphates.
This kind of fluctuation in pH occurs with every attack of sugar on the biofilm.
If the frequency / intensity of the acid attack outweigh the buffering capacity of the oral fluid the physiologic equilibrium in the
microbial colony change.
The continuous acidic environment allows only the aciduric (acid-resistant) organisms such as the S. mutansand lactobacilli to
proliferate in larger numbers.
As they are acidogenic also, the local acid production keeps increasing.
Thus, S. mutansand lactobacilli that were initially low on the list of colonizers later predominatein a mature, cariogenic biofilm.
These are homofermentative in nature, which means that they produce mainly lactic acid instead of the other organic acids.

DISTURBANCE IN MINERAL HOMEOSTASIS

Tooth enamel is composed primarily of hydroxyapatite (HA)—Ca10(PO4)6(OH)2.
Oral fluidis a rich reservoir of calcium, phosphate, and fluoride minerals.
According to the law of saturation, a dynamic equilibrium exists between the mineral contents of the tooth and the oral
fluidwith the mineral content in the HA crystal being equal to that of the oral fluid.
In any aqueous ambience with a ‘neutral pH,’ the HA crystal dissolves minimally and releases the calcium (Ca2+), phosphate
(PO43−) and hydroxyl (OH−) ions into the solution.
Ifthe solution, for instance, is the oral fluid that already contains the same minerals, it becomes ‘supersaturated’, resulting in the
‘precipitation’ of the minerals back onto the tooth enamel.
In an aqueous ambience with ‘acidic pH,’ mainly the phosphate ions, (PO4)3−, and the hydroxyl ions (OH−) react with the
hydrogen ions (H+) in the tooth–biofilm interface, by forming complexes, such as, HPO42−and H20.
In a severe acidic environment hydrogen ions (H+) further combine with HPO42−, to form H2PO42−, a more acidic ion.
Thus the localized acidity is buffered but the oral fluid becomes ‘under saturated’ with respect to the phosphate ions (PO43−).This
leads to the ‘dissolution’ of HA crystals in an attempt to resaturate the oral fluid.
CLASSIFICATION OF DENTAL CARIES
DENTAL CARIES CAN BE CLASSIFIED IN SEVERAL WAYS:
BASED ON LOCATION OF CARIES:
1. Pit and fissure caries:seen in pits and fissures found on occlusal, buccaland lingual surfaces of posterior teeth as well as lingual
surfaces of maxillary anteriors.
2.Smooth surface caries: seen in all smooth surfaces of teeth, without involving pits, fissures or grooves.
3.Root surface caries:occurs on root surfaces of teeth

BASED ON SPEED OF CARIES PROGRESSION:

1.Acute or rampant caries: rapidly invaded caries, involving several teeth.
•Appears soft and light-colored.
•If unattended causes early pulpal involvement.
2.Chronic caries:slowly
progressing, long standing. Hard in consistency, dark colored.
3. Arrested caries: carious lesion, usually incipient, may become arrested if change in oral environment. Appears as a dark brown
pigmentation with smooth surfaces.

BASED ON WHETHER NEW OR RECURRENT CARIES:

1. Initial or primary caries: first attack of caries on tooth.
2. Recurrent or secondary caries: found under or around the margins of existing restoration.Occurs due to microleakage.

BASED ON EXTENT OF CARIES:

1. Incipient caries: consists of demineralizedenamel not extended to DEJ. Can be remineralized, hence also referedas reversible
caries.
2. Cavitatedcaries: caries has spread beyond enamel and dentin. can not be remineralized, hence also referedas irreversible caries.

BASED ON PATHWAY OF CARIES SPREAD WITHIN TOOTH:

1. Forward caries: when caries cone in enamel is larger or same size as that in dentin.
2. Backward caries: spread of caries along DEJ exceeds caries cone in enamel, caries extends into enamel from junction.
BASED ON NUMBER OF TOOTH SURFACE INVOLVED:
1. Simple caries: involving one surface of tooth.
2. Compound caries: involving two surfaces of tooth.
3. Complex caries: involving three or more surfaces of tooth.

BASED ON TREATMENT AND RESTORATION DESIGN: This is G.V.Black’s classification.

1.CLASS I CARIES.
2. CLASS II CARIES.
3. CLASS III CARIES.
4. CLASS IV CARIES.
5. CLASS V CARIES.
6. CLASS VI CARIES.
GV Black’s Classification
CLASS I
 Occlusal 2/3 of
Occlusal surfaces
facial & lingual
of molars &
surfaces of
premolars
molars

Lingual surfaces
of maxillary
incisors

CLASS II
Restorations on proximal surfaces of posterior teeth
CLASS III
Restorations on proximal surfaces of anterior teeth that do not involve the incisal angle
CLASS IV
Restorations on proximal surfaces of anterior teeth that do involve the incisal angle
CLASS V
Restorations on the gingival third of the facial/lingual surfaces of all teeth
CLASS VI
Restorations on the incisal edges of anterior teeth
Restorations on the occlusal cusp heights of posterior teeth

BASED ON AGE OF THE PATIENT

1. Nursing bottle caries: during early infancy, bottle fed babies develop rapidly spreading caries usually on maxillary incisors.
2. Adolescent caries: acute caries frequently seen in teenage population due to dietary habits.
3. Senile caries: occurring in elderly population, mostly characterized by involvement of root surfaces. Occurs because of gingival
recession, reduced salivation and poor oral hygiene.
BASED ON WHETHER CARIES IS COMPLETELY REMOVED OR NOT, DURING TREATMENT:
-Residual caries: caries that remains in prepared cavity even after the restoration is completed.

GRAHAM MOUNT’S CLASSIFICATION BASED ON SIZE AND SITE

BASED ON WHO SYSTEM

D1-clinically detectable enamel lesionswith intact surfaces
D2-clinically detectable cavities limited to enamel
D3-clinically detectable cavities in dentin
D4-lesions extending into the pulp
BASED ON SEVERITY OF DENTAL CARIES
Class 1 –very mild caries
Class 2 –mild caries
Class 3 –moderate caries
Class 4 –severe caries
Class 5 –very severe caries
HISTOpatholoGYOF CARIES
ZONES OF ENAMEL CARIES
ZONE 1-TRANSLUCENT ZONE
It is the deepest zonerepresenting the advancing front of the enamel lesion.In this zone, the pores or voids form along the enamel
prism (rod) boundaries,.The pore volume is 1%, 10 times greater than normal enamel.
ZONE2-DARKZONE
Sonamedbecauseitdoesnottransmitpolarizedlight.
Thetotalporevolumeis2%to4%.
Thereissomespeculationthatthedarkzonemaybeformedbydepositionofionsintoanareapreviouslyonlycontaininglargepores.
Thereisalsoalossofcrystallinestructureinthedarkzone,suggestiveoftheprocessofdemineralizationandremineralization.
•Thesizeofthedarkzoneisprobablyanindicationoftheamountofremineralizationthathasrecentlyoccurred.
ZONE 3-BODY OF THE LESION
The body of the lesion is the largest portion of the incipient lesion while in a demineralizing phase.
It has the largest pore volume, varying from 5% at the periphery to 25% at the center.
The striae of Retziusare well marked in the body of the lesion, indicating preferential mineral dissolution along these areas of
relatively higher porosity.
The first penetration of caries enters the enamel surface via the striaeof Retzius.
The interprismaticareas and these cross-striations provide access to the rod (prism) cores, which are then preferentially attacked.
Bacteria may be present in this zone.
ZONE 4: SURFACE ZONE
The surface zone is relatively unaffected by the caries attack.
It has radiopacitycomparable to unaffected adjacent enamel.
It has been hypothesized that hypermineralization and increased fluoride content of the superficial enamel are responsible for the
relative immunity of the enamel surface.
However, removal of the hypermineralized surface by polishing fails to prevent the reformation of a typical, well-mineralized
surface over the carious lesion.
DENTINAL CARIES
Caries advancement in dentin proceeds through three changes:
1.Weak organic acids demineralize the dentin.
2.The organic material of the dentin , particularly collagen, degenerates and dissolves.
3.Loss of structural integrity is followed by invasion of bacteria.

ZONE 1:NORMAL DENTIN

The deepest area is normal dentin , which has tubules with odontoblastic processes that are smooth & no crystals are in the lumens.
•Nobacteriaareinthetubules.
•Theintertubulardentinhasnormalcrossbandedcollagen&normaldenseapatitecrystals.
ZONE2:SUBTRANSPARENTDENTIN
•Thisisthezoneofdemineralizationoftheintertubulardentin.
•Damagetotheodontoblasticprocessisevidenthowevernobacteriaarefoundinthezone.
•Dentiniscapableofremineralization.
ZONE3:TRANSPARENTZONE
•Thisisthezoneofcariousdentinthatissofterthannormaldentin&showsfurtherlossofmineralsfromtheintertubulardentin.
•Nobacteriaarepresent.
•Althoughorganicacidsattackboththemineral&organiccontentofthedentin,thecollagencross–linkingremainsintactinthiszone.
•Theintactcollagencanserveasatemplateforremineralizationoftheintertubulardentin,&thusthisregionremainscapableofselfrepairprovi
dedthepulpremainsvital.
ZONE4:TURBIDDENTIN
•Itisthezoneofbacterialinvasion&ismarkedbywidening&distortionofdentinaltubules,whicharefilledwithbacteria.
•Thereisverylittlemineralpresentandthecollageninthisregionisirreversiblydenatured.
•Thiszonecannotberemineralized&mustberemovedbeforerestoration.

ZONE5:INFECTEDDENTIN
•Theoutermostzone,infecteddentin,consistsofdecomposeddentinhavingbacteria.
•There is no recognizable structure to the dentin & collagen.
•Great number of bacteria are dispersed in this granular material.
•Removal of infected dentin is essential to sound successful restorative procedures as well as prevention of spreading the infection.
PULPAL RESPONSE TO DENTAL CARIES
Pulpaltissuesubjacenttodeepcarieslesionsoftenshowsthepresenceofchronicinflammation,includinglymphocytes,macrophagesandpla
smacells.
Formationoftertiarydentinisusuallyvisibleonthepulpalaspectandtheincreaseindentinthickness.