DENTAL

CARIES
Prepared by Dr Sundeep Bhagwath
 OVERVIEW

 DEFINATION
 EPIDEMIOLOGY
 ETIOLOGY
 CLASSIFICATION
 HISTOPATHOLOGY
DEFINITION
Dental caries is defined as an “irreversible
disease of calcified tissues of teeth,
characterized by demineralization of the
inorganic portion and destruction of the
organic substance of the tooth, which
often leads to cavitation”.
- Shafer, Hine and Levy
EPIDEMIOLOGY OF
DENTAL CARIES
CARIES IN PREHISTORIC MAN: -
 Caries is considered a disease
mainly of modern civilization, as
prehistoric humans rarely suffered
from it.
 In those instances where it was noted,
it was usually found to occur in older
persons teeth with attrition and food
impaction.
 Caries in such persons was seen to
occur below the contact areas and
also on the CEJ.
CARIES IN MODERN MAN: -
 Occurs universally. No human being
is immune.
 Commonest infection to occur in oral
cavity.
 Directly linked to dietary habits of
modern man – processed, soft food.
 Primitive man’s diet was coarse, raw
and mostly uncooked.
FACTORS AFFECTING CARIES
PREVALENCE: -
1. RACE:
 People living in same geographical
area but belonging to different race
have differing caries incidence.
 Generally, Chinese, Blacks, Indians
have lesser caries incidence than the
Caucasian whites.
2. AGE:
 Dental caries more prevalent in
children up to 12 years.
 Incidence decreases somewhat in
younger and middle age group.
 Incidence increases again by the
older age.
3. GENDER:
 Incidence of caries is significantly
higher in females than males.

 This may be due to the fact that

teeth in females erupt earlier
compared to males.
4. FAMILIAL:
 There appears to be heredity
involved.

 Children of parents with low caries

experience also show lesser caries
incidence and vice versa.
 ETIOLOGY OF
DENTAL CARIES
 No universally accepted opinion of
etiology.
 Many theories have been proposed
but only 3 have stood the test of time
1. Miller’s Chemico – parasitic theory
2. Proteolytic theory
3. Proteolysis - chelation theory
 I. CHEMICO PARASITIC THEORY

 W.D.Miller stated in 1887 that “Dental

decay is a chemico - parasitic process
consisting of two stages, the
decalcification of enamel, which results
in its total destruction and the
decalcification of dentin as a preliminary
stage followed by dissolution of the
softened residue”.
 The acid which caused the decay was
derived from fermentation of starches
and sugars lodged in the retaining
centers on teeth.
 In his experiment he incubated a mixture
of bread, meat and sugar with saliva at
body temperature
 It produced enough lactic acid within 48
hours to decalcify sound dentin
 In his hypothesis, Miller assigned
essential roles to 3 factors –
1. Carbohydrate substrate
2. Acid which caused dissolution of
tooth minerals
3. Oral micro organisms which
produce acid and also cause
proteolysis.
OBJECTIONS TO THE HYPOTHESIS: -
1. Unable to explain predilection of specific sites
on tooth to caries.
2. Initiation of smooth surface caries not
explained.
3. Unable to explain why some populations are
caries free and some are caries prone.
However, this theory is accepted by majority in
unchanged form. Also, bulk of evidence DOES
implicate carbohydrates, acids and
Microorganisms.
1.ROLE OF CARBOHYDRATES: -
 Numerous studies confirm the fact that
presence of readily fermentable
carbohydrates are responsible for
increased caries incidence.
 Cariogenic carbohydrates are dietary in
origin since human saliva contains
negligible amounts of carbohydrates.
 Also, whatever is present, is bound to
salivary proteins and thus not available for
microbial degradation.
 Cariogenicity of carbohydrates depend upon –
frequency of its ingestion, physical form,
chemical composition, route of administration
and presence of other food components.
 Thus, carbs in detergent foods are less
cariogenic than those in sticky, retentive
foods.
 Polysaccharides are less easily fermented
than monosaccharides by the plaque
organisms.
 Meals high in fats, proteins or salt reduce the
retentiveness of carbs.

2. ROLE OF MICROORGANISMS: -
 Two gram positive coccal forms of bacteria
have been implicated in dental caries from
over a century – L.acidophilus and S.mutans.
 However, it is now recognized that one or
more different types of bacteria are involved in
“initiation” of caries and a completely different
species of bacteria may be involved in
“progression” of caries.
 Also, a different diet – bacterial interaction is
involved in producing root and coronal caries.
 The various cariogenic species of bacteria
include – S.mutans, S.salivarius, S.sanguis,
S.mitior, S.millieri, L.acidophilus,
Peptostreptococcus intermedius, A.naeslundi,
A.viscosus etc.
 Different bacteria show selectivity for the tooth
surfaces they localize and attack, e.g.
S.mutans, Lactobacilli species attack the pit
and fissures, while A.naeslundi and
A.viscosus prefer root surfaces.
 The Lactobacilli species and A.naeslundi also
show preference to deep dentinal lesions.
3. ROLE OF ACIDS: -
 It is understood that acids are produced by
enzymatic breakdown of sugars by cariogenic
bacteria.
 Acids produced are – Lactic acid mainly and
butyric acid to some extent.
 However only production of acid is of no
consequence. It must be localized and
retained on the tooth surface for it to cause
the caries.
 Its accepted that dental plaque does this.
4. ROLE OF DENTAL PLAQUE: -
 Plaque defined as a soft,
unmineralized, bacterial deposit
or biofilm which forms on teeth
and dental prostheses that are
not adequately cleaned.
 Resists cleansing by
physiological oral forces like
salivary washing and tongue
movements but is removable by
tooth brushing.
 Considered as a contributing factor
for at least initiation of caries.

 However mere presence of dental

plaque doesn’t necessarily mean
caries will occur.
COMPOSITION OF DENTAL PLAQUE =>
Water – 80%
Solids – 20%
 Dry weight of plaque composed of
Bacterial & Salivary proteins – 50%
Carbohydrates & Lipids - 25%
---
Inorganic ions, mainly Ca++ & Po4 - 10%
CLASSIFICATION OF DENTAL PLAQUE =>
 Plaque classified as – SUPRAGINGIVAL &
SUBGINGIVAL.
 Supragingival plaque – essential role in causing
caries, while subgingival plaque – role in
periodontal diseases.
MECHANISM OF FORMATION =>
 Plaque formation proceeds through
following stages

1. Deposition of a cell free layer,

ACQUIRED PELLICLE which is
derived from salivary glycoproteins.
This layer acts as nutrient for
plaque bacteria.
2. Colonization of pellicle by Gram
positive bacteria like S.sanguis
and S.mutans within 24 hours.

3. Maturation of plaque by further

colonization with filamentous
and other bacteria. Also there is
build up of plaque substance by
polysaccharides produced by
plaque bacteria.
 II. PROTEOLYTIC THEORY
 In contrast to acidogenic theory, this
theory postulated by Gottleib, Diamond
and Applebaum states that caries is
essentially a proteolytic process.

 According to them, the organic or protein

elements like enamel lamellae, rod
sheath etc are the initial pathway of
invasion by microorganisms.
OBJECTIONS TO THE THEORY: -
 Out of 0.56% of organic matrix, 0.18% is
Keratin. However, no enzyme systems capable
of attacking keratins have been isolated so far.
 Studies in germ free rats have shown that
caries can occur in the absence of proteolytic
organisms.
However, even though proteolysis may not play
any role in initiation of caries, their role in
progression of more advanced carious lesions
cannot be ruled out.
 III. PROTEOLYSIS –
CHELATION THEORY

Schatz et al in 1955 proposed

that caries occurred as a result
of simultaneous degradation of
organic substances
(Proteolysis) and dissolution of
tooth minerals by a process
called Chelation.
 Chelation is a process of complexing of a
metallic ion to a complex substance
through a co-ordinate covalent bond
resulting in a highly stable, poorly
dissociated ionized compound.

 Examples are – Chlorophyll molecule in

green plants where 4 pyrrole nuclei are
linked to magnesium and Hemoglobin
where 4 pyrrole nuclei are linked to iron.
 According to this theory, the initial
attack on the tooth is on the organic
components of enamel.
 Breakdown products of the
proteolysis have chelating
properties which form chelates with
mineralized components of enamel
and thereby decalcify the enamel
even in neutral or even alkaline pH.
 OBJECTIONS TO THIS THEORY: -

 Direct evidence for proteolysis – chelation as a

mechanism for causing caries is lacking.

 Recent studies have shown that saliva as well as

plaque do not contain substances in sufficient
concentrations to chelate calcium from enamel.

However, although chelation may not be actually

responsible for initiating caries, it may still have some
role to play in advanced carious lesion where the pH
levels return to neutral.
MULTIFACTORIAL CONCEPT OF
CARIES ETIOLOGY
 Dental caries – a multifactorial
disease – interplay of 3 primary
factors plus time also.
 Mere presence of bacteria and a
suitable substrate on a tooth
surface at a given time is not
enough to cause caries.
 So, variations in caries
incidence occur because of
number of indirect or
CONTRIBUTING FACTORS.
 CONTRIBUTING FACTORS
A. TOOTH 1. Composition
2. Morphologic characteristics
3. Position
B. SALIVA 1. Composition
2. pH
3. Quantity
4. Viscosity
5. Antibacterial factors
C. DIET 1. Physical factors
2. Local factors
D. SYSTEMIC CONDITIONS
 CONTRIBUTING FACTORS -
TOOTH
1. COMPOSITION OF TOOTH: -
 Structure & composition of a tooth determines
initiation and rate of progression of caries.
 Surface enamel more mineralized than
subsurface enamel and is more resistant to
caries. It also accumulates more fluoride, zinc,
lead ions than subsurface enamel.
 Therefore in initial carious lesions, the
subsurface enamel shows marked
demineralization even though the outer
enamel is relatively intact.
2. MORPHOLOGIC CHARACTERISTICS: -
 Deep, narrow occlusal fissures or buccal and
lingual pits predispose to caries as they tend
to trap food and bacteria. Also enamel is quite
thin at the base of such deep pits and fissures.
 Certain surfaces of teeth are more prone to
decay like e.g. in mandibular 1st molars the
likelihood of caries in descending order is
occlusal, buccal, mesial, lingual and distal.
 The most susceptible teeth are mandibular 1st
molars followed by maxillary 1st , mandibular
and maxillary 2nd molars.
3. POSITION: -
 Malaligned, rotated or otherwise
abnormally situated teeth can be
difficult to cleanse and are likely to trap
food debris and bacteria.

 This, in susceptible persons is sufficient

to cause dental caries.
 CONTRIBUTING FACTORS -
SALIVA
1. COMPOSITION: -
 Many inorganic and organic components of
saliva have been investigated for anti
cariogenic effects. However, results have
been conflicting.
 In normal circumstances, saliva is
supersaturated with calcium and phosphate
ions w.r.t enamel hydroxyapatite.
 This not only prevents enamel from dissolving
but even tends to precipitate apatite in the
surface enamel of carious lesions.
2. pH OF SALIVA: -
 The “critical” pH at which the inorganic
material of tooth begins to dissolve is about
5.5, since above this pH, saliva is
supersaturated with Ca and Po4 ions.
 Although much has been discussed about
buffering capacity of saliva, its relation with
caries incidence is not so simple!
 Acid production during caries occurs at a
localized site on tooth, which in initial stages
at least, is covered by dental plaque. This
plaque prevents a free exchange of ions.
3. QUANTITY OF SALIVA: -
 Caries incidence is significantly higher
in people with less or no saliva flow, as
is seen in cases of salivary gland
aplasia and xerostomia.

 Continuous flow of saliva is required for

mechanical removal of bacteria and
food debris from the tooth surfaces.
4. VISCOSITY OF SALIVA: -
 Sound scientific evidence is lacking
to support the view that viscous
saliva is associated with high caries
incidence as some studies have
reported.

 The reverse has also been shown to

be true in some other studies.
5. ANTIBACTERIAL PROPERTIES: -
 Saliva contains many antibacterial
factors like lysozyme, lactoferrin,
sialoperoxidase, bistatin, thiocyanate
ion, IgA etc.
 However their efficacy has been
doubtful as saliva always appears to
contain bacteria capable of causing
caries if carbohydrates are present.
 CONTRIBUTING FACTORS -
DIET
1.PHYSICAL FORM: -
 Very important factor responsible for
difference between caries incidence of
primitive and modern man.

 Already explained that diet of primitive

man contained plenty of roughage
which mechanically cleansed the teeth
of any adhering to the teeth.
 Also, the coarse nature of the diet
induced early attrition of occlusal and
proximal surfaces leading to reduction
in food entrapment.

 Diet of modern man in contrast is soft

and lacking in roughage. As a result,
food sticks tenaciously to teeth and is
not cleansed mechanically.
2. CARBOHYDRATE CONTENT OF
DIET: -
 Accepted all over as one of the most
important factors in caries process.

 Observed that different ethnic

populations have differing caries
incidences – postulated that it could be
due to difference in diet, especially
carbohydrate content.
 Diet of caries free ethnic races contain low
amounts of carbohydrates, that too found
in fruits and vegetables, while diet of
caries prone westerners contains more
carbohydrates due to intake of processed
food.

 Exceptions – certain populations in India

have a high carbohydrate content yet are
relatively caries free.
3. LIPID CONTENT OF DIET: -
 Understood that medium chain fatty
acids and their salts have
antibacterial effects at low pH.
Mechanism of action not understood.

 Its potential as anticariogenic food

needs more investigation.
4. VITAMIN CONTENT OF DIET: -
 Of all vitamins, only Vit D and Vit K appear to
have some role in the caries process.
 Vit D may have an indirect effect on caries
process. Its deficiency can cause enamel
hypoplasia which can make the tooth more
susceptible to caries.
 Vit K has enzyme inhibiting action in
carbohydrate degradation cycle. Can be
utilized as an anticariogenic agent.


5. CALCIUM & PHOSHORUS
CONTENT:-
 Available evidence indicates that there
is no relation between dietary calcium
and phosphorus and dental caries.
6. 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.
 CONTRIBUTING FACTORS –
SYSTEMIC FACTORS
1. 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.
2. 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.
 Thus increased caries incidence during
pregnancy & lactation is more a
problem of neglect !
CLASSIFICATION
OF CARIES
I. BASED ON MORHOPLOGICAL SITE: -
1. Pit and fissure caries
2. Smooth surface caries
II. BASED ON RATE OF PROGRESSION:-
1. Acute dental caries
2. Chronic dental caries
III. BASED ON WHETHER LESION IS NEW OR
UNDER PREVIOUS RESTORATION: -
1. Primary (virgin) caries
2. Secondary (recurrent) caries
 PIT & FISSURE CARIES

 Usually develops
on occlusal
surface of molars
and premolars,
buccal and lingual
surfaces of
molars and on
lingual surface of
maxillary incisors.
Deep pits and fissures are
naturally more prone to
caries due to their poor self
cleansing properties and
tendency to entrap food
debris and bacteria.
 Also, enamel at the base of
such pits and fissures is thin
or even absent, thereby
exposing dentin.
 Early lesions in such
locations appear brown /
black and “catch” a fine
explorer point.
 Upon reaching the DEJ,
there is lateral spread of
caries and penetration of
dentinal tubules.
 All this occurs without apparent
fracturing away of overlying enamel.
 Thus there may be a large carious lesion
inside with only a pinpoint opening seen
on the tooth surface.
 Not all pit and fissure caries progress in
this way.
 In many cases, carious lesion begins as
an open cavity and becomes larger
progressively.
 In such cases, the progress of caries is
much slower and pulpal involvement is
also much delayed.
SMOOTH SURFACE CARIES
 Develops on proximal surfaces of
all teeth or on gingival 1/3rd of
buccal and lingual surfaces.
 Here, the caries is preceded by
formation of dental plaque, quite
unlike the pit and fissure caries.
 Presence of plaque ensures
retention of carbohydrate and
bacteria on tooth surfaces,
leading to subsequent acid
production and demineralization
of enamel.
 Smooth surface caries
usually begins just below the
contact point and appears in
initial stages as a faint white
opacity of enamel without
loss of continuity of enamel
surface.
 The early chalky white spot
becomes roughened owing
to superficial decalcification
of enamel.
 As caries reaches the DEJ, there is rapid
lateral spread.
 Quite often, caries extends buccally and
lingually but not till the actual buccal and
lingual surfaces, as these areas are more
accessible to the toothbrush.
 CERVICAL CARIES
 Cervical caries occurs on
buccal, lingual or labial surfaces.

 Extends occlusally from gingival

crest region to the convexity of
smooth surface that marks the
self cleansing portion of tooth.

 Laterally, it extends towards the

proximal surfaces.

 Thus this lesion is a crescent

shaped cavity beginning in its
initial stages as a chalky white
lesion.
 CERVICAL CARIES
 It almost always occurs as an open cavity
unlike the smooth surface or pit and fissure
caries.

 Occurs on all the teeth without predilection as it

is directly related to lack of oral hygiene.

 No excuse for it to occur on anybody’s teeth

since it can always be prevented by maintaining
good oral hygiene.
 ACUTE DENTAL CARIES
 It is that form of caries that follows a rapid
clinical course and results in early pulpal
involvement by carious process.

 Predominantly affects children and young

adults probably because their dentinal tubules
are larger and show no sclerosis.

 The point of entry of caries is small even though

there is rapid spread of caries at DEJ,
producing large internal cavitation.
 The small point of
opening doesn’t allow
the buffering ions of
saliva to neutralize acids
formed within the cavity.
 The affected dentin is
usually stained light
yellow compared to deep
brown / black of chronic
caries.
 Pain is more likely to be
seen in acute dental
caries than chronic
caries, but this is not a
hard and fast rule.
RAMPANT DENTAL CARIES
 Characterized by sudden, rapid
destruction of teeth affecting
even relatively caries free
surfaces like proximal and
cervical surfaces of mandibular
teeth.
 10 or more carious lesions over
a one year period is
characteristic of rampant caries.
 Prominently observed in deciduous
dentition of young children and
permanent dentition of teenagers.

 Dietary factors like high carbohydrate

intake etc as well as physiological
factors affecting saliva are major
contributors to etiology of rampant
caries.
NURSING BOTTLE CARIES
 Also called baby bottle
syndrome and bottle mouth
syndrome.
 It is a type of rampant caries
and occurs due to –
(a) Nursing bottle containing milk,
milk formula or sweetened
water.
(b) Breast feeding
(c) Sugar or honey sweetened
pacifiers
 Usually, the above aids are used at sleeping time after
one year of age.
 Clinically seen as widespread caries of the 4 maxillary
incisors followed by 1st molars and then canines.
 Absence of caries in mandibular teeth distinguishes
it from ordinary rampant caries.
 If milk or other carbohydrates are rapidly cleared from
mouth, they aren’t cariogenic, but if they pool in the
mouth, then they can cause rampant caries.
 Mandibular teeth usually escape the process as the
pooled milk or sweet products are washed away by
saliva
 CHRONIC DENTAL CARIES
 That type of caries which progresses slowly and
involves the pulp much later than acute caries.

 Most commonly seen in adults.

 Opening to the lesion is invariably large r than that

of acute caries. As a result, there is lesser food
impaction and greater access to saliva.

 Also, the slow progress of caries allows enough

time for dentinal sclerosis and deposition of tertiary
dentin in response to irritation.
 The carious dentin is
stained deep brown
 As compared to acute
caries there is
considerable SURFACE
destruction with a
shallower cavity and little
undermining of enamel,
while there is only
moderate spread of caries
along the DEJ.
 Pain is NOT a prominent
feature here due to the
protection provided to the
pulp by tertiary dentin
formation.
RECURRENT CARIES
 Occurs around or
beneath an existing
restoration.
 Usually due to
inadequate extension of
restoration resulting in
food impaction
 Can also occur if a
restorative material is
not properly adapted to
margins of cavity
leading to leaky cavity
margins.
 This “renewed” carious
process follows a
similar pattern as that of
primary caries.
ARRESTED CARIES
 It is that caries which becomes
static or stationary and does not
progress any further.

 Can occur in both deciduous

and permanent dentition.

 Occurs almost exclusively on

occlusal surface caries.
 Characterized by large, open cavity in
which there is no food retention and the
softened decalcified dentin is gradually
burnished until it assumes a brown
polished appearance.
 Called “Eburnation of dentin”.
 Sometimes arrest can also occur in initial
proximal caries, when the adjacent tooth is
extracted for some reason.
 This is due to the automatic creation of a
self cleansing area
 RADIATION CARIES
 Rampant caries occurring in patients
receiving radiotherapy in head & neck
region is called as RADIATION CARIES.

 Xerostomia is a major complication of

radiotherapy of head & neck region. This,
coupled with increase in viscosity and low
pH of saliva results in decreased
anticariogenic actions of saliva.
HISTOPATHOLOGY OF
CARIES
 HISTOPATHOLOGY OF CARIES -
ENAMEL

 Caries process in enamel progresses

through following stages
A. Early submicroscopic lesion
B. Phase of nonbacterial enamel crystal
destruction
C. Cavity formation
D. Bacterial invasion of enamel
* C & D Occur almost simultaneously
EARLY LESION – SMOOTH
SURFACE
 Earliest visible changes are
seen as a chalky white spot
on the tooth just adjacent to
contact point.
 Electron microscopic study
reveals the early changes as
loss of inter rod enamel,
accentuation of striae of
Retzius and perikymata.
 As caries progresses, the lesion of
smooth surface caries has a
distinctive conical shape with its base
towards enamel surface and apex
towards DEJ.
 This conical lesion when observed in
a light microscope reveals four
different zones as seen from deepest
advancing zone first
1. Translucent zone 2. Dark zone
3. Body of lesion 4. Surface zone
1.TRANSLUCENT ZONE: -
 Unrecognizable clinically &
radiologically.
 Occurs due to formation of
submicroscopic pores at
enamel rod boundaries and
striae of Retzius.
 This zone is slightly more
porous than sound enamel
having a pore volume of 1%
compared to 0.1% of sound
enamel.
2. DARK ZONE: -
 Lies superficial to translucent
zone.
 Called positive zone as it is
always present.
 Pore volume is 2 – 4%.
Increased porosity in this
zone is due to greater
degree of demineralization in
this zone.
3. BODY OF LESION: -
 Forms bulk of the lesion and
lies between relatively
unaffected surface zone and
dark zone.

 Area of greatest
demineralization, having a
pore volume of 5% near the
periphery to about 25% in the
center of body of lesion.
4. SURFACE ZONE: -
 Interestingly, this zone not only
remains intact during the early stages
of attack by caries, but also
REMAINS MORE HEAVILY
MINERALIZED.
 Pore volume of only 1%.
 Ions for remineralization come either
from those within plaque or from
reprecipitation of calcium and
phosphate ions diffusing outwards as
deeper layers are demineralized.
 Eventually, this zone is demineralized
by the time caries penetrates dentin.
EARLY LESION – PIT & FISSURE
 Caries process not much
different from smooth surface.
 Caries most often starts on both
side of fissure and visual
changes like yellow or brown
discoloration are seen.
 Also, enamel being usually thin
at the base of pits and fissures,
dentin involvement occurs much
earlier.
 In contrast to smooth surface caries’ lesion, the caries here
follows direction of enamel rods, forming a cone shaped lesion
with its base towards DEJ and apex directed occlusally.
 As a result therefore, greater number of dentinal tubules are
affected when lesion reaches DEJ.
 CAVITY FORMATION &
BACTERIAL INVASION

 The enamel crystallites are progressively dissolved until the

disintegration becomes visible macroscopically.
 Now the pathways are large enough for the bacteria to
physically enter the enamel, destroy organic matrix by
proteolysis and then proceed to DEJ and dentinal tubules.
HISTOPATHOLOGY OF CARIES –
DENTIN (EARLY CHANGES)
 The initial (non infected) lesion in dentin
forms beneath enamel before any
cavity has formed.
 Even though acids formed from
fermentation of carbohydrate substrate
diffuse into dentin, they leave the organic
matrix intact.
 Once bacteria penetrate enamel, they
spread laterally along DEJ and attack
dentin over a wide area.
 The infected lesion of dentin is helped in
its course by the presence of tubules
within dentin which provide an easy
pathway to the bacteria.

 Bacteria now liberate proteolytic

enzymes and bring about destruction of
organic matrix of dentin which is already
softened by demineralization.
 The first change to occur in the caries process
within dentin is fatty degeneration of the tome’s
fibers, with deposition of lipid globules within
these fibers.
 This is then followed by dentinal sclerosis,
which is minimal in rapidly advancing acute caries
and maximum in slow, chronic caries.
 This is considered as a protective measure by
dentinal tubules to seal off the invading bacteria.
 In spite of all these attempts to prevent
spread of caries process, dentin is
continually destroyed.
 Thus behind the zone of dentinal sclerosis
a narrow zone of decalcification is seen,
just ahead of bacterial invasion of dentinal
tubules.
 At this stage, only a few tubules are
invaded even before clinical evidence of
caries.
 These bacteria are called “Pioneer
bacteria”.
HISTOPATHOLOGY OF CARIES –
DENTIN (ADNANCED CHANGES)

 Continued decalcification of
dentinal tubules leads to their
confluence, although the structure
of organic matrix may still be
maintained for some time.

 Confluence of tubules occurs due

to packing of the tubules with the
invading bacteria.
 The coalescence and breakdown
of adjacent dentinal tubules leads
to formation of “Miller’s
liquefaction foci”.

 It is an ovoid area of destruction

of tubules parallel to the course of
tubules and is packed with
necrotic debris derived from
destruction of tubules.
 Continued dentinal destruction by
decalcification followed by proteolysis
occurs at many focal areas which
ultimately coalesce to form a necrotic
leathery mass of dentin.
 In this mass, clefts occur at right
angles to tubules and parallel to the
course of lateral branches of tubules
or along the collagen fibers of organic
matrix.
 Due to these clefts, carious dentin can
be peeled away in thin layers by hand
instruments.
 ZONES OF DENTINAL CARIES

 Observing from the pulpal side at the advancing

edge of carious lesion following different zones can
be seen –
ZONE 1 – Zone of fatty degeneration of Tomes’ fibers
ZONE 2 – Zone of dentinal sclerosis
ZONE 3 – Zone of decalcification
ZONE 4 – Zone of bacterial invasion
ZONE 5 – Zone of decomposed dentin
  Observing from the pulpal side at the
advancing edge of carious lesion
following different zones can be seen
–
ZONE 1 – Zone of fatty degeneration of
Tomes’ fibers
ZONE 2 – Zone of dentinal sclerosis
5
4 ZONE 3 – Zone of decalcification
3
2 ZONE 4 – Zone of bacterial invasion
1 ZONE 5 – Zone of decomposed dentin
 BIBLIOGRAPHY
 Dental Caries: The disease and its clinical
management. 1st ed. Blackwell Munksgaard,
Iowa.
 Soames JV, Southam JC. Oral pathology/. 3rd
ed. Oxford 2002.
 Shafer WG, Hine MK, Levy BM. A text book of
oral pathology. 6th ed. Elsevier, NOIDA, India
2009.
Acknowledgements:
All pictures used in the presentations are
courtesy of above mentioned authors.