DENTAL CARIES

DR. SHIPRA SINGHAL

JR-1
DEPARTMENT OF CONSERVATIVE DENTISTRY & ENDODONTICS
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CONTENTS
 INTRODUCTION
 HISTORY
 DEFINITION
 DEMINERALIZATION & REMINERALIZATION
 HISTOPATHOLOGICAL CHARACTERSTICS OF LESION
 CONCLUSION
 REFERENCES

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INTRODUCTION

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Dental caries is reported to be one of the oldest and most
common diseases found in humans.

It is a prevalent chronic infectious disease resulting from

tooth-adherent cariogenic bacteria that metabolize sugars
to produce acid, which over time demineralizes tooth
structure.

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HISTORY

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Over a million years ago, hominids such as Australopithecus
suffered from cavities

Archaeological evidence shows that tooth decay is an

ancient disease dating far into prehistory.

Skulls through the neolithic period showed signs of caries

attributed to dietary changes, increased consumption of
plant foods containing carbohydrates and beginning of rice
cultivation. 

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A Sumerian text from 5000 BC describes a "tooth worm" as
the cause of caries.

The term “dental caries” was first reported in the literature

approximately around 1634, and it originates from the Latin
word “caries,” which stands for decay.

The term was initially used to describe holes in the teeth.

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During the European Age of Enlightenment, the belief that a
"tooth worm" caused caries was no longer accepted in the
European medical community.

Pierre Fauchard, who was known as the father of modern

dentistry, was one of the first to reject the idea that worms
caused tooth decay and noted that sugar was detrimental to
the teeth and gingiva.

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In 1850, another sharp increase in the prevalence of
caries occurred and is believed to be a result of
widespread diet changes.

Prior to this time, cervical caries was the most frequent

type of caries, but increased availability of sugar cane,
refined flour, bread, and sweetened tea corresponded with
a greater number of pit and fissure caries.

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In the 1890s, W.D. Miller conducted a series of studies that
led him to propose an explanation for dental caries that was
influential for current theories

He found that bacteria inhabited the mouth and that they

produced acids that dissolved tooth structures when in the
presence of fermentable carbohydrates.

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This explanation is known as the chemoparasitic caries
theory.

Miller's contribution, along with the research on plaque

by G.V. Black and J.L. Williams, served as the
foundation for the current explanation of the etiology of
caries.

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DEFINITION

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Dental Caries is a multifactorial,
transmissible, infectious oral disease caused
primarily by the complex interaction of
cariogenic oral flora (biofilm) with fermentable
dietary carbohydrates on the tooth surface
over time. (sturdevant-5th ed.)

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Traditionally, this tooth-biofilm-carbohydrate interaction has been
illustrated by the classical Keyes-Jordan diagram

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Later, it was estimated that cavitation activity is characterized
by a dynamic process of attack (demineralization) & restitution
(remineralization) of tooth matter.

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DEMINERALIZATION &
REMINERALIZATION

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“ACID PRODUCTION”

In health, the microbiome is in symbiosis, the oral

commensals striving in a neutral pH.

Some bacteria in the biofilm metabolize refined

carbohydrates for energy & produce organic acid
by-products (lactic acid)

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“CRITICAL BIOFILM pH”

These organic acids, if present in the biofilm

ecosystem for extended periods, can lower
the pH in biofilm to below a critical level [5.5
for enamel & 6.2 for dentin]

This low pH has effects both on the biofilm

composition & at the tooth surface level

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“DEMINERALIZATION”

With extended periods of low pH, there is shift in the

microbiome to bacteria that are acidogenic &
acidophilic, causes a dysbiosis in the microbiome.

This change in turn will lead to further acidification of

environment.
The low pH drives calcium & phosphate from the tooth
to the biofilm in an attempt to reach equilibrium, hence
resulting in a net loss of minerals by the tooth or
demineralization
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“REMINERALIZATION”

When the pH in biofilm returns to neutral

& the concentration of soluble calcium &
phosphate is supersaturated relative to
that in the tooth, mineral then can be
added back to partially demineralized
enamel, in a process called
remineralization.

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Thus at the tooth surface &
subsurface level, dental caries
lesions result from a dynamic
process of damage
(demineralisation) & restitution
(remineralization)

These events take place several

times a day over the life of the
tooth

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The balance between demineralization and remineralization
has been illustrated in terms of pathologic factors (i.e.,
those favoring demineralization) and protective factors (i.e.,
those favoring remineralization)

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Individuals in whom the balance tilts predominantly toward protective
factors (remineralization) are much less likely to develop dental caries than
those in which the balance is tilted toward pathologic factors
(demineralization).

Repeated demineralization events may result from a

predominantly pathologic environment causing the localized
dissolution and destruction of the calcified dental tissues,
evidenced as a caries lesion or a “cavity.”

Severe demineralization of enamel results in the formation of a

cavitation in the enamel surface & subsequent
demineralization of the inorganic phase and denaturation and
degradation of the organic phase result in dentin cavitation.
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HISTOPATHOLOGY

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ENAMEL CARIES
 Enamel is composed of tightly packed hydroxyapatite crystallites,
organized into long columnar rods (prisms).

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 Each rod starts at the DEJ and extends as
a wavy, continuous column to the surface
of the crown. The mineralization process
is apparently discontinuous and is
characterized by alternating phases of
high and low activity forms the
incremental lines of retzius

 The striae and the inherent spaces in

prism boundaries provide sufficient
porosity to allow movement of water and
small ions, such as hydrogen ions acting
as a molecular sieve
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 Acidified gels were used over a long exposure time (10-12
weeks), to produce artificial carious lesions that were
histologically identical to natural incipient lesions.

 The ability to produce enamel lesions artificially has resulted

in an identification of a detailed description of the early
stages of caries in enamel

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The four regularly observed zones in a sectioned incipient lesion:

a. SURFACE ZONE
b. BODY OF THE LESION
c. DARK ZONE
d. TRANSLUCENT ZONE

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TRANSLUCENT ZONE

The translucent zone is the deepest zone and represents the

“advancing front” of the enamel lesion

The name refers to its structureless appearance when

perfused with quinoline solution and examined with polarized
light.

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In this zone, the pores or voids form along the enamel prism
(rod) boundaries, presumably because of the ease of hydrogen
ion penetration during the carious process

When these boundary area voids are filled with quinoline

solution, which has the same refractive index as enamel, the
features of the area disappear.

The pore volume of the translucent zone of enamel caries is 1%,

10 times greater than normal enamel.

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DARK ZONE
The next deepest zone is known as the dark zone because it
does not transmit polarized light

This light blockage is caused by the presence of many tiny

pores too small to absorb quinoline

These smaller air-filled or vapor-filled pores make the region

opaque

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The total pore volume is 2% to 4%

There is some speculation that the dark zone is not really

a stage in the sequence of the breakdown of enamel;
rather, the dark zone may be formed by deposition of ions
into an area previously containing only large pores.

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[Caries is an episodic disease with alternating phases of
demineralization and remineralization ]
Experimental remineralization has shown
increases in the size of the dark zone at the
expense of the body of the lesion

There is also a loss of crystalline structure in the

dark zone, suggestive of the process of
demineralization and remineralization

The size of the dark zone is probably an indication

of the amount of remineralization that has recently
occurred
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BODY OF LESION
The body of the lesion is the largest portion of the incipient
lesion while in a demineralizing phase

It has the largest pore volume, varying from 5% at the

periphery to 25% at the center

The striae of Retzius are well marked in the body of the lesion,
indicating preferential mineral dissolution along these areas of
relatively higher porosity.
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The first penetration of caries enters the enamel surface via
the striae of Retzius.

The interprismatic areas and these cross-striations provide

access to the rod (prism) cores, which are preferentially
attacked.

Bacteria may be present in this zone if the pore size is large

enough to permit their entry.

Studies using SEM show the presence of bacteria invading

between the enamel rods (prisms) in the body zone.

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SURFACE ZONE
The surface zone is relatively unaffected by the caries attack. It
has a lower pore volume than the body of the lesion (<5%) and
a radiopacity comparable to unaffected adjacent enamel

The surface of normal enamel is hypermineralized by contact

with saliva and has a greater concentration of fluoride ion than
the immediately subjacent enamel.

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It has been hypothesized that hypermineralization and increased
fluoride content of the superficial enamel are responsible for the
relative immunity of the enamel surface.

Removal of the hypermineralized surface by polishing fails,

however, to prevent the reformation of a typical, well-mineralized
surface over the carious lesion.

The intact surface over incipient caries is a phenomenon of the

caries demineralization process rather than any special
characteristics of the superficial enamel.

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Nevertheless, the importance of the intact surface cannot be
overemphasized because it serves as a barrier to bacterial
invasion

As the enamel lesion progresses, SEM shows conical-shaped

defects in the surface zone

These are probably the first sites where bacteria can gain entry
into a carious lesion. Arresting the caries process at this stage
results in a hard surface that may at times be rough, although
cleanable

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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. The loss of structural integrity is followed by invasion of
bacteria

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 Normal dentin has characteristic tubules that follow a wavy
path from the external surface of the dentin, below the
enamel or cementum, to the inner surface of the dentin.

 Dentin is formed from the external surface and grows

inward. As the dentin grows, the odontoblasts become
increasingly compressed in the shrinking pulp chamber,
and the number of associated tubules becomes more
concentrated per unit area.

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The more recently formed dentin near the
pulp (a) has large tubules with little or no
peritubular dentin and calcified
intertubular dentin filled with collagen
fibers.
(b), is characterized by smaller, more
widely separated tubules and a greater
mineral content in the intertubular dentin.
The older dentin tubules are lined by a
uniform layer of mineral termed
peritubular dentin. These changes occur
gradually from the inner surface to the
external surface of the dentin.

Horizontal lines indicate predentin; diagonal lines indicate increasing density

of minerals; darker horizontal lines indicate densely mineralized dentin and
increased thickness of peritubular dentin.
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Carious Dentin
undergoes several
changes.

The most superficial infected zone of carious dentin (3) is characterized by bacteria filling
the tubules and granular material in the intertubular space.
The granular material contains very little mineral and lacks characteristic cross-banding
of collagen. Pulpal to (below) the infected dentin is a zone where the dentin appears
transparent in mounted whole specimens.

This zone (2) is affected (not infected) carious dentin and is characterized by loss of
mineral in the intertubular and peritubular dentin. Many crystals can be detected in the
lumen of the tubules in this zone. The crystals in the tubule lumen render the refractive
index of the lumen similar to that of the intertubular dentin, making the zone transparent.
Normal dentin (1) is found pulpal to (below) the transparent dentin 43
Five different zones have been described in carious dentin.
The zones are most clearly distinguished in slowly advancing
lesions

In rapidly progressing caries,

the difference between the
zones becomes less distinct

Zone 1- Normal dentin

Zone 2- Subtransparent dentin
Zone 3- Transparent dentin
Zone 4- Turbid dentin
Zone 5- Infected dentin

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ZONE-1 NORMAL DENTIN

The deepest area is normal dentin, which has tubules with

odontoblastic processes that are smooth, and no crystals are
in the lumens.

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The intertubular dentin has normal crossbanded collagen
and normal dense apatite crystals.

No bacteria are in the tubules.

Stimulation of the dentin (e.g., by osmotic gradient [from

applied sucrose or salt], a burr, a dragging instrument, or
desiccation from heat or air) produces a sharp pain

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ZONE-2 SUBTRANSPARENT DENTIN

The subtransparent layer is a zone of demineralization of the

intertubular dentin and initial formation of fine crystals in the
tubule lumen at the advancing front
(dentinal sclerosis)

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Damage to the odontoblastic process is evident; however,
no bacteria are found in the zone

Stimulation of the dentin produces pain, and the dentin is

capable of remineralization

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ZONE-3 TRANSPARENT DENTIN
The transparent layer is a zone of carious dentin that is softer
than normal dentin and shows further loss of mineral from the
intertubular dentin and many large crystals in the lumen of the
dentinal tubules.

Stimulation of this region produces pain.

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No bacteria are present. Although organic acids attack the
mineral and organic content of the dentin, (demineralization)
the collagen cross-linking remains intact in this zone.

The intact collagen can serve as a template for remineralization

of the intertubular dentin, and this region remains capable of
self-repair, provided that the pulp remains vital.

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ZONE-4 TURBID DENTIN
Turbid dentin is the zone of bacterial invasion and is marked by
widening and distortion of the dentinal tubules, which are filled
with bacteria.

There is little mineral present, and the collagen in this zone is

irreversibly denatured.

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The dentin in this zone does not self-repair.

This zone cannot be remineralized and must be removed

before restoration.

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ZONE-5 INFECTED DENTIN
The outermost zone, infected dentin, consists of decomposed
dentin that is teeming with bacteria.

There is no recognizable structure to the dentin, and collagen

and mineral seem to be absent.

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Great numbers of bacteria are dispersed in this granular
material.

Removal of infected dentin is essential to sound, successful

restorative procedures and prevention of spreading the
infection

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CONCLUSION

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 Dental caries is a most common chronic infectious diseases
which is preventable thus research efforts must be continued in
understanding the caries process, & how it affects the pulp
covering layers –enamel & dentin histologically.
Patient education and motivation in the prevention and
treatment of dental caries must be stressed. Finally, the clinical
treatment of cavitated, carious teeth must be accomplished
expeditiously, judiciously, and appropriately.

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REFERENCES
 Sturdevant -5th ed.
 Sturdevant- 6th ed.
 Sturdevant’s art & science of operative dentistry – A south Asian
edition
 Rathee M, Sapra A. Dental Caries. [Updated 2022 Jun 12]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan.
 Yadav, Khushbu & Prakash, Satyam. (2016). Dental Caries: A Review. 06.
01-07.

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THANK YOU……

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