Dental Caries: Dr. Hend Elallaky

Dental caries
Dr. Hend Elallaky

Good oral health is an integral component of good
general health.
Dental caries is not self-limiting like the common

cold, It is not able to treatment with simple antibiotic
course like an ear infection.
Bowen (1991) pointed out that although we
have observed a decline in caries prevalence
for many years, it is clear that dental caries
still remains the most prevalent disease
afflicting humans.
Etiology of
dental caries
Dental caries is a multifactorial disease and the following
four factors influence its progression:
Dental plaque.
substrates.
Host factors. Dental
Time. plaque
No caries No caries
Host caries
substrate
factors
No caries No caries
Time
Today all experts on dental caries
generally agree that it’s an infectious
and communicable disease, and that
multiple factors influence the initiation
and the progression of the disease.
Dental plaque:
The saliva, the substrate, and the bacteria, form a
biofilm (plaque), that adheres to the tooth surface,
over time the presence of substrate serves as a
nutrient.
 In the caries process, once the PH in plaque drops

below a critical level (around 5.5), the acid produced
begins to demineralize enamel, This will last for 20
minutes or longer, depending on the availability of the
substrate.
Substrates: ( a dietary substrate)
Any carbohydrate causes the production of acid, but

glucose and sucrose is more important than weaker by-
products such as alcohols.
The amount of fermentable carbohydrates is relatively

unimportant, as even minute amounts of fermentable
carbohydrates will be utilized immediately.
So the time of consuming carbohydrate is more
important than its amount
Substrates:
 Bacteria utilize fermentable carbohydrates for energy

and to form acids.
 Sucrose and glucose is the fermentable carbohydrate

most frequently implicated.
 Bacteria can use all fermentable carbohydrates

including cooked starches.
Streptococus mutans is the most important bacteria
that may cause caries
Host factors: (tooth in the oral environment)
 Saliva plays several critical roles in the caries

process. In removing substrate and buffering plaque-
acid, saliva helps to slow the caries process, and is
critical in remineralization.
Viscous saliva may increase caries rate
Teeth anatomy as deep pit and fissure may increase
caries rate
Time:
When the acid challenge occurs repeatedly it may

result in the collapse of enough enamel crystals to
produce a visible cavity. Cavitation may take from
months to years.
Dental caries is a preventable disease.
The disease typically begins in the enamel and

progresses slowly in the early stages of the process,
cavitation of the tooth is quite a late stage of the
disease, prior to cavitation the progress of the disease
may be arrested, and/or reversed if a favorable oral
environment exists.
Theories of the cause of dental caries:
Three theories regarding the mechanism of dental

caries have been postulated:
The proteolysis theory.

The proteolytic-chelation theory.
The chemicoparastic or acidogenic theory.
The proteolysis theory:
This theory was developed after identification of
protein in enamel.
The theory proposes that: Initial attack is enzymatic
destruction of the protein of the enamel matrix
followed by acid dissolution of the mineral .
The proteolytic _chelation theory:
This theory postulated that:
oral bacteria attack organic components of enamel,
and that the breakdown products have chelating ability
and thus dissolve the tooth minerals.
products of proteolysis can remove calcium from

mineral phase by chelation , without 'the need for acid
production.
The chemicoparasitic or acidogenic theory:
This theory has been the most popular over the years
and probably the one most widely accepted today.
Most acceptable.
Postulated by W.D. Miller 1989.
Proposes that acid formed from the fermentation of
dietary carbohydrates by oral bacteria leads to
progressive decalcification of the tooth substance with
a subsequent disintegration of the organic matrix.
 classification of dental caries:
According to the site of the attack:
Pit or fissure caries.
Smooth surface caries.
Cemental or root caries.
Recurrent caries.
Classification by the rate of the attack:
Rampant or acute caries.
Slowly progressive or chronic caries.
Arrested caries.
Enamel caries:
Ground section through an early carious lesion shows
the enamel caries is cone-shaped, with the base of the
cone on the enamel surface and the apex pointing
towards the amelodentinal junction.
In ground sections it consists of serious of zones:
Translucent zone.
Dark zone.
Body of the lesion.
Surface zone.
1-Translucent zone.
2-Dark zone.
3-Body of the lesion.
4-Surface zone.
Translucent zone:
It is more porous than normal enamel and contains 1
per cent by volume spaces compared with the 0.1 per
cent pore volume in normal enamel.
Chemical analysis shows that there is a fall in
magnesium and carbonate compared with normal
enamel.
The translucent zone is sometimes missing, or present
along only part of the lesion.
This zone is unrecognizable clinically and
radiographically.
Dark zone:
The zone contains 2-4 per cent by volume pores.
The dark zone is narrow in rapidly advancing lesions
and wider in more slowly advancing lesions when
more remineralization may occur.
Body of the lesion:
This zone has a pore volume between 5 and 25 per cent
and also contains appetite crystals larger than those
found in normal enamel.
Surface zone:
This is about 40 mm thick.
It’s highly mineralized than deeper zones and contains
more fluoride level and a lower magnesium level.
Stages of histological development of enamel caries:
c. Typically d. Cavitation of
a. Subsurface b. Dark zone The surface,spread
zoned
translucent along The
structure of
zone amelodentinal
the early
(white spot) junction,Reactive
lesion. changes in the
dentin.
Micrograph of an early carious lesion
in enamel showing loss of mineral
from the body of the lesion.
Ground section through
an early lesion of fissure
caries in enamel.
Dentin Caries:
Dentin differs from enamel in that it is a living tissue
and as such can respond to caries attack.
It also has a relatively high organic content ,
approximately 20 per cent by weight, which consists
predominantly of collagen.
Dentin Caries:
Caries of the dentin develops from enamel caries:
when the lesion reaches the amelodentinal junction,
lateral extension results in the involvement of great
number of dentinal tubules.
The early lesion is cone shaped or convex with the
base at the amelodentinal junction.
Dentin Caries:
Studies of ground and decalcified sections show a
zoned lesion in which four zones are characteristically
present:
Zone of sclerosis.
Zone of demineralization.
Zone of bacterial invasion.
Zone of destruction.
Reactionary, secondary dentin.
Dentin caries:
Dramatic representation of the development of fissure caries.

Root caries:
The primary tissue affected in root caries is usually the
cementum
The development of cemental caries is preceded by
exposure of the root to the oral environment as a result
of periodontal disease followed by bacterial
colonization.
Actinomysis species are present in large numbers and
have been implicated in the disease, along with other
organisms like S.mutans.
Arrested caries:
Enamel:
Arrest of an approximal smooth-surface lesion prior to
cavity formation can occur when the adjacent tooth is
lost so that the lesion becomes accessible to plaque
control.
Remineralization can occur from saliva or from the
topical application of calcifying solutions , but normal;
crystalline structure is not necessarily formed.
Arrested caries:
Dentin:
The loss of unsupported overlying enamel exposes the
superficially softened carious dentin to the oral
environment and is then removed by attrition and
abrasion, leaving a hard polished surface.
Such dentin is deeply pigmented, brown-black in color.
Its surface is hypermineralized due to remineralization
from oral fluids and has a high fluoride content.
Arrested lesions of root caries have a similar
clinical appearance and develop in a similar
manner following loss of superficially
softened cementum.
Tooth structure remineralized in the presence of
fluoride contains increased concentrations of
fluorohydroxyappatite, which makes the remineralized
tissue more resistance to future attack by acids than
was the original structure.
Thank you

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Dental caries

Dr. Hend Elallaky

Dental caries is not self-limiting like the common

 In the caries process, once the PH in plaque drops

Any carbohydrate causes the production of acid, but

The amount of fermentable carbohydrates is relatively

 Bacteria utilize fermentable carbohydrates for energy

 Sucrose and glucose is the fermentable carbohydrate

 Bacteria can use all fermentable carbohydrates

 Saliva plays several critical roles in the caries

When the acid challenge occurs repeatedly it may

The disease typically begins in the enamel and

Three theories regarding the mechanism of dental

The proteolysis theory.

products of proteolysis can remove calcium from

Dramatic representation of the development of fissure caries.

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