Introduction to

Cariology
Points of Focus

 Definition of Dental Caries

 Etiology of Dental Caries
 Classification of Dental Decay
 Caries progression & sequela
 Ecology of Dental Caries
What is dental caries?

How does dental

caries occur?
 Dental Caries
Dental caries is an infectious,
transmissible, non communicable
disease resulting in destruction of
tooth structure by acid-forming
bacteria found in dental plaque, in the
presence of sugar
 Dental Caries
It is a disease of the calcified tissues of the
teeth caused by the action of
microorganisms on fermentable
carbohydrates. It is characterized by
demineralized of the mineral portion of
enamel and dentin followed by
disintegration of their organic material.
Tooth structure
Dental Caries
Remineralization Vs Demineralization

Caries activity is a dynamic process of

demineralization, stasis & reminaralization
Dental Plaque (Biofilm)
It is a complex soft deposit which is
tenaciously attached to the tooth surface
composed of microorganisms, epithelial
cells, leukocytes, macrophages salivary
proteins and water. (Estonia of periodontics)
Dental Plaque
Dental Caries

During the past few decades, changes

have been observed in the prevalence
of dental caries
It is identified a shift toward improved
diagnosis of non-cavitated, incipient
lesions and treatment for prevention
and arrest of such lesions
Dental Caries
Prevention Vs Restoration

Restorations repair the tooth structure,

do not stop caries, have a finite life
span and are susceptible to disease
Etiology of Dental Caries
Vann diagram of caries causation

Susceptible
tooth
surface
Bac Flora
Strep. Mutans

Tooth Decay Fermenlilble

Carbohydrates/
occurs with ___ _ ___..,:su: g:ar:s,:_ _ _ __
Tooth / Host

Microbial colonization on teeth.

Early childhood smooth surface caries
Later in childhood pits & fissures
Susceptible teeth surfaces to
caries
Deep & narrow pits & fissures (1st molars/ 2nd
molars/ premolars).
Approximal enamel tooth surfaces
Cervical margins of teeth
Badly done restorations or overhanging
restorations.
Exposes root surfaces following gingival
recession
Tooth surfaces adjacent to bridges & dentures
Saliva Role
Essential source of Ca & PO4 ions
Flow rate (stimulated vs unstimulated), <
1.0 ml/min
Acid buffering
Antibacterial enzymes
Oral clearance (cleansing action)
Lubrication
Viscosity
Bacterial Plaque

Plaque biofilm essential to caries.

Among the over 300-500-700 species
of bac in plaque only few are
cariogenic.
Streptococcus Mutans/ Lactobacillus/
Actinomyces
PH Scale
Dental Plaque PH
Change in dental plaque PH in response to
challenge (Diet).
The initial rapid drop in pH is due to the
speed with which plaque microbes are able
to metabolize sucrose.
Larger carbohydrates, such as starch,
would diffuse into plaque more slowly and
would need to be broken down before
assimilation by the microbes.
 rides Disaccharides

glucose ma ltose

fructose sucrose

galactose lactose
The lowest PH
The lowest pH achieved depends greatly on:
1. the microbial composition of the dental
plaque (is it carogenic bac???)

2. the nature of the fermentable carbohydrate

source (mono-saccharide, di-saccharide, poly?)

3. the rate of diffusion of substrates and

metabolites into and out of the plaque.
Effect of Microbial Composition
Rate of Diffusion
The lowest pH attained is
also determined by the rates
of diffusion of substrates.
Molar fissures are the most
caries-prone sites because
they are very sheltered from
saliva flow. The deepest parts
are often inaccessible to
toothbrushes which means
that fissures frequently
contain impacted food for
extended periods of time.
Stephan Curve

The Stephan Curve

describes the
change in dental
plaque pH in
response to
challenge
(fermentable
carbohydrate).
Critical PH
Critical PH

Demineralization starts as the local pH is

lowered below 5.5
Remineralization of the damaged tooth
structure occurs as the local pH rises
above 5.5.
Frequently of the Cariogenic
Challenge
Classification of Dental Caries
Classification of Dental Caries

 According to location

 According to extent

 According to rate of caries (speed)

DC According to location

I. Pits & fissures caries

II. Smooth surface caries

III.Root surface caries

Pits & fissures caries

 Limited to occlusal surfaces of molars and

premolars.

 Irregular surfaces are more prone to

dental decay due to their mechanical
characteristics which result in poor self
cleaning features.
Pits & fissures caries
Smooth surface caries
 Begins in a smooth area of the
enamel surface that is habitually
unclean and is continually or
usually covered by plaque.

 Also called proximal caries

affecting the proximal surfaces
(mesial and distal).
Smooth surface caries
Root surface caries

 It affects old age people mainly those who

have periodontal problems with significant
gingival recession and exposed root
surfaces
Root surface caries
DC According to extent

 Incipient caries (Reversible), first evidence

of caries which appears as an opaque white
spot on the surface of enamel (primary
prevention)
 Cavitated caries (Irreversible), when caries
advances into dentine and the enamel
surface is no more Intact.(secondary
prevention)
DC According to rate of caries
(speed)
 Acute caries (Rampant), which
appears as soft light yellow colored
lesion (rapid & extremely damaging)
with bad smell.
lt describes sudden rapid destruction of
many teeth frequently involving
surfaces of teeth that are ordinarily
free of caries.
Acute caries (Rampant)

 Commonly seen in the

primary dentition of
teeth of infants who
continually suck a
bottle or comforter
containing, or dipped
into, a sugar solution.
Acute caries (Rampant)

 Can also be seen in

permanent dentition
of teenagers due to
the frequent intake
of carlogonic snacks
and sweet drinks
between meals
DC According to rate of caries
(speed)
Chronic caries, (Arrested) which
appears as fairly hard discolored lesion
which is slow or may be arrested
following several active phases.

The demineralized tooth structure is

almost due to changes in environment.
Arrest caries

 The slow caries rate allows time for

extrinsic pigmentation.

 Enamel lesion is brown to black , hard and

due to fluoride may be more caries
resistant
Caries Stages in Teeth
Caries Progression
Caries Progression

 Lost tooth structure.

 Pain and distress.
 Pulpal pathosis.
 Periradicular pathosis
(surrounding bone &
soft tissue)
Caries Progression in children

 Chronic pain
 Poor appearance
 Poor nutrition
 Inability to concentrate
 Low self esteem
Caries Progression in children
Early tooth loss malocclusion
Ecology of dental caries

Ecology : relation to surrounding

environment
Ecology of dental caries

 Host Factors

 Environmental Factors
Host Factors

 Age
 Gender
 Race
 Familial Factors
Host Factors

 Age: it's a disease of children. In Thailand in

2011, 96.3% of children with the age of 6 had
caries
 61% of 12 years of children in Brazil in 2001
 61% of adolescents aged 15 years
experienced DC in USA
Host Factors

 Gender factors: Several studies showed a

small higher caries experience in young
females in comparison to males.

 Explained by the earlier eruption of

permanent teeth in girls longer exposure
carious environment
Host Factors

 Race: in societies characterized with

multicultural nature.
 Blacks and Chinese population have lower
calories than the corresponding white
Environmental Factors

 Diet
 Geographic variations
 Dental care
 Socioeconomic status
 Protective Factors
Salivary flow and components
Proteins, antibacterial components
and agents
Fluoride, calcium and phosphate
Dietary components: protective
NO CARIES
Pathological Factors
Reduced salivary function
Bacteria: mutans streptococci,
lact..a...cilli
Dietary components: frequent
carbohydrate ingestion
CARIES