Dental Caries

Intended Learning Outcomes

By the end of this chapter, you will able to :
 Define dental caries
 Comprehend the etiological factors associated with dental
caries
 Recognize predisposing factors that require intervention to
promote oral health
 Explain the biochemical processes contributed to dental caries
 Identify the sequence of events as regards the caries process
histologically
 Construct a mind map to connect all information as regards
dental caries
 What is dental caries?

It is a progressive microbial disease of hard

tooth structure exposed to the oral environment.
Demineralization of the inorganic portion &
destruction of the organic part of the tooth.
 Etiology
Multifactorial disease

Host

Fermentable
carbohydrates caries Plaque

Cariogenic
Bacteria Time
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1- Cariogenic bacteria
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 Miller’s experiment
Saliva (m.o.)+
fermentable
CHO
Caries
like
lesions
 Orland
Germ
free Sucrose- Caries
rich diet ?
rats
Germ
free
Group 1
rats
(Incubator)
No Caries

Group 2
(Environment
Caries
)
Gnoto Sucrose Caries
biote -rich
?
rats diet

Germ
free
Group 1
The most Cariogenic
rats mutans
Streptococcus
Pit & Fissure
Smooth
GroupSurf.
2
Lactobacilli
Pit & Fissure Caries

Group 3
Actinomyces
Root Surf. Caries
 Essential properties of cariogenic
bacteria
1- Acidogenic
Bacteria ferment CHO produce Lactic Acid

pH < 5.5

Enamel demineralization
2- Aciduric
Survive at low pH

3- Formation of extracellular
polysaccharides
a. Dextran

b. Levan
 Extracellular polysaccharides
Dextran Levan

1. Glucose polymer 1. Fructose polymer

2. Water insoluble 2. Water soluble
3. Highly adhesive, 3. Less adhesive
sticky
4. A store of CHO
4. Forms the bulk of
plaque (smooth
surface caries)
4- Formation of intracellular polysaccharides
Amylopectin: acting as a reserve when sucrose is
absent from diet

5- Have means of attachment to surface

6- Ability to actively transport fermentable sugars

when in competition with other plaque bacteria even
against a concentration gradient
 Streptococcus Mutans
1- Powerful Acidogenic
2- Powerful Aciduric (pH4)
3- Formation of extracellular polysaccharides
(Dextran and Levan)
Attach Bacteria
Dextra adhere Smooth
n ment to surface
adhesive, mecha smooth caries
sticky
nism surface

S.Mutans can produce both smooth surface and pit

and fissure caries.
4- Formation of intracellular polysaccharides
(Amylopectin)
5- It adheres to plaque pellicle by Adhesins
 Lactobacilli

1- Acidogenic Progression of
& Aciduric caries

No Pit &
No Bacteri Fissu
2- No Attach a
Dextra ment adhere re
n mechan to carie
ism smooth s
surface ONLY

Pioneer in Dentin caries

 Actinomyces

Produce Root
Proteolyti surface
c enzymes caries
 2- Fermentable carbohydrates

Factors affecting cariogenicity of CHO:

1. Type:
A. Monosaccharides (e.g. Glucose, Fructose)
B. Disaccharides (e.g. Sucrose, Maltose,
Lactose) * Sucrose is the arch criminal?
C. Polysaccharides (e.g. Starch, Glycogen)
 Sucrose
(Disaccharide= Glucose + Fructose)
Why?
1. It has low molecular weight allowing rapid diffusion in dental
plaque

2. It is rapidly fermented by plaque bacteria producing acid

Sucrose Hydrolysis Glucose + Fructose
(St. mutans)
Glucose Glucokinase Energy + H2O + Lactic Acid
(St. mutans)
Fructose Fructokinase Energy + H2O + Lactic Acid
(St. mutans)
 3-The energy liberated from the break of the
disaccharide bond is used by cariogenic
bacteria to produce dextran.

4- Cheap and common in most food

Monosaccharides are less cariogenic
than disaccharides since they are easily
washed away by saliva and …..?????
 Polysaccharides
Low cariogenic effect
It has larger molecular weight so cannot diffuse
rapidly in dental plaque

It cannot be easily metabolized by bacteria

Polysaccharides S. Amylase Mono. + Di.
 Slow process
 Small amount of Acids
2. Amount
3. Frequency
4. Texture
5. Refinement
High Frequency of CHO intake:
Increase periods of activity of bacteria.
No cleansing effect of fibrous food.
No chance for pH to return to normal as the pH takes a
long time to return to normal after carbohydrates intake
(Stephan’s curve).

Sticky CHO:
It remains for a long time in relation to tooth surface
and it is slowly washed by saliva so it is more
accessible to bacteria for a longer time to produce more
Vipeholm experiment
436 adult patients
in a mental hospital
at Vipeholm city
Over 5-years period
 7 groups
(All receiving a basic low CHO diet)

Control 2 groups 4 groups

group at meal between
time meals

In Sweeten toffee caramel

choclat
e
solution ed bread
 Final conclusion
 Total amount of CHO intake:
showed little effect on caries activity
 Frequency of CHO intake & texture of
CHO: showed a greater effect on caries
activity.

Why?
 3- Dental plaque
It is a tenacious bacterial structure
formed on tooth surfaces.

A biofilm of different species of

bacteria in a surrounding substance
(plaque matrix).
 Composition
30-40% Amorphous Matrix

• Proteins
• CHO
• Inorganic
• Fluoride

60-70% Microorganisms

• Mainly Streptococci and Lactobacilli

 Role of Plaque Matrix

1. Acts as a diffusion limiting membrane

Lactic acid in high concentration

Caries initiation

2. Acts as a diffusion limiting membrane

Slow down Buffers entry from saliva

Delaying their neutralizing action

3. Contributes to adhesiveness, bulk and resistance to wash
 Factors affecting plaque thickness

 1 Position & structure of teeth

 2 Presence of appliances
 3 Friction from diet & masticatory movements
 4 Oral hygiene measures
 5 Composition of diet
 Mechanism of formation of plaque

1- Acquired Enamel Pellicle (0.1-1 µm)

 Structureless
 Cell-free
 Salivary glycoproteins ( selective adsorption)

2- Initial Community
Initial colonizers: S.sanguis & Actinomyces viscosus

Monolayer then perpendicular on tooth surface.

3- Intermediate Community
S.Mutans ( adhesin-receptor interactions)

 Ferment sucrose Acids ( +ve & -ve interactions)

veillonella S. sanguis

 Builds up dextran , levan

Sticky &Bulky plaque

4- Mature Community

Corn cobs
Acid production in dental plaque
Stephan’s curve
To study the changes occurring in the pH of plaque
after glucose intake.
Mouth rinsing with a 10% glucose (10 sec.) solution

Sugar diffuse rapidly through plaque

Bacteria Acids (lactic acid)

 Stephan’s curve
Resting
pH
2-5 minutes:
the pH falls rapidly to the critical pH of 5.5

15-20 minutes:
the pH remains at a low level

Over the next 30 to 60 minutes:

the pH returns slowly to the resting level
Why rapid fall in pH occurs?
1. Rapid diffusion of sugar into the
plaque
2. Large amount of enzymes
produced by bacteria in plaque
Slow return to resting PH:
1. Continuous metabolism of residual
sugar in plaque.
2. Diffusion-limiting properties of
plaque resulted in the delay of
escape of acid into saliva.
3. Diffusion-limiting properties of
plaque hampered diffusion of
salivary buffers into plaque.
4. Continuous acid production from
bacterial Intracellular
polysaccharides (reserve CHO)
Demineralization and Remineralization
• Dental caries is a dynamic process.

• It consists of periods of demineralization and periods of remineralization.

• Remineralization occurs when the sugar intake stops, and the oral hygiene is
established by good tooth brushing.

• When demineralization > remineralization, caries is produced.

• When remineralization > demineralization, arrested caries is produced.

Biochemical Reactions Occurring in Bacterial Plaque
& enamel
 Acid production (Stephan’s experiment)
 Formation of extracellular polysaccharides
 Formation of intracellular polysaccharides
 Demineralization phase
 Remineralization phase
 4- Susceptible tooth
:Factors
1. Position (Upper, Posterior, Crowded)
2. Morphology (Pit & Fissures, Contact area)
3. Structure (Newly erupted, Hypoplasia)
4. Genetic (Families)
5. Fluoride
 Fluoride
Fluorides from drinking water and other sources
During development of •
F>1.2 ppm
teeth

Dental Fluorosis Hydroxyapatite F •

Fluoroapatite

Structure
defects Caries •
Actions of Fluoride on caries:
Cariostatic Why?
1- Formation of fluoroapatite which is
less soluble in acid
Deminerilization Caries
2- Reminerilization
3- Inhibit bacterial enzymes
Prevention of bacterial growth
 Saliva and Dental Caries
1. Washing and cleansing effect
2. Rate of flow & Buffering effect:
Biocarbonate: Buffering & neutralize pH
3. Antibacterial activities (Lyzozymes& peroxide)
4. Immunological defenses (Secretory IgA)
5. Salivary glycoproteins which form acquired
enamel pellicle provide initial protection from
bacteria.
6. Inorganic components ( calcium, phosphate &
fluoride) enhance remineralization
Pathology of dental caries
Caries In Enamel
 Macroscopic appearance
Initial enamel caries
white spot
 Patient with initial caries
If good oral hygiene
+ dec. in sucrose intake
+increase in fluoride

Reminerlization

Arrested caries
 Arrested caries
Brown spot
(Hard)
 Phases of enamel caries
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 1- Phase of initial enamel caries
Smooth surface caries

Longitudinal ground sections

Ordinary light Polarized light Microradiograph
microscope microscope
Quinoline/Canada
balsam
 Microscopic appearance
Smooth surface caries
The caries forms
a triangular pattern
(cone shaped lesion),
 Apex: towards DEJ
 Base: towards the tooth
surface.
 Microscopic appearance
Pit and fissure caries
2 cones appearing as 2 smooth surface lesions
Bases: on the lateral surfaces of the fissure
Apex: towards DEJ
 1. The early lesion
•(Initial enamel caries)
Intact surface
• Due to acid demineralization (No bacterial invasion)
Zone 1: Translucent zone,
Zone 2: Dark zone,
Zone 3: Body of the lesion,
Zone 4: Surface zone,

4--------------

3
2--------
1--------
 Translucent zone 1%

First changes observed

 Dark zone 2-4%
Superficial to trans. Zone

2 pore types

Small pores: the Quinoline does not enter

and thus are filled with air SO the zone
appears dark
 Body of the lesion 5-25%
Bet. Surface & dark zone
Translucent
Radiolucent in x-ray
 Surface Zone
Intact although there are subsurface changes

Remineralization from:
Plaque
Minerals coming outwards from deep layers

More Radiopaque than any layer

 Zones of the early lesion
Zone % of It represents Location Appearance
pore
volume

Zone 1: 1% Initial the advancing

Pores filled with Quinoline (same
demineralization front i.e. towards
Translucent the dentine Refractive Index as Enamel)
zone
Normal structure features disappear
The Enamel appears Translucent

Zone 2: 2-4% Further superficial to the

Two different-sized pores:
demineralization translucent zone
Dark zone & remineralization The large pores undergo
remineralization
Micropores are so minute
Quinoline molecules are unable to
enter
Pores remain filled with Air
producing the dark appearance
 Zones of the early lesion
% of It represents Location Appearance
pore
volume

Zone 3: 5- 25 Progressive extending from

demineralization beneath the Pores
Body of the % surface to the
lesion Filled with Quinoline
dark zone
(The largest)
The Enamel appears Translucent

Zone 4: Remineralization Surface of the

Surface lesion
zone
(Hyper-
mineralized )
2. Phase of bacterial invasion
3. Phase of destruction
 4. Phase of 2ry enamel caries
 When the caries reaches the ADJ

Spreads laterally

1- Enamel may become widely undermined

The enamel is no longer able to
withstand the loads placed upon it

Cavity formation
2-E is Destroyed from below and
(reverse attack)

3-Attack Dentin over a wide area

That explains the clinical finding that a

pinhole lesion occlusaly may be a wide
cavity from below
Pathogenesis of enamel caries

White spot
Caries In Dentin
 Dentin

1. Living tissue
2. High organic content
3. Shape Cone base towards
enamel
4. Lactobacilli plays a major
role
5. The first reaction starts before
cavitation of enamel
 Zones of dentine caries

1- Uninfected lesion ( Acid attack)

2- Infected dentinal lesion ( Bulk of the lesion) (Bacterial invasion)

3- Area of dentinal destruction

I- Uninfected dentinal lesion

1- Zone of fatty degeneration

Acids reach dentin & irritate the odontoblastic processes in the tubules.
2- Zone of hypermineralization (sclerosis)

Ca salts within dentinal tubule obliterating it to protect the

odontoblasts and the pulp (peritubular dentin)
1 Active transport
2 Passively from demineralization
3-Zone of hypomineralization (demineralization)

Acids

Remove minerals from the inner wall of the dentinal tubule

Widening

Allow Bacterial invasion

II- Infected dentinal lesion (after cavitation)

1- Pioneers

Pioneer m.o: Acidogenic bacteria (Lactobacilli)

The second wave: Acidogenic and proteolytic bacteria

2- Beading

M.O proliferate inside the soft dentinal

tubule
Alternating active & resting phases

Separate aggregates
Beads
3- Liquefaction foci & transverse
clefts
Coalescing of adjacent beadings

Liquifaction focus

Lateral spread through incremental lines &

lateral branches of D.T

Transverse clefts
 Uninfected lesion Infected lesion
 No bacteria ( acid attack  Bacteria is involved
only)  Not remineralizable and
 Remineralizable & should be removed
should be preserved
 Pioneer Beading
bacteria

Liquefaction Transverse
focus clefts
III- Area of dentinal destruction
Larger and irregular cavities
 Reactionary changes in dentine

1. Tubular sclerosis (Translucent Dentin)

2. Dead tracts
3. Regular reactionary dentine
4. Irregular reactionary dentine
 Root surface caries
 Gingival recession

 Bacteria invade the demineralized cementum early along

sharpey’s fibers
Thank you