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Caries Process

Anita Rosa
Caries Etiology
A CAVITY occurs if the Demineralization "wins" over the Remineralization over time
Understanding the process

pH Low of
production Hydroxyapatite
Understanding the process

What is Hydroxyapatite?
Tooth Microstructure - Enamel
• Rods are made up of bundles of hydroxyapatite
(Ca10(PO4)6(OH)2) crystals, which are composed
of calcium and phosphate (95% inorganic, 5%
Tooth Microstructures - Dentin
• Dentin is also composed of hydroxyapatite,
(70% inorganic, 30% organic) and has tubules
running through it
Equilibrium at normal pH
Saliva is supersaturated with respect to enamel
Ca+statherin Ca+aPRP
[Ca] [PO4] [Ca] [PO4]


Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop
Saliva [Ca]
Ca+statherin Ca+aPRP
[Ca] [PO4] [Ca] [PO4] exit to


[H+] Enamel
[H+] solubility
Saliva flow clears CHO; salivary HCO3 returns pH to normal
statherin Ca+aPRP
[PO4] [HCO3] CHO
move into [Ca] [PO4] [Ca] [PO4]
enamel [HCO3] [HCO3] CHO

soluble Ca10(PO4)6OH2
Alternating cycles of de/re-min
• Break even - sound enamel or arrested caries

• Net loss
– Subsurface demineralization
– New caries
– Progression of old lesions

• Net gain - remineralization of existing lesions

• Does decay travel faster through dentin or
enamel? Why?
What is Dental Plaque?
Bacteria adherence
Bacteria within the plaque
Micro-Biology of Dental Caries
• The main microorganism involved in the initial
caries process is S. mutans.
• S. sobrinus and lactobacillus are also involved,
but must have s. mutans present to colonize.
• Sobrinus means “distant cousin on mother’s
• Lactobacillus produces lactic acid at higher
concentrations than “helpful” bugs
Micro-Biology of Dental Caries
Streptococcus Mutans
• Ability to stick to tooth surfaces
• Ability to produce lactic acid
• Resist the acidogenic environment
• Produce intracellular polysaccharide

Streptococcus Sobrinus
S. mutans structures
• Tooth adherence
• Promotes aggregation
• Biofilm accumulation
• Retention of bacterial nutrients
• Some antibodies prevent GTF function and are
What is the role of saliva?
Role of Saliva in Caries
• Lubrication
• Also called Liquid Enamel because of high mineral
• Cleansing Action
• Buffering Capacity
• AntibacterialActionbyLysozyme,Lactoperoxidase,hemopr
otein enzyme (Prevents bacterial colonization)
• Reservoir of Calcium and Phosphate
• Most prominent antibody in saliva IGA.
• Proteins like statherin protects hydroxyapetite crystals.
Role of Saliva in Caries

If salivary function is reduced for any reason, such as from illness or medications or
due to radiation therapy, the teeth are at increased risk for decay.
What is the correlation between diet
and dental caries?
Fermentable carbohydrate intake
• The frequency of eating cause caries rather
than total quantity of fermentable
• Why??
Fermentable carbohydrate intake
• Have u ever heard about fluorapatite?
• What is it?
Meet the fluorapatite
Fluoride effect on remineralization
and demineralization of enamel
Promote remineralization1


Inhibit acid generation

Reduce demineralization2,3 from plaque bacteria4

1. Silverstone LM. Clinical uses of fluoride 1985;153-175.

2. Featherstone JD, et al. J Dent Res 1990;69:620-625.
3. Aoba T. Crit Rev Oral Biol Med 1997;8:136-153.
4. Briner WW & Francis MD. Arch Oral Biol 1962;7:541-550.
Fluoride Roles
 Fluoride prevents demineralization through formation of
fluorohydroxyapatite (FAP)
 Fluoride prevents demineralization through inhibition of mineral loss from
 Fluoride promotes remineralization through formation of a fluoride reservoir
 Fluoride promotes remineralization through creation of supersaturated
 inhibits plaque bacteria in vitro1-4
- At low pH, fluoride combines with hydrogen ions and diffuses into oral
bacteria as hydrogen fluoride (HF)  Inside the cell HF dissociates, acidifying
the cell and releasing fluoride ions  Fluoride ions inhibit glycolysis

1. Hamilton IR, et al. Fluoride in dentistry. Copenhagen: Munksgaard; 1996. p23-51.

2. Whitford GM, et al. Infect Immun 1977;18:680-687.
3. Van Loveren C. J Dent Res 1990;69:676-681.
4. ten Cate JM. Acta Odontol Scand 1999;57:325-329.
So do you already understand
the caries process?
The five stages of caries
1 Initial1.subsurface demineralization Reversible
Initial subsurface lesion
2 Extension of demineralized
zone towards dentine

3 Collapse of surface layer to form Irreversible lesion

cavity 3. Collapse of surface layer to form cavity

Extension of caries lesion into dentine

5 Possible
Extension of caries into pulp formation of
apical abscess

1. Collins WJN, et al. A Handbook for Dental Hygienists. 3rd edition. Oxford: Wright, 1992.
2. Clarkson BH, et al. Caries Res 1991;25:166-173.
sub-surface enamel lesion
Frank cavitation

• More plaque accumulation so rapid tooth

• It takes 18 (+- 6 months) to progress from
white lesion to cavitation.

Spread of the Carious

Spread of the Carious Lesions

1. Pit and Fissure

Spread of the Carious Lesions
1-Pit and Fissure Caries:
A conical spread pattern in both enamel and dentin.
In enamel, due to the direction
of enamel prisms, the base of 1
the cone is towards the amelo-
dentinal junction.
When caries reaches the amelodentinal junction, it spreads
laterally along the junction,foming the base of the dentinal
The lesion will then spread along the direction of the
dentinal tubules forming the dentin cone with its apex
directed towards the pulp. i.e. base to base relationship.
Pit And Fissure Caries:
-Here the caries follows the direction of the enamel rods.

-It is triangular in shape with the apex facing the surface of tooth and the

base towards the DEJ.

-when reaches DEJ, greater number of dentinal tubules are involved.

-it produces greater cavitation than the smooth surface caries and there is

more undermining of enamel.

Pit And Fissure Caries
Spread of the Carious Lesions

2. Smooth Surface
Spread of the Carious Lesions

2-Smooth Surface Caries

• In enamel the base of the cone is on
the outer surface of the enamel and 2
its apex towards the amelodentinal
junction, then it spreads laterally along the
junction, forming the base of the dentin
cone while its apex is towards the pulp. i.e.
apex to base relationship.
 Prof. A. El-Sahn
Enamel caries

White spot lesions

• Intact surface Advanced enamel caries
• Subsurface • Intact surface
demineralization • “Sticky” fissures
• Visible in radiographs
• Dentin defensive reaction Enamel caries can be remineralized
Dentinal caries Love et al. Infect. Immun. 68:1359

• Cavitation
• Demineralization + proteolysis
• Bacteria move down tubules
• Pulpal involvement
• Major damage if unchecked

Can be arrested, but generally

must be restored
Smooth surface Caries:
Due to plaque formation on enamel. The earliest manifestation of incipient
caries (early caries) of enamel is usually seen beneath dental plaque as areas
of decalcification (white spots).
The first change seen histologically is the loss of inter-rod substance of
enamel with increased prominence of the rods.
-this is followed by the loss of mucopolysaccharides in the organic substance.
-presence of transverse striations of the enamel rods,
- accentuated incremental lines of Retzius
as it goes deeper, the caries forms a triangular pattern or cone shaped lesion
with the apex towards DEJ and base towards the tooth surface. Finally there
is loss of enamel structure, which gets roughened due to demineralization,
and disintegration of enamel prisms.

Dentin reaction
to caries
The zones seen before complete disintegration of enamel are:
Zone 1: Translucent zone,
-lies at the advancing front of the lesion,
-slightly more porous than sound enamel,
-it is not always present
Zone 2: Dark zone,
-this zone is usually present and referred
to as positive zone
-formed due to demineralization.
Zone 3: Body of the lesion,
-found between the surface and the dark zone,
-it is the area of greatest demineralization,
Zone 4: Surface zone,
-relatively unaffected area,
-greater resistance probably due to greater degree of mineralization and
greater F concentration.
Begins with the natural spread of the process along the DEJ and rapid
involvement of the dentinal tubules. The dentinal tubules act as tracts leading to
the pulp (path for micro-organisms).
Early Dentinal Changes:
-initial penetration of the dentin by caries dentinal sclerosis,
-calcification of dentinal tubules and sealing off from further penetration by
-more prominent in slow chronic caries.

Behind the transparent sclerotic zone, decalcification of dentin appears.
In the earliest stages, when only few tubules are involved, microorganisms may
be found penetrating the tubules Pioneer Bacteria.

. In the deeper caries, proteolytic organisms might appear to predominate

while acidophilic forms are more prominent in
early caries.
Shape of the lesion is triangular with the
apex towards the pulp and the base
towards the enamel.

Zone 1; Zone of Fatty Degeneration of

Tome’s Fibers,(next to pulp)

-due to degeneration of the odontoblastic

process. This occurs before sclerotic
dentin is formed and makes the tubules

Zone 2; Zone of dentinal sclerosis,

-deposition of Ca salts in the tubules.

Zone 3; Zone of decalcification of dentin

Zone 4; Zone of bacterial invasion

Zone 5; Zone of decomposed dentin due to

acids and enzymes.
Dentine Caries
Affected & Infected Dentin:

– Affected dentin: is softened,

demineralized dentin that is
not yet invaded by bacteria
 inner carious dentin ( does
not requires removal ).
– Infected dentin:  outer
carious dentin & Bacterial
plaque is both softened &
contaminated with bacteria
( requires removal ).
Spread of the Carious Lesions

3. Root Caries
Root Caries
Root caries  is a soft, progressive lesion that is found anywhere on the root
surface that has lost its connective tissue attachment and is exposed to the
-the root surface must be exposed to the oral environment before caries can
develop here.
-Plaque and micro-organisms are essential for the cause and progression of the
lesion, mostly Actinomyces,
-micro-organisms invade the cementum either along the Sharpey’s fibers or
between the bundles of fibers.
-spread laterally, since cementum is formed in concentric layers.
-after decalcification of cementum, destruction of matrix occurs similar to
dentin with ultimate softening and destruction of this tissue.
-invasion of micro-organisms into the dentinal tunbules, finally leading to pulp
-the rate is slower due to fewer dentinal tubules than crown area
Thank you