Dental Caries

By
Dr:
Hanan eid gamal
 Definition
Dental caries is a progressive,
largely irreversible bacterial
damage of the hard dental tissues
exposed to the oral environment,
characterized by demineralization
of the inorganic portion and
destruction of the organic
substances of the tooth”
 Classification of Dental Caries
 I. based on morphological site:
1. Pit and fissure caries
2. Smooth surface caries
3. Root caries
 II. Based on rate of progression:

1. Acute dental caries

2. Chronic dental caries
 III. Based on whether lesion is new or under
previous restoration:
1. Primary (virgin) caries
2. Secondary (recurrent) caries
 Pit and fissure caries

Occlusal caries in upper second premolar

Smooth surface caries
Cemental (root) caries
Cemental (root) caries
Recurrent caries
Recurrent caries
Rampant caries
Rampant caries
Rampant caries
 Acute and chronic caries
Acute caries
Rapid clinical course and results in
early pulpal involvement
affects children and young adults
because their dentinal tubules are
larger and show no sclerosis.
The point of entry of caries is small
The affected dentin is usually
stained light yellow
Pain is more likely to be seen in
acute dental caries
Chronic caries
progresses slowly and involves the
pulp much later than acute caries.
commonly seen in adults.
Opening to the lesion is larger than
that of acute caries.
The carious dentin is stained deep
brown
Pain is NOT a prominent feature due
to the protection provided to the
pulp by tertiary dentin formation.
 Sequelae of Dental Caries

 Sequelae of dental caries are either:

1. Sequelae in hard dental structures
2. Sequelae in the plup and the para-
dental tissues
 Sequelae of Dental Caries
 Sequelae in hard dental structures
1. Destruction of enamel
2. Formation of dead tracts
3. Formation of Translucent
( sclerotic) dentine
4. Formation of reparative
(secondary) dentine
5. Destruction of dentine
 Sequelae of Dental Caries
 Sequlae in the pulp and para-dental tissues:
1. Pulp hyperemia
2. Acute pulpitis
3. Chronic pulpitis
4. Chronic hyperplastic pulpitis
5. Apical periodontitis
6. Acute periapical abscess
7. Chronic periapical abscess
8. Periapical granuloma
9. Periapical cyst
10. Osteomyelitis
11. Facial cellulitis
 Etiology of dental caries
Acidogenic theory: ( The most accepted
theory)
 Acidogenic bacteria + fermentable
carbohydrate → Acids, mainly lactic acid
which diffuses into enamel.
 Acid + enamel minerals → demineralization

 Acid + dentine minerals → demineralization

 Proteolytic bacteria→ proteolytic enzymes +

org matrix of dentine→ digesion and
dissolution.
 Contributing Factors of Dental Caries

CHO Bacteria

Caries

Tooth

A fourth factor (dental plaque) is needed for the occurrence

of smooth surface caries
 Contributing Factors of Dental Caries

Dental caries is a multifactorial disease

involving several factors:
1. Tooth (host)
2. Fermentable carbohydrate (substrate)
3. Microorganisms (agent)
4. Dental plaque (means of localization of
micro-organisms and substrate to the site
of attack on the tooth)
 Contributing Factors of Dental Caries

1- Tooth
1) Position of the tooth
2) Morphology or form of the tooth
3) Structure of the tooth
4) Fluorides
5) Genetic factors
 Contributing Factors of Dental Caries

1) Position of the tooth

• Upper > lower due to salivary action is not present
• Posterior > anterior due to prescence of fissures
• Malposed > normally aligned because of the
creation of
stagnations area
 Contributing Factors of Dental Caries
2) Morphology or form of the tooth
• Pits and fissures → teeth with deep pits
and fissures are more liable to caries.
• Contact areas → rounded, tight contact
points are less prone to harbour plaque
and debris interproximally than broad,
flat contact areas.
Contributing Factors of Dental Caries

Contact area Undercut

 Contributing Factors of Dental Caries
3) Structure of the tooth
• Hypoplasia and hypocalcification do not
affect the initiation of caries, yet might
affect the progress of the carious lesion.
• Evidence indicates that the outermost
layers of enamel change in composition
following tooth eruption through a process
of post-eruptive maturation. Therefore,
newly erupted teeth are more susceptible
to caries.
 Contributing Factors of Dental Caries
4) Fluorides
• Fluoride is a naturally occurring
constituent of our food and drinking
water. It is found either in bound form or
ionic form.
• When fluoride is ingested systemically its
ions appear in the blood plasma within
minutes. These ions are responsible for
the conversion of hydroxyapatite into
fluoroapatite in the developing teeth.
 Contributing Factors of Dental Caries
• Ingested fluoride is cleared from the blood
plasma within two hours, thus repeated
ingestion is more beneficial than single dose
ingestion.
• It should be clear that ingestion of fluoridated
water in a concentration more than 1.2 ppm,
at the time of tooth development, is
associated with mottled enamel.
• Are mottled teeth more resistant to caries?
Mottled teeth, though hypoplastic, are more
resistant to caries in the non-pitted areas.
 Contributing Factors of Dental Caries

The cariostatic effect of fluoride is believed

to be through three known mechanisms:
1- Formation of fluoroapatite.
2- Enhancement of remineralization.
3- Antibacterial activity.
 Contributing Factors of Dental Caries
1- Formation of fluoroapatite
When enamel is exposed to ionic fluoride,
fluoride ions become incorporated into the
hydroxyapatite by substituting some of the oH
groups in the center of the calcium triangles.
ca ca
oH F
ca ca ca ca
Contributing Factors of Dental Caries

• It is believed that both the strong ionic

bond between fluoride and calcium ions
and the formation of hydrogen bonds
between fluoride and the oH groups are
responsible for most of the increased
resistance to acid solubility of
fluoroapatite when compared with
hydroxyapatite.
 Contributing Factors of Dental Caries
2- Enhancement of remineralization
• Presence of fluoride ions in the carious
environment might enhance and
accelerate remineralization through the
formation of calcium-fluoro-phosphate
salts.
• These salts render the remineralised site
more resistant to future acidogenic
attacks than was the original enamel.
 Contributing Factors of Dental Caries
3- Antibacterial activity
• The antibacterial effect of fluorides is mainly
directed towards acidogenic bacteria.
• Fluoride inhibits enolase enzyme activity, that is
a key enzyme in glycolysis.
glucose + acidogenic --- glycolysis -- acid + energy
bacteria
This will lead to:
1- Decreased acid production.
2- Decreased glucose uptake by the organisms.
3- Decreased metabolic activity of the orgamisms.
 Contributing Factors of Dental Caries
Conclusion
• Initially, it was believed that the main cariostatic
effect of fluoride is a preeruptive one, through
the formation of fluoroapatite.
• Recently, studies suggested that the
posteruptive effects of fluoride may be of equal
or even greater importance than the
preeruptive effect. These posteruptive effects
are gained through:
o Topical application of fluoride
o Mouth wash
o Tooth paste
 Contributing Factors of Dental Caries

5) Genetic factors
• Hereditary has a minor influence on
resistance to caries.
• Increased incidence of caries in some
families may be due to:
1- Tooth shape or anatomy.
2- Common dietary habits in the family.
 Contributing Factors of Dental Caries

2- Carbohydrates
1) Importance of carbohydrates
- When carbohydrates, proteins and fats
were examined for their cariogenic effect it
was found that carbohydrates are the only
food component that can cause caries
(why?)
- This is because carbohydrates can be
acted upon by the oral bacteria with the
production of acids.
 Contributing Factors of Dental Caries

2) Factors affecting cariogenicity of

carbohydrates:
1. Type of carbohydrate
2. Total amount of carbohydrate intake
3. Frequency of carbohydrate intake
4. Consistency and texture of carbohydrates
5. Refinement of carbohydrates
 Contributing Factors of Dental Caries

 Type of Carbohydrate
Carbohydrates are of three types:
• Monosaccharides → (glucose and fructose)
• Disaccharides → (sucrose, lactose and
maltose)
• Polysaccharides → (glycogen and starch)
Contributing Factors of Dental Caries
• Sucrose, in particular, has been described
as the arch criminal of dental caries, this
may be due to:
• Sucrose is of low molecular weight and
can thus diffuse rapidly into plaque.
• Sucrose is rapidly broken down by plaque
bacteria.
• Cariogenic bacteria can synthesize
dextran faster from sucrose than from
other sugars.
Contributing Factors of Dental Caries
• Polysaccharides, on the other hand, are of
little importance in the etiology of dental
caries. This may be due to:
• Polysaccharides are of larger molecular
weight and hence can not diffuse
rapidly into dental plaque.
• Polysaccharides need the action of
salivary amylase before oral bacteria
can act upon them.
 Contributing Factors of Dental Caries
 Total Amount of Carbohydrate Intake
• Increased intake of fermentable
carbohydrates is followed by increased
caries activity.
• In communities where carbohydrates do
not constitute a major part of the diet
(Eskimos), caries is rare.
• In industrialized countries, (USA and
Europe), where readily fermentable
carbohydrates constitute a considerable
part of the diet, caries activity is severe.
 Contributing Factors of Dental Caries
 Frequency of Intake and Relation to
Meals
• Frequent intake of fermentable
carbohydrates between meals causes
increased caries activity.
 Consistency and Texture of
Carbohydrates
• Sticky carbohydrates are highly cariogenic
because they are more attached to the teeth
thus remain accessible to oral bacteria for
longer periods of time.
 Contributing Factors of Dental Caries
 Refinement of Carbohydrates
• Refinement by definition is the treatment of
carbohydrates in order to make them whiter,
remove fibrous material and improve flavour.
• It is believed that refinement of carbohydrates
increases their cariogenicity due to:
• Increased concentration of the fermentable
fraction.
• Removal of the fibrous material.
• Increased adhesiveness of the carbohydrate.
 Contributing Factors of Dental Caries

3- Microorganisms
1. Historical background
2. Miller's experiment
3. Orland's experiment
4. Types of bacteria involved in caries
5. Discussion of the role of some bacteria
• Lactobacilli
• Streptococci
 Contributing Factors of Dental Caries
2. Miller's experiment
- Miller, in 1890, was the first to suggest that
caries might be caused by the action of
bacteria on fermentable carbohydrates with
the production of acids.
- Miller conducted an experiment in which he
suspended two sound teeth in two test tubes
containing saliva and carbohydrates. one of
the test tubes was subjected to boiling.
 Contributing Factors of Dental Caries

- The tooth suspended in the test tube

subjected to boiling remained caries free,
while the other tooth suffered extensive
caries-like lesions.
 Contributing Factors of Dental Caries
3. Orland's experiment
• Orland, in 1954, proved conclusively that the
micro-organisms must be present for caries
to develop.
• Orland demonstrated that germ-free rats did
not develop caries.
• This proved that, in rats at least, caries
development depends upon the presence of
micro-organisms.
 Contributing Factors of Dental Caries

• Orland created what is known as

gnotobiote rats.
• What are gnotobiote rats?
These are germ-free rats in which a single
known strain of micro-organisms was
introduced.
Germ-free rat ₊ known strain of bacteria

Gnotobiote rat
 Contributing Factors of Dental Caries
4. Types of bacteria involved in caries:
A- Acidogenic bacteria
1) Lactobacilli: L. acidophilus, L. caesi
2) Streptococci: Viridance group which include:
St. mutans, St. sanguis, St. salivarius, St. mitis.
B- Proteolytic bacteria
1) Actinomyces 2) Clostridia
3) Pseudomonas
C- Chromogenic bacteria
Asprigillus niger
 Characteristic features of cariogenic bacteria

 Acidogenic: capable of producing acid rom

ferementable carbohydrate .
 Aciduric: can survive in acidic media.
 Adhere to the tooth surface.
 Produce extracellular polysaccharides for dental
plaque formation especially dextran and levan.
 Produce intracellular polysaccharides
(amylopectin)that is used by organisms at the
time of dietary carbohydrate deficiency.
 Contributing Factors of Dental Caries
5. Discussion of the role of some bacteria
I- Lactobacilli:
• Lactobacilli are powerful acidogenic bacteria
• They are also powerful aciduric
• They are mild proteolytic
• They are found in all stages of caries
• Their number increase in saliva when caries
activity is increased. This was the base for the
lactobacillus count test.
Contributing Factors of Dental Caries
• Lactobacilli produced pit and fissure caries
only in gnotobiotes but failed to produce
smooth surface caries due to their inability to
produce extracellular polysaccharides.
• Recently, evidence indicate that lactobacilli do
not appear to play a major role in the initiation
of enamel caries. This is because:
1. The increase in number of lactobacilli in
saliva where caries is active is a
secondary phenomenon.
2. Lactobacilli failed to produce smooth
surface caries in gnotobiotes.
 Contributing Factors of Dental Caries
Streptococcus mutans:
1- Mutans, comes from the ability to undergo
mutation from a round form to a rod form
2- Classified into 7 types, the most cariogenic is
type c
3- Endogenous
4- Transmissible
5- Powerful acidogenic
6- Powerful aciduric
 Contributing Factors of Dental Caries
7- Able to produce smooth surface caries in
gnotobiote animals. This ability was attributed to
the fact that st. mutans can produce
extracellular polysaccharides.
• Dextran:
Which is formed from glucose by the action of
glucosyletransferase enzyme. Dextran is an insoluble
adhesive material.
• Levan:
Which is formed from fructose by the action of
fructosyletransferase enzyme. Levan is less adhesive
than dextran and acts mainly as a store of
carbohydrates.
Contributing Factors of Dental Caries
8- Streptococcus mutans can synthesize
intracellular polysaccharides in the form of a
glycogen-like material known as amylopectin.
These intracellular polysaccharides are used
as a store of carbohydrates at times of dietary
carbohydrate deficiency.
Main differences between dextran and levan

Dextran Levan
- Glucose polymer - Fructose polymer
- Water insoluble - Water soluble
- Highly adhesive - Less adhesive
- Important in plaque - Act as a store of
formation and carbohydrates
adhesiveness
 Contributing Factors of Dental Caries

Function of bacterial polysaccharides:

1. Increase adhesiveness of dental plaque.
2. Act as a store of carbohydrates.
3. Increase thickness of dental plaque.
 Dental plaque
Definition
 Soft, non-mineralized, bacterial deposit or
biofilm which forms on teeth and dental
prostheses that are not adequately
cleaned.
 Resists cleansing by physiological oral
forces like salivary washing and tongue
movements but is removable by tooth
brushing.
 It is formed of a large number of closely
packed bacteria surrounded by an
extracellular matrix.
 Dental plaque
Types
• Supragingival plaque – Is found at or
above the gingival margin.
• Subgingival plaque – Is found below
the gingival margin.
Importance
• Supragingival  Dental caries
• Subgingival  Periodontal diseases
Dental Plaque – clinical appearance
 Dental Plaque - Composition
Composition of dental plaque
Microorganisms (50-60%) such as cocci,
lactobacilli and filamentous bacteria.
Mucin (glycoprotein 30%).

Glucan (Dextran 10%).

Inorganic salts: ca, ph, cl, k.

Mineral ions: zn, cu, Fe traces.

Desquamated epithelial cells.

Food debris.
 Dental Plaque - Composition
Role of plaque matrix:
1- Act as a diffusion limiting membrane against
the escape of acids.
2- Act as a diffusion limiting membrane against
the entry of buffers from saliva , delaying their
neutralizing action .
3- Contribute to adhesiveness, bulk and
resistance to washing.
 Mechanism of formation:
 Stage I: deposition of the acquired
pellicle
At the beginning a structurless cell free
pellicle of salivary glycoprotein (Protein +
Carbohydrate) which is adsorbed on the
tooth surface (for about 3m). It is also not
usually visible to the naked eye and difficult
to be removed by normal tooth brushing.
 Acquired pellicle acts as a substrate for
adherence, nutrition, growth and
colonization of plaque m.os.
 Mechanism of formation:
 Stage II: colonization of the acquired pellicle
Acquired pellicle becomes visible, when tooth
brushing stops for 12-24 hours and by
proliferated of heterogenous bacterial flora
occurs.
 Adhesion of bacteria to the tooth surfaces is an
essential requirement. Attachment depends on
complex mechanism and again on bacterial
production of extracellular polysaccharides
such as glucans (dextran).
 Colonization here is by aerobic streptococci .
 Mechanism of formation:
 Stage III: Maturation of the dental plaque
 Proliferation of heterogeneous bacterial flora
leading to increase in the thickness of the
dental plaque, oxygen consumption in deeper
layers will cause anaerobic filamentous
microorganisms to colonize the plaque
 The filamentous microorganisms grow in long
interlacing threads in which smaller bacilli and
cocci become entrapped.
 Corn-Cob Appearance

This scanning
electromicrograph at
higher power shows
cocci attached to
filamentous organisms
to produce the corn-
cob arrangement
sometimes seen in
plaque
 Corn-Cob Appearance

Scanning electron micrograph showing corn-cob structures.

Cocci adhering to and surrounding filamentous organisms.
 Role of Saliva in Dental Caries
• Saliva is the medium in which plaque
develops and works.
• Saliva is a complex secretion whose
rate of flow, composition and properties
vary among individuals and even in the
same person at different times and
under different conditions.
 Role of Saliva in Dental Caries
The role of saliva in caries can be
summarized in the following:
1) Formation of acquired enamel pellicle
2) Washing effect of saliva
3) Buffering effect of saliva
4) Salivary antibodies
5) Antibacterial substances
 Role of Saliva in Dental Caries
1) Formation of acquired enamel pellicle
The acquired pellicle is a film of salivary
glycoproteins that masks the residual
charges found on the apatite crystals, thus
protects the enamel from being colonized
by the bacteria.
2) Washing effect of saliva
A free flow of saliva has a cleansing effect
on the teeth. In xerostomia there is
increased caries activity.
 Role of Saliva in Dental Caries
3) Buffering effect of saliva
The bicarbonate and phosphate contents
of saliva act as buffer.
4) Salivary antibodies
Saliva contains IgA which is secreted by
plasma cells found in the connective tissue
stroma of the salivary glands. Salivary
antibodies are specific in action.
 Role of Saliva in Dental Caries
5) Antibacterial substances
These are proteins having a non-specific
antibacterial effect. They include:
• Lysozyme: enzyme having a bacteriolytic
effect through destruction of the bacterial
cell wall.
• Peroxidase: enzyme that promotes
oxidation of various substances necessary
for bacteria.
• Lactoferrin: glycoprotein that binds to iron
preventing it from reaching the bacterial cell.
 Pathology of Caries Enamel

Macroscopic picture
Microscopic picture
1. Phase of Initiation
2. Phase of bacterial invasion
3. Phase of destruction
4. Phase of secondary enamel caries
 Macroscopic Picture

• The early carious enamel lesion appears

as an opaque chalky white hard spot. smooth
• Then it becomes rough by probing.
• Followed by staining due to action of
chromogenic bacteria. brown
• Later on cavitation will occur.
Early Caries Enamel
 Early Caries Enamel

The white
areas
represent the
earliest clinical
evidence of
caries.
 Macroscopic Picture
The carious enamel lesions
are cone shaped.
• In pit and fissure lesions:
the base is towards the
dentino-enamel junction
and the apex towards the
surface
• In smooth surface lesions:
the base is towards the
surface and the apex
towards the dentino-
enamel junction
 Microscopic picture
Microscopically enamel caries consists of four
phases and the first phase consists of four zones.
I- Phase of initiation
- Translucent zone
- Dark zone
- Body of the lesion
- Surface zone
II- Phase of bacterial invasion
III- Phase of destruction
IV- Phase of secondary enamel caries
 Microscopic picture

I- Phase of initiation
• In this phase the enamel lesion is cone
shaped.
• The outer enamel surface is intact.
• Changes in this phase are not due to
bacterial invasion but due to the effect of
acids.
Caries Enamel –
Phase of Initiation

4
3

2 1
Phase of Initiation
1- Translucent Zone
· Lies at the advancing front of the
carious lesion.
· The appearance of this zone is due
to initial demineralization of the 4
enamel creating pores representing
3
about 1 -2 % of enamel volume.
· This zone appears translucent only
when seen with quinoline or Canada 2 1
balsam media which have the same
refractive index as that of enamel.
The molecules of the media will fill
these pores and thus the zone
appears translucent.
 Phase of Initiation
2- Dark zone
· Lies superficial to the translucent
zone.
· The appearance of this zone is
due to further demineralization of 4
the enamel creating pores 3
representing from 2 - 4 % of
enamel volume. Some of these
pores are so small that they are 2 1
called micropores.
· Molecules of Canada balsam or
quinoline are too large that they
are unable to fill these micropores
thus this zone appears dark.
 Phase of Initiation

3- Body of the Lesion

· Lies under the surface zone and
constitutes the largest area in the
carious lesion.
· The appearance of this zone is 4
due to advanced 3
demineralization of the enamel
creating pores representing 5 %
at the periphery and 25 % at the 2 1
center.
. The body of the lesion appears
translucent.
 Phase of Initiation
4- Surface Zone
· One of the characteristic features of
enamel caries is that the greatest
degree of demineralization occurs at a
subsurface level.
· This zone although not merely intact, 4
yet it appears more radiopaque and 3
harder than the deeper zones. This may
be due to:
1. Continuous remineralization from 2 1
saliva
2. It contains much fluoride

3. It contains greater amounts of

insoluble proteins
4. The prismless nature of enamel in
this zone may delay diffusion of acids
 Pathology of Caries Enamel
Ground section
cut through the
center of a small
enamel lesion
examined in
polarized light
after imbibition in
water (A) and
quinoline (B).
Translucent zone
(1), dark zone
(2), body of the
lesion (3) and
surface zone (4)
 Microscopic picture
II- Phase of bacterial invasion
Bacteria start to invade the enamel when
sufficient pathways are created by the
action of acids.
 Microscopic picture

III- Phase of destruction

After loss of the enamel minerals, the
structural integrity of enamel is lost and
the remaining organic material either
collapses or is digested by the action of
proteolytic bacteria.
 Microscopic picture
IV- Phase of secondary enamel caries
• When the acids reach the dentino-enamel
junction, they spread laterally along the
hypomineralized dentino-enamel junction
undermining the enamel.
• This lateral spread will determine the
extent and not the depth of the carious
cavity and will lead to:
 A reverse attack on enamel from beneath.
 Separation of the enamel from the
underlying dentine.
 Phase of secondary enamel caries

Caries enamel
lesion
spreading
laterally along
dentino-enamel
junction,
affecting a
wider surface
area of dentine.
 Phase of secondary enamel caries

More advanced
stage of caries.
Enamel lesion
spreading laterally
along dentino-
enamel junction,
producing
secondary
enamel caries
and affecting a
wider surface
area of dentine.
 Pathology of Caries Dentine

Macroscopic picture
Microscopic picture
I- Initial uninfected lesions
II- Infected lesions
 Pathology of Caries Dentine
Macroscopic Picture
• Pit and fissure lesions:
are conical in shape
with the base toward
the dentino-enamel
junction and a abroad
apex towards the pulp
chamber.
• Smooth surface lesions:
are also conical in shape
with the apex
approaching the pulp
further cervically.
 Pathology of Caries Dentine
Microscopic Picture
I- Initial uninfected lesions
(before enamel cavitation)
1. Zone of reactionary or reparative
dentine formation (zone 1) irregular
2. Zone of sclerotic or translucent dentine
formation (zone 2)
3. Body of the lesion (zone 3) daed tracts
 Pathology of Caries Dentine
Initial uninfected lesions - Animated
Pathology of Caries Dentine
Initial uninfected lesions
Pathology of Caries Dentine
Initial uninfected lesions
Ground section of an active
proximal lesion examined in
transmitted light. The
triangular enamel lesion
reaches the dentine-enamel
junction with demineralization
of the outer dentine (DZ) and
sclerotic reaction (TZ)
corresponding to the less
advanced peripheral parts of
the enamel lesion.
 Pathology of Caries Dentine
Initial uninfected lesions
Caries
enamel Sclerotic
Dead tract Dentine
underneath
enamel caries,
surrounded and
underlaid by
translucent
dentine (slowly
progressing
caries).
Dead Tract Sclerotic Intact
Dentine surface
 Pathology of Caries Dentine
II- Infected lesions
(after enamel cavitation)
1. Zone 1: Mild pulpal inflammation.
2. Zone 2: Reparative or reactionary dentine.
3. Zone 3: Sclerotic dentine.
4. Zone 4: Body of the lesion
a) Decalcified uninfected zone
b) Decalcified infected zone
c) Area of destruction
Pathology of Caries Dentine
Infected lesions
 Pathology of Caries Dentine
The decalcified infected zone shows the
following:
• Pioneer bacteria: which are usually cocci.
• Beading: which is the lateral distension of the
soft dentinal tubules by the action of
proliferating bacteria.
• Liquefaction foci: coalescence of beads parallel
to the long axes of the dentinal tubules.
• Transverse clefts: liquefaction foci occurring
perpendicular to the direction of the dentinal
tubules.
Pathology of Caries Dentine
Decalcified infected zone
 Dentine Caries – Diagrammatic
Invading bacteria

Beading

Liquefaction foci

Transverse clefts
Dentine Caries – beading

Beading Liquefaction
foci
Dentine Caries – Liquefaction Foci & Transverse
Clefts – Low Power

Transverse Liquefaction
cleft foci
Dentine Caries – Liquefaction Foci & Transverse Clefts
 Dentine Caries – Liquefaction Foci

Liquefaction
foci
This frame
reveals infected
dentinal
tubules with
clefting
occurring in the
same direction
as the tubules.
 Dentine Caries – Transverse clefts

Horizontal clefting is
typical of dentinal
caries. The process
of beading,
coalescence, and
clefting typifies
progression of
dental caries.