HISTOPATHOLOGY OF DENTAL CARIES Ground section viewed with transmitted polarized

light in a microscope with a red filter.

Incipient Caries
The image shows the external surface (surface
zone). The whole carious lesion is the body of the
lesion. A Dark zone underneath the body of the
lesion and a translucent zone bordering the incipient
enamel caries.

Zones of Enamel Caries

1.Zone 1 – Translucent Zone
• Deepest portion of carious lesion, advancing
part of lesion.
Location: Pit and fissure caries • Voids are present when exposed to polarized
Clinically, there is only a white spot lesion or white light, they reflect giving a translucent
discoloration in the occlusal surface. Upon cutting appearance.
the tooth, you can distinguish the termination of • Pore Volume (PV) is 1% or 10x of sound
white spot lesion not only superficially but also enamel.
involves enamel portion. 2.Zone II – Dark Zone
• Also called positive zone
Microradiograph of Inicipient Enamel Caries • Called dark zone because does not transmit
polarized light
• Formed due to demineralization
• PV is 2-4%
3.Zone III – Body of Lesion
• Largest portion of incipient caries
• Area where most formation of voids is found
because of the dissolution of the content
• Greatest area of demineralization
• PV is 5-25%
4.Zone IV – Surface of the Lesion
This is not a radiograph but rather a histologic • Full intact because surface is harder than
finding or characteristic; the tooth was sectioned subsurface enamel
and has been processed to appreciate the • Not or least affected by caries
termination of carious lesion histologically. • Greater resistance probably due to greater
degree of mineralization (Inorganic
You can see discoloration on the enamel surface material) and greater fluoride concentration.
that dictates a white spot lesion or a developing • Can be arrested by fluoridation.
carious lesion or an incipient caries.
• Pore volume (PV) is <5%
Zones of Incipient Enamel Caries
Pit and Fissure Enamel Caries
 Advance Smooth Surface Enamel Caries
- Caries follows the direction of the enamel
rods In penetrating the dentin.
- As seen in the diagram, there is a triangular
shape or pattern of caries wherein, the apex
is located towards the surface and base
towards the dentin.

Advanced Pit and Fissure Caries

- Loss of enamel structure, which gets

roughened due to demineralization, and
there is disintegration of enamel prism,
hence cavitation happens.
- Lateral spreading of carious lesion towards
the DEJ.
- Triangular pattern of dental caries that
happens towards the dentin, and base
- When reaches the DEJ, greater number of towards the DEJ, and apex towards the pulp.
dentinal tubules are involved.
- A greater surface has been involved in the Cross-Sectional View of a Carious Lesion of Pit vs
area. Smooth Surface
- Another triangular pattern forms in an
inverted cone. The base is located at the Pit and Smooth
DEJ, and the apex towards the pulp. Fissures Surface
- It produces greater cavitation than the ENAMEL Wedge or Triangular
smooth surface caries and there is more Triangular
undermining of enamel. APEX – DEJ
- Backward type of caries. The enamel carious APEX – BASE -
lesion is smaller but bigger on the dentin. cavosurface cavosurface
BASE - DEJ
Early Smooth Surface Enamel Caries

DENTIN Triangular Triangular

BASE – DEJ BASE – DEJ

APEX – APEX –
toward pulp toward pulp

- Carious lesion follows the direction of

- With regards to histologic manifestation
enamel rods
- Loss of interprismatic/ interrod substance of
- When carious lesion is left untreated, in DEJ
enamel with increased prominence of the
there is a lateral spreading of carious lesion
rods.
and then later on in the dentin.
- The base towards external surface, apex
towards the dentin.
Levels of Dentinal Reaction to Caries:
- Wider scope on the external surface than the
1. Low-Grade Irritation
inner surface of the enamel.
 - Formation of sclerotic dentin - Surrounds the dentinal tubules
Sclerotic Dentin - As protective mechanism, it becomes wider
- The peritubular dentin becomes wider and is and gradually filled with calcified materials
gradually filled with calcified materials. from enamel down to the pulp. It thickens
- Protective mechanism of dentin in terms of and hardens and forms sclerosis.
low-grade irritants. - Results from aging or mild irritation such as
a. Physiologic sclerotic dentin in slowly advancing caries so that in regards
- Sclerotic dentin occurs due to aging. As with the primary dentin. There is a change in
times goes on, we are using our teeth for composition – becomes hard and highly
mastication. Attrition, abrasion, there is calcified so dental caries will not penetrate
already physiologic sclerotic dentin. the dentin.
b. Reactive sclerotic dentin § Primary dentin
- Happens when there are irritants. - Laid down during the
development of the tooth.
Early Dentin Caries • Intertubular dentin
- In between dentinal tubules
• Dentinal tubules
- It is where stimulus enter

2. Moderate Irritation
- Reparative Dentin/Reactionary Dentin
- In some terminologies, it is a.k.a as tertiary
dentin
- The wall of the pulp formed due to moderate
level of irritants will be stimulated then
forms reparative dentin.
- As seen microscopically, there is an initial - The peritubular dentin narrows because of
onset of carious lesion in the enamel surface. the deposition of highly mineralized tissues.
Despite cavitation yet, the dentin is already The normal diameter of dentinal tubules is
triggered to provide protective mechanism narrow protecting the dentin itself.
so dentin will not be easily reached. Hence, - Odontoblastic process are triggered to
dentinal sclerosis happens. protect the pulp.Mesenchymal cells will
trigger the formation of dentin.
§ 3 Types of Dentin
1.Primary dentin
-It forms before tooth eruption
-During tooth development
2.Secondary dentin
-With age, there is continuing
development of secondary dentin.
3.Reparative/Tertiary dentin
-Because of irritants and
stimuli, mesenchymal cells forms
reparative dentin to protect the
pulp.
Oral Histology 3.Severe Irritation
- In dentin, odontoblasts feel the sensitivity or - there’s localize inflammation of the pulp then
pain from stimulants when it is exposed or it dies (Pulp Necrosis).
affected. - happens when tooth left untreated.
• Peritubular dentin
- Highly calcified and mineralized
Advanced Dentin Caries Slowly progressing lesions
- Chronic or arrested lesions
- Commonly without clinical symptoms
- Hard, dry, and dark brown
- Same clinical appearance as arrested caries
lesions
Rapidly progressing lesions
- Often painful or hypersensitive
- Soft, wet and light yellow
- Penetrates deep into the dentin
- Demineralization penetrates deep into dentin
- The dentin can no longer cope with the
advancing lesion although the pulp is doing Dentin Sclerosis in Slowly Progressing Caries
its part to form protective mechanism which

Extensive Carious Lesion

- Penetration in the dentin

Dentin Sclerosis in Rapidly Progressing Lesion

- Layering of dentin to protect the pulp.

- In severe cases, the dentin can no longer
produce odontoblasts that are capable in
producing tertiary dentin, cavitation worsens
then there is already pulp exposure and then
irritation and inflammation happens in the
pulp tissue which leads to pulp necrosis.
-
- It reaches the junction of dentin and pulp
- Formation of tertiary dentin

Reactionary Dentin Formation Induced by Caries in

Dentin

- Dilations of blood vessels inside

- Severe pain and sensitivity is felt.
§ Hyperemia
- dilated congested blood vessels
regardless of whether the pulp was
considered “normal,” “inflamed,”
or “diseased.” - Defense mechanism(tertiary dentin) to
protect the pulp
Diagram of the tooth acidity of the environment. However,
demineralization will happen then white spot
lesion appears in attempt that enamel wants
to neutralize the pH of the mouth.

- Caries starts at the pellicle

§ Pellicle
- Layer of tissue that adheres in - In severe cases, cavitation will lead into the
the enamel. enamel portion. No alteration in the dentin
- Once plaque develops, bacteria starts to set yet. There is odontoblast proliferation in the
in. pulp to form reparative dentin to serve its
- Plaque develops within 24 hours or 1-2 protective mechanism.
days. Formation of soft deposits then later
on hardens.
- Within 9-10 days, it hardens.

- The dentin will give its protective

mechanism by hypermineralization.
- More microflora or amount of bacteria will - Dentinal sclerosis happens.
inhabitate into the plaque - Peritubuluar dentin hardens in attempt to
- Streptococcus and carbohydrates (nutrients protect the dentin surface.
and metabolism of microorganisms) leads to - Pulp produces odontoblastic layer to
formation of lactic acid. produce reactionary dentin.
- Lactic acid initiates demineralization.
- Initially saliva can neutralize the pH and
calcium and phosphate in the saliva initiates
remineralization.

- Continuously penetrate DEJ

- Dentin demineralization starts
- Cavitation in the dentin because of cavity in
the enamel that is left untreated.
- If saliva can no longer capable of
neutralizing the pH, the enamel will secrete
calcium and phosphate to help neutralize the
 Zones of Dentinal caries
1. Normal dentin
2. Subtransparent dentin
3. Transparent dentin
4. Turbid zone
5. Infected zone

- Demineralization of dentin starts

- Deposition of reactionary dentin

If left untreated:
- Pulp becomes necrotic or dead
- Restoration will no longer be the applicable
Infected zone – towards the enamel
treatment of choice.
Normal dentin – towards the pulp
Non-cavitated Lesions
Enamel Dentin Pulp
Non- No alteration Cellular
cavitated proliferatio
lesion n
involving ¼
of enamel
thickness
Enamel Hypermineraliza Alteration
caries tion or dentinal in
involving sclerosis predentin
2/3 and Zone 1: Normal Dentin
reduction - Zone of fatty degeneration of Tome’s fibers.
of - Formed by degeneration of the odontoblastic
thickness process.
of - Otherwise dentin is normal and produces
Odontoblas sharp pain on stimulation.
tic layer Zone 2: Zone of Dentinal Sclerosis
Demineraliz Demineralizatio Deposition • Subtransparent Dentin
ation reaches n of dentin starts of - Intertubular dentin is demineralized.
the DEJ reactionary - Dentinal sclerosis, i.e. deposition of calcium
dentin salts in dentinal tubules takes place.
- Damage to the odontoblastic zone process is
Dentinal Caries apparent.
- There are no bacteria in this zone. Hence,
this zone is capable of remineralization.
Zone 3: Zone of Decalcification of Dentin
• Transparent Dentin
- Further demineralization of intertubular
dentin lead to softer dentin.
- No bacteria present.
- Capable of self-repair
Zone 4: Zone of Bacterial Invasion
• Turbid Dentin
 - Widening and distortion of the dentinal - We may leave it, just place medicaments,
tubules which are filled with bacteria. liner, base, and corresponding filling
- Dentin is not self-repairable, because of less material.
mineral content and irreversibly denatured - Continuously monitor the tooth
collagen.
- This zone should be removed during tooth Indirect Pulp Capping
preparation. - Preserve the vitality of the pulp
Zone 5: Zone of Decomposed Dentin due to Acids - Place medicaments and corresponding
and Enzymes material
• Infected Dentin
- Outermost zone.
- Consists of decomposed dentin filed with
bacteria.
- It must be removed during tooth preparation.

Table Summary in Zones of Dentinal Caries

Sensitivity Presence Capacity to
to stimuli of remineralize
bacteria
Zone 5, - + -
ID
Zone 4, - + -
TD
Zone 3, + - +
TrD
Zone 2, + - +
STrD
Zone 1, + - +
ND

Infected and Affected Dentin

• Infected Dentin = Zones 4 and 5
- Both softened and contaminated with
bacteria
- Significantly discolored
- Can be removed by excavators
- Stained with caries detector usually within 5
seconds
- Needs to be removed unless judged to be
within 0.5mm of pulp
- Direct pulp capping – exposed during
excavation. Place calcium hydroxide. On top
of that is a base. Then corresponding
restorative material.
• Affected Dentin = Zones 2 and 3
- Softened, demineralized dentin that is not
yet invaded by bacteria
- Not significantly discolored
- Feels hard already
- Capable of remineralization