HISTOPATHOLOGY OF DENTAL CARIES

Dental caries is a microbial disease of the calcified tissues of the

teeth, characterized by desensitization of the inorganic portion and

destruction of the organic substance of the tooth.

The caries involvement of the tooth structure is an interesting

process as it progresses as a series of exacerbations and remissions.

This process can be best studied by:

1. Transmission and Scanning Electron Microscopy.

2. Histochemical studies.

3. Use of Radioactive isotopes.

Dental caries can be best studied are:

a. Caries of enamel.

b. Caries of dentin.

c. Caries of cementum / Root caries.

(A) CARIES OF ENAMEL: Depending on the site of

OCCURRENCE is of two types:

1) If the caries occurs in the developmental pit and

fissures / occlusal surface it is termed as PIT & FISSURE

CARIES.

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2) Caries occurring on any other surface is termed

SMOOTH SURFACE CARIES.

I] PIT AND FISSURES are of 2 types:

1. Shallow pit and fissures.

2. Deep pit and fissures.

During the union of enamel lobes in the calcification process

organic elements of enamel forming organs get entrapped resulting in a

natural pit/ thin fin which separates the lobes.

- The caries process begins once the bacterial plaque gets

deposited on these sites of the tooth surface.

The entrapped organic material gets attacked by

the enzymatic and bacterial action which causes a material

passageway into the enamel.

Later, this natural fissure becomes a miniature

culture tube for progress of bacteria which causes dissolution

of the remaining enamel and later creeps in to the dentin.

The basic difference between shallow pit and

fissures and deep pit and fissures.

- A relatively thick layer of enamel is present at the base of

the pit.

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- Hence NO DENTINAL INVOLVEMENT.

DEEP PIT & FISSURES

- The enamel thickness at the base of the pit is thin cause of

increased depth.

- There IS DENTINAL INVOLVEMENT.

Almost all the teeth are effected by pit and fissure

caries except for LOWER INCISORS and CUSPIDS.

The carious lesion starts on the lateral walls of the

fissures that eventually fuse at the base of the fissure.

In PIT AND FISSURE the enamel rods are said to

flare laterally at the bottom of the pit and caries is said to

follow the path of enamel rods hence a characteristic

angular / inverted ‘V’ shaped lesion is formed whose.

BASE --------- is towards DENTIN and

APEX --------- is towards OUTER SURFACE.

Once the caries reaches Dentino-Enamel Junction

it spreads laterally and towards pulp.

A greater number of Dentinal tubules are

involved in pit and fissure compared to smooth surface

caries.

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Thus, clinically:

1. A ‘catch’ may be felt with an explorer.

2. Softening at the base of pit and fissure.

3. Opacity surrounding the pit and fissure indicating undermining /

demineralization of Enamel.

4. Radiographic evidence of dental caries under the occlusal

enamel further indicates the need for:

Treatment:

- Restoration of pit and fissures.

- Topical fluoride application.

- Enameloplasty.

II] SMOOTH SURFACE CARIES : The carious process begins only

following the deposition of a layer of dental plaque.

-(microflora + food debris) 24 to 48 hours later.

THE INCIPIENT LESION

CLINICALLY : The first sign of Dental Caries is an area of

Decalcification / less translucency of the affected area which appears /

resembles a CHALKY WHITE SURFACE.

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- This white spot is seen when the enamel is thoroughly

dried.

- No CAVITATION is evident (but the surface may be

rougher than normal enamel as assessed by a dental

probe).

- The white spot is normally seen in the:

a. Gingival area of the buccal and labial

surfaces of the clinical crown.

b. Proximal subcontact sites.

HOWEVER care must be exercised to distinguish a carious

white spot from a non-carious white spot (Enamel hypoplasia)

CARIES WHITE SPOT

- It will partially / totally disappear visually if moistened.

ENAMEL HYPOPLASIA

- It is unaltered by wetting / drying.

HISTOLOGICALLY : This chalky white area is mainly due to:

a. Loss of interprismatic / inter rod substance

of enamel resulting in increased prominence of the enamel

rods.

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b. Due to the roughening of the ends of enamel

rods hence the enamel rods are more susceptible to acid

attack.

It has been shown experimentally and clinically that Incipient

caries of enamel can REMINERALIZE. Non cavitated enamel lesions

retain most of the original crystalline frame work that severes as a

nucleating agent for remineralization Ca and PO4 ions from saliva

precipitate crystalline surfaces in enamel lesion :- At this stage if there

is availability of F ions. Remineralization lesion will be concentrated

with FLUORAPATITE. The presence of Fluorapatite provides

additional resistance to further caries attack.

- A remineralized lesion appears as a brown / discoloured

spot (trapped organic debris and metallic ions are

presumably the cause of the discolouration).

At this stage, the incipient lesion may be arrested / even revered

by remineralization.

Except / if esthetically objectionable caries restoration of an

incipient lesion is an elective procedure.

CERTAIN STUDIES carried out by WISLOSRI showed that the

interprismatic organic substance of enamel was made up of a certain

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MUCOPOLYSACCHARIDE which is said to undergo degradation

early in the caries process.

As the caries progresses other histopathological changes occurring

are:

(III) Appearance of transverse dark lines / bands at right angles to the

enamel rods. These lines are due to changes occurring in the

enamel prisms.

(IV) The incremental lines of retgins undergo accentuation. This

darkening appearance of the ILR in the carious lesion is an

optimal phenomenon which occurs due to the loss of minerals due

to the carious process (as a result of which – the organic structures

appear more prominent).

- The path of ingress of an advancing carious lesions is

roughly parallel to the long axis of the enamel rods.

- The advanced smooth surface caries obtains a typical ‘V’

shaped/ cone shaped lesion whose base is towards the

enamel and apex towards the dentin.

- Eventually there is a loss of continuity of the enamel

surface.

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HISTOPATHOLOGY : This is due to the disintegration of the enamel

prisms following decalcification of the inter prismatic substance

followed by accentuation of debris and microorganisms.

Before the complete disintegration of enamel several zones can

be appreciated starting from the advancing end of the lesion.

Light microscopic studies of the enamel lesion has revealed 4

zones – which represent various degree of hard tissue transformation.

a) A translucent zone – which is the advancing front of the

lesion.

b) A dark zone – separating the translucent zone from the

body of the lesion.

c) The body of carious lesion – Radioluscent region.

d) A relatively intact enamel surface layer.

These zones should not be interpreted as distinct entities but

represent a continuum of changes in caries process.

ZONE 1 : TRANSLUCENT ZONE : is present at the advancing end

of the enamel lesion. I

- It is not always present.

- 50% of longitudinal sections show this zone.

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- This zone has been shown to be slightly more porous than

sound enamel (at junction sites such as the prism

boundaries) having a pore volume of 1% than 0.1% of

normal enamel.

- This zone is best visualized by polarized light.

- There is no evidence whether the organic matter is

removed / altered in this zone.

- There is less demineralization.

- The loss of carbonate and magnesium along with Ca++ and

PO4 results in pore formation.

ZONE 2 : DARK ZONE

- Lies adjacent to translucent zone.

- It is termed as positive zone because it is usually

presence.

- Zone is present due to mineralization of enamel.

- The pores are not small than in translucent zone

Pore volume – 2% to 4%.

ZONE 3 : BODY OF THE LESION

- It is deep to the relatively unaffected enamel surface

layer.

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- This zone lies inbetween the dark zone and the surface

layer.

- It is the area of greatest demineralization.

- Under light – the ground sections revealed:

1. Enhanced striae of retgins.

2. Cross striations in the enamel prisms.

- It has a pore volume of 5% at the periphery and 25% at

the center of the lesion.

- It is considered as the widest zone.

ZONE 4 : SURFACE ZONE:

- An important feature of an progressing initial carious

lesion is the presence of an apparently intact enamel

surface overlying an area of sub-surface demineralization.

- This is the most superficial zone.

- It is the most unaffected zone – due to the great resistance

of the surface zone to decalcification.

1. Because of the greater degree of mineralization of the

surface (hypermineralized surface).

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2. Increased concentration of fluoride in the surface enamel

– here the pore volume is less than 50%.

Thus when only enamel is affected the patient experiences:

1. Sensitivity.

2. On mastication because of the increased forces, the unsupported

brittle enamel will break down – cavity formation.

Clinically:

- Softened enamel may be flabed away by the explorer.

- Proximal lesions detectable on bite-wing radiographs

should be carefully examined clinically.

(Incipient enamel lesions visible / just detectable on bite-

wing are unlikely to have cavitated surfaces).

Treatment: Preventive measures ie.:

1. Fluoride application.

2. Patient education.

May help in preventing the progress of lesion cause the outer

layer of enamel is the most caries resistant and is capable of

withstanding damage.

(B) CARIES OF DENTIN

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- Spread of caries is more in dentin compared to enamel

because of:

1. Decreased calcification (mineralization).

2. Existence of pathways (dentinal tubules).

- Once the enamel caries reaches the dentino-enamel

junction it spreads laterally along the DEJ with the rapid

involvement of a great number of dentinal tubules. Each

dentinal tubules acts as a tract along which

microorganisms travel to the pulp.

- Thus, there will be pulp response-which forms the

sclerotic and secondary dentin.

- CARIES OF DENTIN: IN CHILDREN IS FASTER

because:

1. Dentinal tubules are shorter and wider.

2. Less amount of mineralization.

3. Thickness of enamel and dentin is less and pulp chamber

is wider and large.

- In cases of caries spreading in an enamel lesion clinically

only a small lesion may be present but the underlying

dentin a large cavity may be formed.

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- As the carious lesions progress is various zones of caries

in dentin can be appreciated which assumes a triangular

shape.

- With BASE – towards dentino-enamel junction.

- And APEX – towards the pulp.

The zones are:

1. Zone of fatty degeneration.

2. Zone of dentinal tubules.

3. Zone of decalcification.

4. Zone of bacterial invasion.

5. Zone of decomposed dentin.

- The initial penetration of caries in the dentinal tubules

causes:

1) Firstly the fatty degeneration of the

tomes dentinal fibres resulting in deposition of fat globules in

the further end of dentinal tubules.

- It has been suggested that this fatty degeneration

contributes to the:

1. Impermeability of the dentinal tubule.

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2. Also sclerosis of dentinal tubule.

2) Secondly as the caries penetrates there is a reaction of the

vital dentinal tubules and vital pulp which lay down a

CALCIFIC BARRIER thus protecting the dentinal tubules

from further invasion of microorganisms.

- This calcific barrier is termed as dentinal sclerosis /

transparent dentin (as this zone appears transparent in

polarized light and dark in reflected light).

SLOW PROGRESSIVE LESION (CHRONIC) LESION

A THICK transparent dentinal zone is present.

Sclerosis resulting from aging is - Physiological

dentinal sclerosis.

Resulting from mild irritation- Reactive dentinal

sclerosis

RAPIDLY ADVANCING (ACUTE) LESION

A thin zone of transparent dentin seen

Physiological S.D.

0.5 mm thick

at 35 years.

The rate at

which caries IN OLDER

Reactive D.S.

Can be seen

radiographically in the form of

a more radio-opaque (light)

area in the S shape of the

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INDIVIDUALS the caries

spread is sclerotic dentin.

SD Shiny

and hard to explorer.

tubules progressive depends

on Age.

IN YOUNGER INDIVIDUALS

the spread of caries is fast.

Fresh D Allows penetration of

a sharp explorer lp.

Even before the carious process becomes EVIDENT clinically a

few bacteria are seen to be present in the dentinal tubules. These are

termed as PIONEER BACTERIA. These bacteria are said to be present

in the dentinal tubules prior to the occurrence of

DECALCIFICATION.

3) Close examination of the dentin behind the zone

of dentinal sclerosis reveals a zone of decalcification of dentin.

This decalcified zone occurs prior to bacterial invasion. The

initial decalcification involves the walls of the dentinal tubules

allowing them to distend slightly.

4) The dentinal tubule packed masses of

microorganisms (closer examination reveals adjacent tubules

with different strains of microorganisms i.e. tubule with social

organism adjacent with bacilli type.

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In the early stages of dental caries acidogenic organisms are

responsible for decalcification of dentinal tubules as these

organisms depend on the carbohydrate substrate present at the

surface.

As the carious lesion progresses deeper the carbohydrate

source moves further away, the organisms found in the dentinal

tubule are proteolytic in nature i.e. they depend on the proteins

of dentinal tubules.

Hence the organisms responsible for the initiation of the

caries (ACIDOGENIC) are replaced by other organisms

(PROTEOLYTIC) as the lesion progresses.

ADVANCED DENTINAL CHANGES:

5) Further decalcification of the individual dentinal

tubule in their confluencing and increasing in diameter.

The dentinal tubules undergo further packing with

microorganisms.

Tiny liquifaction foci form due to breakdown of dentinal tubule.

These foci are ovoid area of destruction parallel to the course of the

dentinal tubules.

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- As areas of liquifaction foci undergo, expansion the

adjacent dentinal tubule undergo. Distortion and their

course is bent around liquifaction foci.

- In areas of globular dentin the decalcification process is

said to be faster.

- In last stages destruction of dentin occurs through a

processes of decalcification and proteolytic breakdown.

These are numerous focal areas of destruction present and

dentin, becomes LEATHERY in consistency.

- The caries extends at angular angles, along brachs of DT

thus resulting in clefts.

- These clefts account for the manner in which carious

dentin can be excavated (as thin layers using hand

instruments).

- Above this is the necrotic layer which histologically is

structureless and granular in appearance and contains

masses of bacteria.

SECONDARY DENTINAL INVOLVEMENT

- The carious process is the same as in primary dentin but

here the process is much slower as:

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1. The dentinal tubules are fewer in number.

2. More irregular in course.

Hence, delaying the penetration of invading

microorganisms but sooner / later the involvement of the pulp

results.

- Sometimes the caries process may spread laterally

between primary and secondary dentin producing

separation of the two layers.

ROOT CARIES : This is mainly said to occur in older individuals / or

as those age suffering from debilitating disease undergoes recession

exposing the cementum covering the root. Hence there is increase in

the prevalence of root caries.

- Root caries is found at the cemento-enamel junction or

more apically, on the cementum.

- Root surface caries progresses round rather than into the

tooth. (proteolyses of Sharpey’s fibres being

fragmentation / cavitation).

- The spread of filamentous organisms along the Sharpeys fibres /

inbetween bundles of Sharpey’s fibres are responsible for caries

spread.

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ACTIVE LESION

- Yellowish / light

brown.

- Soft and leathery

consistency.

INACTIVE LESION

- Darker with

smooth surfaces.

- Harder in

consistency (on probing)

- After decalcification of cementum destruction of the

remaining cementum occurs. As the process continues

microorganisms invade into the underlying dentinal tubule

with subsequent matrix destruction and pulpal

involvement.

Treatment:

Pain : due to stimulation of odontoblastic process when acid

in caries reaches DEJ.

CONCLUSION

SIMPLIFIED EQUATIONS depicting the caries progress is as follows:

Cariogenic bacterial plaque +

Suitable local

substrate Organic acids

Organic acids (in plaque) + Tooth

mineral Loss of enamel

Demineralized tooth (Dentin) +

Bacterial proteolytic enzymes

Cavitation

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