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1. 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. 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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3. - 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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4. 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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5. - 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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6. 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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7. 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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8. 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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9. - 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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10. - 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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11. 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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12. - 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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13. - 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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14. 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
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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15. which caries IN OLDER
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.
In the early stages of dental caries acidogenic organisms are
responsible for decalcification of dentinal tubules as these
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16. 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.
- As areas of liquifaction foci undergo, expansion the
adjacent dentinal tubule undergo. Distortion and their
course is bent around liquifaction foci.
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17. - 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:
1. The dentinal tubules are fewer in number.
2. More irregular in course.
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18. 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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19. 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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