This document provides an overview of the classification of dental caries based on various factors such as anatomical site, progression, extent of involvement, number of tooth surfaces affected, chronology, and whether caries was fully removed during treatment. It discusses 12 different classification systems for dental caries and provides details on types of caries such as pit and fissure, smooth surface, root surface, incipient, occult, and others based on these classification criteria. The document also covers the histopathology of caries in enamel and dentin.
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Clinical features and histopathology of dental caries
1. CLINICAL FEATURES &
HISTOPATHOLOGY OF
DENTAL CARIES
PRESENTATION BY:SAGAR HIWALE
MDS 1ST
YEAR
DEPARTMENT OF CONSERVATIVE AND ENDODONTICS
JAIPUR DENTAL COLLEGE AND HOSPITAL
2. CONTENTS
CLASSIFICATION OF DENTAL CARIES
1.BASED ON ANATOMICAL SITE
2.BASED ON PROGRESSION
3.BASED ON VIRGINITY OF LESION
4.BASED ON EXTEND OF CARIES
5.BASED ON TISSUE INVOLVEMENT
6.BASED ON PATHWAY OF CARIES SPREAD
7. BASED ON NUMBER OF TOOTH SURFACE INVOLVED
8. BASED ON CHRONOLOGY
9 .BASED ON WHETHER CARIES IS COMPLETLY REMOVED OR NOT DURING
TREATMENT.
10.BASED ON TOOTH SURFACE TO BE RESTORED
11.BLACK’S CLASSIFICATION
12.WHO SYSTEM.
13.GJ MOUNT CLASSIFICATION
HISTOPATHOLOGY OF CARIES – ENAMEL
HISTOPATHOLOGY OF CARIES – DENTIN
4. 1.BASED ON ANATOMICAL SITE
OCCLUSAL
(PIT AND
FISSURE)
ROOT
CARIES
SMOOTH
SURFACE
CARIES
(PROXIMAL
AND CERVICAL
CARIES)
LINEAR
ENAMEL
CARIES
5. PIT AND FISSURE CARIES
PIT AND FISSURE CARIES of the primary type
develops in the occlusal surface of molar and
premolar,in the buccal and lingual surface of the
molar and in the palatal surface of the maxillary
incisors.
Shape, morphological variation and depth of pit
and fissures contributes to their high susceptibility
to caries.
Enamel in the extreme depth is very thin or
occasionally absent and thus allows the exposure of
dentin.
6. Pit and fissures affected by early caries may
appear brown or black and will feel slightly soft
and ‘catch’ a fine explorer point.
Entry site may appear much smaller than actual
lesion, making clinical diagnosis difficult.
Carious lesion of pits and fissures develop from
attack on their walls.
In cross section, the gross appearance of pit and
fissure lesion is inverted V with a narrow
entrance and a progressively wider area of
involvement closer to the DEJ.
7. MORPHOLOGY OF FISSURES
NANGO (1960):Based on the alphabetical
description of shape– 4 types
V&U type: self cleansing and somewhat
caries resistant
U type: narrow slit like opening with a larger
base as it extend towards DEJ .Caries
susceptible; also have a number of
different branches
K type: also very susceptible to caries
8.
9.
10.
11. Smooth surface caries
Less favorable site for plaque attachment, usually
attaches on the smooth surface that are near the
gingiva or are under proximal contact..
In very young patients the gingival papilla
completely fills the interproximal space under a
proximal contact and is termed as col. Also
crevicular spaces in them are less favorable
habitats for s.mutans.
Consequently proximal caries is less lightly to
develop where this favorable soft tissue
architecture exists.
12. The proximal surfaces are particularly
susceptible to caries due to extra shelter
provided to resident plaque owing to the
proximal contact area immediately occlusal to
plaque.
Lesion have a broad area of origin and a
conical, or pointed extension towards DEJ.
V shape with apex directed towards DEJ.
After caries penetrate the DEJ softening of
dentin spread rapidly and pulpally
13.
14.
15. Linear enamel caries
Linear enamel caries ( odontoclasia ) is seen to occur in
the region of the neonatal line of the maxillary anterior
teeth.
The line, which represent a metabolic defect such as
hypocalcemia or trauma of birth, may predispose to
caries, leading to gross destruction of the labial surface
of the teeth.
Morphological aspects of this type of caries are atypical
and results in gross destruction of the labial surfaces
incisor teeth
16. ROOT SURFACE CARIES
The proximal root surface, particularly near the cervical line, often
is unaffected by the action of hygiene procedures, such as
flossing, because it may have concave anatomic surface contours
(fluting) and occasional roughness at the termination of the
enamel.
These conditions, when coupled with exposure to the oral
environment (as a result of gingival recession), favor the formation
of mature, caries-producing plaque and proximal root-surface
caries.
Root-surface caries is more common in older patients.
Caries originating on the root is alarming because
1. it has a comparatively rapid progression
2. it is often asymptomatic
3. it is closer to the pulp
4, it is more difficult to restore
17. The root surface is refer the enamel and
readily allows plaque formation in the
absence of good oral hygiene.
The cementum covering the root surface is
extremely thin and provides little resistance
to caries attack.
Root caries lesions have less well-defined
margins, tend to be U-shaped in cross
sections, and progress more rapidly
because of the lack of protection from and
enamel covering.
20. ACUTE CARIES
Acute caries is a rapid process involving a large
number of teeth.
These lesions are lighter colored than the other
types, being light brown or grey, and their caseous
consistency makes the excavation difficult.
Pulp exposures and sensitive teeth are often
observed in patients with acute caries.
It has been suggested that saliva does not easily
penetrate the small opening to the carious lesion, so
there are little opportunity for buffering or
neutralizaton
21. CHRONIC CARIES These lesions are usually of long-standing
involvement, affect a fewer number of teeth, and are
smaller than acute caries.
Pain is not a common feature because of protection
afforded to the pulp by secondary dentin
The decalcified dentin is dark brown and leathery.
Pulp prognosis is hopeful in that the deepest of lesions
usually requires only prophylactic capping and
protective bases.
The lesions range in depth and include those that
have just penetrated the enamel.
22. ARRESTED CARIES:-
Caries which becomes stationary or static and
does not show any tendency for further
progression
Both deciduous and permanent affected
With the shift in the oral conditions, even
advanced lesions may become arrested .
Arrested caries involving dentin shows a
marked brown pigmentation and induration of
the lesion [the so called ‘eburnation of dentin’]
Sclerosis of dentinal tubules and secondary
dentin formation commonly occur
23. Exclusively seen in
caries of occlusal
surface with large open
cavity in which there is
lack of food retention
Also on the proximal
surfaces of tooth in
cases in which the
adjacent approximating
tooth has been extracted
25. PRIMARY CARIES(INITIAL)
A primary caries is one in which the lesion
constitutes the initial attack on the tooth
surface.
The designation of primary is based on
the initial location of the lesion on the
surface rather than the extent of damage.
26. SECONDARY CARIES
(RECURRENT)
This type of caries is observed around the edges and
under restorations.
The common locations of secondary caries are the
rough or overhanging margin and fracture place in all
locations of the mouth.
It may be result of poor adaptation of a restoration,
which allows for a marginal leakage, or it may be due
to inadequate extension of the restoration.
In addition caries may remain if there has not been
complete excavation of the original lesion, which later
may appear as a residual or recurrent caries.
27.
28.
29. 4. BASED ON EXTENT OF
CARIES
INCIPIENT CARIES
OCCULT CARIES
CAVITATION
30. INCIPIENT CARIES
The early caries lesion, best seen on the smooth
surface of teeth, is visible as a ‘white spot’.
Histologically the lesion has an apparently intact
surface layer overlying subsurface
demineralization.
Significantly may such lesion can undergo
remineralization and thus the lesion is not an
indication for restorative treatment
31. These white spot lesion may be confused
initially with white developmental defects of
enamel formation, which can be
differentiated by their position away from the
gingival margin], their shape [unrelated to
plaque accumulation] and their symmetry
[they usually affect the contralateral tooth].
Also on wetting the caries lesion disappear
while the developmental defect persist
32.
33. It is believed that bite wing and OPG radiographs
along with noninvasive adjuncts like fiber optic
transillumination (FOTI),laser luminescence, electrical
resistance method (ERM) are used for diagnosis
these occlusal lesions.
These lesion are not associated with microorganisms
different to those found in other carious lesion.
These carious lesion seem to increase with
increasing age.
Occult carious lesion are usually seen with low caries
rate which is suggestive of increase fluid exposure.
34. It is believed that increased fluid exposure
encourages remineralization and slow down
progress of the caries in the pit and fissure
enamel while the cavitations continues in
dentine, and the lesions become masked by
a relatively intact enamel surface.
These hidden lesions are called as fluoride
bombs or fluoride syndrome.
Recently it is seen that occult caries may
have its origin as pre-eruptive defects which
are detectable only with the use of
radiographs.
35. Once it reaches the
dentinoenamel junction,
the caries process has the
potential to spread to the
pulp along the dentinal
tubules and also spread in
lateral direction.
Thus some amount of
sensitivity may be
associated with this type
of lesion.
This may be generally
accompanied by cavitation
36. 5.Based on tissue
involvement
1. Initial caries
2. Superficial caries
3. Moderate caries
4. Deep caries
5. Deep complicated caries
37. Dental caries can be divided into 4 or 5
stages
Initial caries: Demineralization without
structural defect. This stage can be
reversed by fluoridation and enhanced
mouth hygiene
Superficial caries (Caries
superficialis):Enamel caries, wedge-
shaped structural defect. Caries has
affected the enamel layer, but has not
yet penetrated the dentin.
38. 3. Moderate caries (Caries media): Dentin caries.
Extensive structural defect. Caries has
penetrated up to the dentin and spreads two-
dimensionally beneath the enamel defect where
the dentin offers little resistance.
4. Deep caries (Caries profunda): Deep structural
defect. Caries has penetrated up to the dentin
layers of the tooth close to the pulp.
5. Deep complicated caries (Caries profunda
complicata) :Caries has led to the opening of the
pulp cavity (pulpa aperta or open pulp).
40. “Forward-backward” classification is
considered as graphical representation of the
pathway of dental caries.
ENAMEL
First component of enamel to be involved in
carious process is the interprismatic substance.
The disintegrating chemicals will proceed via the
substance, causing the enamel prism to be
undermined.
The resultant caries involvement in enamel will
have cone shape.
In concave surface (pit and fissures) base
towards DEJ.
In convex surfaces (smooth surface) base
away from DEJ.
41. DENTIN
First component to be involved in dentin is
protoplasmic extension within the dentinal
tubules.
These protoplasmic extension have their
maximum space at the DEJ, but as they
approach the pulp chamber and root canal
walls, the tubules become more densely
arrange with fewer interconnections.
So caries cone in dentin will have their base
towards DEJ.
42. Decay starts in enamel then it involves the
dentin. Wherever the caries cone in enamel
is larger or at least the size as that of dentin,
it is called forward decay (pit decay)
However the carious process in dentin
progresses much faster than in enamel, so
the cone in dentin tends to spread laterally
creating undermined enamel. In addition
decay can attack enamel from its dentinal
side. At this stage it becomes backward
decay.
43. 7.BASED ON NUMBER OF
TOOTH SURFACE INVOLVED
Simple
Compound
Complex
A caries involving only one
tooth surface
A caries involving two
surfaces of tooth
A caries that involves more
than two surfaces of a tooth
44. 8. BASED ON CHRONOLOGY
EARLY CHILDHOOD CARIES
ADOLESCENT CARIES
ADULT CARIES
45. It has been stated that over a lifetime,
caries incidence i.e. the number of new
lesions occurring in a year, shows three
peaks-at the ages 4-8,11-19 and 55-65
years
46. EARLY CHILDHOOD CARIES
Early childhood caries
would include, two
variants: Nursing caries
and rampant caries.
The difference primarily
exist in involvement of
the teeth[ mandibular
incisors ] in the carious
process in rampant
caries as opposed to
nursing caries.
47. CLASSIFICATION OF EARLY CHILDHOOD
CARIES
TypeI
(MILD )
Involves molars and incisors
Seen in 2-5 years
Causecariogenic semisolid food +lack
of oral hygeine
TypeII
(MODE
RATE)
Unaffected mandibular incisors
Soon after first tooth erupts
Causeinappropriate feeding +lack of
oral hygeine
TypeIII
(SEVE
RE)
All teeth including mandibular incisors
Causemultitude of factors
48. NURSING CARIES
Seen in infant and
toddler
Affects primary
dentition
Mandibular incisors
are not involved
ETIOLOGY
Improper bottle
feeding
Pacifier dipped in
honey/other sweetner
RAMPANT CARIES
Seen in all ages,
including adoloscennce
Affects primary and
permanent dentition
Mandibular incisors are
also affected
ETIOLOGY
MULTIFACTORIAL
Frequent snacks
Sticky refined CHO
Decreased salivary
flow
Genetic background
49. TEENAGE CARIES
(ADOLESCENT CARIES)
This type of caries is a variant of rampant caries
where the teeth generally considered immune to
decay are involved.
The caries is also described to be of a rapidly
burrowing type, with a small enamel opening.
The presence of a large pulp chamber adds to
the woes, causing early pulp involvement
50.
51. ADULT CARIES
With the recession of the
gingiva and sometimes
decreased salivary
function due to atrophy, at
the age of 55-60 years, the
third peak of caries is
observed.
Root caries and cervical
caries are more commonly
found in this group.
Sometime they are also
associated with a partial
denture clasp.
52. 9.BASED ON WHETHER CARIES IS
COMPLETLY REMOVED OR NOT
DURING TREATMENT
RESIDUAL CARIES
Residual caries is that which is not removed during
a restorative procedure, either by accident, neglect
or intention.
Sometimes a small amount of acutely carious
dentin close to the pulp is covered with a specific
capping material to stimulate dentin deposition,
isolating caries from pulp.
The carious dentin can be removed at a later time.
53. 10.BASED ON SURFACES TO BE
RESTORED
Most widespread clinical utilization
O for occlusal surfaces
M for mesial surfaces
D for distal surfaces
F for facial surfaces
B for buccal surfaces
L for lingual surface
Various combinations are also possible, such as
MOD –for mesio-occluso-distal surfaces.
54. 11.BLACK’S CLASSIFICATION
Class 1 lesions:
Lesions that begin in the
structural defects of
teeth such as pits,
fissures and defective
grooves.
Locations include
Occlusal surface of
molars and premolars.
occlusal two thirds of
buccal and lingual
surfaces of molars and
premolars.
Lingual surfaces of
anterior tooth.
55. Class 2 lesions:
They are found on the
proximal surfaces of
the bicuspids and
molars.
Class 3 lesions:
Lesions found on the
proximal surfaces of
anterior teeth that do not
involve or necessitate
the removal of the incisal
angle.
56. Class 5 lesions:
Lesions that are found at the
gingival third of the facial and
lingual surfaces of anterior and
posterior teeth.
Class 4 lesions:
Lesions found on the
proximal surfaces of
anterior teeth that
involve the incisal
angle.
58. 12.World health organization
(WHO) system
In this classification the shape and depth of the
caries lesion scored on a four point scale
D1. clinically detectable enamel lesions with intact
(non cavitated) surfaces
D2. Clinically detectable cavities limited to enamel
D3. Clinically detectable cavities in dentin
D4. Lesions extending into the pulp
59. CLASSIFICATION BY GJ
MOUNT AND HUME (1998)
This new system defines the extent and
complexity of a cavity and at the same
time encourages a conservative approach
to the presevation of natural tooth
structure.
This system is designed to utilized the
healing capacity of enamel and dentin.
60. The three sites of carious lesion
Site1- pit and fissure and enamel defects
on occlusal surface of posterior teeth or
other smooth surfaces.
Site2- proximal enamel immediately below
area in contact with adjacent teeth
Site3 – the cervical one third of crown or
following gingival recession,the exposed
root.
61. Four sizes of carious lesion
Size1- minimal involvement of dentin
treatment by remineralization alone.
Size2- moderate involvement of dentin
following cavity preparation,remaning
enamel is sound,well supported by dentin
and not likely to fail under normal occlusal
load.
The remaining tooth structure is sufficient
strong to support the restoration.
62. Size3- the cavity is enlarged beyond
moderate.The remaining tooth structure is
weakened to the extend that cusp or incisal edges
are split or are likely to fail or left exposed to
occlusal or incisal load the cavity need to be
futher enlarged so that the restoration can be
designed to provide support and protection to the
remaining tooth structure.
Size4- extensive caries with bulk loss of tooth
structure has already occurred.
63. RADIATION CARIES
Radiography is frequently associated with
xerostomia due to decreased salivary secretion,an
increase in viscosity and low PH.
lead to a rampant form of caries
Three types of defects due to radiation
1. Lesion usually encircling the neck of teeth
amputation of crowns may occur
2. Begins as brown to black discolouration of tooth
.occlusal surface and incisal edges wear away
3. Spot depression which spreads from any surface
66. HISTOPATHOLOGY OF CARIES -
ENAMEL
Caries process in enamel
progresses through following
stages
A. Early submicroscopic lesion
B. Phase of nonbacterial enamel
crystal destruction
C. Cavity formation
D. Bacterial invasion of enamel
* C & D Occur almost simultaneously
67. EARLY LESION – SMOOTH
SURFACE
Earliest visible changes are
seen as a chalky white spot
on the tooth just adjacent to
contact point.
Electron microscopic study
reveals the early changes as
loss of inter rod enamel,
accentuation of striae of
Retzius and perikymata.
68. As caries progresses, the lesion of
smooth surface caries has a
distinctive conical shape with its base
towards enamel surface and apex
towards DEJ.
This conical lesion when observed in
a light microscope reveals four
different zones as seen from deepest
advancing zone first
1. Translucent zone 2. Dark zone
3. Body of lesion 4. Surface zone
69. 1.TRANSLUCENT ZONE: -
Unrecognizable clinically &
radiologically.
Occurs due to formation of
submicroscopic pores at
enamel rod boundaries.
This zone is slightly more
porous than sound enamel
having a pore volume of 1%
compared to 0.1% of sound
enamel.
70. 2. DARK ZONE: -
Lies superficial to
translucent zone.
Called positive zone as it
is always present.
Pore volume is 2 – 4%.
Increased porosity in this
zone is due to greater
degree of
demineralization in this
zone.
71. 3. BODY OF LESION: -
Forms bulk of the lesion
and lies between
relatively unaffected
surface zone and dark
zone.
Area of greatest
demineralization, having
a pore volume of 5%
near the periphery to
about 25% in the center
of body of lesion.
72. 4. SURFACE ZONE: -
Interestingly, this zone not only
remains intact during the early stages
of attack by caries, but also
REMAINS MORE HEAVILY
MINERALIZED.
Pore volume of only 1%.
Ions for remineralization come either
from those within plaque or from
reprecipitation of calcium and
phosphate ions diffusing outwards as
deeper layers are demineralized.
Eventually, this zone is demineralized
by the time caries penetrates dentin.
73. HISTOPATHOLOGY OF CARIES –
DENTIN (EARLY CHANGES)
The initial (non infected) lesion in dentin
forms beneath enamel before any
cavity has formed.
Even though acids formed from
fermentation of carbohydrate substrate
diffuse into dentin, they leave the organic
matrix intact.
Once bacteria penetrate enamel, they
spread laterally along DEJ and attack
dentin over a wide area.
74. The infected lesion of dentin is
helped in its course by the
presence of tubules within dentin
which provide an easy pathway to
the bacteria.
Bacteria now liberate proteolytic
enzymes and bring about
destruction of organic matrix of
dentin which is already softened by
demineralization.
75. The first change to occur in the caries
process within dentin is fatty degeneration
of the tome’s fibers, with deposition of
lipid globules within these fibers.
This is then followed by dentinal
sclerosis, which is minimal in rapidly
advancing acute caries and maximum in
slow, chronic caries.
This is considered as a protective measure
by dentinal tubules to seal off the invading
bacteria.
76. In spite of all these attempts to prevent
spread of caries process, dentin is
continually destroyed.
Thus behind the zone of dentinal sclerosis
a narrow zone of decalcification is seen,
just ahead of bacterial invasion of dentinal
tubules.
At this stage, only a few tubules are
invaded even before clinical evidence of
caries.
These bacteria are called “Pioneer
bacteria”.
77. HISTOPATHOLOGY OF CARIES –
DENTIN (ADVANCED CHANGES)
Continued decalcification of
dentinal tubules leads to their
confluence, although the
structure of organic matrix
may still be maintained for
some time.
Confluence of tubules occurs
due to packing of the tubules
with the invading bacteria.
78. The coalescence and breakdown
of adjacent dentinal tubules leads
to formation of “Miller’s
liquefaction foci”.
It is an ovoid area of destruction
of tubules parallel to the course of
tubules and is packed with
necrotic debris derived from
destruction of tubules.
79. Continued dentinal destruction by
decalcification followed by proteolysis
occurs at many focal areas which
ultimately coalesce to form a necrotic
leathery mass of dentin.
In this mass, clefts occur at right
angles to tubules and parallel to the
course of lateral branches of tubules
or along the collagen fibers of organic
matrix.
Due to these clefts, carious dentin can
be peeled away in thin layers by hand
instruments.
80. Observing from the pulpal side at the
advancing edge of carious lesion
following different zones can be seen
–
ZONE 1 – Zone of fatty degeneration of
Tomes’ fibers
ZONE 2 – Zone of dentinal sclerosis
ZONE 3 – Zone of decalcification
ZONE 4 – Zone of bacterial invasion
ZONE 5 – Zone of decomposed dentin
1
2
3
4
5
ZONES OF DENTINAL CARIES
81. BIBLIOGRAPHY
Dental Caries: The disease and its clinical
management. 1st
ed. Blackwell Munksgaard, Iowa.
Soames JV, Southam JC. Oral pathology/. 3rd
ed.
Oxford 2002.
Shafer WG, Hine MK, Levy BM. A text book of oral
pathology. 6th
ed. Elsevier
Cawson, R.A: Cawson’s Essentials of OralCawson, R.A: Cawson’s Essentials of Oral
Pathology and Oral Medicine,Pathology and Oral Medicine,
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