Download SMOOTH SURFACE

classification of caries
SMOOTH SURFACE CARIES
• Develops on proximal surfaces of all
teeth or on gingival 1/3rd of buccal
and lingual surfaces.
• Here, the caries is preceded by
retention of carbohydrate and
bacteria on tooth surfaces, leading to
subsequent acid
demineralization of enamel.
• Smooth surface caries usually
begins just below the contact
point and appears in initial
stages as a faint white opacity
of enamel without loss of
continuity of enamel surface.
• The early chalky white spot
becomes roughened owing to
superficial decalcification of
enamel.
• As caries reaches the DEJ, there is rapid
lateral spread.
• Quite often, caries extends buccally and
lingually but not till the actual buccal and
lingual surfaces, as these areas are more
accessible to the toothbrush.
CERVICAL CARIES
• Cervical caries occurs on buccal,
lingual or labial surfaces.
• Extends occlusally from gingival crest
region to the convexity of smooth
surface that marks the self cleansing
portion of tooth.
• Laterally, it extends towards the
proximal surfaces.
• Thus this lesion is a crescent shaped
cavity beginning in its initial stages as a
chalky white lesion.
CERVICAL CARIES
• It almost always occurs as an open cavity unlike the
smooth surface or pit and fissure caries.
• Occurs on all the teeth without predilection as it is
directly related to lack of oral hygiene.
• No excuse for it to occur on anybody’s teeth since it
can always be prevented by maintaining good oral
hygiene.
ACUTE DENTAL CARIES
• It is that form of caries that follows a rapid clinical
course and results in early pulpal involvement by
carious process.
• Predominantly affects children and young adults
probably because their dentinal tubules are larger
and show no sclerosis.
• The point of entry of caries is small even though
there is rapid spread of caries at DEJ, producing
large internal cavitation.
• The small point of opening
doesn’t allow the buffering
ions of saliva to neutralize
acids formed within the
cavity.
• The affected dentin is
usually stained light yellow
compared to deep brown /
black of chronic caries.
• Pain is more likely to be
seen in acute dental caries
than chronic caries, but this
is not a hard and fast
rule.
RAMPANT DENTAL CARIES
• Characterized by sudden, rapid
destruction of teeth affecting even
relatively caries free surfaces like
proximal and cervical surfaces of
mandibular teeth.
• 10 or more carious lesions over a
one year period is characteristic of
rampant caries.
• Prominently observed in deciduous
dentition of young children and
permanent dentition of teenagers.
• Dietary factors like high carbohydrate
intake etc as well as physiological
factors affecting saliva are major
contributors to etiology of rampant
caries.
NURSING BOTTLE CARIES
•
Also called baby bottle syndrome
and bottle mouth syndrome.
• It is a type of rampant caries and
occurs due to –
(a) Nursing bottle containing milk, milk
formula or sweetened water.
(b) Breast feeding
(c) Sugar or honey sweetened
pacifiers
• Usually, the above aids are used at sleeping time after one
year of age.
• Clinically seen as widespread caries of the 4 maxillary incisors
followed by 1st molars and then canines.
• Absence of caries in mandibular teeth distinguishes it from
ordinary rampant caries.
• If milk or other carbohydrates are rapidly cleared from
mouth, they aren’t cariogenic, but if they pool in the mouth,
then they can cause rampant caries.
• Mandibular teeth usually escape the process as the pooled
milk or sweet products are washed away by saliva
CHRONIC DENTAL CARIES
• That type of caries which progresses slowly and involves
the pulp much later than acute caries.
• Most commonly seen in adults.
• Opening to the lesion is invariably larger than that of
acute caries. As a result, there is lesser food impaction
and greater access to saliva.
• Also, the slow progress of caries allows enough time for
dentinal sclerosis and deposition of tertiary dentin in
response to irritation.
• The carious dentin is stained deep
brown
• As compared to acute caries there is
considerable SURFACE destruction with
a shallower cavity and little
undermining of there is only enamel,
while moderate spread of caries along
the DEJ.
• Pain is NOT a prominent feature here
due to the protection provided to the
pulp by tertiary dentin formation.
RECURRENT CARIES
• Occurs around or beneath
an existing restoration.
• Usually due to inadequate
extension of restoration
resulting in food
impaction
• Can also occur if a
restorative material is not
properly adapted to
margins of cavity leading
to leaky cavity margins.
• This “renewed” carious
process follows a similar
pattern as that of primary
caries.
ARRESTED CARIES
•
It is that caries which becomes
static or stationary and does not
progress any further.
•
Can occur in both deciduous and
permanent dentition.
•
Occurs almost exclusively on
occlusal surface caries.
•
•
•
•
Characterized by large, open cavity in which there
is no food retention and the softened decalcified
dentin is gradually burnished until it assumes a
brown polished appearance.
Called “Eburnation of dentin”.
Sometimes arrest can also occur in initial proximal
caries, when the adjacent tooth is extracted for
some reason.
This is due to the automatic creation of a self
cleansing area
RADIATION CARIES
•
Rampant caries occurring in patients receiving
radiotherapy in head & neck region is called as
RADIATION CARIES.
•
Xerostomia (dry mouth )is a major complication
of radiotherapy of head & neck region. This,
coupled with increase in viscosity and low pH of
saliva results in decreased anticariogenic
actions of saliva.
HISTOPATHOLOGY OF CARIES
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
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.
•
•
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
1.TRANSLUCENT ZONE: • Unrecognizable clinically &
radiologically.
• Occurs due to formation of
submicroscopic pores at enamel
rod boundaries and striae of
Retzius.
• This zone is slightly more porous
than sound enamel having a pore
volume of 1% compared to 0.1%
of sound enamel.
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.
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.
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.
EARLY LESION – PIT & FISSURE
• Caries process not much
different from smooth surface.
• Caries most often starts on both
side of fissure and visual changes
like yellow or brown
discoloration are seen.
• Also, enamel being usually thin
at the base of pits and fissures,
dentin involvement occurs much
earlier.
• In contrast to smooth surface caries’ lesion, the caries here follows
direction of enamel rods, forming a cone shaped lesion with its base
towards DEJ and apex directed occlusally.
• As a result therefore, greater number of dentinal tubules are affected
when lesion reaches DEJ.
CAVITY FORMATION & BACTERIAL
INVASION
• The enamel crystallites are progressively dissolved until the
disintegration becomes visible macroscopically.
• Now the pathways are large enough for the bacteria to physically
enter the enamel, destroy organic matrix by proteolysis and then
proceed to DEJ and dentinal tubules.
HISTOLOGY OF ENAMEL & DENTIN
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.
• 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.
• 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.
• 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”.
HISTOPATHOLOGY OF CARIES – DENTIN
(ADNANCED 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.
• 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.
• 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.
ZONES OF DENTINAL CARIES
5
4
3
2
1
• 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