management of deep seated caries

1. ‫د‬ ‫اعداد‬.‫محمد‬ ‫حيدر‬‫اشراف‬‫د‬.‫سمير‬ ‫ممدوح‬

2. What is Dental Caries?
Dental caries is a multifactorial, transmissible, infectious
oral disease caused primarily by the complex interaction of
cariogenic oral flora (biofilm) with fermentable dietary
carbohydrates on the tooth surface over time.
caries activity is characterized by localized
demineralization and loss of tooth structure.

3. Keyes-Jordan diagram.

4. Factors affect caries , including number and
type of microbial flora in the biofilm, diet, oral hygiene,
genetics, dental anatomy, use of fluorides and other chemotherapeutic
agents, salivary flow and buffering capacity; and
inherent resistance of the tooth structure and composition
that will differ from person to person, tooth to tooth, and site
to site.

5. Cariogenic bacteria in the biofilm metabolize refined
carbohydrates for energy and produce organic acid
byproducts. These organic acids, if present in the biofilm
ecosystem for extended periods, can lower the pH in the
biofilm to below a critical level (5.5 for enamel, 6.2 for
dentin). The low pH drives calcium and phosphate from the
tooth to the biofilm in an attempt to reach equilibrium,
hence resulting in a net loss of minerals by the tooth, or
demineralization. When
the pH in the biofilm returns to neutral and the
concentration
of soluble calcium and phosphate is supersaturated relative
to
that in the tooth, mineral can then be added back to
partially
demineralized enamel, in a process called remineralization.
At

6. Enamel Caries
On clean, dry teeth, the earliest evidence of caries on the smooth enamel
surface of a crown is a white spot. These lesions usually are observed on the
facial and lingual surfaces of teeth. White spots are chalky white, opaque
areas that are revealed only when the tooth surface is desiccated and are
termed noncavitated enamel caries lesions. These areas of enamel lose their
translucency because of the extensive subsurface porosity caused by
demineralization.

7. *Care must be exercised in distinguishing white spots of
noncavitated caries from developmental white spot
hypocalcifications of enamel.
Noncavitated (white spot) caries partially or totally disappears
visually when the enamel is hydrated (wet), whereas
hypocalcified
enamel is affected less by drying and wetting.
The surface texture of a non-cavitated lesion is unaltered and is
undetectable by tactile examination with an explorer. A more
advanced lesion develops a rough surface that is softer than
the unaffected, normal enamel. Softened chalky enamel that
can be chipped away with an explorer is a sign of active caries.

8. *It has been shown experimentally and clinically that
noncavitated
caries of enamel can remineralize
A more advanced lesion develops a rough surface that is
softer than
the unaffected, normal enamel. Softened chalky enamel that
can be chipped away with an explorer is a sign of active
caries.

9. Remineralized (arrested) lesions can be observed clinically as
intact, but discolored, usually brown or black, spots. The
change in color is presumably caused by trapped organic
debris and metallic ions within the enamel. These discolored,
remineralized, arrested caries areas are intact and are more
resistant to subsequent caries attack than the adjacent
unaffected enamel. They should not be restored unless they
are esthetically objectionable.

10. 1.TRANSLUCENT ZONE: -
Represent the advancing front of the lesion
– Ten times more porous than sound enamel
2. DARK ZONE: -
– It lies adjacent and superficial to the translucent zone
– Usually present and thus referred as positive zone
– Called dark zone because it does not transmit polarized light
– Formed due to demineralization.

11. 3. BODY OF LESION: -
– Largest portion of caries.
– Found between the surface and the dark zone.
– It is the area of greatest demineralization .
4. SURFACE ZONE: -
–is zone is not or least affected by caries
– Greater resistance probably due to greater degree of mineralization and
greater fluoride concentration
– Its radiopacity is comparable to adjacent enamel.

12. Dentin Caries
Caries advances more rapidly in dentin than in enamel because
dentin provides much less resistance to acid attack owing to less
mineralized content. Caries produces a variety of responses in
dentin, including pain, sensitivity, demineralization, and
remineralization.
*The pulp–dentin complex reacts to caries attacks by attempting
to initiate remineralization and blocking off the open tubules.
Dentin responds to the stimulus of its first caries
demineralization
episode by deposition of crystalline material in the lumen of the
tubules and the intertubular dentin of affected dentin in front of
the advancing infected dentin portion of the lesion.

14. Three different zones have been described
in carious dentin . The zones are most clearly
distinguished in slowly advancing lesions. In
rapidly progressing caries, the difference
between the zones becomes less distinct.

16. ZONE 1: NORMAL DENTIN
The deepest area is normal dentin, which has tubules with
odontoblastic processes that are smooth, and no crystals are
present in the lumens. The intertubular dentin has normal
cross-banded collagen and normal dense apatite crystals. No
bacteria are present in the tubules. Stimulation of dentin (a
bur, a dragging instrument, or desiccation from heat or air)
produces a sharp pain.

17. * Dentin that has more mineral content than normal dentin is
termed sclerotic dentin. Sclerotic dentin formation occurs
ahead of the demineralization front of a slowly advancing
lesion and may be seen under an old restoration. Sclerotic
dentin is usually shiny and darker in color but feels hard to the
explorer tip. By contrast, normal, freshly cut dentin lacks a
shiny, reflective surface and allows some penetration from a
sharp explorer tip. The apparent function of sclerotic dentin is
to wall off a lesion by blocking (sealing) the tubules. The
permeability of sclerotic dentin is greatly reduced compared
with normal dentin because of the decrease in the tubule
lumen diameter.

18. ZONE 2: AFFECTED DENTIN
Also called inner carious dentin, affected dentin is a zone of
demineralization of intertubular dentin and of initial formation of
fine crystals in the tubule lumen at the advancing front.
Damage to the odontoblastic process is evident. Affected
dentin is softer than normal dentin and shows loss of mineral
from intertubular dentin and many large crystals in the lumen of
the dentinal tubules. Stimulation of affected dentin produces
pain. Although organic acids attack the mineral and organic
contents of dentin, the collagen cross-linking remains intact in
this zone. The affected dentin zone can also be subclassified in
three sub-zones:
(1) subtransparent dentin
(2) Transparent dentin (3) and turbid dentin.

19. ZONE 3: INFECTED DENTIN
Also called outer carious dentin, this is the outermost carious
layer, the layer that the clinician would encounter first when
opening a lesion. The infected dentin is the zone of bacterial
invasion and is marked by widening and distortion of the
dentinal tubules, which are filled with bacteria. Little mineral is
present, and the collagen in this zone is irreversibly denatured.
The dentin in this zone does not self-repair. This zone cannot
be remineralized, and its removal is essential to sound,
successful restorative procedures and the prevention of
spreading the infection.

21. *In slowly advancing lesions, it is expedient to remove softened
dentin until the readily identifiable zone of sclerotic dentin is
reached. In rapidly advancing lesions little clinical evidence (as
determined by texture or color change) exists to indicate the
extent of infected dentin. For deep lesions, this lack of clinical
evidence may result in an
excavation that risks pulp exposure.
In a tooth with a deep caries lesion, no history of spontaneous
pain, normal responses to thermal stimuli, and a vital pulp, a
deliberate, incomplete caries excavation may be indicated. This
procedure is termed indirect pulp capping.

22. Necrotic dentin is recognized clinically as a wet, mushy, easily
removable mass. This material is structureless or granular in
histologic appearance and contains masses of bacteria.
Removal of the necrotic material uncovers deeper infected
dentin (turbid dentin), which appears dry and leathery.
Leathery dentin is easily removed by hand instruments .

23. If the lesion is progressing slowly, a zone of hard,
hypermineralized sclerotic dentin may be present, as a result
of remineralization of what formerly was affected (or
transparent) dentin (zone 2). When sclerotic dentin is
encountered, it represents the ideal final excavation depth
because it is a natural barrier that blocks the penetration of
toxins and acids.
*dentin as either infected, which requires removal, or affected,
which does not require removal.

24. The outer layer (infected dentin) can be selectively stained by
caries detection solutions (caries detection dyes).This solution
stains the irreversibly denatured collagen in the outer carious
layer but not the reversibly denatured collagen in the inner
carious layer. Clinical use of staining technique may provide a
more conservative tooth preparation because the boundary
between the two layers differentiated by this technique cannot
easily be detected in a tactile manner.

25. DIAGNOSIS OF DEEP CARIOUS LESION
No particular diagnostic method gives an exact picture of the
involved tissue, like the extent of degenerating changes in pulp
or the reparative capacity of the remaining tissue. A diagnosis is
arrived at combining the results of various clinical tests and from
observation.
*Various clinical tests used for evaluating the pulp condition and
the extent of caries
1. Symptoms
2. Clinical appearance
3. Pulp vitality test
4. radiograph

26. Symptoms
Pain is often the chief complaint of patients with deep caries. The
degree of pain depends on the extent of the lesion and the extent
of
pulpal changes. It can also vary from one person to another. Pain
at night or spontaneous pain are often suggestive of
degenerative changes in the pulp dentin origin. Whereas pain on
thermal or chemical
stimulation which disappears immediately or removal of the
stimuli indicates lesser degree of degenerative changes.

27. Clinical appearance
Dentin which appear grayish brown or grayish pink all
throughout the lesion may indicate a devitalized or devitalizing
pulp. This usually occurs when the dentin has lost its
reparative capacity. Tactile evaluation using an explorer
usually will give us an idea of type of dentin present in the
lesion. If the base of the lesion is soft it means that caries
lesion has extended towards the pulp. Similarly if the dentin is
hard but discolored it indicates formed reparative dentin.

28. Pulp vitality test
Thermal pulp test (heat or cold)
This is accomplished by simple application of heat or cold on
the tooth. Heat stimuli is usually applied by heated compound
of
gutta-percha sticks. In tooth with full coverage from a rubber
cup can be applied to the tooth under pressure to produce
frictional heat, cold stimuli is applied with a aid of cotton pellet
soaked in ethylene chloride or liquid nitrogen or simply by
sticks of ice.
A positive response to any of these

29. Removal of Tooth Structure without Anesthesia
Dentin removal close to the pulp either using a spoon
excavator or rotary instrument is a reliable test to pulp vitality. If
there is pain on such procedure the pulp is vital whereas there
will be no pain if the pulp is devitalized.
Electric Pulp Testing
This is accomplished by device that generate electric current.
Result is compared to adjacent teeth .
False positive can also occur in recently devitalized tooth
because the inflammatory exudates and pus that fill the pulp
chamber
or root canal is a good conductor of electricity.

30. Radiograph
• The proximity of the caries lesion to the pulp chamber or
root canal system.
• The approximate thickness of dentin between the lesion
and the pulp
• Discontinuity of lamina dura most probably indicates
destructive activity of the pulp

31. large carious lesions with healthy pulpal and periapical tissues
should be managed via partial caries excavation and indirect
pulp capping.
*Caries is completely excavated peripherally to a
sound, caries-free DEJ. Axially and pulpally, caries will
be excavated to within approximately 1 mm of the
pulp.
.

32. TECHNIQUE STEPS FOR INDIRECT PULP TREATMENT
1. No history of spontaneous pain.
2. Proper Diagnosis: EPT (Electric Pulp Test), CO2 with (+) normal results.
3. Periapical radiograph with normal periapical structures, no peri-radicular
pathosis
4. Good Isolation (Preferable Rubber Dam).
5. Peripheral caries at the DEJ removed while maintaining thin residual
caries dentin over pulpal and axial walls.
6. Clean DEJ at cavosurface margin to achieve a good restoration seal.
7. Finish cavity preparation (clean and smooth walls) with design depending
on material selection.
8. Liner placement (either calcium hydroxide, resin modified glass ionomer
or a resin-modified calcium silicate filled liner® Theracal (Bisco).
9. Final restoration providing good seal.
10. The treated tooth is re-evaluated approximately 12 weeks after the
restorative appointment..

34. Direct pulp capping
This is indicated, when pulp exposure occurs either during carious
removal due to deep carious or pinpoint exposure mechanically
during cavity preparation. There should not be any degenerative
changes in the pulp. The exposure in such cases should have the
following characteristics.
1. The tooth has been asymptomatic (no spontaneous pain,
normal response to thermal testing, and vital) before the operative
procedure.
2. The exposure is small (<0.5mm in diameter).
3. The hemorrhage from the exposure site is easily controlled.
4. The exposure occurred in a clean, uncontaminated field (such
as that provided by rubber dam isolation).
5. The exposure was relatively atraumatic, and little desiccation of
the tooth occurred, with no evidence of aspiration of blood into
dentin ( (dentin blushing).

36. visible pulpal exposure, should be covered with a calcium
hydroxide liner that can stimulate formation of dentin bridges
(reparative dentin) over the exposure. If used, the calcium
hydroxide liner should always be covered with a glass ionomer
or resinmodified glass ionomer liner before the tooth is restored.
Deep excavations not encroaching on the pulp should be
covered with a glass-ionomer material and then restored with
either a definitive or a temporary restorative material.

38. contraindication

39. References
Sturdevant Art and Science of Operative Dentistry, 6 edition
Essentials of Operative Dentistry
Text book of operative dentistry