2. CONTENTS
1. Introduction
2. Effects of caries on P-D organ
3. Arrested caries
4. Histopathology of dentinal caries
5. Effective depth (remaining dentin) and pulpal
response.
6. Prognosis of deep carious lesions
7. Reparability
8. Treatment modalities 2
3. INTRODUCTION
• Deep carious lesions are those in which caries
penetration is easily observed in the dentin
and may involve more than one half of the
dentin thickness between the DEJ and the
pulp.
• Tooth with a deep cavity will reveal upon
excavation of the carious and necrotic dentin,
an interface of decalcified and softened.
3
4. Introduction
• It can destroy the structural components of
the tooth, if the rate of the carious process
exceeds the speed of the pulpal response.
• One of the basic steps in restorative operative
procedures is removal of carious dentin.
Unfortunately , this process is still empirical,
resulting in a great deal of inconsistency.
4
6. Response of P-D complex in lesion progression
a. Carious lesion advancing in enamel
• A reduction of the odontoblast predentin region can
be observed as the very first cellular changes
subjacent to active progressing enamel lesions.
• Size of odontoblasts decrease, as compared to
unaffected odontoblasts.
• Pulpal cells proliferate into the cell free zone.
• Dentin tubular hypermineralization occurs, as the
demineralization in enamel is reaching the dentino-
enamel junction.
6
7. b. Carious lesion advancing in dentin
• Demineralization of dentin is initiated, as the enamel
lesion comes in contact with the dentinoenamel
junction.
• It presents as a brownish discoloration of dentin.
• This appearance is not lateral spread of the lesion. It
has been shown never to extend beyond the limits of
the enamel lesion contact area with the dentino-
enamel junction. This dentin demineralization is a
reaction of bacterial byproducts passing through
enamel prisms.
Response of P-D complex in lesion progression
7
8. • The advancing front of dentinal caries follows the
direction of dentinal tubules, this being the primary
route for dissolution of the hard dentinal tissue.
• Consequently the zone of dentin demineralization
subjacent to non-cavitated lesions narrows as it
progresses toward the pulp.
• The initial dentin demineralization takes place
without the presence of bacteria in the dentin.
• As bacteria are still far too large to penetrate the
demineralized rod and inter-rod enamel.
Response of P-D complex in lesion progression
8
9. • However, when the enamel crumbles, bacterial
invasion of the demineralized enamel occurs.
On the basis of oral hygiene status of the patient,
persistence of the plaque biofilm and other related
factors, caries may progress as an active lesion, or
slow progressing lesion or may attain quiescence as
arrested caries.
Response of P-D complex in lesion progression
9
10. Acute Caries/Active
lesion
Dentin - yellowish, light
brown in color
The hardness of carious dentin
decreases considerably
Proliferation of cells takes
place from the sub-
odontoblastic cell rich zone
into cell free zone
Chronic caries/slow
progressing lesion
It has a darker brown
color
Relatively less
softening of dentin
occurs
It is not so evident in slow
progressing lesions
10
11. Acute Caries/Active
lesion
Odontolbasts necrosis
occurs at a faster rate
followed by atubular dentin
or fibrodentin deposition
by newly formed
odontoblasts
Rapid demineralization and
tissue destruction occurs
Chronic caries/slow
progressing lesion
Tertiary dentin formed is
tubular dentin at the pulpal
site. It appears as a result of
reactionary dentinogenesis
and dentin produced by new
odontoblast like cells
Organic tissue is more
resistance. Defensive process
predominates
11
13. ARRESTED CARIES
• The conditions under which the arrest of an
active lesion occur are still very not clear and
being studied.
• An arrested dentinal lesion differs from an active
lesion by its darker pigmentation, absence of
visible bacteria within the tubule and
impermeability to dyes and isotopes.
13
14. • Following layers are identified:
1. A narrow surface layer, brown in color and leathery
in consistency.
2. The widest zone, dark brown in color and hard in
consistency.
3. Sclerotic layer, white in color and often harder than
normal dentin.
• One of the major characteristics of an arrested caries
is its high degree of mineralization.
ARRESTED CARIES
14
15. • The possible ways by which the accumulation of
minerals occur can be:
a. Remineralization of the surface layer - source can be
saliva from where calcium and phosphate are
absorbed.
b. Reprecipitation of dissolved apatite - the minerals
dissolved by bacterial acids in the upper
demineralized layer reprecipitate to form large
crystals in the area just below.
ARRESTED CARIES
15
16. • Sclerosis of intratubular calcification and obliteration
of tubules of deeper layers underneath the lesion.
• Probably minerals are mediated by odontoblastic
processes through blood supply.
• In arrested lesions, the bacterial bodies are coalesced
into homogenous masses, degenerated and
disintegrated.
• Another characteristic is the presence of deep
pigmentation. The degenerated bacteria or the
degradation products of their proteins and nucleic
acids are the possible sources of pigmentation.
ARRESTED CARIES
16
18. HISTOPATHOLOGY
• The pathological changes occurring in dentin,
have been divided into various zones, starting
from surface. These are:
a) Zone of decomposed dentin
b) Zone of bacterial invasion
c) Zone of demineralization
d) Zone of dentinal sclerosis or
hypermineralization
a) Zone of fatty degeneration of Tome's fibers
18
19. A. Zone of Decomposed Dentin
• Completely devoid of minerals; more so in acute caries
than in chronic caries
• Organic matrix decomposed completely
• High concentration of micro-organisms in the
destructed dentin mass with substantial amounts of
residual plaque deposits.
• Chronic lesions may be more odiferous, due to
extensive lysis and darker in color due to longer
duration of the decay process.
• Soft consistency
HISTOPATHOLOGY
19
20. B. Zone of Bacterial Invasion
• Highest concentration of micro-organisms
• Dentinal tubules are extremely widened and
cavitated
• This layer may have a slightly greater dimension in
chronic than in acute decay
• Soft consistency, more soft in acute lesion.
HISTOPATHOLOGY
20
21. C. Zone of Demineralization
• Dentin is only demineralized, with the dentinal
matrix intact
• Dentinal tubules may have normal dimensions
• Dimension of this zone is greater in acute lesion
(1750 μm) than a chronic lesion (50 μm)
• Remineralization process is seen to accompany the
demineralization activity in this zone, less so
pronounced in acute decay
HISTOPATHOLOGY
21
22. • Color in acute decay is straw color, and for
chronic decay, the color is always yellow-
brown or dark brown depending upon the
time it has been subjected to microbial and
environmental staining.
• Consistency and hardness in acute decay is
much less than in chronic decay.
HISTOPATHOLOGY
22
23. D. Zone of Dentinal Sclerosis or Hypermineralization
• Appears transparent in ground section and opaque in
radiograph.
• Area of undisturbed mineralization repair
• Zone of dentinal sclerosis and calcific barrier, the two
most impermeable types of dentin
• More pronounced in chronic decay
• Extremely hard when compared with normal dentin
(15 times harder) and more so in chronic lesions.
HISTOPATHOLOGY
23
24. E. Zone of fatty degeneration
• Intra tubular fatty degeneration with lipid deposits
being precipitated from fatty degeneration of the
peripheral odontoblastic processes
• This degeneration predisposes to the sclerosis of the
dentinal tubules
• More pronounced in acute lesions and will appear
radiolucent in radiograph
• The chronic or acute status of a lesion can be changed
if there is a change in the environment i.e . presence
of bacterial substrates
HISTOPATHOLOGY
24
26. EFFECTIVE DEPTH
& PULPAL RESPONSE
• The effective depth is the area of minimum thickness
of sound dentin separating the pulpal tissue from the
carious lesion.
• If remaining dentin thickness is more than 1.0mm, no
significant disturbance in the pulp is seen. 0.25 to 0.5
mm remaining dentin leads to maximal reparative
dentin formation and remineralization of
demineralized dentin, whereas 0.25 mm or less
remaining dentin provokes bacterial growth in pulp.
• Reparative dentin formation and remineralization is
greatly decreased.
26
28. PROGNOSIS OF DEEP CARIOUS LESIONS
The outcome of the treatment of a deep carious lesion
depends on various factors:
1. Reparative capacity of pulpo-dentinal complex
2. Soundness of the dentin in the preparation floors and
walls
3. Reparative capacity of unsound affected dentin
4. Type and extent of any degeneration in the
pulpodentinal complex
5. Sealability of the restorative materials to be used
28
29. 6. Potential further irritation to the pulpo-dentinal
complex resulting from preparation instrumentation,
restorative materials and procedures
29
31. REPARABILITY OF
P-D COMPLEX
• The reparative capacity of pulpo- dentinal complex is
the main agent determining the fate of a carious
lesion advancing into dentin. It is further dependent
on various factors.
I. Status of Pulp
1. Pain:
• Pain could serve as a tool to assess the pulpal
status. The absence of toothache cannot be used as
a deciding criterion for the pulpal health.
• The presence or absence of pain varies with
different pathological conditions of pulp.
31
32. • Spontaneous pain not initiated by thermal/ chemical
stimulation - indicative of pulpodentinal
degeneration.
• Pain initiated by thermal/ chemical stimulation of
pulpo-dentinal organ that disappears immediately
after the removal of the stimulation is a possible
indication of much lesser degree of degenerative
changes.
32
33. 2. Radiographs: A radiograph can indicate:
a. Proximity of the carious lesion to the pulp chamber and
root canal system.
b. The effective depth or the thickness of the dentin bridge
can be evaluated.
c. Any pulpal changes in the form of intrapulpal and
peripulpal calcification (it denotes the consumption of
and reduction of the reparative capacity of the pulp; as
it reduces/prevents the flow of fluids into or out of the
pulp/ root canal system).
33
34. d. Periradicular status- the thickening of the periodontal
ligament with an intact lamina-dura, especially
periapically will indicate increased vascularity and
consequently increased reparative capacity. Discontinuity
in lamina dura indicates degeneration.
e. Size of pulp chamber compared to size of tooth the
higher the pulp size/tooth ratio, the better will be the
reparative capabilities of the pulpodentinal organ (It
must be mentioned that unusually high ratio in
comparison to other teeth may indicate complete
cessation of reparative capacity).
34
35. f. Size of pulp exposure - Size of pulp exposure in
relation to pulp chamber/ root canal system is a
major factor determining the reparability via
dentinal bridging.
g. Permeability of dentin or evaluation of
mineralization - Sclerotic dentin and calcific barrier
can be identified radiologically as radioopaque
regions. Tertiary dentin, appears as a localized
thickening of the dentinal bridge, pulpal to lesion
creating irregularities in the pulp chamber.
35
36. 3. Pulp testing
a. Thermal pulp testing Application of heat or cold stimulates
the nerves present in the pulp to elicit the symptoms of
pain. The character of this pain, helps in arriving at a
primitive diagnosis regarding the condition of the pulp.
b. Electric pulp testing The objective of electric pulp testing is
to stimulate a response by electric excitation of the neural
elements within the pulp by subjecting the tooth to an
increase degree of electric current.
• Positive response - indicates vitality of pulp
• No response - pulp necrosis
36
37. II. Extent of Pulpal Exposure
1. Pin point exposure; sound dentin at periphery, no
haemorrhage, vital pulp, no pulpal inflammation or mild
inflammation restricted to exposure site - successful
repair possible.
2. Exposure having infected dentin at periphery -
reparability doubtful.
3. Exposure with profuse haemorrhage - beyond repair
4. Exposure with inflammatory fluid/pus - beyond repair
5. Exposure near to the anatomical constrictions in root
canals - lesser will be the reparability locally because of
the diminished availability of nutrients.
37
38. Ill. Type of Dentin
• The type of dentin is assessed visually and also using
tactile methods.
• Presence of a calcific barrier/ sclerotic dentin
indicates formation of reparative dentin.
• Generalized discolored dentin ranging from grayish to
grayish-brown may indicate necrosis of underlying
pulp.
38
39. Caries Indicator Dyes
Caries Indicator Dyes
• Various types of dyes are used to indicate the extent
of progress of caries.
• 0.5% basic fuschin in propylene glycol applied to
dentin for 10 seconds and washing it off with water
may guide an operator as to where to stop in
excavating dentin from cavity walls and floors.
• It is the nature of collagen fibers that differ in
infected and affected dentin that accounts for the
different stainability of the two.
39
40. • The affected dentin will have intact collagen fibers
oriented for remineralization and will not stain with
dye.
• The infected dentin or the irreparable damaged
collagen, stains red. 1 % acid solution in propylene
glycol can also be used.
40
44. 1. Indirect Pulp Capping/Indirect Pulp Treatment
• Indirect pulp capping implies treating pulps, which are
near exposure; whereas indirect pulp treatment is a
technique in which an effort is made to avoid
exposure during the treatment of teeth with deep
carious lesions without any evidence of pulpal
degeneration or periapical pathology.
• Indirect pulp capping is a two appointment procedure,
whereas indirect pulp treatment is a single
appointment procedure
TREATMENT MODALITIES
44
45. Indications
• Deep carious lesion with minimal pulpal
inflammation.
• Where complete removal of caries may lead to pulp
exposure.
Contraindications
• A tooth with existing pulp inflammation
• A tooth with periapical pathosis
TREATMENT MODALITIES
45
47. Rationale
• In a carious lesion, dentin decalcification precedes
bacterial invasion within dentin.
• In an active carious lesion, two distinct layers are seen:
i. Infected dentin: It is necrotic, soft dentin, not painful to
stimulation and grossly infected with bacteria. Collagen is
irreversibly denatured.
ii. Affected dentin: It is demineralized, discolored but hard
dentin, painful to stimulation containing very few
bacteria. It is reversibly denatured and capable of being
remineralized
47
49. • When outer layer is removed, most of the bacteria
are removed and the substrate on which they thrive
is also removed.
• When cavity is sealed with a suitable material, any
remaining bacteria are either killed or lie in a stage of
dormancy.
• However affected dentin can be left on pulpal and
axial walls and never on dentinoenamel junction and
cavity margins.
TREATMENT MODALITIES
49
50. • The two layers can be differentiated with
either 0.5% basic fuschin or 1.0% acid red
dyes.
• Acid red is preferred since basic fuschin has
carcinogenic potential.
TREATMENT MODALITIES
50
51. Technique
• The technique involves the
following steps:
Removal of Caries
1. Mechanical Method
• Soft caries can be removed with
a spoon excavator by removing
flakes of carious dentin in
layers.
51
52. • The discolored dentin can be removed
with large round steel bur revolving at
slow speed.
• Pulp damage may result from reaction of
frictional heat with the use of bur while
excessive pressure with a spoon
excavator may force the micro
organisms into the dentinal tubules or
expose the pulp.
• Removal of infected dentin should
continue until the remaining dentin feels
as hard as normal dentin.
TREATMENT MODALITIES
52
53. 2. Chemomechanical Methods
• It is the chemical softening of carious dentin followed
by gentle excavation.
• It is especially indicated in deciduous teeth, dental
phobics and medically compromised patients.
Carisolv and Caridex are the two agents available
which soften the carious dentin.
TREATMENT MODALITIES
53
54. Two-appointment Technique
1st Sitting
• Local anaesthesia is administered and the tooth is
isolated with a rubber dam.
• Cavity outline is established with a high-speed
handpiece.
• Peripheral carious dentin/infected dentin should be
removed with sharp spoon excavators; however,
Cohen recommends the use of a large round bur for
better results.
TREATMENT MODALITIES
54
55. • Cavity should be irrigated and dried with cotton
followed by placement of hard setting calcium hydroxide
over the remaining affected dentin.
TREATMENT MODALITIES
55
56. • The remainder of the cavity is filled with reinforced
zinc oxide eugenol cement or a GIC to achieve a good
seal .
56
57. • This seal should not be disturbed for 6-8 weeks, as
the carious process in the deeper layer gets arrested.
Ilnd Sitting, (6-8 weeks later)
• In the second sitting, carefully all temporary filling
material, especially the Calcium hydroxide dressing
over the deep portions of the cavity floor is removed.
• The color changes from deep red rose to light gray/
light brown.
• The texture would change from spongy to hard and
caries appear to be dehydrated.
TREATMENT MODALITIES
57
58. • Thus, the remaining affected carious
dentin appearing dehydrated and
"flaky" should be removed.
• Do not disturb predentin, which is
the area around the potential
exposure appearing whitish and may
be soft.
• The cavity preparation should be
restored in the similar way as 1st
sitting.
TREATMENT MODALITIES
58
59. Re-enter or Not?
• The re-entry restorative procedure is still questionable.
• It is recommended only if the tooth is asymptomatic,
surrounding soft tissues are free from swelling,
temporary filling is intact, bitewing radiographs of the
treated tooth showing the presence of reparative
dentin.
• Research has shown that carious dentin will
remineralize within the restoration.
• If patient is asymptomatic on recall, the restoration
should be redone.
TREATMENT MODALITIES
59
60. • With re-entry there should be a risk of creating pulp
exposure and further insult to the pulp.
• If a pulp exposure occurs during re-entry, a more
invasive vital pulp therapy techniques such as direct
pulp capping or pulpotomy would be indicated.
TREATMENT MODALITIES
60
61. One Appointment Technique
• Indirect pulp capping is now termed as indirect pulp
treatment.
• The selection for one-appointment indirect pulp
treatment must be based on clinical judgement and
experience with many cases.
• In recent years, rather than complete caries removal in
two appointments, the focus has been to excavate caries
as close as possible to the pulp, i.e. some caries be left in
the tooth to avoid an exposure, placement of a protective
liner, and restoring the tooth without a subsequent re-
entry to remove any remaining caries.
TREATMENT MODALITIES
61
63. • More recently, the step-wise excavation of deep
caries has been revisited and shown to be
successfully in managing reversible pulpitis without
pulpal perforation and/ or endodontic therapy.
• This approach involves a 2-step process.
a. The first step is the removal of carious dentin along
the DEJ and excavation of only the outermost
infected dentin, leaving a carious mass over the pulp.
TREATMENT MODALITIES
63
64. • The objective is to change the cariogenic environment
in order to decrease the number of bacteria, close the
remaining caries from the biofilm of the oral cavity,
and slow or arrest the caries development.
• This allows time for P-D complex reactions to take
place so that at the second excavation visit, there is
less likelyhood of pulpal exposure.
• It is also suggested that changing the cavity
environment from an active lesion into the condition
of a slowly progressing lesion, a more regular and
tubular tertiary dentin formation occurs.
TREATMENT MODALITIES
64
65. B. The second step is the removal of the remaining caries and
placement of a final restoration.
• The most common recommendation for the interval between
steps is 3-6 months, allowing sufficient time for the formation
of tertiary dentin and a definitive pulpal diagnosis.
• Critical to both steps of excavation is the placement of a well-
sealed restoration.
• Since the research available is inconclusive on which approach
is the most successful over time.
• The decision to use a one appointment caries excavation or a
step-wise technique should be based on the individual patient
circumstances.
TREATMENT MODALITIES
65
67. • Direct pulp capping implies treating exposed pulps.
• Exposure caused by trauma or by operators' fault
during tooth preparation can be successfully treated;
whereas, exposure caused by caries usually need
root canal treatment.
• The younger the patient, the better are the chances
of healing and repair.
67
TREATMENT MODALITIES
68. Indications
• Size of exposure should be less than 0.5 mm
• No profuse haemorrhage or serous/purulent
exudates
• In case of trauma, it is not more than few hours old
• Non tender to percussion (a recently traumatized
tooth may be reversibly tender to percussion).
68
TREATMENT MODALITIES
69. Contraindications
• Instrument has not penetrated the pulp, since
infected dentin chips may settle in the pulp
• Tooth should not be periodontally involved
• Symptoms of irreversible pulpitis
69
TREATMENT MODALITIES
70. Ideal Requirements of Pulp Capping Material
• Stimulate reparative dentin formation
• Maintain pulp vitality
• Bactericidal/Bacteriostatic
• Release fluoride to prevent secondary caries
• Adhere to dentin/ restorative material
• Resist forces during restoration placement
• Provide appropriate seal
• Radiopaque
70
TREATMENT MODALITIES
71. Technique
• Tooth is isolated with rubber dam.
• Caries, if present, are removed from side walls using
spoon excavators .
71
72. • The exposed pulp is not allowed to dry.
• The exposed site is washed with weak
disinfectant and covered with a moist cotton
pellet dipped in disinfectant solution.
• Bleeding is controlled with 5% sodium
hypochlorite.
• After controlling bleeding, pulp capping
material is placed .
• It is placed with little pressure because
displacement of capping material/ dentin chips
into the pulp may lead to further pulpal
damage.
72
73. • It is followed by a restoration that seals the tooth
from microleakage .
• It is established that bacterial leakage is responsible
for pulpal response rather than toxicity of materials
which results in only mild and transitory pulpal
response.
73
74. Hypersensitivity to temperature change may persist
for a day or so.
• Tooth is tested periodically for pulp vitality.
• Symptoms usually subside in 4-6 weeks.
• If tooth remains vital, a permanent restoration may
be placed.
• If tooth becomes painful, or exhibits decreased
reading on vitality testing or becomes non vital, root
canal treatment becomes mandatory.
74
75. Materials used
a. Calcium hydroxide
b. Mineral trioxide aggregate (MTA)
c. Bonding agents
d. Resin-resorcinol
75
76. a. Calcium Hydroxide
• Herman (1930) demonstrated that when vital pulps
were covered with calcium hydroxide, it led to the
formation of secondary dentin.
• When calcium hydroxide is applied directly to pulp
tissue, coagulation necrosis of adjacent tissues occur.
• Beneath the region of coagulation necorsis, cells of
underlying pulp differentiate into odontoblasts and
other cells, which help forming dentin matrix.
76
77. • However a blood clot should not be left between
calcium hydroxide and pulp. In these cases, hydroxyl
ions trapped in the clot do not allow differentiation of
odontoblasts.
b. Mineral Trioxide Aggregate (MTA)
• It is modified Portland cement.
• It is of following three types:
• Gray • White • Modified
77
78. Properties
• Setting time: sets within 24 hours
• Compressive strength: 70 MPa after one day
• pH of the set MTA: 11-13 after setting
• Biocompatible and non-mutagenic
• Antibacterial effect is similar to calcium hydroxide
78
79. Manipulation
• MTA powder is mixed with sterile water at a ratio of
3:1 on a glass slab or paper pad a plastic/metal
spatula.
• It is placed over exposure site using plastic/ metal
spatula.
• The chamber is filled with flowable composite and
other interim restorative materials.
• MTA is a difficult material to handle. Once it starts to
dry it looses its cohesiveness and becomes hard to
handle.
79
80. • When compared with calcium hydroxide, MTA
produces more dentinal bridging in a short period of
time with significantly less inflammation.
• It resists microleakage better than calcium hydroxide.
• Presence of blood has little impact on leakage of MTA
80
81. C. Bonding Agents
• It is established that healing is directly related to
capacity of pulp capping agent to provide a biological
seal against immediate and long term micorleakage.
• Adhesive bonding agents have been tried as pulp
capping agent. They provide immediate seal.
• However, when adhesive agents were compared with
calcium hydroxide, they showed more pulp necrosis.
• Direct bonding agents are not preferred as these can
lead to inflammatory reaction, delay in pulpal healing
and failure of dentin bridge formation.
81
82. d. Resin-resorcinol
• Resin-resorcinol has also been successfully tried as pulp
capping material.
• The exposure site is washed immediately with normal
saline solution and isolated with sterilized cotton rolls.
• The exposure site and the rest of the cavity is wiped
with cresophene.
• Two drops of freshly prepared resinifying solution is
poured over the exposure site and allowed to set.
82
83. • The rest of the cavity is filled with zinc phosphate
cement or any other restorative material.
• The effectiveness of resinifying agent as pulp capping
material has been histologically proved.
• Histological sections revealed areas of fibrosis and
hyalinization in the pulp in the coronal area;
83
84. 4. Atraumatic Restorative Treatment (ART)
• This is considered as one form of indirect pulp
treatment.
• The procedure is based on excavating and removing
caries using hand instruments only and then
restoring the tooth with an adhesive filling material.
• The materials used for pulp protection are: • Calcium
hydroxide • Zinc oxide eugenol • Glass-ionomer
cement • Cyanoacrylates • Thymol • Polycarboxylate
cements • Tricalcium phosphate • Resin resorcinol
84
85. • All these materials lead to the formation of
reparative dentin and decrease the dentin
permeability
85
86. 5. Pulp Curettage
• It is well documented that pulp exposure due to
caries usually lead to pulp necrosis with passage of
time.
• During caries removal, carious dentin chips may be
inadvertently pushed into pulp tissue resulting in
inflammation, resorption and encapsulation of
dentin chips which after capping may show foreign
body reaction.
86
87. • It is suggested to remove superficial layer of pulp
tissue by enlargement of the exposure site.
• This procedure is known as 'Pulp curettage'.
• It is followed by control of haemorrhage, placement
of a pulp capping material and sealing of the cavity as
in direct pulp capping.
87
88. Advantages
• It preserves cell zone due to minimal excision, hence
chances of better healing.
• Physiologic apposition of dentin is maintained.
• Natural color/translucency of tooth is maintained.
• Less chance of root canal obliteration.
88
89. 6. Partial Pulpotomy
• It is the removal of only outer layer of damaged
hyperemic tissues in exposed pulps.
• If 2.0 - 3.0 mm of pulp is removed it is called partial
pulpotomy.
• Rationale Based on the rationale that following
surgical amputation of the affected or infected pulp
tissue at the exposure site, the remaining tissue is
capable of healing.
89
90. Indications
• A small and recent pulpal exposure of upto
approximately 14 days in a non-carious primary
incisor
• Highly indicated in a very young tooth with a
wideopen apex and very thin root dentin walls
• Only if sufficient tooth structure is present to allow
proper restoration and full coverage of the crown
with a bonded resin-composite strip crown.
90
91. Contraindications
• If the exposure is very large or when more than two
weeks have passed between injury and treatment
time allowing oral contaminants to cause extension
infection or inflammation beyond 2.0 to 3.0 mm of
the exposure.
91
92. Advantages
• This procedure is quick and easy to perform
• It maintains the natural tooth color and preserves
the tooth structure for better retention of
restoration.
• It is advantageous over complete pulpotomy in the
preservation of cell-rich coronal pulp tissue.
• Its successful outcome will allow the continuation of
normal development of the tooth, including further
root development and maturation.
92
93. 7. Partial Pulpotomy After Carious
Exposures
Indications
• In a young permanent tooth for a
carious pulp exposure in which the
pulpal bleeding can be controlled within
several minutes. The tooth must be
vital, with a diagnosis of normal pulp or
reversible pulpitis.
93
94. Procedure
• In this procedure, the inflamed pulp
beneath an exposure is removed to a
depth of 1.0 to 3.0 mm or deeper to
reach healthy pulp tissue .
• Pulp al bleeding is controlled by
irrigation with a bactericidal agent
such as sodium hypochlorite or
chlorhexidine. Later, the site is
covered with calcium hydroxide or
MTA.
94
95. Calcium Hydroxide
• A dressing of calcium hydroxide
paste should be placed followed by
a base-liner of glass-ionomer .
• The tooth is restored using a
bonded resin-composite strip
crown.
• Scheduled follow-ups should be
made after 1 month, 3 months, and
then every 6 months.
95
96. • A dentin bridge will begin to form, separating the
exposure site from the rest of the pulp.
• The bridge may be evidenced radiographically after 6
to 8 weeks.
96
97. MTA
• After haemorrhage control, MTA is
paced over the pulp stump.
• A thin layer of flowable composite is
placed over it and light cured.
• The tooth is then sealed with etched
bonded composite restoration.
• While calcium hydroxide has been
demonstrated to have long-term
success, MTA has shown more
predictable dentin bridging and pulp
health
97
98. CONCLUSION
• In view of the direct relationship between caries
depth and pulpal pathosis, early excavation of what
might appear to be superficial caries in the dentin is
advocated as sound preventive treatment to
minimize pulpal exposure.
• If pulpal exposure discovered at the time of the early
caries excavation could be routinely treated with
consistently good results, a major problem in
dentistry would be solved; thus care must be taken
to prevent pulp exposure during the removal of deep
caries.
98
99. REFERENCES
• John I. Ingle, DDS, MSD Endodontics fifth edition.
• M.A. Marzouk, A.L.Simonton, R.D. Gross Modern
theory and practice operative dentistry.
• Baum Phillips lund text book of operative
dentistry third edition.
• Vimal K Sikri MDS ,Textbook of Operative
Dentistry 4th edition
99
