This document summarizes pulpal reactions to various restorative materials and dental procedures. It discusses how microbial, physical, and chemical irritants can damage the pulp, including through dental caries, operative procedures, trauma, and restorative materials. It also describes the pulp's defensive reactions like formation of reactionary dentin, reparative dentin, and inflammation. Treatment options for vital pulp like indirect pulp capping, direct pulp capping, and medicaments are outlined, with calcium hydroxide and mineral trioxide aggregate highlighted as common capping materials that stimulate hard tissue formation.

1. PULPAL REACTIONS TO
VARIOUS RESTORATIVE
MATERIALS
Dr. SV.SATISH
Professor & HOD
Dept of Conservative Dentistry & Endodontics
Navodaya Dental College

3. Introduction
⚫There are several noxious stimuli
responsible for pulp
damage, inflammation and
necrosis, these stimuli can be
summarized into the following:
⚫Microbial.
⚫Physical.
⚫Chemical.

4. Microbial Irritants:
⚫Coronal Ingress
 Dental caries
 Crown fracture
⚫Radicular ingress
 Root caries
 Retrograde infection

5. Coronal Ingress
⚫ Dental caries:
The main cause of pulp injury in which carious
dentin and enamel contains numerous
amount of bacteria, recently it has been
shown that deep carious dentin contains
predominantly anaerobic bacteria.
⚫ Crown fracture:
Complete crown fracture seldom devitalizes the
pulp immediately however pulp death is the
result of bacterial ingress through the fracture
the same can be said about incomplete
fracture ( infraction).

6. Radicular ingress
⚫ Root caries:
Is less frequent than coronal caries, these type of lesions
which can occur bucco-gingivally or inter-proximally are the
result of poor oral hygiene accompanied with periodontal
problems.
⚫ Retrograde infection:
Periodontal pocket, is not frequently a cause of pulp damage
unless there is involvement of the apical foremen or the
accessory canals.
Periodontal abscess, pulp infection, either immediately
following or during an acute periodontal abscess is also an
infrequent cause of pulp necrosis.
Hematogenic infection, in which the bacteria gain access to the

7. Physical or Mechanical
irritants:
⚫Operative procedures
⚫Trauma
⚫Orthodontic movement
⚫Deep periodontal curettage

8. Operative procedures
If proper operative procedures are not
taken during cavity preparation the
adjacent odontoblast will be damaged
leading finally to pulp infection, this
damage can result from the following :
⚫Heat generation.
⚫Cavity depth.
⚫ Pulp exposure.
⚫Pin insertion.

9. Trauma
⚫ Acute trauma:
Fractures ( Coronal or Radicular ):
Coronal fracture expose the dentinal tubules to bacterial
invasion which if untreated leads pulpal inflammation.
Radicular fracture is associated with disruption of the vascular
supply to the pulp which results in its calcification or death.
Luxation , the most common type of dental trauma in which the
tooth is displaced rather than completely coming out of it
socket in such case the condition is known as ( avulsion ).
With these types of trauma the integrity of the pulp tissues
depends on the integrity of the blood vessels supplying the
pulp.

10. Trauma
⚫Chronic trauma:
Bruxism , the increased severity of the
trauma may eventually cause pulpal
necrosis.
Attrition, incisal wear rarely causes
pulpal inflammation because the
reparative power of the pulp usually
overcome this chronic stimuli.

11. Orthodontic movement
Deep periodontal curettage
⚫Orthodontic movement, can lead to
devitalization of the pulp and pulpal
hemorrhage.
⚫Deep periodontal curettage, leads to
damaging the pulpal vessels, so it
should be done after R.C.T.

12. Chemical irritants:
⚫Dental materials
⚫Antibacterial agents

13. Dental materials
⚫ Final restorations:-
Composite resin, has been regarded as irritant to
the pulp in which it is important to place a
suitable base material in order to minimize the
irritation.
Amalgam, some of its content showed pronounced
cytotoxic effects.
Cements: some cement materials has potential
irritation to the pulp tissues.
Etching agents, if placed over 15 second in dentin
can cause chronic inflammation of the pulp.

14. Antibacterial agents
Antibacterial agents as silver
nitrate, phenol and eugenol which
was used to sterilize the cavity
preparation have shown cytotoxic
effects and causes inflammatory
changes.

16. RESPONSE DEFENSE
REACTIONS OF PULP
Depends on:
⚫Rate of caries attack: Small or slowly
progressing lesion forms more reactionary
dentin than large or rapidly progressing
lesion.
⚫Pulp Vitality: If the pulp supply is poor the
reactionary dentin is not formed for these
reason the young teeth may form
reactionary dentin more readily than old
teeth.

17. RESPONSE DEFENSE
REACTIONS OF PULP
I. TUBULAR SCLEROSIS
II. TERTIARY DENTIN FORMATION
III. PUP IMFLAMMATION

18. TUBULAR SCLEROSIS
REACTIONARY DENTIN:
⚫ If the injury to the tooth is mild and primary
odontoblast survive, they are stimulated to synthesize
reactionary dentin, which resembles primary dentin
matrix and has a tubular pattern.
⚫ It is a process in which mineral is deposited within the
dentinal tubules, reducing the permeability of the
dentine and making it impermeable to bacteria and
toxic products.
Intratubular dentin is the result of odontoblast activity.
⚫ In case of dental caries, some of the dissolved
mineral salts are reprecipitated within the subjacent

19. TERTIARY DENTIN -
REPARATIVE DENTIN:
⚫ As a response to various external stimuli, such as dental
caries, attrition and trauma, tertiary dentin is synthesized.
⚫ It is a layer of dentin formed at the interface between dentin
and pulp, and its distribution is limited to the area beneath the
stimulus.
⚫ Tertiary dentin provides extra protection for odontoblast and
other cells of the pulp by increasing the distance between
them and the injurious stimulus.
⚫ Is usually shiny and more darkly colored, but feels hard to the
explorer tip (more mineral content) and often can be seen
radiographically in the form of a more radiopaque (lighter)
area.

20. TERTIARY DENTIN -
REPARATIVE DENTIN:
⚫ If the injury is severe and causes odontoblast cell
death, odontoblast-like cells synthesize specific
reparative dentin just the beneath the site of
injury to protect pulp tissue.
⚫ The morphology of the reparative dentin varies
greatly, and is often irregular, with cellular
inclusions.
⚫ The tubular pattern of the reparative dentin
varies from a discontinuous to an atubular
nature, and thus the reparative dentin matrix
permeability is reduced and diffusion of noxious
agents from the tubules is prevented.

21. PULP INFLAMMATION:
⚫ The first inflammatory reactions within the pulp occurs
when caries from an enamel lesion invades the dentin.
⚫ Neutrophils, granulocytes, lymphocytes, and
macrophages are seen in the odontoblastic layer.
⚫ The enzymes released by damaged granulocytes and
macrophages cause necrosis of the endothelial cells
and this results in increased vascular permeability and
extracellular edema.
⚫ PAIN, If the treatment is performed at this
stage, the pulp inflammation is reversible.

22. TREATMENT OF TEETH WITH
VITAL PULP
⚫Vital pulp therapy is recommended in
teeth without evidence of sever of
irreversible pulpal inflammation.
MODALITIES
⚫Caries Control
⚫ Pulp Capping: Indirect or Direct.

23. INDIRECT PULP CAPPING
⚫IPC is employed in the management
of deep carious lesion in which the
removal of all carious dentin would
probably result in pulp exposure.

24. INDICATIONS OF INDIRECT
PULP CAPPING
⚫ NO HISTORY OF SEVERE OR SPONTANEUS PAIN.
⚫ ABSENCE OF PAIN ON MASTICATION.
⚫ NORMAL PULP TEST INCLUDING ELECTRIC PULP TEST
AND THERMAL VITALLY TEST.
⚫ NO PAIN TO PERCUSSION OR PALPATION.
⚫ NO EVIDENCE OF PERIAPICAL PATHOLOGY.
⚫ ABSENCE OF INTERNAL RESORPTION.
⚫ MINIMUM OPERATIVE INSULT TO THE PULP.

25. INDIRECT PULP CAPPING
TECHNIQUE:
⚫Cavity preparation (removal of gross caries
of lateral walls of this cavity which rotary
instruments before final removal of caries at
the cavity base).
⚫ Final removal of carious dentine in the floor
using a large round bur at slow speed.
⚫Apply the calcium hydroxide in the
dentine, near to the pulp and over it must be
aplied polycarboxilate cement or zinc
phosphate as base and the final restoration.

26. DIRECT PULP CAPPING:
⚫ The aim is to stimulate the pulp tissue to close
the exposure by hard tissue formation without
inflammatory changes in the residual pulp.
⚫ THERE ARE TWO INDICATIONS FOR DIRECT
PULP CAPPING:
⚫ DENTAL TRAUMA
⚫ ACCIDENTAL DURING MECHANICAL
PROCEDURES: CAVITY PREPARATION OR
OTHER RESTORATIVE PROCEDURE SUCH
AS THE PLACEMENT OF PINS.

27. CONTRAINDICATIONS OF
DIRECT PULP CAPPING:
1. Superficially necrotic teeth (absence of bleeding at
exposure site ).
2. Severely broken down teeth cannot be adequately
restore.
3. Exposed pulp by caries.
4. Severely inflamed pulp (spontaneous, throbbing pain)
5. Exposure with purulent exudates.
6. Rdiographical changes

28. DIRECT PULP CAPPING
TECHNIQUE
⚫ Complete removal of all caries from the dentinal
walls before final removal of caries at the cavity
base.
⚫ If the risk of exposure is anticipated, rubber dam is
applied.
⚫ The exposed pulp should be rinse by 0.1% solution
of chlorhexidine, normal saline or anesthetic
solution.
⚫ Bleeding at the exposure site is arrested by
pressure with a plain sterile gauze or cotton pellet
moistened with epinephrine.

29. DIRECT PULP CAPPING
TECHNIQUE
⚫ The pulp wound is covered with a calcium
hydroxide powder, calcium hydroxide powder
mixed with sterile water to a creamy consistency
or calcium hydroxide supplied in preloaded
syringes, the dressing is covered by a hard
setting calcium hydroxide cement and over it is
setting phosphate or polycarboxilate cement.
⚫ In order to minimize the risk of microleakage a
final restoration should be made.
⚫ Otherwise a strong cement may be inserted as
temporary filling.

30. The outcome of Direct Pulp
Capping
depends on:
⚫Residue of caries in the cavity.
⚫Age of the patient.
⚫Size and location of the exposure.
⚫Capping material employed.

31. CONTROL OF TREATMENT
⚫ Bridge formation (radiography).
⚫ Pain: absent or present
(spontaneous, kind, duration)
⚫ Reactions to thermal stimulus: absent, short
or prolonged.
⚫ Sensitivity to electrical test: positive or
negative.
⚫ Periapical changes.

32. MEDICAMENTS:
⚫ SEVERAL DRUGS HAVE BEEN USED
WITH VARYING DEGREES OF SUCCESS
FOR PULP CAPPING AND PULPOTOMY
PROCEDURES.
⚫ These include calcium hydroxide, zinc oxide-
eugenol, formaldehyde, steroids, antibiotic
paste, glutardehyde, tricalcium
phosphate, collagen preparation, acid and
alkaline phosphates, chondoitrin
sulphate, and polycarboxylate cement.
⚫ Mineral trioxide aggregate

33. ZINC OXIDE AND EUGENOL:
⚫Eugenol is the most active ingredient in
ZOE and it has been demonstrated that
exhibit tissue toxicity. Near to the pulp
ZOE causes chronic inflammation an
eventual necrosis of the pulp tissue.
⚫Its efficacy in vital pulp therapy is primary
as sedative, secondary is antibacterial.
⚫Reparative dentine formation

34. CALCIUM HYDROXIDE MODE
OF ACTION:
⚫ STIMULATION OF VITAL CELLS: Induces hard tissue formation
by stimulating vital pulp tissue and undifferentiated mesenchymal
cells in the pulp and periodontal ligament. These are then capable
of active mitosis and undergo differentiation into blastic cells
⚫ SOURCE OF CALCIUM ION:Acts as a source of calcium to hard
tissue formation.
⚫ ALKALINE PH: Its high ph is believed to be essential for hard
tissue induction. It creates an environment in the tissue that
neutralizes inflammatory reactions which requires an acidic ph.
The high ph has also neutralized osteoclastic enzyme activity
⚫ ANTIBACTERIAL AGENT: It is an effective antibacterial agent due
to its high ph.
⚫ ENZIMATIC EFFECTS: Calcium hydroxide also activates alkaline
phosphate activity, which is essential for hard tissue deposition..

35. PULP RESPONSE TO
CALCIUM HYDROXIDE
⚫ When calcium hydroxide is applied on the surface of the pulp
occurs a superficial coagulation necrosis which is
characterized by infiltration of leukocytes and macrophages.
⚫ The area below the zone of coagulation necrosis becomes
saturated with calcium ions and after some days the repairing
process starts by collagen formation, which is produced by
undifferentiated pulp cells and fibroblasts.
⚫ Mineralization occurs at the junction of the necrotic tissue
and the remaining vital tissue.
⚫ Gradually the mineralized tissue becomes more dentin like
with structures resembling dentinal tubules
⚫ DENTINE BRIDGE FORMATION