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1. PULPAL RESPONSE TO VARIOUS DENTAL
PROCEDURES & RESTORATIVE
MATERIALS
Dr.V.NAGARAJAN

2. CONTENTS
INTRODUCTION
DENTAL PULP : STRUCTURAL ORGANISATION
 PULP DENTIN ORGAN
 STAGES OF PULPAL INFLAMATION
PULPAL RESPONSE TO
 DENTAL PROCEDURES
RESTORATIVE DENTAL MATERIALS
DO’S AND DONT’S
 CONCLUSION

3. Pulp, a specialized connective tissue, is very sensitive to external stimuli.
 In addition to the dental procedures that threaten the integrity of the
pulp, injury may also result from irritation by a noxious agent brought into
contact with the exposed dentin or the pulpal tissue.
The reaction of the pulp, most of the times, is physiologic; however,
depending upon the intensity of the stimulus pathological changes do occur
in pulp.
INTRODUCTION

4. Structural organisation of pulp
Odontoblast layer
Cell free zone
Cell rich zone
Pulpal core
Beneath the pre- dentiin
Has cell bodies in the pulp and cell
process in the dentinal tubules
Contains few cells,
Nervous plexus and blood vessels
Contains fibroblast ,
Undifferentiated mesenchymal cells
,defence cells, collagen fibers
Central region of pulp
Contains major nerves and blood
vessels and cells of pulp

5. The dentin and the pulp must be considered as one organ (the pulp-
dentin complex) because of the intimate relationship of these
structures :
1. Response of dentin to injury are largely functions of the odontoblasts and other
cells in the pulp
2. Normal form and function of one cannot be maintained without the other.
3.The embryonic dental papilla is responsible for the formation of this coupled tissue.
PULP-DENTIN ORGAN

6.  Dentinal fluid in the tubules, which is continuous with the extracellular fluid of
the pulp serves as a medium for relaying injurious agents to the pulp to induce an
inflammatory response. Thus anything that contacts the living dentin can be
carried into the pulp.
 Also, either positive hydrostatic pressure or negative osmotic pressure may
move the fluid in the dentinal tubules, which may displace the odontoblastic
process or nerve endings resulting in pain.
Hence the response of the pulp to any
restorative material will be influenced by its
surrounding dentin

7. PULPAL
INFLAMMATION
PULPAL INJURY
(ODONTOBLASTIC
SURVIVAL
/DEGENERATION)
PULPAL REPAIR
( TERTIARY
DENTIN
FORMATION)
TYPES OF PULPAL RESPONSES

8. The reaction of the pulp to external stimuli is reflected in two broad processes:
Inflammatory changes and secondary dentin formation.
Slight reaction recognizes the increased number of cells in the cell free zone and in
the adjacent pulpal tissue. These cells are similar to fibroblasts and undifferentiated
cells. However, few inflammatory cells are also observed. The increased number of
capillaries means blood flow is also increased to the affected dentinal tubules. The
irregularities in the odontoblastic layer are also observed
Moderate reaction is characterized by more cells around the injury site. The
mononuclear leucocytes and the neutrophils invade the odontoblast-predentin area.
Some odontoblastic nuclei can be seen in dentinal tubules. The number of capillaries
increased along with the blood flow. The occasional haemorrhage in odontoblastic or
subodontoblastic zone is also observed
STAGES OF PULPAL INFLAMATION

9. Severe reaction is characterized by marked cellular infiltration, including abscess
formation. The odontoblastic layer remains unidentified. This layer is either
destroyed or greatly disrupted. The predentin is not formed. Numerous blood
vessels are found in the tissues surrounding the cellular infiltration

10. B.. Remaining Dentin Thickness
As the length of tubule increases the concentration of the solute reaching the pulp
decreases..
It has been shown that a 0.5 mm thickness of dentin reduces the toxicity level of a
material to 75% and an 1.0 mm thickness over 90%.
Effective remaining dentin thickness of 2 mm provides an adequate insulating
barrier against almost all the techniques and restorative materials.( stanley et al)

11. Pulpal response to dental procedures
1.Local anaesthesia
2.Cavity /crown preparation
3.Etching the dentin /smear layer removal
4.Laser procedures
5.Ultrasonic scaling
6.Bleaching
7.Thermal sensibility testing
8.Polishing of restorations
9.Air abrasion
10.Orthodontic tooth movement and brackets
11. PIN PLACEMENT
12. Cleaning / drying the cavity

12. Local Anesthetics
Local anesthetics reduce pulpal blood flow by approximately
half when they contain vasoconstrictors. This effect is
almost due to the vasoconstrictor.
Significant reduction in
blood flow during
preparation
Significant accumalation
of irritant in the pulp
Use of vasoconstrictor
free local anaesthetics
For cavity /crown
preparation
procedures in vital
teeth

13.  Lidocaine (2%) ,1:100,000 or 1:80,000
epinephrine.
Reduce the blood flow
to the pulp
(vasoconstriction)
Enhance the duration
of anesthesia.
Supplemental techniques –
Severe reduction or even
transient cessation of blood
flow

14. Pulp temperature 11°C Destructive reaction
Pulpal temperature is critical and must not exceed normal
values in dental restorative procedures.
Clinical research has shown irreversible damage to pulp tissues
at levels of 60% at 5.5°C and 100% at 11°C..
Cavity / crown preparation
Cooking the pulp in its own juice – BODCCKER description about tooth
preparation without proper coolent

15. WITHOUT
THE USE OF
PROPER
COOLANT
VASCULAR
STASIS AND
THROMBOSIS

16. Excessive heat generation leads to change in
dentin color due to vascular stasis and hemorrage
in the subodontoblastic vascular
plexus present in the pulp - Dentinal blushing
Long term effects of crown preperation on
pulp vitality
Higher incidence of pulp necrosis
Full crown prep -13.3%
Partial veneer prep -5.5%
Unrestored control tooth – 0.5%

17. HEATPRODUCEDDURINGCUTTINGDEPENDS
ON…
SHARPNESS
OF THE BUR
AMOUNT OF
PRESSURE
EXERTED ON
THE BUR
LENGTH OF
TIME THE
CUTTING
INSTRUMENT
CONTACTING
TOOTH
STRUCTURE

18. SAFEST WAY TO PREPARE…
ULTRA-HIGH SPEEDS OF ROTATION (1,00,000 –
2,50,000 rpm)
EFFICIENT WATER-COOLING SYSTEM
LIGHT PRESSURE & INTERMITTENT CUTTING

19. SMEAR LAYER REMAINS ---- MICROLEAKAGE
SMEAR LAYER REMOVAL ----- INCREASES DENTIN PERMEABILITY
Some evidence indicates that etching, as a step in restoration,
may reduce microleakage.
Other evidences suggest that etching causes pulpal damage, when
the thickness of the remaining dentin is <300 μm (RDT).
Even when placed in deep cavities, acid etchants produce only a
small increase in hydrogen ion concentration in the pulp.
Etching dentin for 15 seconds in practice has no pulp effects but
protecting the pulp when the cavity is deep should be considered .
ACID ETCHING PROCEDURE/ SMEAR LAYER REMOVAL

20. Compressed air , drying agents - acetone or ether
Removal of fluid from the tubules by blast of air
Activates strong capillary forces
Causes rapid outward flow of dentinal fluid
Displacement of odontoblast (drawn into the tubules)
Undergoes autolysis and disappear
Cavities dried with
Cotton pellets and
soft blast of air
CAVITY CLENSING /DRYING

21. Pulp damage may result from pinhole preparation or pin
placement.Coolants do not reach the depth of the pin preparation.
During pinhole preparation, there is always the risk of pulp
exposure.
Furthermore, friction-locked pins often produce micro-fractures that
may extend to the pulp, subjecting the pulp to irritation and the
effects of microleakage.
The use of pins should be
discouraged and, with the
introduction of newer adhesive
materials, their use is no longer
necessary.
PIN PLACEMENT

22. LASER PROCEDURES
Different lasers with different energy levels may also be used .mainly
ER.YAG LASER.
1.Minimal thermal diffusion through tooth
structure
2.Water spray to aid in dispersing ablation
products and cooling of target tissue
3.Wavelength of Er.YAG laser (2094nm)
which falls close to absorption peak of water
.
Properpower setting
time of application
use of water spray

23. ULTRASONIC SCALING
The load of force with which the ultrasonic tip is held against the tooth has a much
greater effect (×4) on the heat generated in the dentin substrate than the power
setting.
In live dogs, ultrasonic scaling did not create heat-induced pulpal damage when
water coolant was used. Interestingly, histologic examination did reveal acute
pulpitis, but it was attributed to the vibratory effects of the ultrasonic device rather
than the temperature.
in vitro measurement of 36°C increase. When water coolant was used, all
measurements were below 4.2°C increase.
Proper water-cooling of both ultrasonic and sonic scalers will prevent excessive
heat production in the pulp.
---INGLE’S TEXT BOOK 7th edition

24. Overnight external bleaching of anterior teeth with 10% carbamide peroxide
causes mild pulpitis that is reversed within 2 weeks.
Heat-activated bleaching agents can cause intrapulpal temperatures to rise by
5–8°C when measured in vitro.
Both short-term and longterm (9–12 years) clinical observations on bleached
teeth reported no significant pulpal changes.
In vitro studies show that the principle bleaching agent, hydrogen peroxide,
can reach the pulp after application to the enamel. Whether this occurs in
vivo is unknown. Outward fluid flow in dentinal tubules and other factors
would reduce the effect.
VITAL TOOTH BLEACHING

25. THERMAL SENSIBILITY TESTING
Thermal sensibility testing utilizes media at temperatures that certainly have the
potential to damage tissues.
Heated gutta-percha reaches a temperature of ~200°C just before the smoke point,
and a cold-test substance such as carbon dioxide snow has an inherent temperature
of –78°C. A heattesting device such as the System B (SybronEndo, Orange, CA, USA)
with the appropriate tip is recommended to be set at a temperature of 200°C.
The question must be asked whether these extreme temperatures are transmitted to
the dental pulp during clinical testing and whether there is any likelihood that the
tissue may be damaged.
Rickoff et al.210 reported combined in vivo
and in vitro findings with no damage to pulp
tissue following use of flame-heated gutta-
percha and carbon dioxide snow.
therefore, safe to conclude that heat and cold testing within normal clinical
parameters will not damage the dental pulp.
In vivo histologic analysis revealed no
alteration from normal tissue appearance after
a 2-minute or a 5-minute

26. POLISHING OF RESTORATION
Polishing glass ionomer and composite restorations does not cause an increased
temperature at the pulp-dentin interface.
Polishing amalgam restorations, however, can produce temperatures that may be
damaging. With high contact pressure, high speed, and no coolant, in vitro
temperature increases of >20°C have been recorded within 30 seconds.
4,000 rpm was found to be safest working speed for finishing amalgam and
composite restorations in continuous pressure without coolent .as any speed of
6000 rpm and above without coolent gave rise in pulpal temperature to above
41.6⁰ c endangering the pulp.
With use of coolant, light pressure, and intermittent contact at 10,000 rpm during
polishing, there is a low likelihood of heat-generated pulp damage.

27. AIR ABRASION PROCEDURE
DURING CAVITY PREPARATION :
Higher pressure and lower particle size ( 160 psi-25ủm) – less pulpal effects
Lower pressures and larger particle size ( 80 psi – 50 ủm )
But reactions are reversible.

28. ORTHODONTIC TOOTH MOVEMENT AND BRACKETS
Orthodontic tooth movement of a routine nature does not cause clinically
significant changes in the dental pulp.
Putting more than the pressure required - increases the blood flow in the
pulp (hyperemia). A variety of growth factors are produced including vascular
endothelial growth factor (VEGF) that may explain this increase in vascularity.
The heavy forces used to reposition impacted canines frequently lead to
pulp necrosis or calcific metamorphosis.
Intrusion but not extrusion reduces pulpal blood flow for a few minutes as
the pressure is applied.
--Ingle’s text book seventh edition

29. A method of bracket removal is use of an electrothermal device (ETD) that
heat-softens the bonding composite expediting removal of the bracket.
Heat transferred from the ETD has been measured as high as 45.6°C on the
pulpal side of dentin in in vitro experiments, though most reports have been
in a lower range
there may be limited peripheral disruption of odontoblasts with slight
inflammation

30. Pulpal response to restorative materials
Restorative Materials and reactions
Zinc oxide eugenol
Zinc phosphate
Zinc polycarboxylate
Silicate cements
Silver amalgam
Glass ionomer cement
Composite resin
Calcium hydroxide, MTA, biodentin

31. MICROLEAKAGE
CYTOTOXICITY
HEAT UPON
SETTING
DESSICATION
BY
HYGROSCOPY

32. Mercury from amalgam restorations does not penetrate dentin, while zinc and
tin ions have been found in high concentrations in dentin beneath amalgam
restorations.
These metals do not appear to exert an effect on the pulp, although the
inflammation accompanying direct placement of amalgam over exposed pulps
was tentatively attributed to zinc toxicity
Other, generally short-lived pulpal effects of amalgam have been described.
neutrophils transiently migrate between the odontoblast layer and predentin;
this has been attributed to condensation pressures during amalgam
placement.
The high thermal conductivity of amalgam results in postoperative sensitivity
unless a liner or base is used
SILVER AMALGAM

33. Silicate cements, though widely used earlier, are rarely used these days.
Slicates in set form consist of glass particles covered with a layer of
alumino-silica gel and a matrix of amorphous insoluble phosphates and
fluoride
The pH of silicate cement at the time of insertion into the cavity is less than
3 and it remains below 7 even after 7 months. ( phosphoric acid)
Fluoride ion concentrations of 15–25 μgm/ ml are also known to reduce
cell growth.
Microleakage
Silicate cement

34. Eugenol liberated from zinc eugenolate can diffuse throughdentin and into the
saliva.
PH 6-8..
Calcium in the dentinal tubules chelates eugenol, limiting its ability to diffuse
through dentin.
Eugenol also binds with the organic matrix of dentin, especially collagen, which
slows the diffusion rate.
Toxic(High Dose) Beneficial (Low Dose)
• Induces cell death • Inhibits white cell chemotaxis
• Unknown vascular • Inhibits prostaglandins
changes
• Inhibits cell growth • Inhibits nerve activity
and respiration
ZINC OXIDE EUGENOL CEMENT

35. Zinc phosphate cement is irritating because of its low pH and the rapid
penetration of its lower molecular weight phosphoric acid into the dentinal
tubules and pulp tissues.
The hydraulic forces, which are induced during the seating of the restoration
or during functional movements phosphoric acid in large quantities is forced
into the dentinal tubules.
Since dentin can be penetrated by phosphoric acid to a depth of more than
1.0 mm - adequate insulation when less RDT
The initial pH of luting mixes ranged from 2.0–3.3, which changes to 3.0–4.2
after one hour.
such a low pH induced vascular thrombosis and necrosis in rodent pulp --
when the duration of exposure was prolonged over thin dentin.
Zinc phosphate

36. Polycarboxylate cements are a combination of aqueous polyacrylic acid and zinc
oxide. excellent biocompatibility equivalent to zinc oxide eugenol cements.
Initial PH 1.7. The pH of the mix rises rapidly as the setting reaction proceeds.
Despite the initial acidic nature of the polycarboxylate cements, these products
produce minimal irritation to the pulp probably because,
The larger size of the polyacrylic acid molecule limits its diffusion through the
dentinal tubules.
Also, in the set cement the acrylic acid ions bind the metallic ions so tightly
that they are not easily leached out from the set cement.
When placed directly on pulpal exposure - ------ reactions range from a mild
chronic inflammation to the appearance of a localized liquefactive necrosis.
Zinc polycarboxylate

37. GLASS IONOMER CEMENT
Freshly mixed GIC –acidic ph 0.9 -1.6 -- mild inflammation in pulp.
Showed greater inflammmatory response than znoe but less than
zinc phosphate,other materials resolved with in 30 days ( Garcia et al
1981)
HISTOLOGICAL pictures shows that
After one week of placement of glass-ionomer cement the odontoblastic
layer is disrupted and dialated blood vessels seen in pulp area .
After about a month the pulp tissue recovers and displays a normal
appearance. The disruption of odontoblasts become normal.repairative
dentin formed.

38. Mc Lean and Wilson 1974
1.Poly acrylic acid is weak acid
2. Tendency of acid to dissociate into H + and polyacrylate ions is reduced after
partial neutralization which makes the acid weaker
3.Acid is readily neutralized by Ca2+ ions in tubules
4. Because of its higher molecular weight and chain enlargement there is
unlikely of diffusion of polyacrylic acid into dentinal tubules

39. The earlier resin bond materials, developed as a tooth colored materials, were
detrimental to the pulp. The free monomer of the materials was injurious to the
health of the pulp.
The polymerization shrinkage of the composite creating vacuum in between
the remaining dentin and the restoration might create problems for the pulp.
It has been established that even after curing the monomer is leached from
composites.
This monomer is managed by the bonding agents and the remaining dentin
thickness. In case the dentin thickness below the composites is less, the
leaching monomer can affect the underlying pulp – adequate pulp protection
should be given
Composite resins

40. Direct pulp capping :
Superficial necrosis of pulp tissue -------with tissue displaying
low grade inflammation
Within 30 days tissue subjacent to the necrotic zone has
reorganised and resumed normal architecture
Indirect pulp capping :
Application to intact dentin –induces sclerosis by promoting
crystal precipitation within tubules ,accompanied by reduction in
permeability
Calcium hydroxide

41. MTA AND BIODENTIN
DIRECT PULP CAPING :
AT Ist week :
No sign of necrosis close to the exposure site
Odontoblast like cells are observed at the periphery with the deposition of
calcified bridge
At 2 nd weeks:
calcified bridge formation begins just below the exposure site
Many other capping materials have been explored such as hydroxyapatite, dentin
chips, growth factors (BMP-1, -7, TFG-B-1,-3, FGF, IGF192–202. The release of
bioactive molecules is a key factor for the reparative dentinogenesis induced by
any of these capping agents.

42. Do’s and don’t’s

43. PULPAL HEALING
PULPAL IRRITATION
CONCLUSION

44. REFERENCES
 TEXT BOOK OF INGLE 7th EDITION
 SELTZER AND BENDER – PULP
 TEXT BOOK OF OPERATIVE DENTISTRY –
VIMAL SIKRI 4th EDITION
 COHENS PATHWAY OF PULP - 6th edition