Biologic response of pulp/ dental implant courses

Response of pulp to operative
procedures and restorative
materials
www.indiandentalacademy.com
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education

Flow chart
Introduction
Pathological Responses to Operative Dentistry
Causes of possible pathological responses
Possible sources of odontoblast injury which may
affect dental repair activity ;(P.E.Murray 2001)
Dental pulp ;Structural elements
Zones of pulp
Cells
Intercellular substance
Intercellular fluid
Systemic factors affecting the pulpwww.indiandentalacademy.com

PULPAL REACTIONS
slight ,moderate, severe
Role of odontoblasts; Changes observed
as the injury increases progressively
Pathophysiology of pulpal inflammation
Possible connective tissue reactions to
irritants
Sequence of pulp reactions to irritation
from operative procedures
Cumulative effects of irritants
Factors affecting resolution
Natural defense mechanism and
compensatory pulpal reaction to outside
insult www.indiandentalacademy.com

Indian Dental academy
• www.indiandentalacademy.com
• Leader continuing dental education
• Offer both online and offline dental courses

Pulpal irritants
mechanical and thermal irritants
Depth Of Cavity Preparation
Relationship of depth of cavity preparation to
reparative dentin formation
Speed of rotation
Heat and pressure
Dry cavity preparation
Nature of cutting instrument
Size of wheel and burs
Coolants
Extensiveness of preparation
The effect of tooth movement on pulp

chemical irritants
 Dentin sterilizing agents
 Cleansing and drying medicaments
 Desensitizing and remineralizing agents
 Acid etchants
 varnishes
 cavity liners ,Temporary restorations, &permanent restorations
 Znic oxide eugenol
 Znic phosphate
 Polycarboxylate cement
 Glass ionomer cement
 Cavit
 Gutta percha
 Dental amalgam
 Gold inlay
 Gold foil
 Restorative resins
 Resin cements www.indiandentalacademy.com

radiant irritants; lasers, x-irradition
Effect of local anesthetic on pulp
Effect of bleaching on pulp
Reaction of pulp capping agents
 Traditional ;calcium hydroxide and znic oxide eugenol
 Other materials; dentin adhesives, glass ionomers, M.T.A, B.M.P’s
 Laser treatment

Current thinking of the cause of pulpal reaction to
restorations
Summary and conclusion

Introduction
The effect of restorative procedures on dentin and pulp
represent a combined response to preparation and to
restoration. Long term effects of preparation events
alone are difficult to assess, because the preparation will
have to receive a provisional or permanent restorative
material or left exposed to oral enviornment. No
restorative material exists that is truly inert in biologic
sense and any pulpal and dentinal change that result
from the preparation can effect the evaluation of
reactions to the entire restorative procedure.
 long term maintenance of a healthy pulp is a result of
atraumatic preparation and the use of biologically
acceptable materials that can seal the tooth restoration
interface to prevent or minimize bacterial leakage

Pathological Responses to Operative
Dentistry
Clinical response: hypersensitivity
Hydrodynamic theory by Brannstrom: dentinal
fluid movement stimulates mechanoreceptor
nerve endings near the pulp
Histopathology
Inflammation
Reparative dentin
Odontoblastic degradation
Replacement odontoblasts
Pulp necrosis

Elbuam et al (1992), Biocompatibility of an enamel-dentin
adhesive, Quintessence Int 23(11), 773-782.
There is no correlation between clinical and
histopathological findings
The absence of postoperative pain is not an
indicator of the absence of pulpal inflammation

Causes of possible pathological responses of
dental pulp related to operative dentistry
Physical: occlusal interference, condensation, air blowing
or dentin dehydration
Thermal: heat from cutting, insufficient pulpal protection
for metallic restoration
Electrochemical: galvanism
Chemical: toxicity of dental materials, acid etching
Bacterial: toxin products
Traumatic stimuli: abrasion, attrition, erosion  dentin
exposed
Operator: poor contour-contact, overhanged margin,
poor anatomy, damage of adjacent tooth

Possible sources of odontoblast injury which may affect
dental repair activity ;(P.E.Murray 2001)
Cavity restoration variables
•Restorative materials
•Dentin conditioning
•Use of primers &
adhesives
•Finishing
•Cytotoxicity
Cavity preparation variables
•Residual dentin thickness
•Cavity dimension
• coolant
•drill speed
•cutting method
•Cutting time
Pulp repair response
•Odontoblasts and
cellular destruction
•Reactionary
dentinogenesis
•Reparative
dentinogenesis
•Inflammatory activity

Dental pulp is a connective tissue system
composed of cells ,ground substance and
fibers. The cells manufacture a
fundamental matrix which then acts as a
site and precursor for the fiber complex.
The fiber complex is composed of
collagen and reticulin. “SELTZER”

Structural elements of dental pulp
Cells
Intercellular substance
Intercellular fluid

Zones of pulp
•Central zone
•Cell rich zone
•Cell free zone
•Odontoblastic zone

Cells
Fibroblasts
Defense cells
reserve cells
special cells ;Odontoblasts

ODONTOBLASTS
SEM finding
•Nucleus
•Nucleolus
•Cytoplasm
•Odontoblastic process
•Periodontoblastic space
•Inter cellular junctions
•Odontoblastic junctional complex
•Odontoblasts nerve ending
•Odontoblastic communications

Defense and other cells
Histiocytes
Undifferentiated mesenchymal cells
Macrophages- lysosomes,pericytes
Mast cells, PMN’s
Immunocompetent dendritic cells

FIBRES
Reticular fibres which may transform into
collagen
Collagen fibres
Argyrophilic fibres(von kroff fibres)
GROUND SUBSTANCE
Proteins like glycoprotein and acid
mucopolysacchride

Systemic factors affecting the pulp
Vitamin deficiency- affects fibroblasts, collagen fibers
Hormones and hormonal imbalance -corticosteroids in
high doses affects collagen synthesis, affects
odontoblasts, inhibits dentinogenesis
Diabetes -rise in plasma glucose level produces glucose
concentration in dental pulp fluid. degenarative
inflammatory changes in pulp affecting dentinogenesis
Thyroid deficiency -reduction in vascularity of pulp, rapid
deposition of dentin with narrowing of pulp
Protein deficiency - affects dental repair after injury to
pulp as it is source of energy

Systemic virus infection -degenarative changes
in pulp producing necrosis
Tumor transplantation - not studies how ever
burkitt’s lymphoma, epithiloma,sarcoma have
been found
Hereditary diseases - lukemia, sickle cell
anaemia, Niemann-pick disease

Pulpal reactions Langeland 1957,Stanley 1968
SLIGHT , MODERATE, SEVERE
Slight
increase number of cells in cell free zone,
and pulp tissue
characterstics of fibroblasts and
undifferentiated mesenchymal cells
Few inflammatory cells
Increase number of capillaries
Few extravasated red blood cells
Localized to affected dentinal tubuleswww.indiandentalacademy.com

Moderate reaction
More cells in area subjacent to affected dentin
Nuterophilic and mononuclear leukocytes invade
odontoblst- predentin area
Odontoblasts cannot be identified in their normal
psudostratified appearance
odontoblastic nuclie can be discerned in the
tubules
Increased number of capillaries and vessels are
found in in infiltrated tissue and its border
Width of predentin may or may not deviate

Severe reactions
Marked cellular infilteration with abcess
formation
PMN’s and mononuclear leucocytes
predominate in affected area
Response is well limited
Odontoblastic layer cannot be identified
No predentin is formed and with in days existing
predentin mineralizes
Odontoblastic nuclie in dentinal tubules
Numerous blood vessels found

PULPITIS FROM OPERATIVE PROCEDURES
Role of odontoblasts; Changes observed as the injury increases
prgrossively
Increase permeability of dentinal tubule
Disturbance of pulpodentinal membrane
Disruption of palisaded dentinoblastic layer
Aspiration of odontoblastic nuclie in the dentinal
tubules
Irreversible dentinoblastic injury releasing tissue
injuring factors
Inflammatory changes
Subodontoblastic inflammatory changes
Central zone inflammation

Related to change in osmotic pressure due to increase in
metabolites
Membranes of endoplasmic reticulum fragment and
mitochondria degenerate
Denaturation of proteins
If demage to cell membrane; alteration in the
permeability of cell
 Nucleus gets affected if greater amount of damage
Cytoplasmic granules are increased

Displacement of odontoblasts; known as
aspirated, displaced or ectopic odontoblasts
Due to negative and positive pressure effect.
Odontoblasts are pulled or pushed into the dentin
Displaced cells undergo autolysis in 6 hours
Mineralization of degenarated nuclie in predentin.

Enzymes in pulpal inflammation
Adenosine triphosphate ATP
Lactate hydrogenase LDH
Malate dehydrogenaseMDH
During inflammation MDH activity decreased
when pulp becomes necrotic increase in LDH activity
and decrease in ATP activity indicating increase rate of
anaerobic glycolysis

Pathophysiology of pulpal inflammation

Possible connective tissue reactions to
irritants
Irritants acting on dental pulp
Little or no reaction Pulpitis
Partial total
Acute chronic
Repair necrosis

Sequence of pulp reactions to irritation from operative procedures
Intact,uninflammed pulp Mildly inflamed pulp,
due to moderate
caries
Pulp with chronic
partial pulpits due
to deep caries
No reaction
Mild reaction
recovery
Acute partial pulpitis (with
restoration)
Chronic partial pulpitis
Chronic partial pulpitis
with partial necrosis
Chronic total pulpitis
necrosis of pulp
chronic apical
periodontitis
With restoration
recovery
No recovery

Character of irritant
Single
multiple
Inflammatory Reaction
Mild
Severe
Mild
severe
Resolution
recovery
chronicity
necrosis
With good
quality
tissue
Poor
quality
tissue

Cumulative effects of irritants
Cavity preparation and pressure
Crown preparation ,heat and pressure
Drugs ,pressure and bacteria
Caries ,operative procedures and bacteria

Factors affecting resolution
In regard to irritant
Severity
Duration
number
In regard to resistance
of the host
Age of patient
Hereditary
Nutritional staus
Systemic disease
Hormonal activity

Natural defense mechanisms
Dentinal sclerosis
Reparative dentin formation
Smear layer; controversial
Best way to solve the problem is to remove the smear layer
and replace it with sterile, nontoxic, artificial smear layer-
ferric oxalate 5% and potassium oxalate looks promising
(Bergenholtz)

Reparative dentin is aReparative dentin is a
tertiary dentin matrixtertiary dentin matrix
formed by newformed by new
odontoblast like cells inodontoblast like cells in
response to a specificresponse to a specific
stimulus, whilestimulus, while
Reactionary dentinReactionary dentin isis
formed by survivingformed by surviving
odontoblasts subjacentodontoblasts subjacent
to diseased or otherwiseto diseased or otherwise
damaged dentin.damaged dentin.

reparative dentin under restorations
Avg. daily reparative dentin reported to be 2.8microns for
deciduous and 1.5 microns for permanent teeth (stanley
1966)
Begins earlier in shallow cavities
In deep cavities, lag period in onset of of new predentin,
followed by elaboration of huge amounts under cut
dentinal tubules .
rate is more rapid but the quality is poorer than dentin
formed under shallow preparation.

Odontoblasts appear to be altered in structure, palisaded
arrangement is changed odontoblasts appear flat like
fibroblasts and reduced in number, odontoblast layer is
only one or two cell in depth ,odontoblasts replaced by
other pulp cells
Intense calciotraumatic response to operative
procedures in dentin
More amorphous or irregular

It has been suggested that for successful outcomes of any operative treatment performed
on vital teeth a prime aim should be reduction of dentin permeability as occurs
physiologically in dentin in response to injury. Possible ways in reduction of dentin
permeability are,
Injury
Primary
dentin
Tertiary
dentin
TubularTubular
discontinuity anddiscontinuity and
decrease indecrease in
density withdensity with
tertiary dentintertiary dentin
deposition.deposition.
TubularTubular
discontinuity anddiscontinuity and
decrease in densitydecrease in density
beneath a thin layerbeneath a thin layer
of tubular hard tissueof tubular hard tissue
formed initially fromformed initially from
poorly differentiatedpoorly differentiated
odontablast like cells.odontablast like cells.
TubularTubular
continuity andcontinuity and
maintenance ofmaintenance of
tubular densitytubular density
but diffusionbut diffusion
distance to pulpdistance to pulp
increased byincreased by
tertiary dentintertiary dentin
depositiondeposition
TubularTubular
dimensionsdimensions
decreased bydecreased by
deposition ofdeposition of
peritubular dentinperitubular dentin
sclerosissclerosis

Possible functional significance of the AVA & ‘U’ turn loop in the
pulp
noxious stimulation
Increased blood flow
Increased tissue pressure to critical level(16-20mmof Hg)
AVA & U turn loops open
Shunting of blood flow away from capillary beds
Maintainence of PBF
Compensatory pulpal reaction to outside insults

MECHANICAL AND
THERMAL IRRITANTS

Depth Of Cavity Preparations
Cavity preparation causes
Increased rate of collagen turn over
Odontoblastic cell damage
Protein synthesis by odontoblasts directly under and adjacent,
to the cavity preparation is curtailed.
As cavity depth if increased more severe is injury to
odontoblasts – increase rate of production of reparative dentin.

• With 0.5mm of dentin between base of cavity and pulp
decrease of 0.1mm produces more severe inflammation
in low speed preparation without coolant
• With coolant the floor can be brought much closer to
pulp (0.3mm)
• Pashley (1979,81)Reduction in dentin thickness
increases permeability (increase in number and diameter
of tubules)
• Medium size cavity Zn phosphate is preferred
• deep cavity – ZOE.

RELATIONSHIP OF DEPTH OF PREPARATION TO
REPARATIVE DENTIN FORMATION
Increased rate of reparative dentin formation and
increase depth of preparation
Only if RDT - between pulp and dentino enamel junction
is half the
original thickness
↓
Maximum threshold of stimulation is reached

if further cutting
Greater injury to odontoblasts
Rate of formation of reparative dentin decreases
irregular structure ,Poorly mineralized.
Even less thickness of dentin - formation of reparative
dentin inhibited temporarily
Odontoblastic cells show signs of atrophy.

THE IMPORTANCE OF REMAINING DENTINE THICKNESS UNDERLYING
CAVITY PREPARATIONS IN MODIFYING PULP RESPONSES TO DENTAL
METERIALS.
STANLEY 1975
MINIMAL RDT TO AVOID PULPAL INJURY
PAMEIJER et al. 1991 – 1mm RDT sufficient to
protect ZnPO4 & RMGI.
STANLEY (1994) SUGGESTED RDT OF 2mm
IN 2000 (MURRAY)
0.5 mm with ZnO2
IRM / CaOH2 + SILVER AMALGAM
Little effect underlying odontoblast numbers evenwww.indiandentalacademy.com

SPEED OF ROTATION
 Greatest damage of odontoblasts at speeds upto 50,000 rpm
 Speeds from 5000-15,000 rpm are more destructive than speed
under 3000rpm without coolants (Marsland & Shorelton 1957)
 Least amount of damage occur at speeds of 150,000rpm to
250,000rpm when coolant is used properly
 Very low speeds 300-500rpm - absence or reduction in odontoblast
damage (langeland 1961)
 At 20,000 rpm odontoblast damage occurs whether or not coolant is
used
 50,000 to 250,000 rpm if coolant is delivered properly reactions are
minimal (Stanley 1958)

Concluded :
 Speeds with 3000 or less and 2,00,000rpm or above
are safest with coolant
Speeds between 3000-30,000 rpm are most deleterious
even with coolant
Riethe 1969
Without use of coolant no high safe speed
At 3000-5000rpm less damage without coolant than at
ultra high speed without coolant

HIGH SPEED CUTTING
Burns of dentin
Integrity of pulp threatened
Charred dentinal tubules – susceptible to decay
Ultra high speed should be used for removal of
superficial enamel and dentin ,finishing done with very
low speed.

With increase in speed of rotation of cutting instrument,
not only greater heat is generated but greater vibrations
also which affects the pulp
Sears 1967 mechanical vibrations may be responsible
for protein denaturation of odontoblasts
Causes morphologic changes leading to destruction of
cells

Heat and Pressure : Impinge on pulp simultaneously
Factors in production of heat within pulp as a result of cavity
preparation are
Depth of preparation
Speed of rotation of bur or stone
Size, shape composition of bur / stone
Amount and direction of pressure on cutting
Amount of moisture
Direction and kind of coolant used
tissue being cut
Length of time instrument in contact.

DRY CAVITY PROCEDURES
(cotton 1965,Hamilton,Kramer 1967)
Dry cavity preparation causes greater trauma than
under water spray
Produces both reversible and irreversible changes
(Morrant 1977) Prolonged dehydration with air
causes
odontoblastic damage, displacement, pulpal
edema which cannot be reversed.
Vasodilation
Increase capillary permeability
Above 46°c – irreversible changes – stasis,
thrombosis

(Beveridge & Brown 1965)
Initially thee is drop of intra pulpal pressure
followed by rise in intra pulpal pressure (van
Hassel and brown 1969)
due to result of chemical mediators (persistent
vasodilation)
Escape of plasma proteins into interstitial fluid
↓
Lowering of osmotic pressure and accumulation
of fluid in pulp chamber.

Kramer (1963),Brown (1978)
Enamel temperature increases with dry preparation
May fracture
May effect dentin and then pulp
Breakdown tooth structure at margins
Marginal leakage
Recurrent caries

Nature of cutting instrument :
Weiss et all (1963)
 Greater thermal damage with steel burs, than carbide
 With proper cooling carbide burs produces negligible pulp damage
 Even with coolant diamond instrument are capable of producing
damage to pulp this may be related to additional pressure.
 Simultaneous increase of rotational speeds and pressure by rotary
instruments cause temperature increase and increase inflammation of
pulp (Stanley, Swerdlow 1959)
 When force above 8 oZ applied – even use of coolant does not resist
minimize inflammation
↓
 Displacement of odontoblastic nuclie into tubules (Brannstorm 1962)

Size of Wheels and burs :
Stanley, Swedlow (1960)
Advocate small size instrument
Larger size produce greater damage
Peripheral speed of larger disc is higher that small disc at
same rpm
When using large instrument greater area is cut. Coolant
cannot get to the tooth as readily resulting in more severe
reactions
Less severe reactions when smaller size instrument used.

Hand instruments
Massler (1959) damage more severe with hand
instruments
no heat generations but pressure causes pulp damage

Coolants
Eliminate heat generation
Air spray
Combination air and water
Water spray
Water applied through hollow bur
Water as a jet stream

Air spray
Air blasts are damaging to pulp ( langeland
1982)
Compressed air for 10seconds – produces
displacement of odontoblastic nuclie.
Although greater cellular damage with air
coolant repair follows in absence of other
irritating factors (Cotton, Daschi,Stigers 1968)
Recovery depends on health of pulp extent and
depth of preparation, extent of damage and no.
of cells present
Cavity should not be dried with air blasts,
instead use cotton pallets

Water spray
Temperature elevation is reduced
Rate of removal of debris increased
Control inflammation reaction in pulp

Bodecker 1939 At high speed/without
cooling
“ Cooking the pulp in its own juice”
Speed 50000 and above – water in form of jet
stream must be used
Delivered directly at contact between bur and
tooth simultaneously
crosses cut fissure burs
shower head type of aperture
cutting done with brush stroke
Temperature of coolants
Clinically no significant damage on pulp

Temperature Rise during Tooth Preparation without Coolant
Time (seconds)
0 2 4 6 8 10 12 14 16
Temperature(degreeCelcius)
-10
0
10
20
30
40
50
60
Temperature(degreeCelcius)
-10
0
10
20
30
40
50
60
No coolant
Air from syringe
Spray from turbine
Water from syringe

Extensiveness of preparation
 Class I and Class V – produce lower heat reaction than
MOD or full crown preparation
 In class I – increase the width, and depth of fissure
gradually by shallow angular cuts
 Cavity preparation with high speed instruments should be
widened and deepened gradually for proper cooling and to
minimize pulp damage
 In crown preparation – high speed for gross cutting finish
the grooving part of preparation with burs at low speed.
 Shoulder preparation are more harmful than shoulder less
ones – as preparations are deeper into dentin closer to pulp
 Hazardous in young tooth
 Crown and bridge preparation – paralleling of walls is
hazardous
 If pulp hemorrhage- pinkish , brownish discoloration of
dentin – difficult to recover.

USE OF PINS
In pinledge preparation – avoid use of high speed
instruments
Insertion of pins introduce dentinal fracture or unnoticed
pulp exposures
Deep insertion can cause pulpal irritation
Cementation with Zn-phosphate can cause irritation
-application of Ca (OH)2 in pinholes (Suzuki etal 1973)
Inflammatory reaction, necrosis

Rebound response
Bernier & Knapp (1958)
High energy which is released by ultrasonic cutting or by
ultrahigh speeds
When cavity prepared at one side of tooth reaction occur
on opposite side
Stanley,Langeland (1961) controversy exist about actual
occurance

Polishing of restorations
Polishing of restorations with out taking precautions for
dissipation of heat is dangerous to pulp (Aplin)
Elevation of temprature because of friction, sandpaper,
disc, rubbercups run at high speeds can generate
sufficient heat to damage the pulp
Heat generated can cause enamel to fracture
Polishing instruments should run intermittently at low
speeds or in conjunction with coolants

Effect of tooth movement on pulp
Orthodontics
In young teeth, Circulatory disturbances
resulting in degenaration of odontoblasts
More severe with increase in orthodontic force
Interference in blood supply, reduction of
nutrient supply
Cells may undergo atrophy increase deposition
of reparative dentin and concurrent increase in
dystrophic mineralization
may undergo atrophy with eventual necrosis, in
most cases pulp response is reversible

Care must be taken in performing operative
procedures on teeth undergoing orthodontic
treatment
Pulp will not with stand readily the combined
irritating effects
More frequent inspection of teeth with incipient
caries is indicated
Cavity preparation is indicated as soon as the
beginning of carious lesion is indicated

Effect of local anesthetics on the pulp
20% Lidocaine with 1:10000 epinephrine decrease the blood
flow
Both infiltration, mandibular block infection decrease blood
flow- lasts for shortime
Ligamental injection –flow ceases completely for 30min
Rate of oxygen consumption in pulp is low-can withstand this
period of ecreased flow-if prolonged interferes with cellular
metabolism
Length of flow cessation propotional to concentration of
vasoconstrictor
Blood flow and sensory activity comes to normal after 3hrs of
total cessation of flow

Irreversible injury – when full crown preparation done
immediately after ligament injection
Due to release of vasoactive agent – substance P into pulp
↓
In Normal condition they are removed from pulp by blood
stream
↓
Accumulation – due to decrease flow- result in permanent
damage of waste products.
↓
Whenever possible use vasoconstrictor free L.A for
restorative procedure on vital teeth

Restorative materials
Properties of material capable of producing
injury involves
Chemical toxicity
Acidity (hydrogen ion concentration)
Absorption of water during setting
Heat generated during setting
Poor marginal adaptation resulting in
bacterial contamination

Dental Response to Bacterial
Invasion
Caries
Microleakage of restorations

Dental Pulpal Response to Bacteria
Positive correlation of presence of bacterial beneath
restorations and inflammation in the underlying pulp
Bergenholtz (1982): dentin permeability to noxious
bacterial agents decrease with time
Smear layer may harbor bacteria. But, evidence
suggests that bacteria will grow underneath a restoration
only in the presences of microleakage

Role of bacteria in dental pulp reactions
Proteolytic enzymes: collagenase, protease
Active substances: toxin products
Stimulate lymphocytes, macrophages, plasma
cells, PMN leukocytes infiltration  inflammation
Persistent inflammation leading to tissue
breakdown exudate pH change from alkaline
to acidic neutrophils disintegration 
lysozymes, trypsin-like enzymes  digestive
products “pus”

Temporary filling materials

ZOE – better thermal insulator than zinc
phosphate and Ca(OH)2
Greater the amount of free eugenol greater pulpal
irritation
Thick mix of eugenol will les likely irritate the pulp
Thrombosis of blood vessel when applied directly
on pulp tissue
Anodyne for pulpal pain (Trowbridge 1982)
Insulating material, Prevent galvanic action of
amalgam.

Block of transmission of action potential in nerve
fiber
Adapts very closely to dentin to provide good
seal
antibacterial properties
(Brannstrom 1981) in deep cavities RDT <
0.5mm cause inflammation
Fluoride modified ZOE : ZOE + CaFPO4(14%)
Final product (2% fluoride) fluoride content and
microhardness of dentin increased.

Polyacrylic cement (polycarboxylate
cement)
Adhesion to tooth structure reduces micro
leakage
strong antibacterial properties
Well tolerated by pulp- equivalent to ZOE

Zn phosphate :
severe pulpal damage because of its
inherent irritating property.
More toxic in Deep cavities –should not be used
without intervening liner
Less severe in shallow and medium depth cavities
Thick mixes should be used to minimize pulp
irritation and marginal leakage
Thin mix – pH 2.14 delay in crystallization ,which
prolong irritating effect and greater heat generated
After 24 hours pH5.5 is maintained neutralization
is never achieved even after crystallization
associated with greatest temperature rise 2.14°c

Pulp may be affected by
•Components of material
•Heat liberated in setting
•Marginal leakage
( Brannstorm, Nyborg, Watts)

Glass ionomer cement
pulpal response was first classified as bland, moderate
and less irritating than other cements or composite
Screening tests in cell culture indicate that they can be
cytotoxic and therefore calcium hydroxide liner are
recommended when RDT not certain
(Brannstorm 1979,Mount 1984,Kawahara 1979)
Higher molecular weight of polymer liquid,
use of weaker acids and
less toxic monomers ;guard against permeation of
material through the dentinal tubules to the pulp

More severe pulp response with powder liquid ratios used for
luting cements
Freshly mixed glass ionomer cements cause more damage
than set cement .longer the set before placing on cell culture
less the effect.
More powder that is incorporated into the mix, less toxic the mix
will be to cell cultures Mjor 1977,Kawahara 1979,1988
Good adhesion accounts for its good biocompatibility, less
leakage and thus decreased invasion of bacteria at tooth filling
interface
Leaching of component material is an advantage, fluoride is
released slowly.

RMGIC –
For both indirect and direct pulp capping
•Histological response of pulp in both situations was similar to
Ca (OH)2 – (Cox et al)
•Kanoka 1991 did not find adverse response with visible light
cured composition in cell cultures
Action as pulp capping agent attributed to
Anti bacterial property
Stable long term ionic bonding – prevents
microleakage
Ability to assist remineralization of inner carious dentin (W.
Gado et. al.)

Dental Pulpal Responses to Luting Cements

Gutta percha
Poor marginal sealing and other irritating properties of
gutta percha has injurious effects on pulp
It does not seals the dentinal tubules, tooth is sensitive
Fluids and bacteria are pumped and odontoblasts are
injured heat damage in shallow cavities no pulpal
damage

cavit
Material sets when saliva reacts with calcium
sulfate and znic oxide-znic sulfate
Excellent sealing qualities less antibacterial than
ZOE
Mildly toxic
No severe pathologic alterations in the pulp
Antrim,Brannstorm 1976

Permanent restorations

Gold inlays
Potentially damaging to pulp due to;
Large amount of pressure in seating causes injury to
odontoblastic layer
marginal leakage due to poorly adapted margins or
excessive use of cement resulting in dissolution of
cement, recurrent caries, pulp involvement (Going
1979)
Inflammation reduced in shallow or moderately deep
preparation
With deep inlay preparation pulp is placed in great
danger

Poorly fitting inlays results in future pulpal disease due to
percolation and recurrent decay
Pressure of cementation of tight fitting inlay cause
pulpitis and pain
Preparation of inlay subject the tooth to superimposition
of many irritants thus difficult chance of recovery
Application of two layers of cavity varnish to cavosurface
cavity margins afford the best protection against
marginal leakage

Thomas et al 1969 insertion of gold foils irritates the pulp
Mechanical malleting of dentin is the offending factor
If the duration of application is short there is reasonable
chance of pulp recovery
Inflammatory reaction due to the pressure transmitted
through dentin
Should be avoided in youngsters because of larger pulps
and less thick dentin and wide dentinal tubules
Gold foil

Amalgam
Considered to be either inert or mildly irritating to pulp
in dogs rats and humans (Massler Welder 1956)
Mainly related to physical insertion to amalgam, i.e.
condensation (Stanley 1991) and is of short duration.
Mjor 1979 indicated that alloys containing higher
percentage of copper causes slightly more pulpal
response than conventional alloy
With passage of time pulp under high copper amalgam
showed slight inflammation and extensive irregular
reparative dentin formation

In shallow cavities pulp reactions are lacking or minimal
In deep cavities mild to moderate and pulp recovers
readily
According to some investigators -Inhibition of reparative
dentin formation, due to paralysis of odntoblasts
Use of varnishes under amalgam has been
recommended

Kurosak & fusiyama(1973)showed that mercury from
amalgam in humans and dogs did not reach the pulp it
does not dissolves, but ,rather penetrates back into the
amalgam and reacts further with previously unreacted
alloy cores, (Stephan and ingram(1969),van aken(1973)

Resin based composites :
If adequately polymerized composites are biocompatible –
minimum solubility, Unreacted species leached in
minimum amount
Inadequately polymerized composites induce long term
pulpal inflammation
If too thick layer is polymerized
If inadequate exposure time
Shrinkage of composite
Marginal leakage
Bacterial ingrowth
causing;Secondary carries ,pulpal reactions.
stasis ,hemolysis cessation of blood flowwww.indiandentalacademy.com

Pulp response is intensified in deep cavities when
incomplete curing permits an higher concentration of
residual unpolymerized monomer to leach into the pulp
(shwartz et al 1983)
Reactions to composite materials has been related more
to bacterial leakage than to toxicity of the material
(Brannstorm 1985,stanley 1989)
Leakage, adverse pulp reactions ,development of
recurrent caries are associated with polymerization
shrinkage of composite and imperfect adhesive bonding
of the material to the cavity

Thermal stress also increase the marginal leakage as
does the use of composites with higher viscosity and
lower water absorption values
Less leakage with heat and light treated composite
inlays (shortall 1989)
Pain has been reported following insertion of composite
resin (Jordan,wilson 1986,leinfelder 1991 )especially with
large restorations

Bonding agents are at greatest risk of incomplete cure
as they thin and oxygen inhibition of polymerization is
significant factor (Magresom 1990)
Unpolymerized monomer leaches towards the pulp,
recent evidence suggests that extracellular or salivary
enzyme may degrade the polymerized network over
time, making the hydrolyzed products available to
tissues (Santerre et al 2001)

Risk of biologic harm from unpolymerized or degraded
monomers are dependent on many factors
Component must be free of polymers to diffuse into pulp
tissue
Must have properties like solubility that encourages its
diffusion
Time and dose of pulpal exposure sufficient to cause a
biological reaction
Must have biological properties in cell to cause problems

Rakich et al 1999 demonstrated that resin
monomers are a hazard to inflammatory cells
that are common in pulpal tissue
Noda et al 2003 have shown that resins alter the
secretion of inflammatory mediators from
human macrophages
HEMA is able to diffuse rapidly through dentin in
vitro in sufficient concentration to cause
cytotoxicity.
And bonding agent ,as used clinically elute
sufficient amount of monomer though dentin to
cause significant cellular toxicity after one week;
(Bouillaguet 1996,1998)

(Bouillaguet et al 2000,Lefebvre et al 1999)
Long term studies that used sublethal concentration of
HEMA,TEGDMA or BISGMA for 5-6 weeks showed that
resin clearly altered the cellular mitochondrial activity
and total protein content per cell ,even at concentration
of 1-10% of those used in short term experiments

Gwinnett and Tay 1998 observed persistant
inflammation and granulomatous reaction in human pulp
in response to application of total etch adhesives to deep
dentin
Reported the presence of resin globules displaced into
dentin tubules and penetrating the pulp.

Shallow cavities located in superficial or sclerotic dentin
where the permeability is low and RDT is adequate to
prevent any adverse effects from diffusing materials
there fore total etch adhesives are recommended.
Deep cavities closer to the pulp are more challenging
because of the intrinsic permeability and wetness of the
substrate therefore use of self etch adhesives is
indicated for young deep permiable dentin,
because these adhesives leave residual smear plug
material in tubules that limits the diffusion of uncured
monomers towards the pulp (Tay et al 2000)

Resin Cements
Self- cured resin cements:
 Cured chemically by the combination of two
components, one containing the catalyst for
resin polymerization.
 Examples: Panavia 21 (J. Morita USA).
Bisco C& B (Bisco Dental Products)
Enforce(L. D. Caulk)

 Light -- cured resin cements
Used when restorations are completely
penetrable by light from standard intraoral
curing devices.
Examples: Insure ( Cosmedent Inc.)
Nexus (Kerr Corp.)
Variolink II ( Ivoclar NorthAmerica),
without catalyst added.

Dual -- cured resin cements
For restorations that are translucent
enough to allow some light penetration,
but so thick that full polymerization would
not be achieved light curing alone.
 Examples: Nexus and Variolink II, both
used with their respective catalyst.

Postoperative sensitivity
 Post -op sensitivity within the first year after
cementation in about 37 percent of their patients
with crowns; with some brand of cement and
bonding agents, up to 11 percent of the teeth
require endodontic treatment within the first
year.
(Clinical Research Associates. Filled polymer crowns: 1
and 2 year status reports. CRA Newsletter 1998; 22( 10):
3)

For acceptable tooth desensitization, most
resin cements require adequate use of a
bonding sealing agent between the tooth
preparation and the crown.

Use self- etching primer and bond
desensitizing concept by Christensen
 http:// www. hsdm. med. harvard. edu/ pages/ intranet/ courses/
resotrative/ articlesjada/ resinCementsSensitivity. htm
 The smear layer of the tooth preparation is left
on the tooth, and the self etching, self -curing
primer is incorporated into the existing smear
layer
Examples: Panavia 21 or Panavia F
(J.MoritaUSA)

Dental Pulp Responses Resin Cements

CHEMICAL IRRITANTS
DENTIN STERILIZING AGENTS
Phenol : cytotoxic, poor sterilizing agent increase
permeability of dentin tubules
Silver nitrate : causes irritation to pulp – inflammation
reaction
Camphorated Parachlorophenol : pulpal inflammation

Eugenol : Inhibitory not destructive of microbial growth
(due to hydroscopic property)
Not irritating to dentin. beneficial in deep seated cavities
when placed directly over pulp marked inflammatory
reaction occurs.

Cleansing and drying medicaments:
Smear layer removal
Enhances bonding of resin
Hydrogen peroxide – formation of emboli in pulp
Potentially damaging
Rupture of blood muscles
35% Hydrogen peroxide on enamel – severe but
reversible changes.
Alchohol : Injures odontoblsts
denatures protein
Drying of cavity by rinsing with warm water and
rubbing with cotton pellets produce least damage

Smear layer
Cutting of dentin with high speed tungston carbide bur,
or diamond points or hand chisels produce smear layer
(Brannstorm 1979)
Effective removal
Polishing with pumice (Dold 1978)
Acid etching ( Branstorm,Nordenvall 1977 )
Microbiocidal fluoride solution (Brannstorm, Johnson
1974)
Combination of 0.2% EDTA with surface active
antibacterial solution.

Acid etchants :
Pashley 1979 : Increase dentin permeability
Allow penetration of streptococcus mutans into
dentinal tubules
Rated as mid to moderate reaction
Use of Ca(OH)2 base or liner before
pretreatment
Negligible – Rapid buffering of acid by dentinal
fluid.
Reversed by 3% solution of potassium hydrogen
oxalate

Controversies of acid etching in deep dentin
• Total etching of deep dentin or exposed pulp does not cause
pulpal inflammation. – Brannstrom et. al.
• Acidic environment is well tolerated by pulp – Snuggs et. al.
• Marked increase in dental permeability is due to-
- Enlargement of dentinal tubules
- Removal of smear layer and plugs
- Hypertonic property of acidic gel –
C.A. D’souza Costa et. al.
- Further increase in deep dentin permeability
- Inner carious dentin more permeable than normal
dentin.
“Increased diameter and increased number of tubules close to the
pulp.”
- A Hamid, W.R. Humewww.indiandentalacademy.com

•Increased permeability –
- Interferes with resin permeation
- Unprotected collagen below the diffusion zone
- Vulnerable to hydrolysis
•Faster outward dentinal fluid movement- displacement or
rupture of odontoblasts
•Outward fluid movement, pooling on to the surface -
incomplete polymerization of primer and adhesive.
• Heat generated by polymerization - inward fluid shift –
unpolymerized resin fragments enter the tubules – pulp foreign
body type of reaction with persistent inflammation.

Smear Layer Removal with Various Solutions

Dental Pulpal Response to Acid
Etching

Desensitizing and remineralizing
agents
Calcium fluoride (2%) reduced the sensitivity
permeability
Sodium fluoride : For desensitization
Stimulate reparative dentin (less permeable)
Mechanical barrier
Human pulp effects are controversial
,odontolasts may be injured.
Should not be applied on freshly cut dentin is
high concentration.

Ionization : Iontophpresis Increase permeation of
therapeutic agents through dentin for hypersensitive
dentin
Murthy 1973 – with 1% sodium fluoride produce best
result than topical applicaton of 33.5% NaF
Carlo 1982- cervical hypersensitivity treated , effectively
by 2% sodium fluoride

Stannous fluoride : Reduce solubility of enamel dentin
root surface (mayers Nyborg ,Brannstorm 1971
Minimal pulp response to lower concentration
0.4% stannous fluoride gel – effective for hypersensitivity
of root surface exposed by periodontal disease.
10% capable of remineralizing carious dentin
Other sodium fluoride solutions :
0.9% sols of sodium silicofluoride
6% sol of sodium monofluorophospahte
Acidualted sodium fluoride solution – forms calcium
fluoride which interfaces with pain transmission of pain to
pulp.
. www.indiandentalacademy.com

Strontium chloride : 10% strontium chloride reduces
hypersensitivity
Block neural transmission of stimuli
Calcium Acid phosphate : Block dentinal tubules
Potassium nitrate : (1-15%)
No adverse effect
Prevent nerve exitation

Reducing sensitivity
(Pashley)
 Oxalate salts are effective in Blocking tubules
Formation of microcomplexes of calcium oxalate
↓
Reduce hydraulic conductance
↓
Reduce permeability 95%
 Ca-fluoride silver nitrate
 Plasma proteins – fibrinogen
 increasing in potassium concentration around nerve endings
 Eugenol

Pit and Fissure sealants :
Low number of microorganism from dentin of sealed
teeth
 effect of acid etching of enamel on the dental pulp not
harmful
Varnishes - 5-6 µm thick
They reduce but do not inhibit pulpal irritation
Limited value for pulp protection even following three
subsequent varnish application permeability of dentin
was not reduced (Dippel 1979)
Deep cavities – base of calcium hydroxide or ZOE-
varnish application

Polystyrene + Methyl cellulose liners :
Liners composed of polystyrene, Ca(OH)2 and ZOE – a
thin film acts as barrier, prevent,penetration
Liners composed of Ca(OH)2 in methylcellulose-
effective in protecting pulp and reduces sensitivitiy to
thermal stimuli
Fluoride Liners :
Calcium monoflurophosphate potassium fluorozirconate
–reduce thermal conduction, decrease acid solubility of
dentin
Absence of irritating effects on pulp

Biocompatibility consideration of dental
restorative materials
Dental amalgam
 No adverse pulpal response
from mercury
 Corrosion may limit
marginal leakage, in long
term may lead to break
down of marginal integrity,
especially. with low copper
amalgam
 Innocuous to gingival tissue
 Lichenoid reactions
reported
 Thermal conduction to pulp

 Resin based composites
 Few documented systemic side effects
 Very little research on systemic
biocompatibility
 Associated with many organic compounds,
the effect of which are not known
 Incomplete polymerization leading to
degradation, leaching and imperfect bonding
 Predispose to polymerization shrinkage
 Associated with adverse local pulpal and
dentin reactions, development of recurrent
caries,and pain
 May lead to increase plaque accumulation
 Lichenoid reactions reported.

 Glass ionomer cements
 Few documented systemic side effects
 Early pulpal reactions, although less than
with cements or composite resins, with
rapid recovery
 Composition guards against the
permeation of material through the dentinal
tubules to pulp
 When used as luting agent liners are
advocated
 Hydraulic pressure and acid etching during
placement may irritate the pulp
 No undue reactions in the gingival tissue
 Good adhesion, minimal leakage at
margins, high biocompatibility
 Leaching of component materials offers
opportunity for slow release of fluoride

 Gold foils and cast alloys
 ceramics
 Inert, sensitivity is rare
 Potential pulp reactions due to
condensation
 Rare allergic reactions to alloy
metals
 No known reaction except
wear on opposite dentition and
restoration
 No long term data on
biocompatibility

Effects of bleaching on pulp
Pulp penetration during bleaching vary among
commercial 10% carbamide peroxide Resulting
in different level of tooth sensitivity or bleaching
efficacy
Potential for pulp damage as result of enamel
and dentin penetration (Powel and Bales 1992)
Cooper et al 1992- pulp penetration can occur
with in 15 mins
Less penetration from carbamide peroxide than
hydrogen peroxide

3% solution of hydrogen peroxide cause a transient
reduction pulpal blood circulation and occlusion of pulpal
blood vessels (Robertson And Melfi 1980)
Most common side effect experienced by patients is
transient, mild temperature sensitivity (Heymann et al
1998)
increased sensitivity in patients overzealous to achieve
faster whitening and increase the frequency of
application
More dose related than pH related

Effects of vital bleaching on pulp histology.
Researchers have observed that vital tooth bleaching
produces histological evidence of minor inflammation of
superficial layers of pulp adjacent to the pulp-dentin
junction (Robertson and Melfi, 1980)
(Cohen and Chase, 1979 and Anderson et al., 1999).
minor inflammatory response of the pulp to the
introduction of bleaching is concurrent with the pain
response expressed by consumers having
hypersensitivity.

 The histological and immunostaining studies confirm in
vivo observations that the response of pulp to bleaching
appeared self-limiting.
 Evidence of pulp inflammation did not worsen with
increased Time of bleaching, and in all cases, responses
appeared self-resolving
 Studies support that controlled home bleaching is safe to
pulp (Kelleher and roe 1999, Li 1998)
 minor, self-limiting and rapidly resolving (even during
treatment) effects of peroxides on pulp tissues

(Varvara et al., 2003) found significant quantities of
active catalase in vital pulp – supporting that rapid
degradation of peroxide would take place during the
limited penetration of peroxide associated with tooth
bleaching.
 In addition, they found that the catalase activity was3-
fold increased in inflamed pulps as opposed to normal
pulp tissue
the concentrations of hydrogen peroxide required to
produce enzyme inhibition were some 1000-10,000 fold
higher than concentration observed to penetrate pulp
under even idealized in vitro treatment conditions

Impression and imaging of prepared teeth
Rubber base impression materials Cause significantly
less damage than impression made with hot wax in
copper band. no heat and little pressure
Langeland found no irritation on pulp.
Hydrocolloid impression material employs no pressure
and heat
The use of a gingival retraction chord with
vasoconstrictor results in significant changes in blood
flow

Imaging of teeth for computer designed
restorations
requires the application of an adhesive and uniform
reflecting material to produce evenly reflecting surface,
titanium dioxide powder is used for this purpose.
No studies have been performed to assess the effects
of such treatment to dentin and pulp.
It is critical to isolate the gingival extent of preparation,
use of rubber dam is essential
Do not allow the preparation to dehydrate, this alone
may cause changes in dentin and pulp

Radiation irritants
Depends on dose source ,type of irradiation,
exposure factors, stage of tooth development
Mature odontoblast appear to be extremely radio
resistant
How ever pulp cells exposed to radiation may
become necrotic
Affect vascularity and interfere with mitosis

Effects of lasing on the pulp dentin complex
Clinically Er;YAG and Carbon dioxide laser do less harm
to the pulp than Nd;YAG laser.
Carbon dioxide laser; animal studies .
increases blood flow,
dilatation of blood vessels.
moderately high energy output caused irreversible
blood flow indicating damage to pulp
Pashley- permeability increases after lasing

NdYAG with 1.06 mm wavelength (white et al) is safe for
the human pulp when used with in safe parameters
Depends on RDT
Using 100mj10ppssecond pulpal flow did not change
with lasing of intact enamel
Flow increased moderately after lasing in cavities with
RDT of 1mm and was irreversibly altered at high energy
levels.
when applied to one area for more than 10sec significant
structural damage is caused.
when lasing for longer than 15 sec, crater resulted
(almost exposing the pulp)

Comparison of cavity preparation by high speed handpiece
and bur and ER:YAG laser(100-200mj at 10 pulses per
second) Sekine y etal 1995
High speed cutting Shows a smooth surface, with smear
layer covering the surface
Laser cutting surfaces is granulated and rough, with
exposed dentin tubules with a sparse smear layer
One day post operatively- displacement and aspiration
of odontoblasts, infilteration of inflammatory cells,
haemorrhage below the prepared cavities. more severe
in case of ER-YAG laser

In seven days pulpal reaction was milder under
shallow cavities inflammation was limited to area
of pulp below the cavities in both the groups
28 days post operatively – repair of
odontoblastic layer in both laser and high speed
handpiece groups
In low RDT groups pulp was almost normal with
no difference between both the groups
In general there was no little or no pulpal reaction
suggesting that there complete healing took place
and cavity preparation to laser is safe to pulp

Reactions of pulp capping agents
Choice of pulp capping agent
a. Biocompatible
b. Provide biological seal
c. Prevent bacterial micro leakage
Traditional – Ca (OH)2 & ZnOE
Other materials tried – Dentin Adhesives, Glass-
ionomers, M.T.A., B.M. P’s.

ZnOE
• Obtundant and more comfortable
• Interferes with polymerization of resins
• Used only when R.D.T > 0.6 mm
Ca (OH)2
• Induces reparative dentin formation
• Does not interfere with resin polymerization
• Used when RDT< 0.6 mm

Ca (OH)2.
Relatively insoluble, acts as mechanical barrier,
neutralize acid from cements, sclerosis of primary
tubules (Major 1968)
Microscopic exposure – deep cavities ca (OH)2 followed
by ZOE
No exposure – ZOË, least irritating-hygroscopic,
anodyne
Calcium hydroxide does not alter nerve impulse activity
,there fore not used to treat painful pulpitis

Calcium hydroxide
Mechanism of action – not very clear
1. Initiates the process of repair – Not a substrate of repair
2. High Alkalinity
a. Local buffer against acidic reaction of the inflammatory
process
b. Neutralizes lactic acid secreted by Bacteria
c. Reduces capillary permeability – reduced serum flow –
increased Ca at the mineralization site – reduces the
concentration of inhibitory pyrophosphate – increased
levels of Ca dependent pyrophosphate – uncontrolled
mineralization
d. Activates alkaline phosphotase activity – plays a role in
hard tissue mineralization
e. Antibacterial action
f. Solubilization of T.G.F.Beta and B.M.P.’s, of dentin
matrix – induces cytodifferentiation.www.indiandentalacademy.com

Disadvantages
•Dissolution over a period of time – recurrent carries
•May degrade upon tooth flexure
•Tunnel defects – 89% of Dentin bridges – contain multiple
defects – permits microleakage of bacteria into pulp
•May exert persistent stimulatory effect
•Does not adhere to composite resin or amalgam
•Acids may degrade the interface while etching
•Does not exclusively stimulate dentinogenesis
Charles F. Cox

Calcium hydroxide
Non-setting type (pH 11-13)
Setting type (pH 9-10)
Chemical cure
Light cure
Healing – Ca (OH)2
High pH Material
Zone of obliteration followed by
Zone of coagulation necrosis
Mummification
1. Dentin bridge – forms below the necrotic zone and pulp void
is formed when necrotic zone resorbs subsequently.

Low Ph material
1. Zone of obliteration but no zone of mummification
2. Dentin bridge – formed
a. Subjacent to capped material
b. As necrotic zone resorbs prior to the formation of dentin
bridge.
Low Ph materials preferred – favorable healing pattern

Dentin Adhesives
•Remaining Dentin thickness – plays major role in pulp
protection
•RDT < 300 µm – Inflammatory pulpal response even in the
absence of Bacteria due to toxic effect of D.B.A. – (Hebling et
al)
•Although many components of D.B.A are toxic to the pulp –
Their release is rapid - slows down dramatically with time – not
a source of chronic exposure to healing pulp tissue –
(Ferracane & Condon )
•Anti Bacterial activity – all the 3 components have shown
some antibacterial activity when tested separately
•After polymerization – Not clearwww.indiandentalacademy.com

Self-etching primer Vs Separate acid conditioner
Self-etching primer
•More favorable results in deep dentin
•Hydrophilic resin infiltrates the collagen and decalcifies the
inorganic component simultaneously without altering dentin
permeability to a great extent
•Better as a pulp capping agent ( Gorden et al)

Cytotoxicity of dentine-bonding agents on human pulp cells
in vitro. International Endodontic Journal, 35, 905 909, 2002.
Set specimens from Clearfil SE Bond (CB), Heliobond
(HB), Prime & Bond NT (PB), Single Bond (SB), and
Syntac Single Component (SC) were eluted with culture
medium for 2 and 5 days. The cytotoxic response
decreased in an order of SB > PB > SC > HB > CB.
Conclusions The influence of the cytotoxicity depended
on the materials tested. Dentine-bonding agents have
significant potential for pulpal toxicity.

Dent Mater 2001 May;17(3):230-40
Response of human pulps capped with a self-etching
adhesive system. De Souza Costa CA, Lopes do
Nascimento AB, Teixeira HM, Fontana UF
evaluate the human pulp response following direct pulp
capping with a current self-etching bonding agent and
calcium hydroxide
 The pulps were capped with Clearfil Liner Bond 2 (CLB-
2) or calcium hydroxide

 CLB-2 elicited a mild to moderate inflammatory pulp response with
dilated and congested blood vessels adjacent to pulp exposure site.
With time, macrophages and giant cells engulfing globules and
particulates of resinous material displaced into the pulp space were
observed.
 This did not allow pulp repair interfering with the dentin bridging.
 pulps capped with CH exhibited an initial organization of elongated
pulp cells underneath the coagulation necrosis. Pulp repair and
complete dentin bridge formation was observed at long-term
evaluation.
Significance:
 The present study demonstrated that CH remains the pulp capping
agent of choice for mechanically exposed human pulps. CLB-2 did
not allow complete connective tissue repair adjacent to the pulp
exposure site. Consequently, this bonding agent cannot be
recommended for pulp therapy of sound human teeth.www.indiandentalacademy.com

Pulpal healing following direct pulp capping with bonding
agents; favourable views
Formation of dentin bridge– although thickness of dentin bridge was less
compared to calcium hydroxide
 Akimoto, Cox et al Noticed tunnel defects in dentin bridge (79%) due to
presence of vascular channels below the bridging interface.
Yet, no inflammation since the cavity is adequately sealed by adhesive – Cox
et al.
Dentin bridge formation after adhesive pulp capping –
D.H.Pashley.
Pulp has a high tolerance for acidic conditioners – Snuggs.
Acid etching of exposed pulp does not produce pulpal inflammation -
Brannstrom.

Pulpal reactions following capping – unfavorable views
Dentin adhesives may be cytotoxic –
Resin monomers –
•immunosuppression of pulpal immunocompentent cells
•decreased resistance to infectious agents
• increased susceptibility of pulp to bacterial attack (Luster et.
al.)
•Globules of resin monomers in pulp cause foreign body
reaction – (Hussey et. al.)

Laser treatment
Effects:
•Sterilizes exposed pulp and surrounding dentin
•Scar formation owing to thermal effect
•Both above – preserve pulp from bacterial invasion and
help efficiently control hemorrhage
•Direct stimulation of dentinogenesis.
(Mortiz et al, Paschand & Holz)

Conflicting reports:
Exercise caution in selecting the parameters
(Y. Kimura, P. Wilder Smith)
Inert materials like Teflon to Bioactive materials like
B.M.P.’s explored.

Mineral Trioxide Aggregate:
Composition: Tricalcium silicate, tricalcium
aluminate, tricalcium oxide and certain mineral oxides
Advantages:
Highly biocompatible with living tissues
Excellent sealing ability
Sets in presence of water
Alkaline (pH 12) – may induce dentinogenesis like
Ca (OH)2 – (Thomas &R.Pittford et. al.)

Hydroxy apatite
Most thermodynamic, stable of all synthetic calcium
phosphate ceramic.
Advantages
1.Hydroxyapatite layer – used as scaffolding for newly
forming mineralized tissue.
2.Wound healing is more desirable than that of
Ca(OH)2

Antoxidants (Catalase)
Essential enzymes necessary for proper functioning
of body’s defense mechanism – helps in tissue
healing.
Mechanism:
a)Free radicals generated during normal oxidative
mechanism --- begin inflammatory process.
Antoxidants – act as free radical scavengers and
aid in healing process.

Growth factors in pulp capping
Physiologic approach to regeneration.
•Bio-active materials - Family transforming growth factor.
•T.G.F.Beta
•B.M.P – Bone Morphogenic Protein
•T.G.F.Beta & B.M.P.- Large signaling molecules that control
differentiation of cell types.
•T.G.F.1,Beta2 and B.M.P. 2-4-6- regulates pulp cell
differentiation, human morphogenesis during odontogenesis,
stimulate synthesis of extra-cellular matrix components including
collagen and proteoglycans.

BONE MORPHOGENIC PROTEINS (B.M.P)
•Direct pulp capping – directly in contact with the pulp
•Indirect pulp capping – permeates through dentinal tubules
•Limits inflammatory response
•Induces cyto-differentiation
•Accelerates tissue regeneration and Dentin Bridge of
physiological quality
•Biologically directed approach / simple mechanical approach
•Bio active material – decrease risk of pulpal necrosis
•Avoids excessive calcification unlike calcium hydroxide dose
dependent dentin deposition.www.indiandentalacademy.com

Collagen:
Advantages: induces dentinogenesis without pulpal
necrosis
Disadvantages: Antigenicity of collagen is high.

Current thinking of the cause of pulpal
reaction to restoration
Microleakage
Three possible routes of microleakage
 with in or via the smear layer
 Between the smear layer and the cavity varnish and
cement
 Between the cavity varnish or cement and the restorative
material
Rate of diffusion of substance depend on
 Concentration gradient of substance
 Surface area available for diffusion
Pashley 1984 diffusible surface area is 1% of total dentin
surface area at the DEJ, where as it is 22% at the pulpwww.indiandentalacademy.com

Marginal leakage
None of the filling materials exhibit perfect marginal seal
against oral fluids
With temporary filling materials greatest leakage around
guttapercha and least around zinc oxide eugenol.
Permanent filing materials exhibit varying degree of
microleakage
Preponderant evidence that Microleakage is responsible
for most pulp irritation and the microflora under
composite resin produce same inflammatory reaction as
produced by dental plaque( Mjor & Tronstad
1972,bergenholtz and lindhe 1975,Mejare et al 1979)
Amalgam produces leakage with in first few days and it
decreases with time (Hembree and Andrews1979)

Restorative Pulpal and Repair Responses Murray P.E.1
JADA The Journal of the American Dental Association,
April 2001,
 authors investigated and compared pulpal reactions to
different types of restorative materials

The results showed that RMGI was the best material for
preventing bacterial microleakage, and resin-based
composite bonded to enamel was the worst.
In regard to minimizing pulpal inflammatory activity,
ZnOE was the best material and resin-based composite
bonded to enamel was the worst.
In terms of maximizing odontoblast survival beneath
deep cavity preparations, Ca(OH)2, was the best
material and RMGI was the worst.
Clinical Implications.; RMGI be used to restore teeth with
cavities that are shallow to moderate in depth, with the
floor of deep cavities being lined with Ca(OH)2 before
the teeth are restored with RMGI.

Bacterial microleakage and pulp inflammation
associated with various restorative materials
Peter E. Murray 2002,
Cavities were restored with a number of materials in the
following categories: Zinc oxide eugenol (ZnOE),
Calcium hydroxide [Ca(OH)2], zinc phosphate (ZP),
Resin-modified glass ionomer (RMGI), Composite resin
(CR), Bonded amalgam (BA), Gutta-percha (GP),
Compomer and Silicate.

In rank order of preventing bacterial
microleakage from best to the worst; RMGI
(100%), BA (88%), ZnOE (86%), CR (80%), GP
(64%), Ca(OH)2 (58%), compomer (42%),
silicate (36%) and ZP (0%).
Significance: The most effective restorative
materials to prevent bacterial microleakage and
pulp injury from inflammatory activity were
RMGI, BA, ZnOE and CR restorations

PREVENTION ;to preserve integrity of
dental pulp
Cutting procedures; use light, intermittent
cutting, an efficient cooling system, high speed
of rotation
Avoid desiccating the dentin
Do not apply irritating chemicals to freshly cut
dentin
Choose restorative materials carefully,
considering physical and biological property of
the material
Do not use caustic sterilizing agents

Assume all restorative materials will leak; use a
cavity liner or base to seal the openings of
exposed tubules
Do not use excessive force when inserting a
restoration
Employ polishing procedure that do not subject
dental pulp to excessive heat.
Establish a patient recall system that ensures
periodic evaluation of status of the pulp that
have been exposed to injury.

Summary and conclusion
Restorative dentistry is an intricate form of microsurgery.
When removing caries, it is often difficult for clinicians to
know how, when, and where to start, and vice versa for
when to stop. Yet there are biological indicators as well as
records of longevity, radiographs, stimuli
testing, and patient opinions to be used for predicting the
outcomes of different caries-treatment strategies, cavity
cutting methods, and restorative materials.

From the bio-logical perspective, each restorative
variable has some effect on pulp vitality, injury,
and regeneration. Deviations from normal pulp
regeneration may be used to diagnose the onset
of complications, such as bacterial leakage and
pulp inflammation. Minimizing pulp injury during
cavity preparation and placing materials which
prevent bacterial microleakage will preserve
pulp vitality.

Furthermore, pulp regeneration will be used as the
basis for tissue engineering to radically alter
restorative dentistry and the prognosis of
restored teeth. Restorative materials may
contain a "cocktail" of growth factors, delivered
in a slow-release vehicle to regenerate
replacement dentin from intra-coronal pulp
matrix.

Biologic response of pulp/ dental implant courses

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Biologic response of pulp/ dental implant courses

Similar to Biologic response of pulp/ dental implant courses (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Biologic response of pulp/ dental implant courses