VITAL PULP THERAPY

Introduction
1. Pulp : A peculiar tissue
2. Skepticism towards vital pulp therapy
3. Present concept
4. Preserving tooth vitality.
5. Development of tooth
Bell stage in detail
Odontoblast
Formation of enamel - dentin complex
Types of dentin
1. Primary dentin
2. Secondary dentin
3. Circum-pulpal dentin
4. Intertubular dentin
5. Peritubular dentin
6. Reactionary dentin
7. Reparative dentin
Types of reparative dentin
Blood supply of teeth
Venous drainage of teeth
Lymphatic drainage
Nerve supply and pain perception
Materials of importance
Calcium hydroxide
Mineral Trioxide Aggregate (MTA) / Portland
cement (PC)
Bone Morphogenic Proteins (BMP)
Remaining dentin thickness and its importance
Indirect pulp capping
Definition
Rationale
Case selection
Caries excavation
Mechanical - Rotary and non rotary
Chemomechanical - Carisolv
Photoablation - Laser
Difference between infected and affected
dentin
Procedure
Choice of capping agent
Calcium hydroxide
Dentin adhesives
Pre-requisites
Rationale
Effectiveness
Biological testing
Controversies
Remaining dentin thickness
Quality and durability of bond
Glass ionomer cement
Re-entry?
Direct pulp capping
Case selection
Factors determining success
Control of haemorrhage and pre-treatment
Materials used
Laser
Calcium hydroxide
Dentin bonding agents
Mineral trioxide aggregate
Collagen
Antoxidants
Growth factors
Pulpotomy
Definition
Partial
Complete
Indications
Procedure
Materials used
Calcium hydroxide
Dentin adhesives
BMP
Re-entry?
Molecular biology
Designing new strategies in vital pulp therapy
Summary and conclusion
 INTRODUCTION

An over view vital pulp therapy

Some pulps die if you stare at them,
while others won’t die even if you cut them with an
axe. Some pulps die kicking and screaming, while
others die a slow painless death.
Skepticism toward V.P.T
Scant knowledge of pulpal physiology
Awareness & therefore acceptance lacking
Indication & criteria for success: controversial
Present concept

Conviction towards V.P.T.

Improved knowledge of pulpal physiology
Better understanding of indications
Clarity of criteria for success
Better utilization of healing potential of pulp
 Aims at preserving the vitality of the tooth

Why preserve?
1. Loss of vitality – loss of intradental sensory function
Registration of masticatory load:

Vital tooth Non vital tooth

a) Periodontal ligament fibers a) periodontal
ligament fibers
b) Intradental nerves

Non-vital tooth requires 2.5 times more load to register a

proprioceptive response than its vital counterpart.
Loss of natural protection of tooth to overload………….
Increased susceptibility to fracture.

2. Cumulative loss of tooth structure after pulp space therapy –

reduces tooth strength
CALCIUM HYDROXIDE
Mineral trioxide aggregate
Bone morphogenic proteins
Signaling Pathway of TGF-
SIGMA-ALDRICH
HOMOLOGY HUMAN BMP

BMP 2

92
%
59% BMP 5
BMP 4

BMP 6
82
% BMP 7

BMP 8

BMP 9

BMP 3
Bone Morphogenetic Protein Receptors
SIGMA-ALDRICH
 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 even after
38days in patient
 INDIRECT PULP CAPPING

Definition
“A procedure where in a small amount of carious
dentin is retained in deep areas of cavity preparation to
avoid exposure of the pulp and placement of a
medicament to seal the dentin, and encourage pulp
recovery.”

“The application of a suspension of calcium hydroxide

to a thin layer of dentin overlying the pulp, in order to
stimulate secondary dentin formation and protect the
pulp.”
Medical Dictionary Search
Rationale:

Demineralization precedes bacterial invasion

Asymptomatic till bacteria within 0.5 mm from pulp
Softened dentin close to pulp – no bacteria
Absence of substrate kills or inactivates the few left
behind
Therapeutic pulp capping agents may aid in dentin-
bridge formation
Case selection : Reversible pulpitis

Symptoms : Thermal stimulus –

momentary pain

Percussion : Non tender

Vitality : Normal or slightly

exaggerated

Radiography : Absence of –
Periodontal ligament
thickening
Periapical rarefaction
 PROCEDURE
Caries removal
Placement of indirect pulp capping agent
Final restoration

Carries excavation
a) Mechanical
Rotary- High and low speed

Non rotary – spoon excavators

Air abrasion – Sono abrasion –Ultrasonics
(Not effective in removing soft caries)
Slow speed drills preferable to the spoon excavators
b) Chemomechanical – carisolv
c) Photoablation – laser
 Infected dentin Affected dentin
1.Softened demineralized 1.Softened deminerlized dentin
dentin teeming with not yet invaded by bacteria
bacteria
2.Collagen is irreversibly 2.Collagen cross linking remains
denatured
3.Cannot remineralize 3.Acts as a template for
remineralization
4.Soft necrotic tissue, 4.Softer than normal dentin,
followed by dry leathery discoloured but does not flake
dentin – flakes away with easily
an instrument
5.Dyes: 1% Acid red in 5.Does not stain
propylene glycol stains
only irreversibly denatured
collagen
Chemomechanical caries removal

Carisolv – modified hand excavation with the aid of gel

Excavation aided by Gel:

a) Lubricating effect to aid mechanical removal
b) Chemical effects on carious dentin
- Chlorination of partially degraded collagen
- Cleavage by oxidation of Glycine residue
- Resulting in collagen fibril disruption
- Collagen fibrils – more friable and easily removed
Advantages
• Selective removal of softened dentin
• Conserves sound tooth structure
• No iatrogenic pulp exposures
• Painless procedure
• Biocompatible – No adverse reactions on pulp
• Removes smear layer – aids in bonding of adhesive
restorations

Disadvantage: Time consuming (9-12 minutes)

 Caries excavation by Photoablation

Lasers : Cut – incise - ablade

Hard and soft tissue lasers

Mechanism: Water molecules within the microscopic

dentinal surface absorbs energy on laser irradiation.
- Builds up pressure within the dentinal surface
- Micro explosion and vaporization.

Laser used: Carbon dioxide, Diode

and Excimer lasers, Nd:YAG, Ho:YAG
and Er:YAG lasers.
 Demonstration of Biolase Waterlase cutting
system combining laser energy with water
droplets to create high-speed hydrokinetic water
particles that can mechanically cut both hard
and soft tissues.
Advantages
• Selective ablation of carious dentin
• Mild thermal irritation – induces dentinogenesis
• Sterilization of dentin
• Reduces permeability and sensitivity of dentin
• Painless when compared to drills
• Irregularities on dentinal surface – (Aids in resin
bonding without altering permeability)
Limitations

• Concern regarding the thermal effects on pulp

• Appropriate parameters to be selected, to avoid
thermal injury to pulp
• To be used with caution
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
 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.
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
Dentin Adhesives

Pre-requisites:

Acid, Primer, Adhesive- should not be cytotoxic or

atleast neutral to living tissue
Effectively seal and prevent microleakage permanently
Preferably antimicrobial
Able to stimulate reparative dentinogenesis
Rationale:
Bacterial microleakage – pulpal irritation
Pulpal healing –depends on biological sealing
Hybrid layer – morphological impregnation of vital dentin
with resin – permanent seal against bacterial invasion.

Effectiveness of DBA – factors responsible

Quality and durability of bond in deep dentin
Chemical nature of its components and its effects on
pulpal tissue

Biological testing of DBA – Complex

DBA are made up of more than one material
Each component being altered to further
improve bond strength and clinical performance
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. Hume
•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.
Dentin Adhesives

Remaining Dentin thickness – plays major role in pulp

protection
RDT < 300 m – 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 clear
 Self-etching primer Vs Separate acid conditioner

S.E.P.’s

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)
Quality and durability of bond in deep carious
dentin
1) Bonding in deep dentin < Superficial dentin
a) Reduced amount of intertubular dentin and
collagen
2) Bonding to carious dentin < sound dentin
a) Disturbed collagen network
3) Acid etching – increased permeability –

a) Reduces polymerization
b) Reduces bond strength
c) Therefore integrity of Bond - ?
 Indirect pulp capping

Conventional
Ca (OH)2 or ZOE

- Time tested
- Considerable degree of success
- Long term studies available
- Certain limitations

Dentin Bonding Agent

- Initial encouraging result

- Dispute over long term seal
- Conflicting reports on risk of cytotoxicity
Glass Ionomer
Indirect pulp capping agent

RMGIC – For both indirect and direct pulp capping

Histological response of pulp in both situations was
similar to Ca (OH)2 – (Cox et al)

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.)
Re-entry – Is it necessary?

Re-entry is not necessary: Majority opinion

a) Additional operative procedure – overzealous
excavation of inactive lesion – Irritate healing pulp
b) Restoration placed provides permanent seal against
bacterial ingress and prevention of microleakage and
its consequences periodic clinical and radiological
checkup would suffice.

Re-entry necessary:
Re-entry and stepwise excavation suggested (Pittford)
 DIRECT VITAL PULP THERAPY
“An exposed pulp is doomed organ” – Rebel
Research ongoing to disprove this axiom – Stanely Cox
and others
Doomed organ ---------- “Hope & Recovery”

“A procedure for covering and protecting an

exposed vital pulp.”
Medical Dictionary Search
Case selection

a) Traumatic exposure of pulp provided the patient reports

early
b) Small mechanical exposure of the pulp in an asymptomatic
vital tooth with sound dentin at the periphery
c) Small carious exposures in an asymptomatic vital tooth
with incomplete root information
Benefits far out weigh the risks

d) Carious exposures in mature teeth – should be

discouraged (Not a contraindication) – (Seltzer & Bender)
i. Microbes and inflammation invariably associated
ii. Operative procedures add insult to injury
iii. Ailing pulp may not respond favorably
iv. Therefore advocated only when time, economics or any
other factors don not permit R.C.T. (Cohen)
Factors determining success of direct pulp capping
Size of exposure : Large exposure – poor prognosis
Traumatic exposure – size does not
interfere as long as pulp is healthy.

Hemorrhage : Necessary to arrest bleeding

Continued bleeding indicates
irreversible inflammation
Location of exposure : Compared to occlusal or incisal,
exposure on the axial wall poor
prognosis.
Isolation from saliva : Rubber dam isolation to prevent
flooding of microorganisms mandatory.
Dentin chips intrusion: Severe foreign body reaction
worsens inflammation –
“Chipitis”
Marginal seal: coronal seal crucial to prevent microbial
leakage irrespective of pulp capping material. Improper
seal worsens pulpal inflammation.

Age of Tooth: Younger tooth responds better than

older ones- capacity to heal better.

Extrapulpal clot: Presence of extrapulpal clot impairs

healing
- Acts as bacterial substrate
- Barrier between capping material and the pulp
Direct pulp capping

a. Control of hemorrhage and pre-treatment

b. Pressure application
c. Haemostatic agents
d. Sodium hypochlorite pre-treatment : 2.5%
i. Controls hemorrhage
ii. Provides disinfection
iii. Removes dentin chips from subjacent pulp tissue
iv.Removes fibrin and clot (chemical amputation)
e. Pretreatment with chlorhexidine to disinfect prior to
capping
f. Steroid antibiotic paste – Symptomatic tooth for 3-4
days prior to capping (Stanley)
DIRECT PULP CAPPING
 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:

Lasers are a boon –but could be a bane

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

Rationale:
1. Cohesive hybridization – seal against bacterial
invasion
2. Resinous film layered over wet pulp without
damaging or displacing pulp tissue
3. Primer and adhesive work in wet environment –
reduces potential for dehydration injury
4. Resinous covering effectively prevent displacement
of composite resin into pulp chamber
Pulpal healing following direct pulp capping views
Formation of dentin bridge in primates – 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 resistacne 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.)

Why controversial reports?

Excellent results with dentin bridge formation
Mild to moderate reaction
Disastrous results
Studies are short term.
Varying evaluation period.
Trials done on primates on non carious teeth.
Technique sensitive material.
Histological findings – don’t correlate with clinical
picture.
Dentin bridge formation – criteria for success ?

Criteria Not criteria

Hess Zonder Kanca Gutman et al.
J. Cvek etc Santini et al etc.
Mineral Trioxide Aggregate:

Composition: Tricalcium silicate, tricalcium

aluminate, tricalcium oxide and certain mineral oxides

Advantages:
Highly biocompatible with living tissues
Hydrophillic – sets hard in presence of water
Alkaline (pH 12) – may induce dentinogenesis like
Ca (OH)2 – (Thomas &R.Pittford et. al.)
Collagen:
Advantages: induces dentinogenesis with out pulpal
necrosis

Mechanism
• Collagen fibrils catalyses calcium phosphate
crystallization from physiologic concentration of Ca
and PO4 ions
• 3 dimensional collagen net work is formed
Can be used as frame work for healing
process.

Disadvantages: Antigenicity of collagen is high.

Hydroxy apatite

Most thermodynamic, stable or 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)
In direct and indirect pulp capping
•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.
Considerations for usage
•Delivery vehicle – appropriate carrier facilitates
proper clinical handling
•Dose response – active in picogram level – Dose
effect relationship to avoid uncontrolled calcification
•Possible immunological problems associated
•Half-life of molecules and local tissue factor which
may modulate their activity.

Clinical trials on way with commercially available

B.M.P.’s
If successful B.M.P.’s will help transcend all other
treatment modalities currently available –
(DM. Ranly et al)
 PULPOTOMY

Definition: “Surgical removal of inflamed or infected

coronal pulp leaving intact vital tissue in the canals. A
suitable medicament is placed over remaining tissue
attempt to promote healing and retention of vital
tisuues.”

Partial pulpotomy
Introduced by Cvek, differs from Sweet’s pulpotomy in
that, only a portion of the coronal pulp, (Superficial
layers – just sufficient depth to reach the tissue that is
free of inflammation) is removed before placing a
medicament.
Indications:

1. Traumatic exposures where coronal pulp is likely to

be inflamed in young healthy teeth.

2.Mechanical or carious exposure in teeth with

incomplete root formation
Procedure:

 Pulp amputation

 Hemorrhage control

 Placement of medicament

 Final restoration
PARTIAL
PULPOTOMY
COMPLETE
PULPOTOMY
1- Completely
remove caries.
2- Open pulp
chamber by
completely
removing the
roof with 330 high
speed bur.
3- Remove pulp from
pulp chamber with
a sharp curette or
a large round low-
speed bur or a 330
high speed bur.
4- Stop bleeding by
applying a moist
cotton pellet in the
pulp chamber for 3
minutes
5- Place a cotton
pellet with
formocresol for 5
minutes in the
pulp chamber.
6- Remove cotton
pellet and
confirm pulp
fixation, by the
“black eye”
appearance of “Black eye”
the pulp stumps .
7- Fill the pulp chamber
with ZOE-eugenol
Pulp amputation
• Sharp spoon excavator
• Large rotating round bur in slow speed.
• Diamond drill – High speed
• Electro surgery
• Lasers

High speed drill with coolant – superior to spoon

excavator or slow speed round bur - Least trauma to
under lying pulp
Control of hemorrhage – most crucial for successful
outcome.

Control of hemorrhage :
a. Pressure application with moist cotton pellet
b. Haemostatic agent e.g. – aluminum chloride, gel
foam, sodium hypochlorite – good results with
additional advantages
c. Electro surgery
d. Laser energy
i. Blood less tissue incision
ii. Sterilization of pulp, promotes healing
iii. Scarring
Choice of pulpotomy agent

 Calcium hydroxide
 Formocresol
 Gluteraldehyde
 Dentin adhesives
 Light cure glass ionomers
 Collagen, cyanoacrylates
 B.M.P’s etc.
Calcium hydroxide: traditionally used over many
decades with considerable degree of success.

Limitations:
May precipitate dystrophic calcification,
complicating pulp space therapy later.
 Dentin adhesives as pulpotomy agent

Rationale – similar to direct pulp capping. In fact

chances of success should be better since the
diseased pulp is removed – response of remaining
healthy pulp should be more favorable provided,
hemorrhage, isolation and prevention of bacterial
leakage is take care of.
• Normal healing on monkey pulps
• Supports use of D.B.A. for sealing
pulpotomized teeth.
(Abeer A Hafeez, M.S. Hugn et. al.)
Bone Morphogenic Proteins in pulpotomy:

A physiological regenerative approach under trial.

Advantages
Predictably induces sound dentin bridges
leaving radicular tissue completely enclosed in
healthy dentin.
Need for pulp space therapy after pulpotomy
eliminated.

If successful
Vital pulp therapy will acquire more importance
in preventive endodontics.
Pulpotomy – permanent treatment procedure
even in mature teeth.
RECENT CONCEPTS – MOLECULAR
BIOLOGY
 MILD INJURY:

Odontoblast responsible for primary dentin

secretion can survive the challenge and are
stimulated to secrete a reactionary dentin. Since
original primary odontoblast are responsible for this
matrix, there will be tubular continuity and
communicates with the primary dentin matrix.
ODONTOBLAST SECRETORY ACTIVITY

PRIMARY DENTIN

ODONTOBLASTS
ODONTOBLAST SECRETORY ACTIVITY

PRIMARY DENTIN

PHYSIOLOGICAL
SECONDARY DENTIN

ODONTOBLASTS
ODONTOBLAST SECRETORY ACTIVITY

INJURY

PRIMARY DENTIN

TERTIARY DENTIN
SEVERE INJURY:

Odontoblast beneath the injury die and odontoblast like

cells differentiate and form reparative dentin matrix.

The distinction between reparative and reactionary dentin

is based upon the origin of the odontoblasts responsible
for its production.

Reparative dentin is a tertiary dentin matrix formed by new

odontoblast like cells in response to a specific stimulus,
while reactionary dentin is formed by surviving
odontoblasts subjacent to diseased or otherwise
damaged dentin.
Reparative dentin is a
tertiary dentin matrix
formed by new
odontoblast like cells in
response to a specific
stimulus, while
Reactionary dentin is
formed by surviving
odontoblasts subjacent
to diseased or otherwise
damaged dentin.
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,
Tubular Tubular Tubular Tubular
discontinuity and discontinuity and continuity and dimensions
decrease in decrease in density maintenance of decreased by
density with beneath a thin layer tubular density deposition of
tertiary dentin of tubular hard tissue but diffusion peritubular dentin
deposition. formed initially from distance to pulp sclerosis
poorly differentiated increased by
odontablast like cells. tertiary dentin
deposition

Injury

Primary
dentin

Tertiary
dentin
MOLECULAR AND CELLULAR UNDERSTANDING OF
ODONTO BLAST DIFFERENTIATION :
 Differentiation of tooth germ is triggered by various molecular
signals.


.Molecular signals are responsible for the cytodifferentiation of

dentin secreting odontoblast.

Molecular signals are helpful for
There are two types of Molecular
both,
signals,
 Induction of odontoblast
differentiation  Endogenous signaling molecules
 Stimulation of odontoblast
 Exogenous signaling molecule
metabolism
Exogenous signalling Endogenous signalling
molecules molecules
BIO-ACTIVE MOLECULES IN ODONTOBLAST
DIFFERENTIATION :

Inner dental enamel epithelium

Dental basement membrane

Dental papilla
IMPORTANCE OF MATRIX
SUB-STRATUM
• The presence of an
Endogenous
insoluble substrate signalling
molecules

to which pulp cells

Fibrodentine
can attach and
express the
Pulpal
progenitor
phenotype of cell Odontoblast – like cell

odontoblast like
Fibrodentin formed as an intermediate
cells seems to be
matrix zone during the wound healing
of critical
process has been suggested to
importance during
represent the stereotypic requirement
reparative for initiation of reparative dentin
dentinogenesis. formation.
Differentiation of odontoblast like cells in pulp capping situations
has been observed when healing processes occur in contact
with a collagenous matrix formed as a response of vital pulp
tissue to superficial necrosis or with some calcium hydroxide
containing cements.

Calcium hydroxide

Firm zone of
tissue reaction
binding

Endogenous
signalling
Pulpal progenitor cell molecules
Odontoblast – like cell
• The role of these surfaces in the mechanisms,
which control odontoblast like cell differentiation,
has not been adequately investigated.

• The substrate adhesion molecule fibronectin

seems to mediate interactions between these
substrates and pulp cells.
Dentine matrix containing
signalling molecules

Pulpal Odontoblast – like

progenitor cell
cell
ADVANTAGES AND LIMITATIONS OF NEW
STRATEGIES:

One of the major advantages of stimulating a

reactionary or reparative dentinogenic response
beneath injury in the tooth is to promote
deposition of a protective hard tissue barrier
which is an integral part of the function of the
tooth between the pulpal cells and the injury.
Stimulation of a specific cellular response in the
dentin pulp complex at the site of injury would
allow a biologically directed approach to tissue
repair rather than a simple mechanical
approach.
However, new strategies based on these
approaches will have to address the problems of
delivery and control of the bioactive molecules
and also the spatial pattern of dentinogenesis
leading to matrix deposition in a pulpal direction
whereas tissue loss occurs from the opposite
direction.

Whilst the latter point may be of lesser importance

in situations of pulpal exposure, it will be
significant where residual dentin remains.
Re – entry after direct vital pulp therapy

Should direct vital pulp therapy be followed by

pulpectomy and pulp space therapy?

Controversial
Seltzer and Bender
• Routine re-entry not necessary
• Follow proper technique with utmost care to avoid
microbial contamination – progressive calcification
is infrequent sequelae.
• Periodic recall will suffice – Cohen C. Burns
Conclusion
Ultimate goal of Vital Pulp Therapy is to maintain the
vitality and function of pulp dentin complex.
 Natural defense mechanism of pulp have been
fully recognized.
 Healing and recuperation of pulp largely
depends on providing an irritation free environment.
 Varieties of materials are tested for V.P.T. with
variable degree of success – therefore dentin
bridge formation does not seem to be material
specific.
 Do not employ procedures and materials, which
will over power pulpal defenses and push the pulp
beyond a point of no return.
“Do the right thing at the right time –the right
way for the right patient – to get the best
possible results”
 List of references
1. Orban’s Oral histology & Embryology. 2004 mosby 11th edition.
2. The dental pulp. 2000 Samuel seltzer & I.B.Bender 3rd edition
3. Tissue engineering (qb) 1999. Samuel E lynch, Robert J Genco & Robert E
Marx.
4. Evaluation of clinical & Microbiological features of deep Carious lesions in
primary molars, Buket ayna et al (J Dent Child 2003;70 15-18).
5. Desinging new treatment strategies in vital pulp therapy, D. Tziafas et al, (J
of dentistry 2000;28 77-92).
6. Calcium hydroxide pastes : Classification and clinical indications, L.R.G.
Fava et al, (INT. Endo J 1999; 32 257-282
7. Formaldehyde in dentistry : A review for the millenium, Bradley Lewis (J Clin,
Pediatr Dent 1998; 22(2) 167-177
8. Er: YAG Laser Effects on Oral Hard and Soft Tissues, Ulrich Keller &
Raimund Hibst (Lasers in Dentistry)
9. Identification of Hard Tissue After Experimental Pulp Capping Using Dentin
sialoprotein (DSP) as a marker (JOE, 2003 29(10) 646-650)
10.Reparative dentin: affecting its deposition, Charles F. Cox et al (QI, 1992 23
257-270
11.Pulp capping of dental pulp mechanically exposed to oral microflora: a 1-2
year observation of wound healing in the monkey. C.F.Cox et al ( J of oral
pathology 1985: 14 156-168).
12.Pulpotomy therapy in primary teeth: new modalities for old rationales, Don
M. Ranly.(Pediatric dentistry 1994 16(6) 403-408)
13.Pulpal healing and dentinal bridge formation in an acidic environment.
C.F.Cox et al ( QI 1993; 24 501-510)
14.Histopathologic study on Pulp response to single-bottle and self Etching
adhesive systems VO Medina et al . (Operative dentistry 2002 27 330-342).
15.Direct pulp capping with bonding resin, without calcium hydroxide H.S. Cho
et al (Int J of paed Dent 13(suppl 1 ): 5 -68