INTRODUCTION:

During the last 200yrs there have been many changes in the

rationale governing the treatment of dental pulp.

Question concerning which technique gives the highest % of

success. It is essential to have thorough understandings of the

compatibility of the material, its physiological response, and the

histological changes that takes place during and after the use of

medicaments

HISTORY

Mid – 18th century - Pierre Fauchard

Mid – 19th century - John Tomes

“ Layer of discolored dentin” (indirect)

1756 – Philip Ptaff – “golf leaf” (direct pulp capping)

1850 – ‘Principles of indirect pulp capping – Foster

1860 – Taft – ‘mixture of sorghum molasses/sparrow

1866 – Atkinson - Creosote

1891 – W.D. Miller – Antiseptics

1930 – Teucner – New era

1980 – Calcium phosphate cement

1990 – Dentin bonding agent

1993 – Mineral trioxide aggregate

Zones of early enamel caries:

I Translucent: More porous (1% pore volume/0.1% normal enamel)

1.2% mineral loss

II Dark zone: Positive – more porous (2-4%) – 6% mineral loss

III Body of lesion: 5% in periphery & 25% center – 25% mineral loss

IV: Surface zone: Unaffected (20-100µm) – 10% mineral loss

Zones of dentinal caries:

I Normal dentin: No bacteria

II Sub-transparent dentin: Demineralization of intertubular – crystals

– odontoblastic process are damaged

III Transparent dentin: Softer

IV Turbid dentin: Bacterial invasion – widening & destruction of

tubules– little mineral – denatured collagen

V Infected dentin: Decomposed dentin

Infected dentin Affected dentin

Highly deminerlized Less

Unremineralizable Remineralizable

Superficial layer Deeper

Lacking sensation Sensitive

Can be stained Does not stain

Should be excavated Left behind

DIRECT PULP CAPPING

Application of a medicament to exposed pulp to preserve the vitality

1. Pinpoint – sound dentin – no hemorrhage - mild infl. – repaired

2. Pinpoint – sound dentin – drop of blood – mild infl.

3. Infected dentin – considerable – site far – doubtful

4. Profuse – greater infl. – very doubtful

5. Infl. Pus/fluid – destruction – not indicated

Indications: No H/O pain.

Exposure size < 4 mm

No observable hemorrhage

Clean uncontaminated field

Dentin at periphery is repairable

No pathologic changes

Contraindications: Severe toothache

Tooth mobility

Excess hemorrhage

Purulent discharge

Radiographic changes

Direct Pulp Capping

INDIRECT PULP CAPPING

Gross caries is removed and the cavity is sealed with a biocompatible material

Indication: Pulp inflammation is minimal – complete removal of caries would cause an exposure

Contraindication: Severe toothache

Tooth mobility

Purulent discharge

Radiographic changes

Indirect Pulp Capping

Objectives: Seal completely

Vitality.

No prolonged post-treatment

Pulp healing & tertiary dentin

No pathological changes.

Failures:

Degree of trauma

Sealing pressure

Low threshold of host resistance

Presence of microorganisms

Failure of an aseptic technique

Ivory Quill Gold-beaters skin Oiled skin

Paper Plaster of paris Canada balsam Asbestos Gutta percha

Lactophosphate of lime Oxychloride Oxyphosphate Oxyxulphate of zinc cement

Calcium hydroxide Pulp Caps – Celluloid Dome

Zinc phosphate

Zinc oxide eugenol

Zinc polycarboxylate

Glass ionomer

Calcium phosphate Freezed dried bone MTA

Bone cement

Demineralized dentin matrix Bioactive glass

Dentin chips Collagen matrix

Zinc phosphate cement

– Most irritating (acidity / exothermic)

- Solubility (0.06%), pH 3.5 (neutral)

ED >2.5 mm – Healthy reparative, but occ. unhealthy

ED 1.5 - 2.5 mm – Unhealthy reparative, sometimes destruction

ED <1.5 mm – destruction of pulp tissue

Zinc oxide eugenol:- Least irritating (eugenol / impurities)- Solubility (0.4%), pH 6.6-8- Obtudent (sedative)

1. Pulp is healthy, site is controlled microbially & reparable

Limited Propagate Firbosis Acute infl.

Fibrous tissue Pulp/root canal No bridge Necrosis

Matrix formation Necrosis (slow/symptomless)

Mineralization

Bridging

2. Acute inflammation – bridging is unlikely to occur

3. Dentin chips – fibrous – bridging. (nucleation)

4. Impingement (force, thin matrix) – interfere healing.

Zinc polycarboxylate

- minimally irritant

- Solubility (0.6%), pH 3-4 (5-6)

ED >1mm = healthy reparative dentin

ED <1mm = Unhealthy / frequently destruction

BORISSOV 2003 – 5% potassium nitrate (anti-inflammatory effect of

alkaline medium) – reparative dentin.

Glass ionomer cement

- irritant

ED > 1.5 mm = healthy dentin

ED 0.5 – 1 mm = unhealthy dentin

ED < 0.5 mm = destruction

Cyanoacrylate cements

- Composite-type polymers

- methyl, ethyl, n-butyl or isobutyl cyanoacrylate

Rapid hemostasis, biocompatible & reparative dentin

formation – without necrotic zone. (Berkman & Bhasker et al, 1971)

On degradation – low-grade degeneration – cellular layer – chemical

equilibrium – attract calcium - mineralization

Spray form

Fine drop of liquid

Additive in capping material:

Diff. Substance – to reduce infl./eliminate infection

Corticosteriods: Degenerative changes – interfere hard tissue

(Hansen, 1963, Everett 1969, Barker 1969, Mitchell 1970,

Soto-Feine 1982)

Antibiotics: Little information on topical application (cytotoxic/hypersensitivity)

[Tetracycline, neomycin, penicillin, vancomycin – Obersztyn 1968, Baker 1969, Gardner 1971, Page 1973, Bergenholtz

1977]

Antiseptics: Cytotoxcity

(Dankert 1976, Martin 1978, Kopel 1980, Cunningham 1982)

Calcium Hydroxide

In 1920, Herman- irritant (alkalinity)- Solubility (0.4-7.8%), pH 9.2-11.7

ED > 1mm = healthy reparative dentinED < 1mm = unhealthy reparative dentin

Direct Contact1. Zone of obliteration (compressed tissue) –

debris, dentinal fragment, hemorrhage, blood clots, Ca(OH).2. Zone of edema3. Zone of coagulative necrosis(mummifying) -

24-hours

2-3 weeks

4-5 weeks

2-months

Ca(OH)2

Ca2+ OH-

Reduced capillary permeability Neutralize acid -osteoblast

Reduced serum flow Pyrophosphates activity (pH)

Reduced – level of inhibitory Increased Ca2+ dependent pyrophosphate pyrophosphate

Uncontrolled mineralization

Advantages:

Bactericidal & bacteriostatic

Promote healing & repair

pH – fibroblasts

Inexpensive and easy to use

Disadvantages:

Does not exclusively – dentinogenesis/reparative dentin

Degrade during acid etching

Do not adhere to dentin / resin restoration

Solubility

Settable calcium hydroxide:

Dycal

Hydrex

Reolit

Life

Nu-Cap

Dycal VLC

Reocap

Procal

Water-Based Calcium Hydroxide • Direct pulp-capping • Radiopaque •63% Ca(oH)2•"Save cap"

Self-Curing Calcium Hydroxide • Indirect pulp capping• 25 % Ca(oH)2

Light-Curing Calcium Hydroxide • Cures in 30 seconds • Compressive strength (135 MPa)

COX et al – capacity of the capping agents to provide a biologic

seal against immediate & long-term bacterial microleakage along

the entire tooth surface

Hybridization of dentin

Superior ability to adhere to both demineralized enamel and dentin

Inoue et al, 1992 – excellent pulp healing

Katoh et al, 1993 – good healing with adhesive resin

Miyakoshi et al, 1994 – protective layer on the pulpal surface

Jontell et al, 1995 – immunosuppression -pulpal immunocompetent cells

Tsuneda et al, 1995 – histopathologic – best healing(absence infl.)

Mijakoshi et al – 4-META-MMB-TBB – effective biological seal

Ability to seal the exposure site from bacterial microleakage

• Cytotoxic – pulpal inflammation

• Leachable nonpolymerized monomers

• Accumulation of DBA fragments

In vitro/ In vivo – components are cytotoxic to pulp cells (fibroblast)

Current adhesives (SEP) – suitable property – lack of diffusion of resin

globules (DT) – may be useful and safe

While bonding system have greatly improved sealing

ability in recent years, there is a clear evidence that even with the

best bonding system, there is microleakage of bacteria around the

restoration

Need long-term clinical performance

MTYA1-Ca (resinous agent)

Powder: Microfiller 89%

Calcium hydroxide 10%

Benzyl peroxide (catalyst) 1%BPO

Liquid: Triethylene glycol dimethacrylate 67.5%(3G)

Glyceryl methacrylate 30%GM

Methacryloyl tyrosine amide(MTYA) – adhesive

Dimethyaminoethylmethacrylate (initiator) DMAEMA

Camphoroqiunone ( catalyst)

• Powder:Liquid = 3:5

• MTYA – good adhesion (adhesive monomer)

• Triethylene glycol dimethacrylate – Mechanical prop

• Glyceryl methacrylate – bond strength

MTYA1-Ca – good physicalproperties.

Potential to be used as a direct pulp capping agent

Niinuma et al,1999

Calcium phosphate cements (1980)Ca:P

Octacalcium phosphate, (Ca4H(PO4)3)3H2O 1.33

Tricalcium phosphate, (Ca3(PO4)2) 1.50

Calcium hydroxyapatite, (Ca5(OH)(PO4)3) 1.67

Dicalcium phosphate dihydrate, (CaHPO4 2H2O) 1.0

Nucleation/growth – amorphous

solid – crystalline HAP

Further investigations – explain

how exactly – contribute RD formations

Bioactive glass

Calcium 24.5%Sodium 24.5%

Silica 45.0%

Phosphorus 6.0%

Grainy particles Porous

Negative charge, - attract building blocks

Framework of hydroxy-carbonate-apatite crystals - trapping & bonding building blocks

Amorphous non-crystalline – ionic release

MTA

Fine hydrophilic particles – Tricalcium silicate

- Tricalcium aluminate

- Tricalcium oxide

- Silicate oxide

Hydration – colloidal gel - < 4 hours – pH 10.2

to 12.5

• Resistant to marginal leakage

• Allows normal healing response

• Set in the presence of moisture

• Reduces bacterial migration

• Open a single pouch

• Mix with the water ampule (sterile water) provided to a creamy consistency

• Condense with a condenser

•Approximately 5 - 15 minutes' working time and 4 - 6 hours' setting time

•Action: Stimulate cytokine release – hard tissue

formation

Dentinogenesis – sealing ability, biocompatibility & alkalinity

Portland Cement

• Ingredients in common with MTA, (calcium phosphate, calcium oxide, & silica.)

• MTA - bismuth oxide (radiopacity), - absent PC

• Induce dentin bridge - excellent sealing, fast ST 5 minutes.

BONE CEMENT

Powder - (polymethyl) methacrylate polymer, methyl methacrylate – styrene copolymer & barium sulphate

Liquid - methylmethacrylate monomer.

Antibiotics - 2% weight by weight (gentamicin sulphate)

Advantage: Moist environment.

Gary Mathew Holt & Thom C Dumsha - dye leakage

In vitro bacteriological study by High et al - bacteriocidal

An ideal repair material is one that will support osteogenesis and

cementogenesis and biocompatible, non toxic, non carcinogenic, easily

obtainable, convenient to use, biodegradable. No such “ideal material”

has yet been identified

LASER

First laser use in endodontics – Weichman & Johnson, 1971• CO2• Argon• Nd YAG• Er. YAG

Immense heat & power – sterilizes scar formation – preserve

pulp from bacterial invasion

Blood extravasation – gradual organization – hard tissue formation

Melcer et al, 1987 – exposed pulp tissue (CO2) – hemostasis

Ebihara et al, 1992 – Nd:YAG – 89% success

Moritz et al, 1998 – CO2 – direct pulp capping

Sekine et al – No reparative dentin formation (28 days)

Wigdor et al – No reparative dentin – after 4 days (CO2 laser)

Tankano et al - Reparative dentin (Er.YAG)

With the development of thinner, more flexible and durable

laser fibers, laser application in endodontics will increase, but

acceptance of this technology by clinicians has remained limited

Two concepts

Mechanical concepts Biological properties

Disappearing Bioactive molecules

Bioactive molecules: Materials that induce a specific biological activity in the body

With the development of tissue engineering, a new era that will

lead to modifications in daily practice in the near future

Bioengineered reconstruction, regeneration – four components

Undifferentiated / STEM cells

- repair site – cells prog. specifically – tissue

3D-ECM

- Specific – possess intrinsic mineralizing prop

Signaling molecules

- cytokines, growth factors, hormones

Carrier

- important factor, scaffold

DSPP

DPP DSP

- nucleator for mineralization

- dentin mineralization

• Dentin matrix protein (DMP-1)

• Bone sialoprotein –I (osteopontin) Bone sialoprotein

• Bone sialoprotein –II

TGF-ß

BMP-7 / OP1

IGF – I & II

Rutherford et al - hOP-1/ bovine type-1 collagen, sterile saline, reparative dentine

Nakashima - BMP-2 & BMP–4 - dentin formation

Hu et al - (i.e.EGF, FGF, IGFII, PDGF-BB, and TGF-ß) - TGF-ß1 = enhanced reparative dentin

Six et al - the effect of dose-dependent BMP-7 - collagen pellets containing 1, 3 or 10 µg = No difference

BMP-7/OP-1

Enamel matrix (EMD) induces hard tissue formation in the pulp and that it may be a suitable capping agent.

Emdogain®Gel consists of EMD in propylene glycol alginate.

Two vials - a vehicle solution and freeze dried enamel matrix

proteins (amelogenin fraction). When mixed,

they create a viscous,

easy to use,

syringable gel

Treatment of dentine matrix with various cavity conditioning

agents -solubilize TGF-b1

EDTA was the most effective agent

Calcium hydroxide is also able to solubilise TGFb-1 from dentine matrix

Questions concerning the application of these biological modulators:

1. Development & classification of biological modulators.

2. Interaction - artificial barriers, biological modulators, & restorative

materials.

3. Effects - status (i.e. normal, inflamed or infected). Most of the

research - vital, non-inflamed

4. The effect of aging on pulpal response.

5. The delivery vehicle used for the molecules.

6. The dose response effects of the molecules.

7. The half-life of the molecules.

8. Immunological problems due to repeated implantation

Reparative Dentin Formation by Ultrasound-Mediated Gene Delivery of Growth/Differentiation Factor 11

BMPs - Odontogenic differentiation.

Gene therapy - induce reparative dentin. Gene transfer

(Gdf11)/Bmp11 plasmid DNA into dental pulp stem cells by

sonoporation & stimulated by ultrasound (1 MHz, 0.5 W/cm2, 30 sec) -

stimulated a large amount of reparative dentin formation on the

amputated dental pulp in canine teeth in vivo.

Gdf11 cDNA plasmid - by sonoporation in vitro, induced Dsp

(marker for odontoblasts.)

Thus, the result suggested the possible use of BMP using

ultrasound-mediated gene therapy for endodontic treatment.

• Endodontic & restorative challenge

• Debridement & obturation - impossible

APEXIFICATION

Process of creating an environment with in the root canal & periapical tissue after pulp death that allows a calcified barrier to form across the open apex.

Indication: Immature tooth with pulp necrosis.

Contraindication: - Root #

- Replacement resorption

- Very short roots.

Objective: Calcified barrier / artificial barrier

• Nygaard-Ostby – Lacerate the apical tissue – cementum-like tissue

Elimination of residues/bacteria – stimulate the radicular formation – not necessary – chemical stimulator – cementum

• Baouchon et al – Walkoff’paste

• Kaiser at al – Calcium hydroxide (1956)

• Frank - Published

MATERIALS

Ca(OH)2

MTA

Tricalcium Phosphate

TECHNIQUE:

Anesthesia and Rubber Dam Isolation

Bigger Access Cavity

EWL

Hypochlorite

Ultrasonic Devices Recommended

Ca(OH)2

Permanent filling

4-6 week, 3rd, 6th,& 24 month recall

• Duration of treatment

• Marginal adaptability

• Sealing ability

1. Good sealing ability2. Marginal adaptation3. Biocompatible4. Used in moisture presence5. Speed of completion of therapy

One Visit Apexification

MTA Angelus

Composition

SiO2, K2O, Al2O3, Na2O, Fe2O3, SO3, CaO, Bi2O3, MgO and insoluble residues of CaO, KSO4, NaSO4 and crystalline silica.

ST - Gel - in 10 -15 minutes.

Success: Absence of signs / symptoms

Calcified barrier

Failure: Bacterial contamination (seal / debridement)

Infected necrotic material

Undetected root #

Conclusion:

The last decade has proved to be an exciting time for pulp

biology & has led to rapid advances in repair of this tissue. At the start

of a new millennium, the use of biological molecules for the

development of novel treatment modalities is in sight.

These approaches have potential applications in unexposed as

well as in exposed pulp situations for the restoration of the structural

integrity of the dentin wall by reparative dentinogenesis