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vital pulp therapy in endodontics dental

Vital pulp therapy

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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 BMP 4 82 % BMP 5 BMP 6 BMP 7 BMP 8 BMP 9 BMP 3 92 % 59%
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 dentin teeming with bacteria 2.Collagen is irreversibly denatured 3.Cannot remineralize 4.Soft necrotic tissue, followed by dry leathery dentin – flakes away with an instrument 5.Dyes: 1% Acid red in propylene glycol stains only irreversibly denatured collagen 1.Softened deminerlized dentin not yet invaded by bacteria 2.Collagen cross linking remains 3.Acts as a template for remineralization 4.Softer than normal dentin, discoloured but does not flake easily 5.Does not stain
Chemomechanical caries removal Carisolv – modified hand excavation with the aid of gel Excavation aided by Gel: ) Lubricating effect to aid mechanical removal ) 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- 1- Completely Completely remove caries. remove caries.
2- 2- Open pulp Open pulp chamber by chamber by completely completely removing the removing the roof with 330 high roof with 330 high speed bur. speed bur.
3- 3- Remove pulp from Remove pulp from pulp chamber with pulp chamber with a sharp curette or a sharp curette or a large round low- a large round low- speed bur or a 330 speed bur or a 330 high speed bur. high speed bur.
4- 4- Stop bleeding by Stop bleeding by applying a moist applying a moist cotton pellet in the cotton pellet in the pulp chamber for 3 pulp chamber for 3 minutes minutes
5- 5- Place a cotton Place a cotton pellet with pellet with formocresol for formocresol for 5 minutes in the 5 minutes in the pulp chamber. pulp chamber.
6- 6- Remove cotton Remove cotton pellet and pellet and confirm pulp confirm pulp fixation, by the fixation, by the “black eye” “black eye” appearance of appearance of the pulp stumps . the pulp stumps . “ “Black eye” Black eye”
7- 7- Fill the pulp chamber Fill the pulp chamber with ZOE-eugenol 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.
PRIMARY DENTIN ODONTOBLASTS ODONTOBLAST SECRETORY ACTIVITY
PRIMARY DENTIN PHYSIOLOGICAL SECONDARY DENTIN ODONTOBLASTS ODONTOBLAST SECRETORY ACTIVITY
INJURY PRIMARY DENTIN TERTIARY DENTIN ODONTOBLAST SECRETORY ACTIVITY
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 Reparative dentin is a tertiary dentin matrix tertiary dentin matrix formed by new formed by new odontoblast like cells in odontoblast like cells in response to a specific response to a specific stimulus, while stimulus, while Reactionary dentin Reactionary dentin is is formed by surviving formed by surviving odontoblasts subjacent odontoblasts subjacent to diseased or otherwise to diseased or otherwise damaged dentin. 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, Injury Primary dentin Tertiary dentin Tubular Tubular discontinuity and discontinuity and decrease in decrease in density with density with tertiary dentin tertiary dentin deposition. deposition. Tubular Tubular discontinuity and discontinuity and decrease in density decrease in density beneath a thin layer beneath a thin layer of tubular hard tissue of tubular hard tissue formed initially from formed initially from poorly differentiated poorly differentiated odontablast like cells. odontablast like cells. Tubular Tubular continuity and continuity and maintenance of maintenance of tubular density tubular density but diffusion but diffusion distance to pulp distance to pulp increased by increased by tertiary dentin tertiary dentin deposition deposition Tubular Tubular dimensions dimensions decreased by decreased by deposition of deposition of peritubular dentin peritubular dentin sclerosis sclerosis
MOLECULAR AND CELLULAR UNDERSTANDING OF ODONTO BLAST DIFFERENTIATION : . There are two types of Molecular There are two types of Molecular signals, signals,  Endogenous signaling molecules Endogenous signaling molecules  Exogenous signaling molecule Exogenous signaling molecule Molecular signals are helpful for Molecular signals are helpful for both, both,  Induction of odontoblast Induction of odontoblast differentiation differentiation  Stimulation of odontoblast Stimulation of odontoblast metabolism metabolism  Differentiation of tooth germ is triggered by various molecular Differentiation of tooth germ is triggered by various molecular signals. signals.  Molecular signals are responsible for the cytodifferentiation of Molecular signals are responsible for the cytodifferentiation of dentin secreting odontoblast. dentin secreting odontoblast.
Exogenous signalling molecules Endogenous signalling 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 insoluble substrate to which pulp cells can attach and express the phenotype of odontoblast like cells seems to be of critical importance during reparative dentinogenesis. Fibrodentin formed as an intermediate Fibrodentin formed as an intermediate matrix zone during the wound healing matrix zone during the wound healing process has been suggested to process has been suggested to represent the stereotypic requirement represent the stereotypic requirement for initiation of reparative dentin for initiation of reparative dentin formation. formation. Fibrodentine Endogenous signalling molecules Pulpal progenitor cell Odontoblast – like cell
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 molecules Pulpal progenitor cell 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 progenitor cell Odontoblast – like 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
vital pulp therapy in endodontics dental

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vital pulp therapy in endodontics dental

  • 2.
  • 3.
    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
  • 4.
    Types of reparativedentin 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
  • 5.
    Indirect pulp capping Definition Rationale Caseselection Caries excavation Mechanical - Rotary and non rotary Chemomechanical - Carisolv Photoablation - Laser Difference between infected and affected dentin Procedure
  • 6.
    Choice of cappingagent Calcium hydroxide Dentin adhesives Pre-requisites Rationale Effectiveness Biological testing Controversies Remaining dentin thickness Quality and durability of bond Glass ionomer cement Re-entry?
  • 7.
    Direct pulp capping Caseselection Factors determining success Control of haemorrhage and pre-treatment Materials used Laser Calcium hydroxide Dentin bonding agents Mineral trioxide aggregate Collagen Antoxidants Growth factors
  • 8.
    Pulpotomy Definition Partial Complete Indications Procedure Materials used Calcium hydroxide Dentinadhesives BMP Re-entry? Molecular biology Designing new strategies in vital pulp therapy Summary and conclusion
  • 9.
    INTRODUCTION An over viewvital 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
  • 10.
    Present concept Conviction towardsV.P.T. Improved knowledge of pulpal physiology Better understanding of indications Clarity of criteria for success Better utilization of healing potential of pulp
  • 11.
    Aims at preservingthe 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
  • 25.
  • 26.
  • 29.
  • 30.
    Signaling Pathway ofTGF- SIGMA-ALDRICH
  • 31.
    HOMOLOGY HUMAN BMP BMP2 BMP 4 82 % BMP 5 BMP 6 BMP 7 BMP 8 BMP 9 BMP 3 92 % 59%
  • 32.
    Bone Morphogenetic ProteinReceptors SIGMA-ALDRICH
  • 39.
    THE IMPORTANCE OFREMAINING 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
  • 40.
    INDIRECT PULP CAPPING Definition “Aprocedure 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
  • 41.
    Rationale: Demineralization precedes bacterialinvasion 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
  • 42.
    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
  • 43.
    PROCEDURE Caries removal Placement ofindirect 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
  • 47.
    Infected dentin Affecteddentin 1.Softened demineralized dentin teeming with bacteria 2.Collagen is irreversibly denatured 3.Cannot remineralize 4.Soft necrotic tissue, followed by dry leathery dentin – flakes away with an instrument 5.Dyes: 1% Acid red in propylene glycol stains only irreversibly denatured collagen 1.Softened deminerlized dentin not yet invaded by bacteria 2.Collagen cross linking remains 3.Acts as a template for remineralization 4.Softer than normal dentin, discoloured but does not flake easily 5.Does not stain
  • 48.
    Chemomechanical caries removal Carisolv– modified hand excavation with the aid of gel Excavation aided by Gel: ) Lubricating effect to aid mechanical removal ) 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
  • 49.
    Advantages • Selective removalof 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)
  • 50.
    Caries excavation byPhotoablation 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.
  • 51.
    Demonstration of BiolaseWaterlase cutting system combining laser energy with water droplets to create high-speed hydrokinetic water particles that can mechanically cut both hard and soft tissues.
  • 52.
    Advantages • Selective ablationof 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)
  • 53.
    Limitations • Concern regardingthe thermal effects on pulp • Appropriate parameters to be selected, to avoid thermal injury to pulp • To be used with caution
  • 54.
    Choice of pulpcapping 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.
  • 55.
    ZnOE • Obtundant andmore 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
  • 56.
    Calcium hydroxide Mechanism ofaction – 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.
  • 57.
    Disadvantages Dissolution over aperiod 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
  • 58.
    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
  • 59.
    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
  • 60.
    Controversies of acidetching 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
  • 61.
    •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.
  • 62.
    Dentin Adhesives Remaining Dentinthickness – 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
  • 63.
    Self-etching primer VsSeparate 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)
  • 64.
    Quality and durabilityof 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 - ?
  • 65.
    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
  • 66.
    Glass Ionomer Indirect pulpcapping 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.)
  • 67.
    Re-entry – Isit 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)
  • 68.
    DIRECT VITAL PULPTHERAPY “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
  • 69.
    Case selection a) Traumaticexposure 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)
  • 70.
    Factors determining successof 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.
  • 71.
    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
  • 72.
    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)
  • 73.
  • 77.
    Laser treatment Effects: •Sterilizes exposedpulp 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)
  • 78.
    Conflicting reports: Lasers area 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.
  • 79.
    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.
  • 80.
    Low Ph material 1.Zoneof 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
  • 81.
    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
  • 82.
    Pulpal healing followingdirect 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.
  • 83.
    Pulpal reactions followingcapping – 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
  • 84.
    Studies are shortterm. 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.
  • 85.
    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.)
  • 93.
    Collagen: Advantages: induces dentinogenesiswith 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.
  • 94.
    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
  • 95.
    Antoxidants (Catalase) Essential enzymesnecessary 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.
  • 96.
    Growth factors inpulp 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.
  • 97.
    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.
  • 98.
    Considerations for usage •Deliveryvehicle – 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)
  • 99.
    PULPOTOMY Definition: “Surgical removalof 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.
  • 100.
    Indications: 1.Traumatic exposures wherecoronal pulp is likely to be inflamed in young healthy teeth. 2.Mechanical or carious exposure in teeth with incomplete root formation
  • 101.
    Procedure:  Pulp amputation Hemorrhage control  Placement of medicament  Final restoration
  • 102.
  • 103.
  • 107.
  • 108.
    2- 2- Open pulp Openpulp chamber by chamber by completely completely removing the removing the roof with 330 high roof with 330 high speed bur. speed bur.
  • 109.
    3- 3- Remove pulpfrom Remove pulp from pulp chamber with pulp chamber with a sharp curette or a sharp curette or a large round low- a large round low- speed bur or a 330 speed bur or a 330 high speed bur. high speed bur.
  • 110.
    4- 4- Stop bleedingby Stop bleeding by applying a moist applying a moist cotton pellet in the cotton pellet in the pulp chamber for 3 pulp chamber for 3 minutes minutes
  • 111.
    5- 5- Place acotton Place a cotton pellet with pellet with formocresol for formocresol for 5 minutes in the 5 minutes in the pulp chamber. pulp chamber.
  • 112.
    6- 6- Remove cotton Removecotton pellet and pellet and confirm pulp confirm pulp fixation, by the fixation, by the “black eye” “black eye” appearance of appearance of the pulp stumps . the pulp stumps . “ “Black eye” Black eye”
  • 113.
    7- 7- Fill thepulp chamber Fill the pulp chamber with ZOE-eugenol with ZOE-eugenol
  • 114.
    Pulp amputation • Sharpspoon 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
  • 115.
    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
  • 116.
    Choice of pulpotomyagent  Calcium hydroxide  Formocresol  Gluteraldehyde  Dentin adhesives  Light cure glass ionomers  Collagen, cyanoacrylates  B.M.P’s etc.
  • 117.
    Calcium hydroxide: traditionallyused over many decades with considerable degree of success. Limitations: May precipitate dystrophic calcification, complicating pulp space therapy later.
  • 118.
    Dentin adhesives aspulpotomy 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.)
  • 119.
    Bone Morphogenic Proteinsin 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.
  • 120.
    RECENT CONCEPTS –MOLECULAR BIOLOGY
  • 121.
    MILD INJURY: Odontoblast responsiblefor 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.
  • 122.
  • 123.
  • 124.
  • 125.
    SEVERE INJURY: Odontoblast beneaththe 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.
  • 126.
    Reparative dentin isa Reparative dentin is a tertiary dentin matrix tertiary dentin matrix formed by new formed by new odontoblast like cells in odontoblast like cells in response to a specific response to a specific stimulus, while stimulus, while Reactionary dentin Reactionary dentin is is formed by surviving formed by surviving odontoblasts subjacent odontoblasts subjacent to diseased or otherwise to diseased or otherwise damaged dentin. damaged dentin.
  • 127.
    It has beensuggested 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 Tubular Tubular discontinuity and discontinuity and decrease in decrease in density with density with tertiary dentin tertiary dentin deposition. deposition. Tubular Tubular discontinuity and discontinuity and decrease in density decrease in density beneath a thin layer beneath a thin layer of tubular hard tissue of tubular hard tissue formed initially from formed initially from poorly differentiated poorly differentiated odontablast like cells. odontablast like cells. Tubular Tubular continuity and continuity and maintenance of maintenance of tubular density tubular density but diffusion but diffusion distance to pulp distance to pulp increased by increased by tertiary dentin tertiary dentin deposition deposition Tubular Tubular dimensions dimensions decreased by decreased by deposition of deposition of peritubular dentin peritubular dentin sclerosis sclerosis
  • 128.
    MOLECULAR AND CELLULARUNDERSTANDING OF ODONTO BLAST DIFFERENTIATION : . There are two types of Molecular There are two types of Molecular signals, signals,  Endogenous signaling molecules Endogenous signaling molecules  Exogenous signaling molecule Exogenous signaling molecule Molecular signals are helpful for Molecular signals are helpful for both, both,  Induction of odontoblast Induction of odontoblast differentiation differentiation  Stimulation of odontoblast Stimulation of odontoblast metabolism metabolism  Differentiation of tooth germ is triggered by various molecular Differentiation of tooth germ is triggered by various molecular signals. signals.  Molecular signals are responsible for the cytodifferentiation of Molecular signals are responsible for the cytodifferentiation of dentin secreting odontoblast. dentin secreting odontoblast.
  • 129.
  • 130.
    BIO-ACTIVE MOLECULES INODONTOBLAST DIFFERENTIATION : Inner dental enamel epithelium Dental basement membrane Dental papilla
  • 131.
  • 132.
    • The presenceof an insoluble substrate to which pulp cells can attach and express the phenotype of odontoblast like cells seems to be of critical importance during reparative dentinogenesis. Fibrodentin formed as an intermediate Fibrodentin formed as an intermediate matrix zone during the wound healing matrix zone during the wound healing process has been suggested to process has been suggested to represent the stereotypic requirement represent the stereotypic requirement for initiation of reparative dentin for initiation of reparative dentin formation. formation. Fibrodentine Endogenous signalling molecules Pulpal progenitor cell Odontoblast – like cell
  • 133.
    Differentiation of odontoblastlike 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 molecules Pulpal progenitor cell Odontoblast – like cell
  • 134.
    • The roleof 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 progenitor cell Odontoblast – like cell
  • 135.
    ADVANTAGES AND LIMITATIONSOF 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.
  • 136.
    However, new strategiesbased 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.
  • 137.
    Re – entryafter 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
  • 138.
    Conclusion Ultimate goal ofVital 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.
  • 139.
    “Do the rightthing at the right time –the right way for the right patient – to get the best possible results”
  • 140.
    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)
  • 141.
    9. Identification ofHard 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