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Young Permanent TeethIntroduction Are those in which root development & apical closure have not been completed.Present in children from 6 yrs of age until 2-3 yrs after eruption of 3rd molarsThe aim of all treatment planning for young permanent teeth is to preserve pulp vitality, so providing conditions for continuous root development & physiologic dentin apposition

DevelopmentRoot developmentMaturation Diagnosis Vitality testingTreatment planningApexogenesisApexification

What makes them special???Tooth developmentEnamel and dentin future CE junctionIEE & OEE separated by Stratum intermediun & stellat reticulum hertwigs epithelial root sheathHERS - Shape of root and number Epithelial diaphragm apical foramenHertwigs & Epithelial diaphragm - sensitive to trauma

Apical ForamenAverage sizeMaxillary 0.4mmMandibular 0.3mmLocation and shape changes as a result of functional influence on the teeth.

Eruption and MaturationAlthough eruption commences at the time the root of the tooth begins to form, a growing root is not required for eruption to proceed2-4 yrs for complete eruptionLength of root 2/3rd complete- Erupts most rapidlyOnce emerged in oral cavity: 1-2 yrs to reach occlusal plane.

Posteruption maturationContinues 2-4 yrs after eruption.Teeth more susceptible to cariesPresence of Fluoride increases rate of posteruptive maturationAid enamel to form fluorapatite, which increases surface hardness : especially effective in preventing smooth surface cariesDifference between posteruptive maturation & remineralizationRoot completionIn permanent teeth, root formation is not completed until 14 years after eruption into the oral cavity. Because of the shorter roots of primary teeth, root formation is completed faster than for permanent teeth..

Diagnosis of pulp statusCorrect pulpal and periapical diagnosis is of paramount importancePreserve the vitality - until maturation has occurred. Loss of pulpal vitality before completion of dentin deposition leaves a weak root more prone to fracture as a result of the thin dentinal walls.

In teeth with incomplete root formation, correct pulpal and periapical diagnosis is of paramount importance before proceeding with any endodontic treatment because of the devastating result of loss of vitality. Every attempt should be made to preserve the vitality of these immature teeth until maturation has occurred. Loss of pulpal vitality before completion of dentin deposition leaves a weak root more prone to fracture as a result of the thin dentinal walls

12The diagnosis begins with a thorough medical history and any implications related to the anticipated treatment. The dental history and characteristics of associated pain might be helpful in determining pulpal status. The nature, type, length, and distinction between provoked and spontaneous pain are recorded. Provoked pain caused by thermal, chemical, or mechanical irritants usually indicates pulpal inflammation of a lesser degree and is often reversible. Spontaneous pain, on the other hand, is usually associated with widespread, extensive, degenerative, irreversible pulpal inflammation or necrosis.

Vitality testingElectric pulp tests and thermal tests are of limited valueFull development of the plexus of Rashkow does not occur until 5 years after tooth eruption (Johnsen 1985).Unreliable responses from children because of fear, management problems, and inability to understand or communicate accurately

Advisable to compare the results with those of an antimere or with an uninvolved tooth.

The EPT is often unreliable in testing immature permanent teeth (Fulling & Andreasen 1976b, Klein 1978, Brandt et al. 1988) as full development of the plexus of Rashkow does not occur until 5 years after tooth eruption (Johnsen 1985). Several years elapse before the root apex closes, and the maturation of innervation is slow. Pulpal nerves fail to terminate among the odontoblasts and reach the predentine or dentine, as is found in fully developed teeth in occlusion (Fulling & Andreasen 1976b, Klein 1978). Consequently, most diagnoses are made on observation of clinical symptoms and radiographic evidence of pathosis.14In immature permanent teeth testing with cold is a more effective method (Fuss et al. 1986).Most diagnoses - observation of clinical symptoms and radiographic evidence of pathosis.

In the pulp chamber coronal nerve bundles diverge and branch out towards the pulpo-dentine border (Dahl & Mjor 1973, Gunji 1982).Nerve divergence continues until each bundle looses its integrity and smaller fibre groups travel towards the dentine. This route is relatively straight until the nerve fibres form a loop resulting in a mesh that is termed the plexus of Rashkow. The density of this nerve plexus is well developed in the peripheral pulp along the lateral wall of coronal and cervical dentine and along the occlusal wall of the pulp chamber. The nerve fibres emerge from their myelin sheaths and branch repeatedly to form the subodontoblastic plexus. Finally, the terminal axons exit from their Schwann cell investiture and pass between the odontoblasts as free nerve endings (Byers & Narhi 2002).

Two types of sensory fibres are present in the pulp, the myelinated (A fibres) and unmyelinated C fibresThe A fibres predominantly innervate the dentine and are grouped according to their diameter and conduction velocities into Ab and Ad fibresThe Ab fibres may be more sensitive to stimulation than the Ad fibres, but functionally these fibres are grouped together. Approximately 90% of A fibres are Ad fibresThe C fibres innervate the body of the pulp

The Ad fibres have lower electrical thresholds than the C fibres and respond to a number of stimuli which do not activate C fibres (Olgart 1974). Ad fibres mediate acute, sharp pain and are excited by hydromechanical events in dentinal tubules such as drilling or air-drying (Byers 1984).Ad fibres may act as mechanoreceptors that trigger withdrawal reflexes so that potentially damaging forces may be avoided (Dong et al. 1985, Olgart et al. 1988, Byers & Narhi 1999). The C fibres mediate a dull, burning and poorly located pain and are activated only by stimuli reaching the pulp proper (Narhi 1985, Markowitz & Kim 1990).

C fibres have a high threshold and can be activated by intense heating or cooling of the tooth crown. C fibre pain is associated with tissue injury and is modulated by inflammatory mediators, vascular changes in blood volume and flow, and increases in pressure (Narhi 1990). As the intensity of the stimulus increases, more sensory nerves are activated and this results in a progressive increase in the sensory response

Numerous studies have reported the unreliability of electric pulp tests in permanent teeth with open and developing apices. Inconsistent results ranging from 11percent in 6- to 11-year-olds with completely open apices to 79 percent in older children have been reported. It is also possible to obtain a false-positive in teeth with liquefaction necrosis.Thus, electric pulp tests are of little value during the period of root formation, because the data are not reliable.

Radiographic interpretation:Can be difficult, due to their normally large & open apexBecause the faciolingual width of most roots and canals is greater than the mesiodistal width, apical closure cannot usually be determined radiographically.

Universal agreement exists that immature teeth have the greatest potential to heal after trauma or caries, particularly when the apical foramen is wide open. This group of teeth also has the greatest chance of misdiagnosis and mistreatment. To avoid mistakes, treatment must not be undertaken on the basis of negative responses to pulp testing. Radiographic and symptomatic assessment is currently the principal diagnostic criterion. The following factors are key in making the diagnostic determination: symptoms of irreversible pulpitis or apical periodontitis;clinical signs of periradicular infection including swelling, tenderness to percussionMobilityparulis formationradiographically detectible bone loss; progressive root resorption; and arrested root development compared with other adjacent teeth.

Because pulp vitality is purely the function of vasculature health, a vital pulp with an intact vasculature may test nonvital if only the nerve fibers are injured. This situation is commonly encountered in recently traumatized teeth. On the other hand, pulp fibres are more resistant to necrosis than the vascular tissue.Therefore, thermal and electric tests may give a false-positive response if only the pulp vasculature is damagedLaser Doppler flowmetry Very reliableHistologic studyIn nonvital pulp : accurate in 95 % cases, vital :74%Cautioned against relying solely on this test.Blood pigment within a discolored tooth crown interferes with laser light transmission

Photons that hit stationary tissue cells are scattered, but their frequency is not shifted. Photons that hit moving blood cells are scattered, and the light frequency is shifted according to the Doppler principle. A small proportion of the light, containing both Doppler-shifted and transmitted light, is backscattered to a photodetector (or more commonly, in newer instruments, to two or more photodetectors) built into the probe from which the laser light is beamed. A signal is then calculated with a preset algorithm in the LDF machine

Threats to developing teeth???Loss of pulpal vitality in young permanent teeth creates special problems. Because pulp is necessary for the production of dentin, if the pulp is lost before root length is completed, the tooth has a poor crown to root ratio.Vital pulpOpen apexClosed apexPulpotomy (vital) RCTRestorationPulpotomyPulpectomy RCT (with or without associated periapical pathology)Non vitalOpen apexClosed apexApexification RCTRCTPit and fissure sealantsPattern of cusp form and fissure pattern genetically determined- AxelsonNewly erupted, immature tooth enamel is more permeable and therefore more susceptible to caries attack because of its relatively high organic content. As enamel matures, the organic content of enamel reduces, and permeability decreases. Therefore, it is critical to protect newly erupting tooth surfaces to enhance overall longevity. Additionally, the operculum covering the distal half of teeth during eruption allows for the retention of plaque and the initiation of the caries process before complete eruption.

Pits and fissures present a challenging environment for caries control.Inherently, the morphology of pits and fissures provides an environment for plaque and bacteria retention. Moreover, enamel is thinner in pits and fissures, which allows accelerated demineralization into the dentin.This is especially true for erupting molars that are in the process of maturation.The eruption time for first molars and second molars is roughly 11/2 to 21/2 years, respectively. accounts for the increased decay rate of the molars.Fluorides aid enamel to form fluorapatite, which increases surface hardness. This treatment is especially effective in preventing smooth surface caries.

Retention rates???Newly erupted & 1st molars higherMandibular > maxillaryOperator access is betterGravity assists the sealant in flowing into the fissures.

Candidates for vital pulp therapy??? Teeth exhibiting provoked pain of short duration relieved with over-the-counter analgesics, by brushing, or upon the removal of the stimulus and without signs or symptoms of irreversible pulpitis, have a clinical diagnosis of reversible pulpitisApexogenesis A vital pulp therapy procedure performed to encourage continued physiological development and formation of the root end.Maturogenesis physiologic root development, not restricted to apical segment. The continued deposition of dentin occurs throughout the length of the root, providing greater strength and resistance to fracture

Continued development of root lengthFavourable crown root ratioRemaining odontoblasts to lay down dentinThicker rootResistance to fractureNatural apical constrictionBridging is not essential for the success of the procedureSuggests that pulp is vitalGoals: (Webber, 1984) -Sustaining a viable HERS -Maintaining the pulpal vitality -Promoting root end closure -Generating a dentinal bridge at the site of the pulpotomyIndirect pulp cappingA 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.RationaleDemineralization precedes bacterial invasionAsymptomatic till bacteria within 0.5 mm from pulpSoftened dentin close to pulp no bacteriaAbsence of substrate kills or inactivates the few left behindTherapeutic 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

Direct pulp cappingCase selectionTraumatic exposure of pulp provided the patient reports earlySmall mechanical exposure of the pulp in an asymptomatic vital tooth with sound dentin at the peripherySmall carious exposures in an asymptomatic vital tooth with incomplete root formationBenefits far out weigh the risks

Carious exposures in mature teeth should be discouraged (Not a contraindication) (Seltzer & Bender)Microbes and inflammation invariably associatedOperative procedures add insult to injuryAiling pulp may not respond favorablyTherefore advocated only when time, economics or any other factors don not permit R.C.T. (Cohen)

Factors determining success of direct pulp cappingSize 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 inflammationLocation 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 ChipitisMarginal 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

More recently, the step-wise excavation of deep caries has been revisited

3-6 monthsRemoval of carious dentin along the DEJ infected dentin Objective Change the cariogenic environment to decrease the number of bacteria,close the remaining caries from the biofilmslow or arrest the caries developmentRemoval of remaining caries- final restoration78 More recently, the step-wise excavation of deep caries has been revisited70-82 and shown to be successful in managing reversible pulpitis without pulpal perforation and/or endodontic therapy.83 This approach involves a 2-step process. The first step is the removal of carious dentin along the dentin-enamel junction (DEJ) and excavation of only the outermost infected dentin, leaving a carious mass over the pulp. The objective is to change the cariogenic environment in order to decrease the number of bacteria, close the remaining caries from the biofilm of the oral cavity, and slow or arrest the caries development.83-85 The second step is the removal of the remaining caries and placement of a final restoration. The most common recommendation for the interval between steps is 3-6 months, allowing sufficient time for the formation of tertiary dentin and a definitive pulpal diagnosis. Critical to both steps of excavation is the placement of a well-sealed restoration.17,18 The decision to use a one-appointment caries excavation or a step-wise technique should be based on the individual patient circumstances since the research available is inconclusive on which approach is the most successful over time.36,37

43Pulpotomy Surgical removal of a portion of an affected vital coronal pulp tissue, while leaving the radicular tissue in situ to allow for normal root development.

Following the closure of the apex, it is generally recommended that conventional root canalobturation be accomplished to avoid the potentiallong-term outcome of root canal calcification.Partial pulpotomyA procedure in which the inflamed pulp tissue beneath an exposure is removed to a depth of 1 to 3 mm or deeper to reach healthy pulp tissue. Pulpal bleeding must be controlled by irrigation -covered with calcium hydroxide or MTA. Calcium hydroxide : long-term success.MTA : predictable dentin bridging and pulp health.

Nonvital teeth5 methods(Morse et al )1. A customized cone (Blunt end, rolled cone)2. A short fill technique3. Periapical surgery (with or without a retro grade seal)4. Apexification (Apical closure induction)5. One visit apexification

According to Morse et al there areat least 5 methods of treating a tooth that has a necrotic pulp and an open apex. These methods are----- 1. A customized cone (Blunt end, rolled cone)Filling the root canal with the large (Blunt) end of a gutta percha cone or customized gutta percha cones with a sealer.2. A short fill techniqueFilling the root canal well short of the apex (before the walls have diverged) with gutta percha and sealer or zinc oxide eugenol (ZOE) alone.3. Periapical surgery (with or without a retro grade seal)Filling the root canal with gutta percha and sealer as well as possible and then performing periapical surgery with or without a reverse seal.4. Apexification (Apical closure Induction) Inducing apical closure by the formation of an apical stop (Calcium hydroxide, Ca(OH)2 is generally used)against which a permanent root canal filling can subsequently be inserted.5. One visit apexificationPlacing a biologically acceptable substance in the apical portion of the root canal (Dentinal chips or Tricalcium phosphate have been used) thus forming an apical barrier. This is followed by filling the root canal with gutta percha and sealer.

48ApexificationA method to induce a calcified barrier in a root with an open apex or the continued apical development of an incomplete root in teeth with necrotic pulpIs a method of inducing development of the root apex of an immature pulpless tooth by formation of osteocementum / bone like tissueMorse et al (1990) Apexification is a method of inducing apical closure through the formation of mineralized tissue in the apical pulp region of a non vital tooth with an incompletely formed root

A method of inducing root end closure of an incompletely formed nonvital permanent tooth by removing the coronal and nonvital radicular tissue just short of the root end and placing a biocompatible agent such as calcium hydroxide in the canals for 2-4 weeks to disinfect the canal space.

49Frank (1966)Described a technique based on the normal physiologic pattern of root development that brings about the resumption of apical development so that the root canal can be obliterated by conventional RCT

Weine, 2004Recommended two appointmentsFirst appointmentSealing a sterile, dry cotton for 1 to 2 weeksPlacing calcium hydroxide dressing is optionalSecond appointmentCalcium hydroxide and CMCPOne/two appointmentDetermined by clinical signs and symptomsActive infection To be elminatedAbsence of tenderness to percussion-a good signWide open apexDifficult to achieve drynessIf canal continue to weep, but other signs and symptoms of active infection is absentProceed with calcium hydroxide paste treatmentGeneral ruleTreatment paste -6 monthsReopened to assess the apical stopRadiographic assessmentFrank, 1966No apparent radiographic changebut positive stop at apexDome shaped apical closure with canal retaining a blunderbuss appearanceContinued root growth and closureof canal and apex to a normalappearanceA positive stop and radiographicevidence of a barrier coronal to the anatomic apex of the tooth

If apical closure not occurred in 6 monthsRetreat with calcium hydroxideUsually apical closure in 6 months, may take upto 2 yearsRetreatment at 3 to 6 month intervalCurrently, CMCP not usedCalcium hydroxide is the major ingredientIts also an antibacterialCMCP does not enhance repair

According to Sheehy and Roberts the use of calcium hydroxide for apical barrier formation is successful in 74-100% of casesMorse et al - antibacterial action and the calcification-inducing action of calcium hydroxideCalcific barrierCementumBone DentinCombination of all three tissues, with connective tissue and calcium hydroxide sometimes mixed in with themHistologically, its characteristics may be of dentin, cementum or osteodentin.

Limitations of Ca(OH)2 Apexification Long Duration 3 to 21 monthsSize of apical opening, age of PatientPorous & not continues Apical barriers not allows root developmentCa(OH)2 makes tooth more brittle hydroscopic and proteolytic propertiesCvek et al 77%Anderson et al - >100 days increases chances upto 81%High pH toxic to normal vital cells

How Ca(OH)2 induces hard tissue formation???It may provide a source of Ca ions for mineralizationMay stimulate the activity of Ca-dependent pyrophosphatase, which reduces the level of mineralization inhibitory pyrophosphate ions within the tissues.Several theories exist as to how calcium hydroxide induces hard-tissue formation. These include the high alkalinity (a pH of 11), which produces a favorable environment for the activation of alkaline phosphatase, an enzyme involved in mineralization. The calcium ions reduce the permeability of new capillaries formed in repairing tissue, decreasing the amount of intercellular fluid and increasing the concentration of calcium ions derived from the blood supply at the mineralization front. This may have two effects on the mineralization process; it may provide a source of calcium ions for mineralization, and it may stimulate the activity of calcium-dependent pyrophosphatase, which reduces the level of mineralization inhibitory pyrophosphate ions within the tissues.31-

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Antibacterial Ca(OH)2the hydroxyl ions destroy phospholipids, so the cellular membrane is destroyed;the high alkalinity breaks down ionic bonds so that bacterial proteins are denatured;the hydroxyl ions react with bacterial DNA, inhibiting replication

Single visit apexificationNonsurgical condensation of a biocompatible material into the apical end of root canal. Morse et alGupta, Sharma and Dang, 1999 conducted a single visit apexification in a non-vital and immature mandibular premolar and concluded that frequent changing of the calcium hydroxide dressing is not always required to induce apical closure.

This procedureShould induce root end closure. No adverse post-treatment clinical signs or symptoms.No radiographic evidence of external root resorption, lateral root pathosis, root fracture, or breakdown of periradicular supporting tissues during or following therapy. The tooth should continue to erupt, and the alveolus should continue to grow in conjunction with the adjacent teeth.

Guiliani et al, ,1998Use MTA to form apical plug for apexification

Revascularization Nygard Ostby , a pioneer of regenerative endodontic procedures in the early 1960s, showed that new vascularized tissue could be induced in the apical third of the root canal of endodontically treated mature teeth with necrotic pulps and apical lesions. This was accomplished by the creation of a blood clot in the apical third of a cleaned and disinfected root canal by using an apically extended root canal file just before root canal filling. He proposed that through formation of a clot (scaffold), a vasculature could be established to support growth of new tissue into the unfilled portion of the root canal. He provided histologic evidence in support of his concept that was taken surgically from teeth that had been treated in this manner.In 2001, Iwaya et al described a procedure, which they termed revascularization, that was undertaken on a necrotic immature mandibular second premolar with a chronic apical abscess.

After 30 months they noted thickening of the root canal walls by mineralized tissue and continued root development.

Subsequent to this case report, Banchs and Trope, 2004 described a revascularization procedure for the treatment of a necrotic immature mandibular second premolar with an open apex and a large apical lesion. They stated that many thought that regeneration of pulp tissue in a necrotic infected tooth with apical periodontitis was impossible.

It had been radiographically proven that regeneration was possible in a re-implanted tooth, the same could be accomplished in an infected tooth if a favorable environment was established.

After accessing the root canal, they irrigated it with sodium hypochlorite (NaOCl) and chlorhexidine gluconate (CHX) and sealed in a combination of 3 antibiotics in an attempt to disinfect it and stimulate periapical repair.

After 24 months, they found that the root development in the treated tooth was progressing in a manner similar to that of adjacent and contralateral teeth. Although the predictability of this procedure and the true nature of the tissue that developed in the root canal posttreatment were unknown, they believed that the benefits of the procedure, when successful, made it one worth the attempt.

Supported by Murray et al 2007 , who also added that the procedure was technically simple, inexpensive, and adapted to currently available instruments and medicaments.

At present, the use of the term revascularization is debatable.

Trope , 2008 claimed that the term revascularization was chosen because the nature of the tissue formed posttreatment was unpredictable, and the only certainty was the presence of a blood supply; hence it was revascularized. Huang and Lin , 2008 challenged the term revascularization as applied to endodontic procedures and believed it was more applicable to events that followed dental trauma. suggested the term induced or guided tissue generation and regeneration.

Lenzi and Trope 2012 suggested the term revitalization as being more appropriate because it is descriptive of the nonspecific vital tissue that forms in the root canal.

In 2003, Weisleder and Benitez suggested the term maturogenesis for a direct pulp-capping procedure of a tooth with deep caries that resulted in the complete development of the tooth.They claimed maturogenesis best describes the physiologic development of the root that occurs rather than development restricted to the apical segment. Patel and Cohenca (2006) also agreed that the term maturogenesis was equated with physiological root development and not simply apical development.

Regenerative endodontic procedures are biologically based procedures designed to restore function to a damaged and nonfunctioning pulp by stimulation of existing stem and progenitor cells present in the root canal and/or the introduction and stimulation of new stem and dental pulp progenitor cells into the root canal under conditions that are favorable to their differentiation and reestablishment of functionGuidelines for revascularizationAppointment - IAn assessment of the patient should be performedstate of tooth developmentextent and history of the endodontic infectionrestorability of the crownImmature permanent teeth with necrotic pulp, with or without apical pathosis, and an incomplete developed root with an apical opening that measures 1 mm or larger are considered suitable candidates for treatment, providing the crown, when damaged, is restorable

Appointment - IAnesthesia, isolation, access cavityDebridement and DisinfectionRemoval of necrotic pulp tissueMechanical cleaning is contraindicated because it may weaken the thin dentinal root wallsremove vital tissue remnants that might be present in the apical part of the canalWL determinationRemoval of necrotic tissue from the root canal is accomplished by gently irrigating the root canal with a minimum of 20 mL 2.5% NaOCl dispensed through a syringe and a 20-gauge needleirrigation with 5 mL sterile saline10 mL 2% CHXCHX is recommended because of its antimicrobial activity and its substantivity, ie, the ability to extend antimicrobial action by interacting with the dentinAppointment- IRoot Canal Medicationcarefully dried with large, sterile paper pointsroot canal can then be medicated with 1 of 2 dressingsAntibiotic CombinationHoshino et al 1996 introduced a triple antibiotic combination of ciprofloxacin, metronidazole, and minocycline that they claimed was sufficiently potent to eradicate bacteria from the dentin of the infected root and promote healing of the apical tissues.Problems associatedAntibiotic resistanceAllergic reactionCytotoxic to apical cellsDiscolorationCefaclor (Thibodeau and Trope)Bonding agent (Reynolds et al)Appointment- ITemporary RestorationPreventing coronal leakage of bacteriaDouble coronal restoration is recommendedplacing a sterile cotton pellet over the root canal medicament and then covering the pellet with Cavit cementcovered with glass ionomer cementadvisable to use non-eugenol temporary cementsCan contaminate the preparationinhibiting the polymerization of certain resin composites subsequently used as permanent restorative filling materialMedication PeriodNo agreement exists concerning the preferred medication or the optimal period for leaving medication in the root canal. Different clinicians have used different periods that have ranged from 7 days to several weeksAppointment- IIensure that all clinical signs and symptoms have abatedIf clinical signs or symptoms persistprocedures performed in the first appointment should be repeatedAnesthesiaAn anesthetic without vasoconstrictor should be chosen to prevent constriction of the blood vessels in the apical region or a limited flow of blood when bleeding is mechanically inducedRemove temporary restoration20 mL 2.5% NaOCl10 mL 17% EDTA instead of CHX as a final rinsing solutionchelating agent, it can decalcify the surface of the root canal dentin and expose its collagen fibers Collagen possesses adhesion motifs for the adhesion of new cells, whereas the decalcification of the dentin releases bound growth factors that can attract new cells and promote their differentiation into cells with odontoblast-like propertiesScaffoldScaffolds are used in regenerative procedures to provide a framework through which cells and a vasculature can growa stable blood clot can act as a scaffold in the revascularizationintroduction of a sterile #20 K-file into the apical tissues 2 mm past the apical foramen to initiate bleeding into the root canalBleeding should be controlled so that it does not extend beyond a point approximately 3 mm apical to the CEJ. Tapplying intracanal pressure with a sterile saline soaked cotton pellet until a clot is formed.Estimated mean time for the establishment of a stable blood clot is 15 minutesThe clot can be carefully touched with the reverse end of a large sterile paper point to confirm its stability. Once stability is confirmed, the clot should be carefully covered with MTA cement that is back-filled to the level of the CEJ.Shah , 2008Possible mechanism for the process of revascularizationFew vital cells may remain at the apical endMultipotent dental pulp stem cells Stem cells in the PDLStem cells from the apical papilla or bone marrowBlood clot itselfTrauma - AvulsionExtra oral dry time < 60 minSoaked in doxycycline 0.005% for 5 min before replantation.Extra oral dry time > 60 minEliminate the necrotic tissue from the root surface mechanically-curettageChemically- EDTA, citric acid, sodium hypochloriteHold the tooth by the crown and irrigate the root surface with sterile saline.Soak the tooth in a 2% stannous flouride for 5 min and replanted .Splinting- 7-10 days

Conclusion Common problems associated with open apicesThin dentinal wallsShort rootsFractures of crown.Discoloration in long standing cases.Over the years, there have been significant changes in the clinical management of infected immature permanent teethLike all dental procedures, careful case selection and understanding the goals and limitations of the treatment are essential

Thin dentinal walls- Which are susceptible to fracture before, during or after treatment. Short roots- Thus compromising crown-root ratio Fractures of crown.- Compromising esthetics especially in the anterior region - Necessitating post endodontic Rehabilitation of both crown and root.Discoloration in long standing cases80Frank AL. Therapy for the divergent pulpless tooth by continued apical formation. J Am Dent Assoc 1966;72:8793Murray PE, Garcia-Godoy F, Hargreaves KM. Regenerative endodontics: a review of current status and a call for action. J Endod 2007;33:377390.Trope M. Regenerative potential of dental pulp. J Endod 2008;34:S137.Hargreaves KM, Giesler T, Henry M, Wang Y. Regeneration potential of the young permanent tooth: what does the future hold? J Endod 2008;34:S516.Fundamentals of pediatric dentistry, 3rd edition: Mathewson R J and Primosch R E.Pediatric dentistry: infancy through adolescence, 4th edition: Pinkham CasamassimoPediatric dentistry: scientific foundations and clinical practice: Stewart RE, Barber TK.Pediatric Dentistry: Total Patient care Stephen WeiGrossmans endodontic practice