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Pulp Symposium S1 AAE and AAPD Symposium Overview: Emerging Science in Pulp TherapyNew Insights Into Dilemmas and ControversiesGerald N. Glickman and N. Sue Seale

S2 The Caries Process and Its Effect on the Pulp: The Science Is Changing andSo Is Our Understanding

Lars Bjrndal

S6 Diagnosis Dilemmas in Vital Pulp Therapy: Treatment for the Toothache IsChanging, Especially in Young, Immature Teeth

Joe H. Camp

S13 Regenerative Potential of Dental PulpMartin Trope

S18 Vital Pulp Therapy with New Materials for Primary Teeth: New Directions andTreatment Perspectives

Anna B. Fuks

S25 Vital Pulp Therapy with New Materials: New Directions and TreatmentPerspectivesPermanent Teeth

David E. Witherspoon

S29 Indirect Pulp Therapy and Stepwise ExcavationLars Bjrndal

S34 Indirect Pulp Capping and Primary Teeth: Is the Primary Tooth PulpotomyOut of Date?

James A. Coll

S40 Is Formocresol Obsolete? A Fresh Look at the Evidence Concerning Safety IssuesAlan R. Milnes

S47 New Age Pulp Therapy: Personal Thoughts on a Hot DebatePaula Jane Waterhouse

S51 Regeneration Potential of the Young Permanent Tooth: What Does the FutureHold?

Kenneth M. Hargreaves, Todd Geisler, Michael Henry, and Yan Wang

S57 Contemporary Perspectives on Vital Pulp Therapy: Views From the Endodontistsand Pediatric Dentists

N. Sue Seale and Gerald N. Glickman

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AAE and AAPD Symposium Overview: Emerging Sciencein Pulp TherapyNew Insights Into Dilemmas andControversies

Evidence-based best practices are yet to be established for themanagement of caries-associated pulpal disease in young perma-nent and primary teeth. Controversies still remain among practi-

tioners, including pediatric dentists andendodontists, as to which treat-ment modalities are most predictable in the contemporary practice ofpulp therapy. Many clinicians still remain divided as to whether indirectpulp capping is a viable procedure in primary and young permanentteeth, or whether formocresol remains the medicament of choice forpulpotomies in primary teeth. To begin the process of establishing evi-dence-based best practicesin pulpaltherapy aswell as highlightsomeofthe future directions in pulp therapy including pulp regeneration withstem cells and root canal revascularization, the American Academy ofPediatric Dentistry (AAPD) and the American Association of Endodon-tists (AAE) jointly sponsored Emerging Science in Pulp Therapy: New

InsightsintoDilemmasandControversies.ThesymposiumwasheldonNovember 23, 2007, in Chicago, Illinois.The convening of this pulp therapy symposium was heralded as a

major event in that it was a first time conjoint symposium sponsored bythese 2 national specialty organizations. The genesis of the idea for jointsponsorship was the needto examine the shared procedures performedby the 2 specialties. With specialty organizations routinely producingevidence-based practice guidelines that provide the foundation fortreatments performed, it is critical that when 2 specialties perform thesame or similar treatments, their guidelines areparallel in language andin content. Without these guidelines, confusion and uncertainty willresult in clinical practice when a rational treatment plan is required tomanage a specific pathologic entity such as caries.

Pediatric dentistry and endodontics share in the important treat-

ment decisionsassociated withpulpal therapy for thecariously involved young permanent tooth. In addition, endodontists are consultants toand involved in pulp therapy treatment decisions for the cariously in-

volved primary tooth. With the eventual expectation that the 2 organi-zations could come together andproduce practice guidelines that sharecommon goals and language for caries-associated pulp therapy for pri-mary and young permanent teeth, the decision was made to bring to-gethera panel of world-renown experts from both specialties to presentthe current best evidence as a first step in developing the anticipatedguidelines.

Individuals identified to be on the planning committee from theAAE were DrsGerald N. Glickman, Alan Gluskin, andBradfordJohnson.From the AAPD, Drs Suzi Seale, Elizabeth Barr, and James Coll wereselected. These individuals met and identified the following areas as

appropriate forfocus: thenature of thecarious lesionof dentin; indirectpulp therapy, including stepwise excavation for both young permanentteeth and primary teeth; primary tooth pulpotomy agents with specialemphasis on formocresol and the controversy surrounding its use; andrevascularization of young permanent teeth and pulpal regeneration byusing stem cells. To that end, a cadre of 9 experts was identified andinvited to present evidence for assigned topics. The articles resultingfrom their presentations appear in this publication.

During the conference Professor Lars Bjrndal discussed the car-ies process and its effect on the pulp. He applied this information to thedilemma of the deep carious lesion and indirect pulp capping, withspecial emphasis on the coronal seal. Dr Joe Camp focused on diagnos-tic dilemmas in vital pulp therapy for young immature teeth. Dr Martin

J. Trope spoke on how new trends are changing our understanding ofthe regenerative potential of the dental pulp, whereas Dr David Wither-spoon spoke on new directions and treatment perspectives involvingpulpal revascularization for permanent teeth. Dr Anna Fuks presented acompilation of the evidence for different pulpotomy agents in treatingthe vital cariously involved primary tooth. Dr Jim Coll provided infor-mationaboutindirect pulp capping forprimary teeth as an alternative topulpotomy. Drs Alan Milnes and P. J. Waterhouse presented opposing

views about the controversy over formocresol as a pulpotomy agent for

human teeth. Finally, Dr Ken Hargreaves provided evidence for thefuture of pulpal regeneration for the young permanent tooth.Because 2 specialty groups were represented, the planning com-

mitteesought to determine, through a brief pretest completedbefore thefirst speaker, the baseline opinions of the audience about the varioustopics to be presented. After the last speaker, a more lengthy set ofquestions about the same topics were presented to the audience fortheir opinions by using an audience response system. Attendees re-sponses were identified by specialty, and the results of the comparisonsof the presymposium and postsymposium opinions within specialty andacross specialties are also presented in this publication.

We believe this symposium represented an important landmark inbringing together different disciplines with potentially different opin-ions to reach an evidence-based consensus about common treatment

dilemmas. Because practice guidelines increasingly driveour treatmentdecisions, it is important that we are in agreement about their content,ultimately for the care and benefit of our patients.

Gerald N. Glickman, DDS, MSVice-President, American Association of Endodontists

and

Professor and Chairman, Department of Endodontics

Baylor College of Dentistry

Texas A&M University Health Science Center

Dallas, Texas

N. Sue Seale, DDS, MSDRegents Professor and Chairman, Department of Pediatric Dentistry

Baylor College of Dentistry

Texas A&M University Health Science Center

Dallas, Texas

Conflict of Interest: Gerald N. Glickman, DDS, MS, reports no financialinterests or potential conflicts of interest. N. Sue Seale, DDS, MSD, reports nofinancial interests or potential conflicts of interest.

Copyright 2008 American Academy of Pediatric Dentistry and AmericanAssociation of Endodontists.

This article is being published concurrently in Pediatric Dentistry, May/June2008; Volume 30, Issue 3. The articles are identical. Either citation can be usedwhen citing this article.doi:10.1016/j.joen.2008.02.036

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The Caries Process and Its Effect on the Pulp: The ScienceIs Changing and So Is Our UnderstandingLars Bjrndal, DDS, PhD

AbstractThe understanding of the caries process and its effecton the pulp is presented in the context that caries doesdevelop in various rates of progression. Early in thecaries process, the pulp reflects changes within lesionactivity. Thus, the early pulp response is reversible.Later, the rate of caries progression is reflected by thequality of the tertiary dentin. Slowly progressing lesionscreate tertiary dentin resembling normal tubular dentin.Rapidly progressing lesions lead to the production ofatubular dentin or complete absence of tertiary dentin,as well as pulp necrosis and apical pathology. Finally,

the nature of the untreated deep carious lesion is anecosystem that might undergo significant changes. Theuntreated lesion is temporarily converted from an activeand closed lesion environment into one that is openand slowly progressing. The analysis of untreated car-ious lesions has transformed the treatment philosophyof deep carious lesions. (J Endod 2008;34:S2-S5)

Key WordsDental caries, dental pulp, dentin, indirect pulp treat-ment, stepwise excavation, tertiary dentin

Can We Obtain Consensus on Caries Pathology?Caries can be compared with a train that passes through many stations. Imagine

that each station represents a specific stage of caries progression. The first stationrepresents the initial surface etching at the outer enamel layer, leading to the dull whiteappearanceof the activeprogressing enamel lesion. Thelast station representsthe deepestlayer of the carious tooth, with a necrotic, infected root canal system and the presence ofapical pathosis. Investigators,clinicians, andresearcherswho enter the caries train havetypically focused on only a few stations. They might also have different understandingsand opinions about how to treat dental caries. Their opinions have developed from amixture of clinical empirical tradition and an understanding from research. Theseopinions could be named the cariologist opinion, the operative opinion, and the end-

odontic opinion.

Some Opinions about the Approach to Dental CariesThe classic cariologist opinion is focused on the prevention of caries and further

progression of theestablishedlesion. Theinitial focus is on thewhite spot lesion, whosehistologic picture is visualized in the laboratory via transmitted or polarized light.Treatment philosophies here are typically related to nonoperative and preventive ap-proaches. If caries has progressed into the dentin, with demineralized dentin being

visible on the x-ray or, at most, extending through half the thickness of the dentin,excavation procedures are planned to avoid pulp exposures.

The operative opinion is typically initiated when caries has progressed into aclinical breakdown of the enamel surface and with carious dentin exposure. Withoutfocusing on specific details about caries pathology, the cavity needs to be drilled and

filled. A lesion means an exposure of the pulp, and this might be avoided by leavingcarious dentin behind. The operative opinion also tends to be a two-edged sword,because sometimes thedesign of thecavityoverrides thefact that thecaries lesion mightnot be in need of operative intervention. However, for esthetic or other reasons, theoperative intervention is carried out with a minimally invasive approach, even thoughthe actual lesion is dark, discolored, arrested caries.

Finally, the endodontic opinion deals with the prevention of an infected pulp andsubsequent apicalpathosis; theissueof a lesionmainlyconcerns this region. Therefore,allcarious dentinshould be removed, even if theresult is a pulp exposure.The existenceof these virtual opinions was reflected in a recent practice-based research network todetermine dentists treatment methods for deep caries lesions in which one wouldexpect pulpal exposure (1). The survey findings showed that 62% of the respondingdentists would remove all caries (operative opinion), 18% would partially removecaries (cariologist opinion), and 21% would initiate endodontic treatment (endodontic

opinion). Differences in decision making for treating deep carious lesions in primarymolars have also recently been reported (2).Actually,thistopicisnotnew,asshowninthefollowingquotations:Itisbetterthat

a layer of discolored dentin should be allowed to remain for the protection of the pulprather than run the risk of sacrificing the tooth (3). In contrast, Black (4) wrote:. . . it will oftenbe a questionwhether ornot the pulp will beexposed whenall decayeddentin overlaying it is removed . . . It is better to expose the pulp of a tooth than to leaveit covered only with softened dentin.

It is necessary to remain within the historical perspective to understand how thesedifferent opinions have justified various treatment concepts. The endodontic opinionadvocating an invasive pulp treatment in relation to caries might very well have gained

From the Department of Cariology and Endodontics,School of Dentistry, Faculty of Health Sciences, University ofCopenhagen, Denmark.

Address requests for reprints to Dr Bjrndal at [email protected].

Conflict of Interest: Lars Bjrndal, DDS, PhD, is a GrantRecipient from the Danish Agency for Science Technology andInnovation.0099-2399/$0 - see front matter

Copyright 2008 American Academy of Pediatric Den-tistry and American Association of Endodontists.

This article is being published concurrently in PediatricDentistry, May/June 2008; Volume 30, Issue 3. The articles areidentical. Either citation can be used when citing this article.doi:10.1016/j.joen.2008.02.037

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inspiration from pulp studies carried out on animal models by usingstandardized test cavities in sound dentin, in which the pulp reacts veryearly to the influx of various external stimuli. These stimuli might in-clude samples of plaqueor soft carious dentin(5, 6).Inthiscontext,thestudy by Brnnstrm and Lind (7) has been a key reference, showingthat the early enamel lesion in human teeth could also lead to odonto-blast alterations and signs of pulpal infiltration. This is a key referencebecause in this symposium presentation it is hypothesized that thesefindings have been used as evidence for the early onset of irreversiblepulpal inflammation caused by caries progression. Taken together, it istempting to suggest that the observation of the early influx pulp datamight have led to the clinical interpretation that irreversible pulp in-flammation is also reached relatively early in relation to caries. There-fore, radical interventions have been advocated. A recent Cochranereview of pulp management in extensive caries deals with clinical stud-ies in which deep lesions without clinical symptoms were treated ( 8).One could question why a pulp-preserving treatment was not an option.

In contrast, the cariologist opinion, and to some extent the oper-ative opinion, can be traced back decades to Massler (9). Massler,among others, integrated a sophisticated and advanced biologic under-standing of cariesinto cariestreatment. He describedacuteand chroniccaries on the basis of clinical criteria and histologic descriptions. Con-sequently, different pulpal reaction patterns were to be expected thatcould lead to differing means of treating caries as opposed to only aradical approach.

With the metaphor of the caries train in mind, it is too much toforce everyone to get on and off at all the stations, but during a sympo-sium such as this, a natural goal would be to reach a consensus ofunderstanding caries in between thesegroup opinions. Therefore, whenentering a caries discussion aiming to cross invisible lines of dentalsubspecialities, it is necessary to be clear and precise with the use of

well-defined terms. Why? Because the interpretation of the very sameclinical situation even today might reflect completely different treat-ments (1, 2), and misunderstandings might very well occur in commu-nication between clinicians and researchers. Let us update our under-standing of caries pathology by considering that the caries train might

use more than one track. This reflects the understanding and impor-tance of caries as a disease that can progress at varying rates.What is the sequence of the various zones in carious dentin, be-

ginning with early lesions? When and how does the pulp begin to pro-duce extradentinal matrix and tertiary dentin? What is the spreadingpattern of caries? When will microorganisms invade the demineralizeddentin? Can we say something about the prehistory of caries, when

viewing the histologic picture of tertiary dentin? Why do we sometimesfind tertiary dentin produced during caries, whereas at other times it isdifficult to detect? Is knowledge about lesion activity important?

An Update of Caries Pathology: The Non-cavitatedEnamel Lesion ComplexUnderstanding the Early

PulpDentinal Response to CariesThe proximal white spot lesion is triangular when viewed in 2

dimensions and conical when viewed in 3 dimensions. On the basis ofquantitative data related to the degree of porosity in the enamel lesion,the lesion comprises a multitude of many microlesions following thedirection of the enamel rods. Hence, the topography of the lesion re-flects the acidogenic potential of the cariogenic biofilm at the enamelsurface. Thecentral lesion area is the oldest part and shows the deepestpenetration, whereas the peripheral parts represent new beginnersfollowing the direction of the rods (10).

In short, the shape of the enamel lesion represents a transmissionof stimuli from the enamel surface that can be related to time and

provides the possibility for understanding the subjacent pulpal-dentinalresponse in relation to time. Thus, the deepest penetration of the entirecaries lesion complex can also be seen as the oldest lesion area alongthe dentin-pulp interface following the direction of the dentinal tubules.Consequently, the peripheral areas represent younger and less pro-gressed areas along the dentin-pulp interface, guided by the cariogenicbiofilm covering the surface of the enamel lesion. The morphology ofreactionary dentinogenesis, defined as tertiary dentin produced by pri-mary odontoblasts, hasbeendescribed by using thisconcept(11).Iwillreturn to this subject later.

Examples of Improved Laboratory Methods That HaveCreated a Better Understanding

One approach that has improved our understanding from the his-tologic findings of Brnnstrm and Lind (7) was the use of thin, un-demineralized tooth sections in the examination of well-definedcariouslesions. The normal structural relationships between enamel, dentin,and the pulp were preserved with this new histologic method. There-fore, it waspossibleto describe morphologicchanges in theenamel andthe subjacent pulp-dentinal organ within the same section (12). Also,the application of immunohistochemistry has improved our under-standing of the underlying molecular events (13), as well as reactions

leading to reactionary and reparative dentinogenesis (14).

The Sequence of the Carious Development inthe Tooth

Morphologic changes in odontoblasts have been found in well-defined enamel lesions in freshly extracted third molars (14). More-over, morphologic andmolecular features in theodontoblastcells lead-ing to the production of extradentinal matrix can also be detected (15,16). During our daily clinical practice we might only recall the earlyodontoblast response from thelibrary,but when we experience thepulpin relation to caries, it is duringa verylate stage of lesionprogression as

we consider whether pulp exposure should be avoided.How should we interpret the early pulp response? An updated

interpretation and understanding would be that the pulpal responsefollowsthe carieslesion from thevery beginning. However, it shouldnotbe considered as a station along the track of irreversible pulp inflam-mation, hence a point of no return. Some observations even indicatethat the pulp might react to the signals passing through the enamel evenbefore histologic caries reactions can be observed in the dentin (14).

The first visible histologic change in the dentin subjacent to anenamel lesion is the formation of hypermineralized dentinal tubules.This reaction is seen in the dentin before any signs of demineralization.The reaction might represent activity of the odontoblasts, and it might

very well resemble the age-related intratubular physiologic sclerosis(17). When the enamel lesion reaches the dentinoenamel junction(DEJ), dentin demineralization is initiated. Note that the initial dentindemineralization takes place not in unaffected sound dentin but in den-

tin with a decreased permeability as a result of the presence of thehypermineralized dentin.After the dentin begins the process of demineralization, the ad-

vancing front of demineralization also reflects the dynamic natureof thecariogenic biofilm, expressed as different pH gradient creating eitherdissolution or reprecipitation of dentin mineral. Thus, the hyperminer-alized dentin is probably theresult of physiologic activity from theodon-toblast, but it also contains reprecipitation of previously dissolved den-tin crystals. However, this topic requires additional study (18).

No serious microbial invasion takes place in the dentin as long asthe highly organized enamel layer (even though being demineralized)separates the biofilm from the dentin. The bacteria are not able to

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penetrate throughtheenamelrodstructure(19). Themicrobial invasionisrelated to the gradual structural breakdown of the enamel layer (20).

Another important change in our understanding is the misinter-preted concept of caries spreading along the DEJ subjacent the non-cavitated enamel lesion (21). The extent of the demineralized dentin isrestricted to the histologic enamel lesion contact, and no spreading ofdemineralized hard tissue is noted undermining sound enamel. Thelateral spread of demineralized dentin and enamel is related to the totalbreakdown of theenamel layer andtherefore describesa relatively laterstage of tissue destruction than previously believed.

During the stages of dentin exposure a completely different situa-tion is created under heavy bacterial invasion. A moist, soft, disinte-grated, demineralized, andnecrotic zone is observed.At this activestagethe carious dentin can easily be separated from the enamel. The outfluxof mineral has been extensive, and as the moisture is decreased, even-tually the dentin shrinks, and a clinically visible gap develops betweenthe enamel and dentin (Fig. 1a). Subsequently, the cariogenic biofilmgains improved growth conditions along the lateral spread of caries orretrograde caries (23). If the carious tooth is left untreated, furthertissue breakdown occurs. Eventually the caries process willbring aboutirreversible changes in the pulp,leading to necrosisandpulpal infection

with apical pathosis. This worst case scenario is often what we find inmany textbooks. It also represents what takes place several times a weekin dental practice. In Denmark caries is still the most frequent reasonfor endodontic treatment (24).

Lesion Activity and Pulpal ResponseWhat is the significance of how rapidly caries progresses in rela-

tion to a pulpal response? Let us once again benefit from the histologicfindings of the early pulp response to enamel caries (14).Inadditiontoodontoblastcellreactionperse,theodontoblastsalsodisplayadifferentresponse to active versus arrested caries. When the non-cavitatedenamel lesion has histologic contact with the DEJ, the odontoblasts

within active lesions have a significantly lower cytoplasm:nucleus ratio

comparedwithcontrolsites.Incontrast,thissituationisnotfoundinthearrested or slowly progressing enamel lesion. Moreover, only activeenamel lesions show evidence of proliferation of cells from the sub-odontoblastic cell-rich zone into the cell-free zone. In short, the pulpalresponse follows notonly theearlycaries lesion; it also mirrors changesin lesion activity.

In cavitated lesions, different patterns of tertiary dentin can beexpected relative to the prehistory of each lesion. The presence orabsence of tertiary dentin, as well as its quality, should be seen as areflection of the nature of the external stimuli that have previouslypassed through the dentin. As an additional example, the rapidly pro-gressing caries lesions would typically follow the sequence of odonto-

blast necrosis (25), eventually followed by the presence of atubulardentin formation, also known as fibrodentin. Let us in this contextreturn to the morphology of the reactionary dentinogenesis defined astertiary dentin produced by primary odontoblasts. A few studies havedescribedthis sequence by comparing central andold lesion areas withperipheral andlateral parts of younger lesion areas (11,14). It appearsthat the primary odontoblasts are involved in the early onset of newextradentinal matrix in the younger portions of the lesion, whereas theolder central lesion area shows the gradual development of atubularfibrodentin (26).

In contrast, slowly progressing lesions characteristically displaytubular dentin formation at the pulpal site. This tertiary dentin shows amixture of reactionary dentinogenesis and dentin produced by newodontoblast-like cells. It appears that this takes place in the same man-ner as the primary odontoblast cells, with finger-like projections butinto the reactionary dentin (16). Very little attention has been givenpreviously to the potential capacity of the primary odontoblast to be partof tertiary dentin formation.

Also within deep carious lesions (Fig. 1), large variation in lesionactivity might appear (27). As the lesion progresses, the enamel breaks

down (Fig. 1b), and at the same time the growth conditions change forthe cariogenic biofilm. The cavitated lesion transforms from a closedecosystem into an open ecosystem (Fig. 1c). Different rates of progres-sion can therefore be present within one tooth. After the enamel break-down, the occlusal part of the tooth has no heavy plaque accumulation,as the degree of protection of the biofilm has decreased. The sub-jacent dentin discloses the clinical signs of slowly progressingcariesby its brownish discoloration (Fig. 2a). In contrast, the peripheralparts are protected, and accumulations of cariogenic biomass areapparent. On the basis of these observations, pulp vitality is notnecessarily maintained, but it indicates that deep exposed dentinlesions are not unconditionally related to an irreversible pattern ofpulp pathology, as traditionally taught in textbooks advocating in-

vasive pulp treatments (28). Of course, if nothing is done with thedeep lesion even though it might be temporarily arrested, eventuallythe caries activity in the peripheral parts of the lesion leads to thebreakdown of the tooth (Fig. 2b, c).

The pulpal response in lesions with a conversion of lesion activitycanbereflectedbythepresenceofreparativedentinogenesis,definedasthecombinationof fibrodentinand newtubulardentinproduced bynewodontoblast-like cells (29). The presence of fibrodentin or interfacedentin indicates that all primary odontoblasts have died. After thechange in caries activity, the pulp might respond with reparative dentinresembling thedentin-bridge formationafter a direct pulp capping pro-cedure (16).

Figure1. Diagrams showing the temporaryconversion of the cariogenicecosystemduringuntreatedlesion progress. A closed lesion environment develops in relationto an occlusal lesion(a). Eventually thewhitedemineralizedand undermined enamelbreaks as a resultof mechanical stress, changing theenvironmentinto an openecosystem (b). Consequently, a stage of mixed lesion activity develops. In the occlusal part, classic signs of slow lesion progress are noted in terms of a darkerappearance of the demineralized dentin, whereas at the margins, optimal growth conditions for the plaque are apparent, and active lesion progress continues (c).Red zones indicate plaque. Reprinted with permission from Blackwell Munksgaard from Bjrndal L. Dentin and pulp reactions to caries and operative treatment:biological variables affecting treatment outcome. Endodontic Topics 2002;2:1023. (22)

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Understanding of Caries Pathology Creates theTreatment Philosophy Related to Deep Caries

In the past, the following have all been clear justification for theperformance of radical operative intervention: (1) early microbial in-

vasion of carious dentin, (2) early spreading along the DEJ that under-mines sound enamel, and (3) the early onset of an irreversible pulpresponse. Even though textbooks often illustrate the worst case sce-nario, this doesnot meanthat weshould wait forit tohappen! Weshouldbemotivated to understand the lesion activity and use this information in the

treatment of caries. Instead of accepting that there is a steady progressionthrough the tooth leading toward the same results if left untreated, it mightbe more appropriate to understand that caries activity constitutes manydifferent rates of progression, each of them leading to different pulp reac-tions. Perhaps with theappropriateclinical intervention we can reduce therate of caries progression, perhaps even arresting the subjacent pulpal in-flammation. Only well-designed clinical trials will answer this question,given that we do not yet have noninvasive tools for the measurement of theseverityof the inflamedpulp. Therefore, theclinicaldiscussion of reversibleor irreversible development of pulpitis will continue to be controversial inrelation to the actual state of pulp pathology. However, when diagnosingdeep carious lesions,wemustmakea choice onthebasis ofourknowledgeof the caries process and its effect on the pulp and on the basis of existingdiagnostic methods. The noninvasive pulp treatment of deep caries lesions

will be the focus of my second presentation.

References1. Oen KT, Thompson VP, Vena D, et al. Attitudes and expectations of treating deep

caries: a PEARL network survey. Gen Dent 2007;55:197203.2. Qudeimat MA, Al-Saiegh FA, AL-Omari Q, Omar R. Restorative decisions for deep

proximal cariouslesionsin primary molars.Eur Arch Paediatr Dent 2007; 8:3742.3. Tomes J. A system of dental surgery. London: John Churchill, 1859:336.4. Black GV. A work on operative dentistry in two volumes, vol. II. The technical pro-

cedures in filling teeth. 2nd ed. Chicago: Medico-Dental Publishing Co, 1908.5. BergenholtzG, LindheJ. Effectof solubleplaquefactors oninflammatoryreactionsin

the dental pulp. Scand J Dent Res 1975;83:1538.6. Mjr IA, Tronstad L. Experimentally induced pulpitis. Oral Surg 1972;34:102 8.7. Brnnstrm M, Lind PO. Pulpal response to early caries. J Dent Res 1965;44:104550.8. Nadin G, Goel BR, Yeung CA, Glenny AM. Pulp treatment for extensive decay in

primary teeth. Cochrane Database Syst Rev 2003;1:CD003220.

9. Massler M. Pulpal reactions to dental caries. Int Dent J 1967;17:441 60.10. Bjrndal L, Thylstrup A: A structuralanalysisof approximalenamel caries lesions and

subjacent dentin reactions. Eur J Oral Sci 1995;103:2531.

11. Lee Y-L,Liu J, Clarkson BH,Lin C-P, Godovikova V, Ritchie HH.Dentin-pulp complexresponses to carious lesions. Caries Res 2006;40:25664.

12. Bjrndal L, Thylstrup A, Ekstrand KR. A method for light microscopy examination ofcellular and structural interrelations in undemineralized tooth specimens. Acta Od-ontol Scand 1994;52:18290.

13. Yoshiba N, Yoshiba K, Nakamura H, Iwaka M, Ozawa H. Immunohistochemical lo-calization of HLA-DR-positive cells in unerupted and erupted normal and carioushuman teeth. J Dent Res 1996;75:15859.

14. Bjrndal L, Darvann T, Thylstrup A. A quantitative light microscopic study of odon-toblast and subodontoblastic reactions to active and arrested enamel caries withoutcavitation. Caries Res 1998;32:59 69.

15. Lukinmaa PL, Vaahtokari A, Vainio S, Thesleff I. Expression of type I collagen pro-2chain mRNA in Adult human permanent teeth as revealed by in situ hybridization. JDent Res 1992;71:36 42.

16. Bjrndal L, Darvann T. A light microscopic study of odontoblastic and non-odonto-blastic cells involved in tertiary dentinogenesis in well-defined cavitated cariouslesions. Caries Res 1999;33:50 60.

17. Tagami J, Hosoda H, Burrow MF, Nakajima M. Effect of ageing and caries in dentinpermeability. Proc Finn Dent Soc 1992;88(Suppl 1):14954.

18. Kidd EAM, Bjrndal L, Beighton D, Fejerskov O. Caries removal and the pulpo-dentinal complex. In: Fejerskov O, Kidd EAM, eds. Dental caries: the disease and itsclinical management. 2nd ed. Oxford: Blackwell Munksgaard, 2008:36783.

19. Ekstrand KR, Bjrndal L. Structural analyses of plaque and caries in relation to themorphology of the groove-fossa system on erupting mandibular third molars. CariesRes 1997;31:336 48.

20. Ricketts D, Ekstrand KR, Kidd EAM, Larsen T. Relating visual and radiographicranked scoring systems for occlusal caries detection to histological and microbio-

logical evidence. Oper Dent 2002;27:2317.21. Silverstone LM, Hicks MJ. The structure and ultrastructure of the carious lesion in

human dentin. Gerodontics 1985;1:18593.22. Bjrndal L. Dentin and pulp reactions to caries and operative treatment: biological

variables affecting treatment outcome. Endodontic Topics 2002;2:1023.23. Bjrndal L, Kidd EAM, The treatment of deep dentine carious lesions. Dent Update

2005;32:40213.24. Bjrndal L, Laustsen MH, Reit C. Root canal treatment in Denmark is most often

carried out in carious vital molar teeth and retreatments are rare. Int Endod J2006;39:78590.

25. Magloire H, Bouvier M, Joffre A. Odontoblast response under carious lesions. ProcFinn Dent Soc 1992;88(Suppl.1):25774.

26. Bjrndal L. Presence or absence of tertiary dentinogenesis in relation to cariesprogression. Adv Dent Res 2001;33: 803.

27. Edwardsson S. Bacteriology of dentin caries. In: Thylstrup A, Leach SA, Qvist V, eds.Dentine and dentine reactions in the oral cavity. Oxford: IRL Press, 1987:95102.

28. Tronstad L. Clinical endodontics. 2nd ed. Stuttgard: Thieme, 2003:81.29. Smith AJ, Tobias RS, Cassidy N, et al. Odontoblast stimulation in ferrets by dentine

matrix components. Arch Oral Biol 1994;39:1322.

Figure 2. The pattern of untreated deep lesions might involve a decrease in lesion activity (a), but it might be temporary because the enamel margins will obtainprotection for the cariogenic process (b). Eventually the entire crown breaks, leaving remnants of roots behind (c). Red zones indicate plaque. Reprinted withpermission from Blackwell Munksgaard from Bjrndal L. Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatmentoutcome. Endodontic Topics 2002;2:1023. (22)

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Diagnosis Dilemmas in Vital Pulp Therapy: Treatment forthe Toothache Is Changing, Especially in Young,Immature Teeth

Joe H. Camp, DDS, MSD

AbstractThe literature is almost devoid of scientific studies ofdiagnosis of pulpal pathology in primary and perma-nent teeth with open apices. Most reports are empiricalor retrospective studies without adequate prior knowl-edge of preexisting conditions or histologic findingsleading to the necessity of pulpal procedures. Appro-priate diagnostic tests and their effectiveness are doc-umented for both groups. This article reviews the avail-able literature and current techniques of indirect pulp

therapy, pulp capping, and pulpotomy for primary teethand permanent teeth with open apex. The apical bar-rier with mineral trioxide aggregate followed by rootstrengthening with bonded composite is reviewed.(J Endod 2008;34:S6-S12)

Key WordsDiagnosis, pulp, pulp capping, pulpotomy

Diagnosis in primary and young, permanent, immature teeth varies greatly from thatin fully formed permanent teeth. Most of the diagnostic tests used in conventionalendodontic therapy are of very little or no value in primary teeth and of limited value inpermanent immature teeth. While admittedly poor for diagnosing the degree of inflam-mation in this group of teeth, diagnostic tests must be performed to obtain as muchinformation as possible before arriving at treatment options.

Diagnostic literature based on scientific studies is almost nonexistent. Most out-come reports are supported by empirical treatment and anecdotal case reports (1).Many outcome studies are conducted retrospectively on the basis of clinical signs and

symptoms and make assumptions regarding the pulpal status before treatment withouthistologic or bacterial data to support the preoperative diagnosis. Without histologicexamination an accurate determination of the extent of inflammation is impossible(2).Correlation between clinical symptoms and histopathologic conditions is poor andcomplicates diagnosis of pulpal health in exposed pulps of children (3).

Many of our treatments are based on our diagnosis of the root development stage.Consequently, to properly diagnose and treat primary and young permanent teeth, it isnecessary to have a thorough knowledge of normal root formation and the differencesbetween developing and fully formed teeth. The decision to render conservative vitaltreatment to allow root formation completion or more radical treatment such as rootcanal therapy might hinge on our diagnosis of root development.

According to Orban (4), the tooth roots development begins after enamel anddentin formation has reached the cementoenamel junction (CEJ). Hertwigs epithelialroot sheath is formed by the epithelial dental organ, with one tube for each of the future

roots. As root formation proceeds apically, each root is wide open, diverging apicallyand limited by the epithelial diaphragm. Each roots internal surface is lined by odon-toblasts. Once root length is established, the sheath disappears, whereas dentin depo-sition is continued until root formation is completed.

Depending on each roots external anatomy, differentiation into multiple canalsmight occur. During this formative stage, communication exists between the canals inthe form of isthmuses. As growth continues, the opposing walls meet and coalesce, andislands of dentin are formed, which eventually expand to divide the root into separatecanals. Continued dentin deposition narrows the canals, and the apex is eventuallyclosed with dentin and cementum, creating apical convergence. Isthmuses and finsextending toward the roots center might persist in fully formed teeth.

In permanentteeth,root formationis not completeduntil 14 years after eruptioninto the oral cavity. Because of the shorter roots of primary teeth, root formation is

completed faster than forpermanent teeth. Because thefaciolingual width of most rootsand canals is greater than the mesiodistal width, apical closure cannot usually bedetermined radiographically. The x-ray beam is exposed in the faciolingual plane, butthe radiograph is read mesiodistally. Because of this anatomy, with the exception of themaxillary central and lateral incisors and some single canal lower premolars, radio-graphs cannot determine apical closure. Therefore, the clinician must rely on time todetermine root closure in all other teeth to prevent treatment protocols that cannot besuccessfully completed without apical convergence (5).

During this formative period, treatments should be oriented toward maintenanceof vitality to allow completion of root formation. Further deposition of dentin willstrengthen the roots thin dentinal walls and help diminish future root fracture.

From private practice of endodontics, Charlotte, NorthCarolina, and Department of Endodontics, University of NorthCarolina, Chapel Hill, North Carolina.

Address requests for reprints to Dr Camp at E-mail address:

[email protected] of Interest: Joe H. Camp, DDS, MSD, is the Uni-

versity Clinical Consultant for Dentsply Tulsa Dental Special-ties, a part-time, paid position.0099-2399/$0 - see front matter



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The root canals of primary teeth differ greatly from those of per-manent teeth, and treatment is complicated by apical resorption toallow for eruption of the succeeding teeth. At the time of root lengthcompletion, the root canals roughly correspond to the externalanatomys form and shape. At this time, resorption of the rootsbegins and, combined with additional dentin deposition internally,might significantly change the number, size, and shape of the canals

within the primary roots. Continued physiologic, apical resorption ofthe roots makes the teeth progressively shorter. In addition, resorptionon the roots internal surfaces adjacent to the forming permanent toothmight open other communications with the periapical tissues. Thesefactors complicate establishment of working lengths if root canal ther-apy is necessary.

In the primary anterior teeth (incisors and canines), the perma-nent tooth buds lie apically and lingually near the primary roots. Re-sorption is initiated on the primary roots lingual surface. This causesthe apical foramen to move coronally, resulting in a difference in theapical foramen and the anatomic apex and complicating determinationof root canal length. One study demonstrated that half of the primaryincisors root might be resorbed lingually beforeit becomes obvious ona radiograph(6). Primary anterior teeth have onesimple root canal andrarely have lateral or accessory canals.

The primary molar teeth normally have the same number andposition of roots androot canalsas thecorresponding permanent teeth.

At root length completion, most roots have only 1 canal, but continueddeposition of dentin might divide the root into 2 or more canals (79).During this time, communication exists between the canals in the formofisthmusesorfins(Fig.1). Secondarydentin depositioncontributestothis change in morphology(10, 11). Like the permanent molars, most

variations occur in the mesial roots of mandibular molars and facialroots of the maxillary molars. Also, these variations are usually in thefacial to lingual plane and cannot be visualized on radiographs (7, 9).

Accessory and lateral canals and apical ramifications of the pulparecommon in primary molars (8). In addition, othercommunicationsbetween the pulp and the periapical tissues are formed by physiologicresorption of the internal surfaces of the roots adjacent to the perma-

nent tooth buds.Diagnosis of Pulpal Status in Primary Teeth

As with any dental procedure, a thorough medical history must becompleted, and any implications related to treatment must be consid-

ered. A child withsystemic disease might necessitate different treatmentthan a healthy one.

The examination should begin with a thorough history and char-acteristics of any pain, because these are often important in helping todetermine pulpal status and eventual treatment. Whereas pain usuallyaccompanies pulpal inflammation, extensive problems might arise

without any history of pain. If possible, a distinction between provokedandspontaneouspain should be ascertained.Provokedpain that ceasesafter removal of the causative stimulation is usually reversible and in-dicative of minorinflammatory changes. Stimuli include thermal, chem-ical, and mechanical irritants and many times are due to deep caries,faultyrestorations,sorenessaround a primary toothnearing exfoliation,or an erupting permanent tooth.

Spontaneous pain is a constant or throbbingpain that occurswith-out stimulation or continues long after the causative factor has beenremoved. In a well-controlled histologic study of primary teeth withdeep carious lesions, Guthrie et al. (12) demonstrated that a history ofspontaneous toothache is usually associatedwith extensivedegenerativechanges extending into the root canals. Primary teeth with a history ofspontaneous pain should not receive vital pulpal treatments and arecandidates for pulpectomy or extraction.

The clinical examination might produce evidence of pulpal patho-sis. Redness, swelling, fluctuance, severe dental decay, defective ormissing restorations, and draining parulis mightindicate pulpal involve-ment. Percussion sensitivity might be valuable to the diagnosis, but it iscomplicated by the reliability of the childs response because of thepsychological aspects involved. Tooth mobility might be present nor-mally because of physiologic resorption, and many pulpally involvedteeth have no mobility.

Electric pulp tests arenot valid in primary teeth (1).LaserDopplerflowmetry might be of greater help in determining vitality, butthis equip-ment has not been perfected, and the price is prohibitive (13).

Thermal tests are usually not conducted on primary teeth becauseof their unreliability(1, 5).

After the clinical examination, radiographs of good quality areessential. Like permanent teeth, periapical radiolucencies appear at the

apicesin primary anterior teeth. In primary molars, pathologic changesare most often apparent in the bifurcation or trifurcation areas. Conse-quently, bite-wing radiographs are often best to observe pathologicchanges in posterior primary teeth. Pathologic bone and root resorp-tions are signs of advanced pulpal pathosis that has spread into theperiapical tissues and is usually treatable only with extraction.

Mild, chronic pulpal irritation such as seen in caries might stim-ulate the deposition of tertiary reactionary dentin over the pulp (5).

With acute or rapid onset as the disease reaches the pulp, calcifiedmasses might form away from the exposure site. Such calcified massesare always indicative of advanced pulpal degeneration extending intothe root canals (14). Primary teeth with such calcified masses arecandidates for only pulpectomy or extraction (Fig. 2).

Internal resorption in primary teeth is always associated with ex-

tensive inflammation (12).Becauseofthethinnessoftheprimarymolarroots, if internal resorption can be seen radiographically, a perforationusually exists, and the tooth must be extracted (Fig. 3).

Interpretation of radiographs of primary teeth is always compli-cated by the presence of the succedaneous tooth and surrounding fol-licle. Misinterpretation of the follicle can easily lead to an erroneousdiagnosis of periapical pathology. Superimposition of the permanenttooth might obscure visibility of thefurcaand roots of the primary tooth,causing misdiagnosis. Added to this is the normal physiologic resorp-tion process.

Radiographs might also reveal evidence of: previous pulpal treat-ment;calcification changes in pulpchambers androotcanals; oversized

Figure1. Silicone models of the pulps of 2 primary mandibular second molars.Note the communication between the facial and lingual canals in the mesialroots.

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canalsindicative of cessationof root formationand pulpalnecrosis; andafter trauma, root fractures, bone fractures, displacement of teeth, im-bedded tooth fragments, or foreign bodies in soft tissues.

The size of a pulpal exposure and the amount and color of hem-orrhage have been reported as important factors in diagnosing theextent of inflammation under a carious lesion. Although all cariousexposures are accompanied by pulpal inflammation, the larger the ex-posure, the more likely it is to be widespread or necrotic.

Excessive (2,5,14,15) or deep purple (15) colored hemorrhageis evidence of extensiveinflammation, andtheseteethare candidates forpulpectomyor extraction.Hemorrhage that cannot be controlledwithin12 minutes by light pressure with a damp cotton pellet at an exposuresite indicates more extensive treatment is necessary. The same is trueafter removal of tissue when doing a pulpotomy. A pulpectomy or ex-traction would then be indicated.

In addition to the aforementioned tests and observations whendealing with traumatic injuries to the primary teeth, other factors must

be considered.Studies have shown that 1 in 3 children receive traumatic injuriesto the primary dentition (16, 17). Because of the less dense bone andshorter roots as compared with permanent teeth, most injuries aredisplacements rather than fractures. Such injuries might heal normally

without sequelae by formation of an amorphous diffuse calcificationhistologically resembling osteodentin, formation of a partial or com-plete obliteration of the canal (18, 19), or result in pulpal necrosis.

In a study of 545 traumatized primary maxillary incisors, Borumand Andreasen (20) found that 53% of subjects developed pulpal ne-crosis, and25% developedpulp canal obliteration. Thefactors found toinfluence development of pulp necrosis were age of the patient, degreeof displacement and loosening, and concurrent crown fracture. Calcificobliteration of the canal was influenced by tooth displacement and

amount of root resorption. Crown fracture decreased canal oblitera-tion. They also pointed outthat no well-established treatmentguidelinesexist concerning healing processes and complications in primary teeth.

It has been suggested that the proximity to the succedaneoustoothis an important factor when deciding on treatment for the injured pri-mary tooth. The treatment least likely to damage the permanent toothshould be chosen (1, 20). Conflicting data exist regarding treatment ofprimary injuries. Studies have shown no relationship between treatinginjured primary teeth compared with extraction regarding disturbanceof the permanent teeth (16, 21). Others have shown a tendency towardmore extensive disturbances in the mineralization when injured pri-mary teeth were retained (22).

Near universal agreement exists that avulsed primary incisorsshould not be replanted because of the possibility of danger to thepermanent tooth bud (1).

Roughly half of traumatizedprimary teeth presentingfor treatmentdevelop transient or permanent discoloration. These colors vary from

yellow to dark gray andusually becomeevident 13weeksaftertrauma.Primary teeth with yellow discoloration frequently have radiographicsigns of pulp canal calcification and have a low incidence of pulpalnecrosis (20, 23).

Injured primary teeth withdark gray discoloration arereported tohave necrotic pulps in 50%82% of the cases. Conversely, necrosis ofthe pulp occurred in teeth with no discoloration in approximately 25%of injured primary incisors (20, 2325). Attempts to correlate discol-orationto pathologic, radiographic, andhistologic changes in the pulpsof injured primary incisors present mixed findings. Color change of thetooth alone without other findings is not a reliable indicator of pulpalhealth (26). Diagnosis of pulp necrosis in primary incisors is primarilybased on dark gray color change and radiographic evidence of peria-pical pathology or lack of root formation (1) (Fig. 4). Schroder et al.(25) reported development of periapical osteitis in 82% of gray discol-orations within 1 month. Andreasenand Riis(27) have shown that pulpnecrosis and periapical inflammation of 6 weeks duration did not leadto developmental disturbances of permanent teeth. Thus, when diagno-sis cannot be established, it is justifiable to wait for further develop-ments.

Diagnosis of Pulpal Status in PermanentImmature Teeth

In teeth with incomplete root formation, correct pulpal and peri-apical diagnosis is of paramount importance before proceeding withany endodontic treatment because of the devastating result of loss of

vitality. Every attempt should be made to preserve the vitality of theseimmature teeth until maturation has occurred. Loss of pulpal vitalitybefore completion of dentin deposition leaves a weak root more proneto fracture as a result of the thin dentinal walls.

In a 4-yearstudy, Cvek(28) noted a significant increase in cervical

root fracturesin treated immature teeth compared with those withcom-pleted roots. In immature teeth, the frequency of fractures was depen-dent on the stage of root development, ranging from 77% in teeth withthe least to 28% in teeth with the most developed roots (28). Thus, evenif treatment is successful, prognosisfor prolongedretentionof thetooth

Figure 2. Calcified masses within the pulp (arrow), which form away from theexposure site, and internal resorption (as in this primary mandibular firstmolar) are indicative of advanced degeneration.

Figure3. Internal resorption(arrow), as seen in this primary maxillary secondmolar, will always be perforated and a candidate for extraction. Note the per-forated root after extraction and the periodontal probe in the resorptiveperforation.

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is greatly diminished. Loss of vitality before completion of root lengthwill lead to a poorer crown-to-root ratio, with possible periodontalbreakdownas a resultof increasedmobility. Therefore, alltreatments inthis group of teeth are oriented toward vital procedures. If these moreconservative procedures fail, the tooth can still be treated with apexifi-cation, apical barrier techniques, or conventional root canal treatment.

Although numerous scientific studies have been reported on the

treatment of permanent teeth with immature apices, the literature isalmost devoid in the area of diagnosis of pulpal status in this group ofteeth.

The diagnosis begins with a thorough medical history and anyimplications related to the anticipated treatment. The dental history andcharacteristics of associated pain might be helpful in determining pul-pal status. History of any traumatic injury to the facial area should beexplored in depth and recorded for future medical, dental, legal, andinsurance purposes.

The nature, type, length, and distinction between provoked andspontaneous pain are recorded. Provoked pain caused by thermal,chemical, or mechanical irritants usually indicates pulpal inflammationof a lesser degree and is often reversible. Spontaneous pain, on theother hand, is usually associated with widespread, extensive, degener-

ative, irreversible pulpal inflammation or necrosis.The medical and dental histories are followed by a thorough clin-ical examination. Any areas of redness, swelling, fluctuance, tissue ten-derness, dental decay, defective or missing restorations, or fractured ormobile teeth are noted. Presence of discolored crowns or a parulismight indicate pulpalnecrosis. Thealignment of theteeth, includinganyinfrapositioned or suprapositioned teeth, might provide valuable infor-mation.

Electric pulp tests andthermal tests areof limited value because ofthe varied responses as roots mature. In addit ion, invalid data mightbe obtained as a result of the often unreliable responses from chil-dren because of fear, management problems, and inability to un-

derstand or communicate accurately. Consequently, most diagnosesare made on observation of clinical symptoms and radiographicevidence of pathosis.

Numerousstudies (2932) havereportedtheunreliabilityofelec-tric pulp tests in permanent teeth with open and developing apices.Inconsistent results ranging from 11% in 6- to 11-year-olds with com-pletely open apices (29) to 79% in older children (31) have beenreported. It is also possible to obtain a false-positive in teeth with liq-

uefaction necrosis (33). Thus, electric pulp tests are of little valueduring the period of root formation, because the data are not reliable.Electric and thermal tests were shown to be unreliable after

traumatic injury to a tooth, and no response might be elicited evenafter circulation has been restored (34, 35). The potential for heal-ing is greater with incomplete root development than in fully formedteeth.

Laser Doppler flowmetry has been reported to be very reliable fordiagnosing pulpal vitality(13, 36, 37). In a very detailed histologic andradiographic study of revitalization of dogs teeth after reimplantation,

Yanpiset et al. (36) were able to make a correct diagnosis 84% of thetime. In nonvital pulps, the histologic study proved to be accurate in95% of cases, whereas in vital ones the data were correct 74% of thetime. This significant difference in readings was observed at as early

as 4 weeks. Although the authors pointed out the validity of deter-mining nonvital teeth, they cautioned against relying solely on thistest and would only initiate pulpal therapy after observing othersigns of pathology.

It has also been shown that blood pigment within a discoloredtoothcrowninterferes with laserlight transmission (38).Thislimitationis significant, because discoloration after trauma is frequent. Also, thisequipment has not been perfected for routine dental diagnosis and iscost-prohibitive for the practicing dentist.

Thermal testing with ice and ethyl chloride are of limited valuediagnostically. Iceand ethyl chloride have consistently been reported tobe inferior to carbon dioxide snow (2932) and dichlorodiflu-oromethane (DDM)(31, 39). Researchers have shown carbon dioxide

snow to consistently give positive responses near 100% even with openapices (2932).

Figure 4. The dark gray discoloration of the crown of this primary maxillarycentral incisor is indicative of pulpal necrosis.

Figure 5. Dark gray discoloration of the crown of this permanent maxillarycentral incisor indicates pulpal necrosis.

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Thermal tests with heat in permanent teeth with developing apicesare of limited value because of inconsistent responses (32) and arerarely performed.

Radiographic examination and interpretation are key elements in thediagnosis of pulpal pathology in teeth with developing apices. Good qualityperiapical radiographs of any involved teeth are used to assess root devel-

opment anddiscoverperiapical rarefaction androotresorption.After trau-matic injury, radiographs are essential to determine the presence of frac-tured bone and roots, displaced teeth, and imbedded foreign objects.

In posterior teeth, bite-wing radiographs are also necessary todetect caries, proximity of lesions to the pulp, previous pulpal treat-ments, and quality of any restorations.

Figure6. Apicalbarrier with MTA andstrengthening of thethin root with bondedcomposite.(A) Preoperative radiographof permanentmaxillaryleft central incisor.The pulp is necrotic, and the apex is open. (B) 4-mm plug of MTA placed at the apex. (C) Remainder of canal restored with bonded composite resin.(D) Two-and-a-halfyear follow-up showing covering of MTA with cementum and healing of a periapical lesion.

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Discoloration of a tooth crown after trauma is a common sequelaand one of the foremost diagnostic indicators (4042). Yellow discol-orationis usually indicative of pulp space calcification, anda gray colorusually signifies pulpal necrosis (40) (Fig. 5).

Transient coronal discoloration has been reported (42) in 4% ofteeth after luxation injuries as a result of vascular damage and hemor-rhage immediately after injury. In these cases, it was speculated thatpulpal healing depends on the bacterial status. With bacterial infection,healing is unlikely. In this group of teeth, determination of bacterialstatus could not be ascertained on the basis of coronal discoloration,loss of pulpal sensibility, or periapical rarefaction (42).

Transient apical breakdown occurs after displacement injuriesand might lead to misdiagnosis (42, 43). The development of transientperiapicalradiolucencytogether with coronal discoloration, negativeelectric pulp test, and cold response up to 4 monthswas shown tosubsequently regain the original color and normal pulpal responses(43). Transient apical breakdown apparently is linked to the repairprocess in the pulp and periapical tissues and returns to normal whenhealing is complete (42). Bone loss, which produces the radiolucency,eventually heals with new bone.

Universal agreement exists that immature teeth have the greatestpotential to heal after trauma or caries, particularly when the apicalforamen is wide open. This group of teeth also has the greatest chanceof misdiagnosis and mistreatment. To avoid mistakes, treatment mustnot be undertaken on the basis of negative responses to pulp testing.Radiographic and symptomatic assessment is currently the principaldiagnostic criterion. The following factors are key in making the diag-nostic determination: symptoms of irreversible pulpitis or apical peri-odontitis; clinical signs of periradicular infection including swelling,tenderness to percussion, mobility, or parulis formation; radiographi-cally detectible bone loss; progressive root resorption; and arrestedroot development compared with other adjacent teeth (44).

If doubtful, do not start treatment. Keep the patient under closeobservation and continue to reassess the diagnostic criteria until a de-finitive diagnosis can be established.

The treatment of primary and young permanent teeth has changed

dramatically in recent years as new materials have been developed andresearched. Theuse of calcium hydroxide (for decades thestandardforpulp protection), pulp capping, and pulpotomy procedures in perma-nent teeth is being replaced with composite resins(45, 46)and mineraltrioxide aggregate (MTA) (ProRoot; Dentsply Tulsa Dental, Tulsa, OK).Pulp capping with resin composites in monkeys produced the lowestincidence of bacterial microleakage, pulpal inflammation, and inci-dence of pulpal necrosis when compared with calcium hydroxide andglass ionomer cement(46).

When compared with calcium hydroxide, MTA produced signifi-cantly more dentinal bridging in a shorter time with significantly lessinflammation and less pulpal necrosis (4749). MTA has been shownto be cementoconductive, with attachment of cementoblasts to the ma-terial (49). Sarkar et al. (50) studied the interactions of MTA, a syn-

thetic tissue fluid, and dentin of extracted teeth. They concluded thatcalcium from theMTA reacted withphosphate in tissuefluid, producinghydroxyapatite. The sealing ability, biocompatibility, and dentinogenicactivity of the material occurbecauseof thesephysiochemical reactions.

Once considered taboo, vital pulpal treatment of symptomatic per-manent teeth with MTA has been reported (5, 51, 52) to be successful,allowing continued root development. Stronger roots with greatly im-proved prognosis for permanent retention are now possible.

Loss of pulpal vitality in open apex teeth in the past led to pro-tracted treatment and often ended in early tooth loss caused by fractureof weak roots. Apical barrier techniques with MTA now allow timelycompletion of apexification and have eliminated the use of calcium

hydroxide, except as a temporary canal disinfectant. The use of MTA asan apical barrier has become the standard for treatment of the openapex pulpless tooth (Fig. 6). The development of bonded compositetechniques now allows strengthening of these weak roots to levels ofintact,fully formedrootsand hasvirtuallyended root fractures(5356)(Fig. 6C).

Revascularization of teeth with necrotic infected canals has beenreported by using combinations of antibiotics (57, 58). The canals areaccessed and disinfected with copious irrigation of sodium hypochlo-rite. The canals are not instrumented. A paste of metronidazole, cipro-floxacin, and minocycline is placed in the canals and left for 1 month.The tooth is re-entered, and endodontic files are inserted through theapices to stimulate bleeding to produce a blood clot at the level of theCEJ. After clotting, MTA is placed over the blood clot, and a permanentexternal seal is placed. Theclot is then revascularized, producing thick-ening of the canal walls and apical closure.

Stem cell research holds great hope for the future, with the aim ofhealing impaired dental tissues including dentin, pulp, cementum, andperiodontal tissues. By stimulating the bodys intrinsic capacities, we

will be able to regenerate tissues, allowing further development of teethand bone or possibly the formation of new teeth to replace those rav-aged by decay or lost to traumatic injuries.

References1. Flores MT, Holan G, Borum M, Andreasen JO. Injuries to the primary dentition. In:

Andreasen JO, Andreasen F, Andersson L, eds. Textbook and color atlas of traumaticinjuries to the teeth. 4th ed. Oxford, UK: Blackwell Munksgaard, 2007.

2. Starkey PE. Management of deep caries of pulpally involved teeth in children. In:Goldman HM, Forrest SP, Byrd DL, et al, eds. Current therapy in dentistry. vol 3. StLouis, MO: Mosby, 1968.

3. Mass E, Zilberman U, Fuks AB. Partial pulpotomy: another treatment option forcariously exposed permanent molars. J Dent Child 1995;62:3425.

4. Orban BJ, ed. Oral histology and embryology. 4th ed. St Louis, MO: CV Mosby Co,1957.

5. Camp JH, Fuks AB. Pediatric endodontics: endodontic treatment for the primary andyoung,permanentdentition. In:CohenS, Hargreaves K,eds:Pathwaysof thepulp.9thed. St Louis, MO: Mosby, 2006:82282.

6. Kamijo Y. Studies on morphological change in the alveolar region of the jaw bone

with development of the permanent tooth from the standpoint of clinical anatomy.Bull Tokyo Dent Coll 1967;8:41.

7. Zurcher E. Theanatomy of theroot canalsof theteethof thedeciduousdentitionandof the first permanent molars. New York: William Wood & Co, 1925.

8. Hibbard E, Ireland RL. Morphology of the root canals of the primary molar teeth.J Dent Child 1957;24:250.

9. Finn SB. Morphology of the primary teeth. In: Finn SB, Caldwell RC, Cheraskin E,et al, eds. Clinical pedodontics. 3rd ed. Philadelphia: WB Saunders, 1967.

10. Ireland RL. Secondary dentin formation in deciduous teeth. J Am Dent Assoc1941;28:1626.

11. Bevelander G, Benzer D. Morphology and incidence in secondary dentin in humanteeth. J Am Dent Assoc 1943;30:1079.

12. Guthrie TJ, McDonald RE, Mitchell DF. Dental hemogram. J Dent Res 1965;44:67882.

13. Evans D, Reid J, Strang R, Stirrups D. A comparison of laser Doppler flowmetry withother methods of assessing the vitality of traumatized anterior teeth. Endod DentTraumatol 1999;15:28490.

14. McDonald RE, Avery DR. Treatment of deep caries, vital pulp exposure, and pulplessteeth in children. In: McDonald RE, Avery DR, eds. Dentistry for the child and ado-lescent. 7th ed. St Louis, MO: Mosby, 1999.

15. Pinkham JR. Diagnosis. In: Pinkham JR, ed. Pediatric dentistry: infancy throughadolescence. Philadelphia: WB Saunders, 1988.

16. Andreasen JO, Ravn JJ. Epidemiology of traumatic dental injuries to primary andpermanent teeth in a Danish population sample. Int J Oral Surg 1972;1:2359.

17. Glendor U.On dentaltrauma in children andadolescents: incidence,risk,treatment,time, and cost. Swed Dent J 2000;140(Suppl):152.

18. Robertson A, Lundgren T, Andreasen JO, Dietz W, Hoyer I, Noren JG. Pulp calcifica-tions in traumatized primary incisors: a morphologic and inductive analysis study.Eur J Oral Sci 1997;105:196206.

19. HolanG. Tubelike mineralizations in thedental pulpof traumatizedprimaryincisors.Endod Dent Traumatol 1998;14:279 84.

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developed thick dentinal walls and the apices are closed, a full pulpec-tomy can be performed (Fig. 3).

Revascularization of Infected Pulp Space

Pulp RevascularizationRevascularization of an immature necrotic tooth has many poten-

tial advantages.It has been shown that under certain conditions revascularization

can be achieved in young teeth that have been traumatically avulsed,leaving a necrotic but uninfected pulp. Skoglund et al. (10) demon-strated that in extracted dog teeth, pulpal revascularization started im-mediately after reimplantation and was completed after approximately45 days (Fig. 4). It is important to understand the biologic featurespermitting revascularization in young avulsed teeth, so that we mightattempt to reproduce these unique conditions when the pulp space isinfected. The immature avulsed tooth has an open apex, short root, andintact but necrotic pulp tissue. Therefore, thenew tissuehas easy accessto the root canal system and a relatively short distance for proliferationto reach the coronal pulp horns. It has been experimentally shown thatthe apical portion of a pulp might remain vital and proliferate coronallyafter reimplantation, replacing the necrotized coronal portion of thepulp (1113). The speed with which the tissue completely revascular-izes the pulp space is important because bacteria from the outside arecontinually attempting to enter the pulp space, and the presence of vitalpulpal tissuegreatly slows or prevents thebacterial penetration into thistissue compartment. The ischemically necrotic pulp that is unique to anavulsion injuryacts asa scaffold into which thenew tissuegrows, and the

fact that the crown is usually intact (rather than carious or with an accesscavity) slows bacterial penetration because their only access to the pulp isthrough cracks (14) or enamel defects. Thus, the race between prolifera-tion of new tissue and infection of the pulp space favors the new tissue.

Revascularization of the pulp space in a necrotic, infected toothwith apical periodontitis was attempted by Nygaard-Ostby and Hjortdal(15) in the 1960s but was mostly unsuccessful. However, the materialsandinstruments available 4050 years agowere probably not sufficient

to create an environment similar to the avulsed tooth, ie, a canal that isfree of bacteria, containing a scaffold for new tissue to grow and to belargely resistant to further bacterial penetration. With currently avail-able technologies it could be possible to effectively disinfect an infectedpulp, artificially place a scaffold, and then effectively seal the accesscavity to resist subsequent infection.

A recent case report by Banchs and Trope (16) has reproducedresultsin cases reported by others, indicating that it might be possible toreplicate the unique circumstances of an avulsed tooth to revascularizethepulp in infected necrotic immature roots (1113).Ourcase(Fig.5)described the treatment of an immature second lower right premolar

with radiographic and clinical signs of apical periodontitis with thepresence of a sinus tract. The canal was disinfected without mechanicalinstrumentation but with copious irrigation with 5.25% sodium hypo-

chlorite and the use of a mixture of ciprofloxacin, metronidazole, andminocycline (17), mixed as described in Fig. 6.

A blood clot was produced to the level of the cementoenameljunction to provide a scaffold for the ingrowth of new tissue followed bya double seal of mineral trioxide aggregate in the cervical area and abonded resin coronal restoration above it. Clinical and radiographicevidence of healing was observed as early as 22 days. The large radi-olucency had disappeared within 2 months, and at the 24-month recallit was obviousthatthe rootwallswerethick,and thedevelopment ofthe rootbelow the restoration was similar to the adjacent and contralateral teeth.

The antibacterial effectiveness of the triantibioticpaste reported byHoshino et al. (17) was confirmed by our group in a dog model withinfected immature roots (18). In addition, our group demonstrated in

dogs that the potential for revascularization does exist (Fig. 7), and thatthe blood clot was essential as a scaffold (19). At this point, we areunsure of which factors in the blood clot are important. When thesefactors are isolated, they can be incorporated into a synthetic scaffoldthat willbe easierto for clinicians to manipulate compared with a bloodclot.

The procedure described in this section can be attempted in mostcases. If no signs of regeneration are present after 3 months, then moretraditional treatment methods can be initiated.

Figure 1. Histologic section of a pulp after a traumatic exposure 24 hourspreviously. Only about 1 mm of superficial pulp is inflamed.

Figure 2. Carious exposure caused by caries. The underlying inflamed pulp is removed, and a partial pulpotomy is performed on the remaining healthy pulp withcalcium hydroxide (Courtesy Dr. Francisco Banchs).

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Figure3. Inthiscaseafullpulpotomywasperformed(thusremovingthecoronallyinflamedpulp)andtreatingthepresumablyhealthypulpatthecanalorifices.Whenthe root canal has developed thick dentinal walls and the apices are closed, a full pulpectomy can be done (Courtesy Dr. Francisco Banchs).

Figure 4. Revascularization of immature dog teeth during period of 45 days. The teeth were extracted and immediately replanted. During the course of 45 days theblood supply moves into the pulp space.

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Figure 5. Immature tooth with a necrotic infected canal with apical periodontitis. The canal is disinfected with copious irrigation with sodium hypochloriteand triantibiotic paste. After 4 weeks the antibiotic is removed, and a blood clot is created in the canal space. The access is filled with a mineral trioxideaggregate base and bonded resin above it. At 7 months the patient is asymptomatic, and the apex shows healing of the apical periodontitis and some closureof the apex. Reproduced with permission fr om Banchs F, Trope M. Revascularization of i mmature permanent teeth with apical periodontitis: new treatmentprotocol? J Endod 2004;30:196-200.

Figure 6. Composition and mixing instructions for the triantibiotic paste (adapted from Hoshino et al. (17)).

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There has been a great deal of discussion as to the correct termi-nology for what has been called pulp revascularization in this article.Some have used the cases shown as examples of pulp regeneration andthe beginning of stem cell technology in endodontics. It is clearly notapexificationbecause notonly theapex is closed, butthe canal walls arethicker as well. Apexogenesis accomplishes a closed apex and thickerdentinal walls but by definition uses remaining vital root pulp to attainthis goal, which is not the case here. Guided tissue regeneration hasbeen used in periodontics and has some merit. However, guided tissueregeneration in periodontics assumes regeneration of periodontalstructures, yet this is not the casefor pulp. Inthe present cases, wemustdistinguishbetween revascularization and pulp regeneration. Presently,

we can only say with certainty that the pulp space has returned to a vitalstate. On the basis of research in avulsed teeth and a recent study oninfected teeth, however, it is more likely that the tissue in the pulp spaceis similar to a periodontal ligament than to pulp tissue (19). It appearsthat there is approximately a 30% chance of pulp tissue reentering thepulpspace(20). Futureresearch willneed to be performed to stimulatepulp regeneration from the pluripotential cells in the periapical region(21).

References1. Bergenholtz G. Micro-organisms from necrotic pulps of traumatized teeth. Odont

Revy 1974;25:34758.2. Dummer PM, Hicks R, Huws D. Clinical signs and symptoms in pulp disease. Int

Endod J 1980;13:2735.3. Cvek M. A clinical report on partial pulpotomy and capping with calcium hy-

droxide in permanent incisors with complicated crown fracture, J Endod1978;4:2327.

4. Barthel CR, Rosenkranz B, Leuenberg A, Roulet JF. Pulp capping of carious expo-sures: treatment outcome after 5 and 10 years: a retrospective study. J Endod2000;26;5258.

5. Tronstad L, Mjor IA. Capping of the inflamed pulp. Oral Surg 1972;34:477 83.6. Mjor IA, Tronstad L. The healing of experimentally induced pulpitis. Oral Surg

1974;38:1159.

7. Cvek M, Cleaton-Jones PE, Austin JC, Andreasen JO. Pulp reactions to exposureafter experimental crown fractures or grinding in adult monkeys, J Endod1982;8:3919.

8. Cox CF, Keall HJ, Ostro E, Bergenholtz G. Biocompatibility of surface-sealed dentalmaterials against exposed pulps. Prosthet Dent 1987;57:19.

9. Sato T, Hoshino E, Uematsu H, Noda T. In vitro antimicrobial susceptibility to com-binations of drugs on bacteria from carious and endodontic lesions of human de-ciduous teeth. Oral Microbiol Immunol 1993;8:1726.

10. Skoglund A, Tronstad L, Wallenius K. A microradiographic study of vascular changesin replanted and autotransplanted teeth in young dogs. Oral Surg Oral Med OralPathol 1978;1:1728.

11. Barrett AP, Reade PC. Revascularization of mouse tooth isografts and allo-grafts using autoradiography and carbon-perfusion. Arch Oral Biol 1981;26:5415.

12. Rule DC, Winter GB. Root growth and apical repair subsequent to pulpal necrosis inchildren. Br Dent J 1966;120:58690.

13. Iwaya SI, Ikawa M, Kubota M. Revascularization of an immature perma-nent tooth with apical periodontitis and sinus tract. Dent Traumatol 2001;17:1857.

14. Love RM. Bacterial penetration of the root canal of intact incisor teeth after a simu-lated traumatic injury. Endod Dent Traumatol 1996;12:28993.

15. Nygaard-Ostby B, Hjortdal O. Tissue formation in the root canal following pulpremoval. Scand J Dent Res 1971:79:33348.

16. Banchs F, Trope M. Revascularization of immature permanent teeth with apicalperiodontitis: new treatment protocol? J Endod 2004;30 :196200.

17. Hoshino E, Kurihara-Ando N, Sato I, et al. In-vitro antibacterial susceptibility ofbacteria taken from infected root dentine to a mixture of ciprofloxacin, metronida-zole and minocycline. Int Endod J 1996;29:12530.

18. Windley W III, Teixeira F, Levin L, Sigurdsson A, Trope M. Disinfection of immatureteeth with a triple antibiotic paste. J Endod 2005;6:43943.

19. Thibodeau B, Teixeira F, Yamauchi M, CaplanDJ, Trope M. Pulp revascularization of

immature dog teeth with apical periodontitis. J Endod 2007;33:6809.20. Ritter AL, Ritter AV, Murrah V, Sigurdsson A, Trope M. Pulp revascularization of

replanted immature dog teeth after treatment with minocycline and doxycyclineassessed by laser Doppler flowmetry, radiography, and histology. Dent Traumatol2004;20:7584.

21. Sonoyama W, Liu Y, Yamaza T, et al. Characterization of the apical papilla and itsresiding stem cells from human immature permanent teeth: a pilot study. J Endod2008;34:16671.

Figure 7. Revascularization of an immature dog tooth with apical periodontitis. The root was artificially infected, producing apical periodontitis. After treatment

similar to that described in Fig. 5, revascularization has occurred.

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Vital Pulp Therapy with New Materials for Primary Teeth:New Directions and Treatment PerspectivesAnna B. Fuks, CD

AbstractVital pulp therapy aims to treat reversible pulpal injuryand includes 2 therapeutic approaches: (1) indirect pulptreatment for deep dentinal cavities and (2) direct pulpcapping or pulpotomy in cases of pulp exposure. Indi-rect pulp treatment is recommended as the most ap-propriate procedure for treating primary teeth withdeep caries and reversible pulp inflammation, providedthat this diagnosis is based on a good history, a properclinical and radiographic examination, and that thetooth has been sealed with a leakage-free restoration.Formocresol has been a popular pulpotomy medica-

ment in the primary dentition and is still the mostuniversally taught pulp treatment for primary teeth.Concerns have been raised over the use of formocresolin humans, and several alternatives have been pro-posed. Controlled clinical studies have been criticallyreviewed, and mineral trioxide aggregate and ferricsulfate have been considered appropriate alternativesto formocresol for pulpotomies in primary teeth withexposed pulps. In most of the studies reviewed, thecaries removal method has not been described. The useof a high-speed handpiece or laser might result in anexposure of a normal pulp that would otherwise notbe exposed. (J Endod 2008;34:S18-S24)

Key WordsFerric sulfate, formocresol, mineral trioxide aggregate,primary teeth, pulp therapy

The aim of vital pulp therapy is to treat reversible pulpal injuries in both permanentandprimary teeth, maintaining pulp vitality andfunction (1). In addition to these, inprimary teeth it is important to preserve the tooth until its natural exfoliation time, thuspreserving arch integrity (2). Vital pulp therapy includes 2 therapeutic approaches:indirect pulp treatment (IPT) in cases of deep dentinal cavities and direct pulp capping(DPC) or pulpotomy in cases of pulp exposure (1).

Advances in biomedical research open avenues for the design of new methods ofdental treatment, aiming at regeneration of the dentin-pulp complex. New approacheshave been based on the understanding of the molecular and cellular mechanismsregulating dentinogenesis during dental tissue repair and their potential for clinicalexploitation (1).

The dental pulp possesses the ability to form a dentin-like matrix (tertiary dentin)as part of the repair in the dentin-pulp organ (3). Vital pulp therapy aims to treatreversiblepulpal injury in cases in which dentin and pulp are affected by caries, restor-ative procedures, or trauma. Whenever the dentin-pulp complex is affected by injury, 3different physiopathologic conditions might be observed at the dentin-pulp border:

1. In thecase of mild injuries as in noncavitated enamelcaries or slowlyprogressingdentinal caries, the odontoblasts might survive, and the odontoblastic layer isstimulated to form a tertiary dentin matrix beneath the injury (reactionary den-tin). Reactionary dentin shows many similarities to the primary and secondarydentin and can effectively oppose exogenous destructive stimuli to protect thepulp (4).

2. With severe dentinal injuries without pulp exposure as in rapidly progressingcarious lesions or in severe tissue damage caused by cavity preparation, odon-

toblasts are destroyed subjacent to the affected dentin (5, 6). In an appropriatemetabolic state of the dentin-pulp complex, a new generation of odontoblast-likecells might differentiate and form tubular tertiary dentin (reparative dentinogen-esis) (3, 7). It must be emphasized that under clinical conditions, the matrixformed at the pulp-dentin interface often comprises reactionary dentin, repara-tive dentin, or fibrodentin formation. It is impossible to distinguish these pro-cesses at the in vivo level, and the process might also be indistinguishable from abiochemical and molecular point of view.

3. In the case of pulp exposure, theamputatedpulpcan be repairedby itself orafterapplication of capping materials (810). Pulp exposure caused by caries shows

verylimited potentialfor pulp recoveryas a resultof bacterialinfectionof thepulpfor a substantial period of time, which compromises the defense reaction (11).

As part of the wound healing process in the repairing pulp, the dentinogenicpotential of pulp cells can be expressed. Proliferation, migration, and differen-

tiation of progenitor cells can give rise to a new generation of reparative dentin-forming cells (odontoblast-like cells), reconstituting the lost continuum at thepulp-dentin border (12, 13).

Indirect Pulp TreatmentAfter this brief review of the cellular changes during tooth development and how

they are mimicked during tissue repair, we are able to assess the biologic validity of thevarious vital pulp treatments. In thislight,IPT, contrary to what wasbelieved in the past,can also be an acceptable procedure for primary teeth with reversible pulp inflamma-tion, provided that the diagnosis is based on a good history and proper clinical and

Professor Emeritus, Department of Pediatric Dentistry, Ha-dassah School of Dental Medicine, Hebrew University, Jerusa-lem, Israel.

Address requests for reprints to Dr Fuks at [email protected].

Conflict of Interest: Anna B. Fuks, CD, reports no financialinterests or potential conflicts of interest.0099-2399/$0 - see front matter



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radiographic examination, and the tooth has been sealed with a leak-age-free restoration (2).

In a recent systematic review on complete or ultraconservativeremoval of decayed tissue, Ricketts et al. (14) concluded that in deeplesions, partial caries removal is preferable to complete caries removalto reduce the risk of carious exposure.

Several articles reported the success of this technique in primaryteeth (1519). On the basis of the biologic changes previously de-scribed andthe growing evidence of the success of IPT in primary teeth,

wecan recommendIPT as themostappropriatetreatment forsymptom-free primary teeth withdeepcaries, provided that a proper, leakage-freerestoration can be placed. This issue will be discussed in greater detailfurther in this symposium.

Direct Pulp CappingDPC is carried out when a healthy pulp has been inadvertently

exposed during an operative procedure. The tooth must be asymptom-atic, and the exposuresite must be pinpoint in diameter and free of oralcontaminants. A calcium hydroxide medicament is placed over the ex-posuresite to stimulatedentinformation andthus healthe wound andmaintain the pulps vitality(20).

DPC of a carious pulp exposure in a primary tooth is not recom-mended but can be used with success on immature permanent teeth.DPC is indicated for small mechanical or traumatic exposures whenconditionsfor a favorableresponseare optimal.

journal of endodontics_pulp symposium_july 2008 issue vol 34

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