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July 2008, Volume 34, Number 7S Pulp Symposium
S1 AAE and AAPD Symposium Overview: Emerging Science in Pulp Therapy— New Insights Into Dilemmas and Controversies
Gerald N. Glickman and N. Sue Seale
The Caries Process and Its Effect on the Pulp: The Science Is Changing and So Is Our Understanding
Diagnosis Dilemmas in Vital Pulp Therapy: Treatment for the Toothache Is Changing, Especially in Young, Immature Teeth
Joe H. Camp
Regenerative Potential of Dental Pulp
Vital Pulp Therapy with New Materials for Primary Teeth: New Directions and Treatment Perspectives
Anna B. Fuks
Vital Pulp Therapy with New Materials: New Directions and Treatment Perspectives—Permanent Teeth
David E. Witherspoon
Indirect Pulp Therapy and Stepwise Excavation
Indirect Pulp Capping and Primary Teeth: Is the Primary Tooth Pulpotomy Out of Date?
James A. Coll
S40 S47 S51
Is Formocresol Obsolete? A Fresh Look at the Evidence Concerning Safety Issues
Alan R. Milnes
“New Age” Pulp Therapy: Personal Thoughts on a Hot Debate
Paula Jane Waterhouse
Regeneration Potential of the Young Permanent Tooth: What Does the Future Hold?
Kenneth M. Hargreaves, Todd Geisler, Michael Henry, and Yan Wang
Contemporary Perspectives on Vital Pulp Therapy: Views From the Endodontists and Pediatric Dentists
N. Sue Seale and Gerald N. Glickman
AAE and AAPD Symposium Overview: Emerging Science in Pulp Therapy—New Insights Into Dilemmas and Controversies
vidence-based best practices are yet to be established for the management of caries-associated pulpal disease in young permanent and primary teeth. Controversies still remain among practitioners, including pediatric dentists and endodontists, as to which treatment modalities are most predictable in the contemporary practice of pulp therapy. Many clinicians still remain divided as to whether indirect pulp capping is a viable procedure in primary and young permanent teeth, or whether formocresol remains the medicament of choice for pulpotomies in primary teeth. To begin the process of establishing evidence-based best practices in pulpal therapy as well as highlight some of the future directions in pulp therapy including pulp regeneration with stem cells and root canal revascularization, the American Academy of Pediatric Dentistry (AAPD) and the American Association of Endodontists (AAE) jointly sponsored “Emerging Science in Pulp Therapy: New Insights into Dilemmas and Controversies.” The symposium was held on November 2–3, 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 by these 2 national specialty organizations. The genesis of the idea for joint sponsorship was the need to examine the shared procedures performed by the 2 specialties. With specialty organizations routinely producing evidence-based practice guidelines that provide the foundation for treatments performed, it is critical that when 2 specialties perform the same or similar treatments, their guidelines are parallel in language and in content. Without these guidelines, confusion and uncertainty will result in clinical practice when a rational treatment plan is required to manage a specific pathologic entity such as caries. Pediatric dentistry and endodontics share in the important treatment decisions associated with pulpal therapy for the cariously involved young permanent tooth. In addition, endodontists are consultants to and involved in pulp therapy treatment decisions for the cariously involved primary tooth. With the eventual expectation that the 2 organizations could come together and produce practice guidelines that share common goals and language for caries-associated pulp therapy for primary and young permanent teeth, the decision was made to bring together a panel of world-renown experts from both specialties to present the current best evidence as a first step in developing the anticipated guidelines. Individuals identified to be on the planning committee from the AAE were Drs Gerald N. Glickman, Alan Gluskin, and Bradford Johnson. From the AAPD, Drs Suzi Seale, Elizabeth Barr, and James Coll were selected. These individuals met and identified the following areas as appropriate for focus: the nature of the carious lesion of dentin; indirect pulp therapy, including stepwise excavation for both young permanent teeth and primary teeth; primary tooth pulpotomy agents with special emphasis on formocresol and the controversy surrounding its use; and revascularization of young permanent teeth and pulpal regeneration by using stem cells. To that end, a cadre of 9 experts was identified and invited to present evidence for assigned topics. The articles resulting from their presentations appear in this publication.
During the conference Professor Lars Bjørndal discussed the caries process and its effect on the pulp. He applied this information to the dilemma of the deep carious lesion and indirect pulp capping, with special emphasis on the coronal seal. Dr Joe Camp focused on diagnostic dilemmas in vital pulp therapy for young immature teeth. Dr Martin J. Trope spoke on how new trends are changing our understanding of the regenerative potential of the dental pulp, whereas Dr David Witherspoon spoke on new directions and treatment perspectives involving pulpal revascularization for permanent teeth. Dr Anna Fuks presented a compilation of the evidence for different pulpotomy agents in treating the vital cariously involved primary tooth. Dr Jim Coll provided information about indirect pulp capping for primary teeth as an alternative to pulpotomy. 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 the future of pulpal regeneration for the young permanent tooth. Because 2 specialty groups were represented, the planning committee sought to determine, through a brief pretest completed before the first speaker, the baseline opinions of the audience about the various topics to be presented. After the last speaker, a more lengthy set of questions about the same topics were presented to the audience for their opinions by using an audience response system. Attendees’ responses were identified by specialty, and the results of the comparisons of the presymposium and postsymposium opinions within specialty and across specialties are also presented in this publication. We believe this symposium represented an important landmark in bringing together different disciplines with potentially different opinions to reach an evidence-based consensus about common treatment dilemmas. Because practice guidelines increasingly drive our treatment decisions, it is important that we are in agreement about their content, ultimately for the care and benefit of our patients. Gerald N. Glickman, DDS, MS
Vice-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, MSD
Regents 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 financial interests or potential conflicts of interest. N. Sue Seale, DDS, MSD, reports no financial interests or potential conflicts of interest. Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. This article is being published concurrently in Pediatric Dentistry, May/June 2008; Volume 30, Issue 3. The articles are identical. Either citation can be used when citing this article. doi:10.1016/j.joen.2008.02.036
JOE — Volume 34, Number 7S, July 2008
AAE and AAPD Symposium Overview
The Caries Process and Its Effect on the Pulp: The Science Is Changing and So Is Our Understanding
Lars Bjørndal, DDS, PhD
The understanding of the caries process and its effect on the pulp is presented in the context that caries does develop in various rates of progression. Early in the caries process, the pulp reflects changes within lesion activity. Thus, the early pulp response is reversible. Later, the rate of caries progression is reflected by the quality of the tertiary dentin. Slowly progressing lesions create tertiary dentin resembling normal tubular dentin. Rapidly progressing lesions lead to the production of atubular 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 an ecosystem that might undergo significant changes. The untreated lesion is temporarily converted from an active and closed lesion environment into one that is open and slowly progressing. The analysis of untreated carious lesions has transformed the treatment philosophy of deep carious lesions. (J Endod 2008;34:S2-S5)
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 station represents the initial surface etching at the outer enamel layer, leading to the dull white appearance of the active progressing enamel lesion. The last station represents the deepest layer of the carious tooth, with a necrotic, infected root canal system and the presence of apical pathosis. Investigators, clinicians, and researchers who enter the “caries train” have typically focused on only a few stations. They might also have different understandings and opinions about how to treat dental caries. Their opinions have developed from a mixture of clinical empirical tradition and an understanding from research. These opinions could be named the cariologist opinion, the operative opinion, and the endodontic opinion.
Some Opinions about the Approach to Dental Caries
The classic cariologist opinion is focused on the prevention of caries and further progression of the established lesion. The initial focus is on the white spot lesion, whose histologic picture is visualized in the laboratory via transmitted or polarized light. Treatment philosophies here are typically related to nonoperative and preventive approaches. 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 a clinical breakdown of the enamel surface and with carious dentin exposure. Without focusing 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 leaving carious dentin behind. The operative opinion also tends to be a two-edged sword, because sometimes the design of the cavity overrides the fact that the caries lesion might not be in need of operative intervention. However, for esthetic or other reasons, the operative intervention is carried out with a minimally invasive approach, even though the actual lesion is dark, discolored, arrested caries. Finally, the endodontic opinion deals with the prevention of an infected pulp and subsequent apical pathosis; the issue of a lesion mainly concerns this region. Therefore, all carious dentin should be removed, even if the result is a pulp exposure. The existence of these virtual opinions was reflected in a recent practice-based research network to determine dentists’ treatment methods for deep caries lesions in which one would expect pulpal exposure (1). The survey findings showed that 62% of the responding dentists would remove all caries (operative opinion), 18% would partially remove caries (cariologist opinion), and 21% would initiate endodontic treatment (endodontic opinion). Differences in decision making for treating deep carious lesions in primary molars have also recently been reported (2). Actually, this topic is not new, as shown in the following quotations: “It is better that a layer of discolored dentin should be allowed to remain for the protection of the pulp rather than run the risk of sacrificing the tooth” (3). In contrast, Black (4) wrote: “. . . it will often be a question whether or not the pulp will be exposed when all decayed dentin overlaying it is removed . . . It is better to expose the pulp of a tooth than to leave it covered only with softened dentin.” It is necessary to remain within the historical perspective to understand how these different opinions have justified various treatment concepts. The endodontic opinion advocating an invasive pulp treatment in relation to caries might very well have gained
Dental caries, dental pulp, dentin, indirect pulp treatment, stepwise excavation, tertiary dentin
From the Department of Cariology and Endodontics, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Denmark. Address requests for reprints to Dr Bjørndal at lb@odont. ku.dk. Conflict of Interest: Lars Bjørndal, DDS, PhD, is a Grant Recipient from the Danish Agency for Science Technology and Innovation. 0099-2399/$0 - see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. This article is being published concurrently in Pediatric Dentistry, May/June 2008; Volume 30, Issue 3. The articles are identical. Either citation can be used when citing this article. doi:10.1016/j.joen.2008.02.037
JOE — Volume 34, Number 7S, July 2008
Taken together. the application of immunohistochemistry has improved our understanding of the underlying molecular events (13). the deepest penetration of the entire caries lesion complex can also be seen as the oldest lesion area along the dentin-pulp interface following the direction of the dentinal tubules. the advancing front of demineralization also reflects the dynamic nature of the cariogenic biofilm. radical interventions have been advocated. Therefore. Number 7S. The bacteria are not able to S3 An Update of Caries Pathology: The Non-cavitated Enamel Lesion Complex—Understanding the Early Pulp–Dentinal Response to Caries The proximal white spot lesion is triangular when viewed in 2 dimensions and conical when viewed in 3 dimensions. No serious microbial invasion takes place in the dentin as long as the highly organized enamel layer (even though being demineralized) separates the biofilm from the dentin. in which the pulp reacts very early to the influx of various external stimuli. showing that the early enamel lesion in human teeth could also lead to odontoblast alterations and signs of pulpal infiltration. Why? Because the interpretation of the very same clinical situation even today might reflect completely different treatments (1. 2). beginning with early lesions? When and how does the pulp begin to produce extradentinal matrix and tertiary dentin? What is the spreading pattern of caries? When will microorganisms invade the demineralized dentin? Can we say something about the prehistory of caries. 16). has been described by using this concept (11). Therefore.” Some observations even indicate that the pulp might react to the signals passing through the enamel even before histologic caries reactions can be observed in the dentin (14). However. and it might very well resemble the age-related intratubular physiologic sclerosis (17). This is a key reference because in this symposium presentation it is hypothesized that these findings have been used as evidence for the early onset of irreversible pulpal inflammation caused by caries progression. but it also contains reprecipitation of previously dissolved dentin crystals. morphologic and molecular features in the odontoblast cells leading to the production of extradentinal matrix can also be detected (15. These stimuli might include samples of plaque or soft carious dentin (5. In contrast. it is too much to force everyone to get on and off at all the stations. different pulpal reaction patterns were to be expected that could lead to differing means of treating caries as opposed to only a radical approach. Massler. In this context. as well as reactions leading to reactionary and reparative dentinogenesis (14). it was possible to describe morphologic changes in the enamel and the subjacent pulp-dentinal organ within the same section (12). dentin demineralization is initiated. guided by the cariogenic biofilm covering the surface of the enamel lesion. Moreover. but when we experience the pulp in relation to caries. dentin. Examples of Improved Laboratory Methods That Have Created a Better Understanding One approach that has improved our understanding from the histologic findings of Brännström and Lind (7) was the use of thin. integrated a sophisticated and advanced biologic understanding of caries into caries treatment. the study by Brännström and Lind (7) has been a key reference. and misunderstandings might very well occur in communication between clinicians and researchers. Thus. the topography of the lesion reflects the acidogenic potential of the cariogenic biofilm at the enamel surface. The reaction might represent activity of the odontoblasts. I will return to this subject later.Pulp Symposium inspiration from pulp studies carried out on animal models by using standardized test cavities in sound dentin. expressed as different pH gradient creating either dissolution or reprecipitation of dentin mineral. it should not be considered as a “station” along the track of irreversible pulp inflammation. During our daily clinical practice we might only recall the early odontoblast response from the library. Note that the initial dentin demineralization takes place not in unaffected sound dentin but in dentin with a decreased permeability as a result of the presence of the hypermineralized dentin. The morphology of reactionary dentinogenesis. This reaction is seen in the dentin before any signs of demineralization. hence a “point of no return. When the enamel lesion reaches the dentinoenamel junction (DEJ). He described acute and chronic caries on the basis of clinical criteria and histologic descriptions. it is necessary to be clear and precise with the use of well-defined terms. The first visible histologic change in the dentin subjacent to an enamel lesion is the formation of hypermineralized dentinal tubules. Consequently. After the dentin begins the process of demineralization. when viewing the histologic picture of tertiary dentin? Why do we sometimes find tertiary dentin produced during caries. whereas the peripheral parts represent “new beginners” following the direction of the rods (10). whereas at other times it is difficult to detect? Is knowledge about lesion activity important? provides the possibility for understanding the subjacent pulpal-dentinal response in relation to time. Hence. it is during a very late stage of lesion progression as we consider whether pulp exposure should be avoided. Thus. it is tempting to suggest that the observation of the “early influx pulp data” might have led to the clinical interpretation that irreversible pulp inflammation is also reached relatively early in relation to caries. How should we interpret the early pulp response? An updated interpretation and understanding would be that the pulpal response follows the caries lesion from the very beginning. One could question why a pulp-preserving treatment was not an option. the shape of the enamel lesion represents a transmission of stimuli from the enamel surface that can be related to time and JOE — Volume 34. This reflects the understanding and importance of caries as a disease that can progress at varying rates. the cariologist opinion. A recent Cochrane review of pulp management in extensive caries deals with clinical studies in which deep lesions without clinical symptoms were treated (8). can be traced back decades to Massler (9). but during a symposium such as this. Also. and the pulp were preserved with this new histologic method. undemineralized tooth sections in the examination of well-defined carious lesions. On the basis of quantitative data related to the degree of porosity in the enamel lesion. when entering a caries discussion aiming to cross invisible lines of dental subspecialities. However. a natural goal would be to reach a consensus of understanding caries in between these group opinions. The normal structural relationships between enamel. Consequently. the peripheral areas represent younger and less progressed areas along the dentin-pulp interface. Let us update our understanding of caries pathology by considering that the caries train might use more than one track. In short. 6). With the metaphor of the caries train in mind. and to some extent the operative opinion. The Sequence of the Carious Development in the Tooth Morphologic changes in odontoblasts have been found in welldefined enamel lesions in freshly extracted third molars (14). defined as tertiary dentin produced by primary odontoblasts. among others. the lesion comprises a multitude of many microlesions following the direction of the enamel rods. the hypermineralized dentin is probably the result of physiologic activity from the odontoblast. What is the sequence of the various zones in carious dentin. Therefore. this topic requires additional study (18). July 2008 The Caries Process and Its Effect on the Pulp . The central lesion area is the oldest part and shows the deepest penetration.
as well as its quality. whereas the older central lesion area shows the gradual development of atubular fibrodentin (26). The microbial invasion is related to the gradual structural breakdown of the enamel layer (20). Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatment outcome. In Denmark caries is still the most frequent reason for endodontic treatment (24). In short. 2b. whereas at the margins. The subjacent dentin discloses the clinical signs of slowly progressing caries by its brownish discoloration (Fig. defined as the combination of fibrodentin and new tubular dentin produced by new odontoblast-like cells (29). the rapidly progressing caries lesions would typically follow the sequence of odontoS4 blast necrosis (25). the enamel breaks down (Fig. also known as fibrodentin. Eventually the white demineralized and undermined enamel breaks as a result of mechanical stress. Red zones indicate plaque. slowly progressing lesions characteristically display tubular dentin formation at the pulpal site. and necrotic zone is observed. 1c). the pulp might respond with reparative dentin resembling the dentin-bridge formation after a direct pulp capping procedure (16). and at the same time the growth conditions change for the cariogenic biofilm. The lateral spread of demineralized dentin and enamel is related to the total breakdown of the enamel layer and therefore describes a relatively later stage of tissue destruction than previously believed. Lesion Activity and Pulpal Response What is the significance of how rapidly caries progresses in relation to a pulpal response? Let us once again benefit from the histologic findings of the early pulp response to enamel caries (14). This tertiary dentin shows a mixture of reactionary dentinogenesis and dentin produced by new odontoblast-like cells. 1a). Reprinted with permission from Blackwell Munksgaard from Bjørndal L. Of course. After the change in caries activity. soft. only active enamel lesions show evidence of proliferation of cells from the subodontoblastic cell-rich zone into the cell-free zone. as traditionally taught in textbooks advocating invasive pulp treatments (28). As an additional example. disintegrated. When the non-cavitated enamel lesion has histologic contact with the DEJ.2:10 –23. It also represents what takes place several times a week in dental practice. Endodontic Topics 2002. large variation in lesion activity might appear (27). It appears that the primary odontoblasts are involved in the early onset of new extradentinal matrix in the younger portions of the lesion. The pulpal response in lesions with a conversion of lesion activity can be reflected by the presence of reparative dentinogenesis. After the enamel breakdown. and a clinically visible gap develops between the enamel and dentin (Fig. with finger-like projections but into the reactionary dentin (16). should be seen as a reflection of the nature of the external stimuli that have previously passed through the dentin. On the basis of these observations. changing the environment into an open ecosystem (b). Different rates of progression can therefore be present within one tooth. the odontoblasts within active lesions have a significantly lower cytoplasm:nucleus ratio compared with control sites. In contrast. The presence of fibrodentin or interface dentin indicates that all primary odontoblasts have died. if nothing is done with the deep lesion even though it might be temporarily arrested. The cavitated lesion transforms from a closed ecosystem into an open ecosystem (Fig. Number 7S. Consequently. eventually the dentin shrinks. and accumulations of cariogenic biomass are apparent. 14). A few studies have described this sequence by comparing central and old lesion areas with peripheral and lateral parts of younger lesion areas (11. optimal growth conditions for the plaque are apparent. The presence or absence of tertiary dentin. The extent of the demineralized dentin is restricted to the histologic enamel lesion contact. It appears that this takes place in the same manner as the primary odontoblast cells. as the degree of protection of the biofilm has decreased. a stage of mixed lesion activity develops. At this active stage the carious dentin can easily be separated from the enamel. (22) penetrate through the enamel rod structure (19). leading to necrosis and pulpal infection with apical pathosis.Pulp Symposium Figure 1. the cariogenic biofilm gains improved growth conditions along the lateral spread of caries or retrograde caries (23). Diagrams showing the temporary conversion of the cariogenic ecosystem during untreated lesion progress. pulp vitality is not necessarily maintained. This worst case scenario is often what we find in many textbooks. the occlusal part of the tooth has no heavy plaque accumulation. In addition to odontoblast cell reaction per se. Subsequently. Let us in this context return to the morphology of the reactionary dentinogenesis defined as tertiary dentin produced by primary odontoblasts. Moreover. Eventually the caries process will bring about irreversible changes in the pulp. In the occlusal part. Another important change in our understanding is the misinterpreted concept of caries spreading along the DEJ subjacent the noncavitated enamel lesion (21). and active lesion progress continues (c). In contrast. the pulpal response follows not only the early caries lesion. classic signs of slow lesion progress are noted in terms of a darker appearance of the demineralized dentin. demineralized. eventually followed by the presence of atubular dentin formation. Also within deep carious lesions (Fig. and as the moisture is decreased. 2a). In contrast. If the carious tooth is left untreated. c). The outflux of mineral has been extensive. 1). further tissue breakdown occurs. As the lesion progresses. this situation is not found in the arrested or slowly progressing enamel lesion. and no spreading of demineralized hard tissue is noted undermining sound enamel. the odontoblasts also display a different response to active versus arrested caries. Bjørndal JOE — Volume 34. it also mirrors changes in lesion activity. different patterns of tertiary dentin can be expected relative to the prehistory of each lesion. 1b). July 2008 . Very little attention has been given previously to the potential capacity of the primary odontoblast to be part of tertiary dentin formation. but it indicates that deep exposed dentin lesions are not unconditionally related to an irreversible pattern of pulp pathology. A closed lesion environment develops in relation to an occlusal lesion (a). the peripheral parts are protected. A moist. In cavitated lesions. During the stages of dentin exposure a completely different situation is created under heavy bacterial invasion. eventually the caries activity in the peripheral parts of the lesion leads to the breakdown of the tooth (Fig.
19. 25. Bjørndal L. 15. Bjørndal L. Odontoblast response under carious lesions. Caries Res 2006. Oxford: IRL Press. Effect of ageing and caries in dentin permeability. Tomes J. Clarkson BH. 20. The technical procedures in filling teeth. 2003:81. Attitudes and expectations of treating deep caries: a PEARL network survey. Ekstrand KR.88(Suppl 1):149 –54. Darvann T. Number 7S. 7. 6. Dental caries: the disease and its clinical management.34:102– 8. Lind PO. 2nd ed. 12. 1908. Oral Surg 1972. Bjørndal L.52:182–90.103:25–31. Black GV. References 1. each of them leading to different pulp reactions. Root canal treatment in Denmark is most often carried out in carious vital molar teeth and retreatments are rare. when diagnosing deep carious lesions. Pulp treatment for extensive decay in primary teeth. The structure and ultrastructure of the carious lesion in human dentin. (22) Understanding of Caries Pathology Creates the Treatment Philosophy Related to Deep Caries In the past. J Dent Res 1992. Int Endod J 2006. Silverstone LM. Thylstrup A: A structural analysis of approximal enamel caries lesions and subjacent dentin reactions. Ekstrand KR. Acta Odontol Scand 1994. Eur Arch Paediatr Dent 2007. Only well-designed clinical trials will answer this question. July 2008 The Caries Process and Its Effect on the Pulp S5 .39:785–90. Tronstad L. Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatment outcome. Ekstrand KR. 3. 9. Effect of soluble plaque factors on inflammatory reactions in the dental pulp. 24.44:1045–50. et al. Bjørndal L. Pulpal response to early caries. Dentine and dentine reactions in the oral cavity. perhaps even arresting the subjacent pulpal inflammation. Qvist V. Eur J Oral Sci 1995.33: 80 –3. Dentin-pulp complex responses to carious lesions. Structural analyses of plaque and caries in relation to the morphology of the groove-fossa system on erupting mandibular third molars. 10. Ritchie HH. Proc Finn Dent Soc 1992. 8:37– 42.Pulp Symposium Figure 2. Joffre A. Qudeimat MA. 18. this does not mean that we should wait for it to happen! We should be motivated to understand the lesion activity and use this information in the treatment of caries. eds. Brännström M.1):257–74. A work on operative dentistry in two volumes.40:256 – 64. Beighton D. A method for light microscopy examination of cellular and structural interrelations in undemineralized tooth specimens.27:231–7. 14.88(Suppl.39:13–22. Oxford: Blackwell Munksgaard. Scand J Dent Res 1975. 2. Cochrane Database Syst Rev 2003. Dent Update 2005. Oper Dent 2002. vol. Bjørndal L. Perhaps with the appropriate clinical intervention we can reduce the rate of caries progression. given that we do not yet have noninvasive tools for the measurement of the severity of the inflamed pulp. Therefore. 29. Thylstrup A. Yeung CA. Lee Y-L. Relating visual and radiographic ranked scoring systems for occlusal caries detection to histological and microbiological evidence.31:336 – 48. Darvann T. The treatment of deep dentine carious lesions. J Dent Res 1996. A light microscopic study of odontoblastic and non-odontoblastic cells involved in tertiary dentinogenesis in well-defined cavitated carious lesions. Reit C. Bacteriology of dentin caries. 26. Lin C-P. 21.17:441– 60.2:10 –23. Iwaka M. Thesleff I. Caries Res 1998. Bjørndal L. Goel BR. Hosoda H. Proc Finn Dent Soc 1992. 27. Al-Saiegh FA. Bergenholtz G. 11. 2008:367– 83. However.33:50 – 60. Omar R. but it might be temporary because the enamel margins will obtain protection for the cariogenic process (b). Experimentally induced pulpitis. the following have all been clear justification for the performance of radical operative intervention: (1) early microbial invasion of carious dentin. Arch Oral Biol 1994. Ozawa H. Vaahtokari A. The noninvasive pulp treatment of deep caries lesions will be the focus of my second presentation. eds. et al.32:59 – 69. Tronstad L. 2nd ed. Instead of accepting that there is a steady progression through the tooth leading toward the same results if left untreated. Larsen T. Godovikova V. Liu J. Lukinmaa PL. the clinical discussion of reversible or irreversible development of pulpitis will continue to be controversial in relation to the actual state of pulp pathology. Massler M. Tobias RS. Endodontic Topics 2002. Immunohistochemical localization of HLA-DR-positive cells in unerupted and erupted normal and carious human teeth. 23. Bjørndal L. Smith AJ. A system of dental surgery. 5. Clinical endodontics. Red zones indicate plaque. Hicks MJ. 1987:95–102. AL-Omari Q. Restorative decisions for deep proximal carious lesions in primary molars. 2nd ed.1:CD003220. Gen Dent 2007. Adv Dent Res 2001. Glenny AM. The pattern of untreated deep lesions might involve a decrease in lesion activity (a). Ricketts D. 17. Lindhe J. Kidd EAM. 13.83:153– 8. Fejerskov O. Reprinted with permission from Blackwell Munksgaard from Bjørndal L. Oen KT. Nakajima M.75:1585–9. Stuttgard: Thieme. leaving remnants of roots behind (c). Burrow MF. Nadin G. we must make a choice on the basis of our knowledge of the caries process and its effect on the pulp and on the basis of existing diagnostic methods. Edwardsson S. Pulpal reactions to dental caries.55:197–203. Vena D. Nakamura H.2 chain mRNA in Adult human permanent teeth as revealed by in situ hybridization. (2) early spreading along the DEJ that undermines sound enamel. Bjørndal L. In: Thylstrup A. Bjørndal L. Even though textbooks often illustrate the worst case scenario. Kidd EAM. 22.1:185–93. Caries Res 1997. Yoshiba K. Chicago: Medico-Dental Publishing Co. Thompson VP. JOE — Volume 34. Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatment outcome. Caries removal and the pulpodentinal complex.32:402–13. A quantitative light microscopic study of odontoblast and subodontoblastic reactions to active and arrested enamel caries without cavitation. 4. 8. Presence or absence of tertiary dentinogenesis in relation to caries progression.71:36 – 42. Eventually the entire crown breaks. Bouvier M. Leach SA. 16. Kidd EAM.2:10 –23. London: John Churchill. Int Dent J 1967. Kidd EAM. Mjör IA. and (3) the early onset of an irreversible pulp response. 28. Caries Res 1999. Vainio S. J Dent Res 1965. Endodontic Topics 2002. Odontoblast stimulation in ferrets by dentine matrix components. Tagami J. Laustsen MH. Expression of type I collagen pro. Thylstrup A. Gerodontics 1985. In: Fejerskov O. Magloire H. Yoshiba N. Bjørndal L. II. Cassidy N. it might be more appropriate to understand that caries activity constitutes many different rates of progression. 1859:336.
University of North Carolina. DDS. Because of this anatomy. pulp capping. a part-time. During this formative period. Depending on each root’s external anatomy. each root is wide open. D S6 Camp JOE — Volume 34. (J Endod 2008. pulpotomy From private practice of endodontics. The decision to render conservative vital treatment to allow root formation completion or more radical treatment such as root canal therapy might hinge on our diagnosis of root development. MSD Abstract The literature is almost devoid of scientific studies of diagnosis of pulpal pathology in primary and permanent teeth with open apices. treatments should be oriented toward maintenance of vitality to allow completion of root formation. Issue 3. Conflict of Interest: Joe H. Because of the shorter roots of primary teeth. The articles are identical. the clinician must rely on time to determine root closure in all other teeth to prevent treatment protocols that cannot be successfully completed without apical convergence (5).com. pulp capping. the tooth root’s development begins after enamel and dentin formation has reached the cementoenamel junction (CEJ). doi:10. Volume 30. but the radiograph is read mesiodistally. paid position.2008. whereas dentin deposition is continued until root formation is completed. Either citation can be used when citing this article. Because the faciolingual width of most roots and canals is greater than the mesiodistal width. pulp. the sheath disappears. During this formative stage.03. The x-ray beam is exposed in the faciolingual plane. and islands of dentin are formed. the opposing walls meet and coalesce. July 2008 . According to Orban (4). Most outcome reports are supported by empirical treatment and anecdotal case reports (1). Once root length is established. North Carolina. DDS. and the apex is eventually closed with dentin and cementum. Camp. Address requests for reprints to Dr Camp at E-mail address: joecamp@carolina. Without histologic examination an accurate determination of the extent of inflammation is impossible (2). with the exception of the maxillary central and lateral incisors and some single canal lower premolars. it is necessary to have a thorough knowledge of normal root formation and the differences between developing and fully formed teeth. and pulpotomy for primary teeth and permanent teeth with open apex. While admittedly poor for diagnosing the degree of inflammation in this group of teeth. Camp. As root formation proceeds apically. Many outcome studies are conducted retrospectively on the basis of clinical signs and symptoms and make assumptions regarding the pulpal status before treatment without histologic or bacterial data to support the preoperative diagnosis. Most reports are empirical or retrospective studies without adequate prior knowledge of preexisting conditions or histologic findings leading to the necessity of pulpal procedures. Most of the diagnostic tests used in conventional endodontic therapy are of very little or no value in primary teeth and of limited value in permanent immature teeth.020 iagnosis in primary and young. creating apical convergence. The apical barrier with mineral trioxide aggregate followed by root strengthening with bonded composite is reviewed. is the University Clinical Consultant for Dentsply Tulsa Dental Specialties. differentiation into multiple canals might occur. radiographs cannot determine apical closure. Hertwig’s epithelial root sheath is formed by the epithelial dental organ. Many of our treatments are based on our diagnosis of the root development stage. permanent. which eventually expand to divide the root into separate canals.1016/j. communication exists between the canals in the form of isthmuses. In permanent teeth. MSD. May/June 2008. to properly diagnose and treat primary and young permanent teeth. Charlotte. Chapel Hill.Pulp Symposium Diagnosis Dilemmas in Vital Pulp Therapy: Treatment for the Toothache Is Changing. Correlation between clinical symptoms and histopathologic conditions is poor and complicates diagnosis of pulpal health in exposed pulps of children (3). Continued dentin deposition narrows the canals. 0099-2399/$0 . diagnostic tests must be performed to obtain as much information as possible before arriving at treatment options. immature teeth varies greatly from that in fully formed permanent teeth.34:S6-S12) Key Words Diagnosis. Appropriate diagnostic tests and their effectiveness are documented for both groups. Diagnostic literature based on scientific studies is almost nonexistent.joen.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. North Carolina. Therefore. apical closure cannot usually be determined radiographically. This article is being published concurrently in Pediatric Dentistry. As growth continues.rr. This article reviews the available literature and current techniques of indirect pulp therapy. Immature Teeth Joe H. with one tube for each of the future roots. root formation is completed faster than for permanent teeth. Further deposition of dentin will strengthen the roots’ thin dentinal walls and help diminish future root fracture. Especially in Young. root formation is not completed until 1– 4 years after eruption into the oral cavity. Number 7S. Isthmuses and fins extending toward the root’s center might persist in fully formed teeth. Each root’s internal surface is lined by odontoblasts. Consequently. and Department of Endodontics. diverging apically and limited by the epithelial diaphragm.
radiographs of good quality are essential. combined with additional dentin deposition internally. Laser Doppler flowmetry might be of greater help in determining vitality. calcified masses might form away from the exposure site. but continued deposition of dentin might divide the root into 2 or more canals (7–9). With acute or rapid onset as the disease reaches the pulp. Primary teeth with a history of spontaneous pain should not receive vital pulpal treatments and are candidates for pulpectomy or extraction. and many pulpally involved teeth have no mobility. In primary molars. Note the communication between the facial and lingual canals in the mesial roots. periapical radiolucencies appear at the apices in primary anterior teeth. the root canals roughly correspond to the external anatomy’s form and shape. communication exists between the canals in the form of isthmuses or fins (Fig. 2). Like the permanent molars. causing misdiagnosis. Guthrie et al. The primary molar teeth normally have the same number and position of roots and root canals as the corresponding permanent teeth. These factors complicate establishment of working lengths if root canal therapy is necessary. Tooth mobility might be present normally because of physiologic resorption.Pulp Symposium The root canals of primary teeth differ greatly from those of permanent teeth. At the time of root length completion. Number 7S. Accessory and lateral canals and apical ramifications of the pulp are common in primary molars (8). swelling. Interpretation of radiographs of primary teeth is always complicated by the presence of the succedaneous tooth and surrounding follicle. because these are often important in helping to determine pulpal status and eventual treatment. Thermal tests are usually not conducted on primary teeth because of their unreliability (1. the permanent tooth buds lie apically and lingually near the primary roots. extensive problems might arise without any history of pain. Internal resorption in primary teeth is always associated with extensive inflammation (12). Spontaneous pain is a constant or throbbing pain that occurs without stimulation or continues long after the causative factor has been removed. and treatment is complicated by apical resorption to allow for eruption of the succeeding teeth. and mechanical irritants and many times are due to deep caries. but it is complicated by the reliability of the child’s response because of the psychological aspects involved. ered. Pathologic bone and root resorptions are signs of advanced pulpal pathosis that has spread into the periapical tissues and is usually treatable only with extraction. The clinical examination might produce evidence of pulpal pathosis. 1). Provoked pain that ceases after removal of the causative stimulation is usually reversible and indicative of minor inflammatory changes. Stimuli include thermal. apical resorption of the roots makes the teeth progressively shorter. (12) demonstrated that a history of spontaneous toothache is usually associated with extensive degenerative changes extending into the root canals. Radiographs might also reveal evidence of: previous pulpal treatment. After the clinical examination. resorption of the roots begins and. Superimposition of the permanent tooth might obscure visibility of the furca and roots of the primary tooth. a perforation usually exists. chronic pulpal irritation such as seen in caries might stimulate the deposition of tertiary reactionary dentin over the pulp (5). and the tooth must be extracted (Fig. and draining parulis might indicate pulpal involvement. The examination should begin with a thorough history and characteristics of any pain. and shape of the canals within the primary roots. other communications between the pulp and the periapical tissues are formed by physiologic resorption of the internal surfaces of the roots adjacent to the permanent tooth buds. pathologic changes are most often apparent in the bifurcation or trifurcation areas. resulting in a difference in the apical foramen and the anatomic apex and complicating determination of root canal length. severe dental decay. soreness around a primary tooth nearing exfoliation. most variations occur in the mesial roots of mandibular molars and facial roots of the maxillary molars. July 2008 Diagnosis Dilemmas in Vital Pulp Therapy . Whereas pain usually accompanies pulpal inflammation. One study demonstrated that half of the primary incisor’s root might be resorbed lingually before it becomes obvious on a radiograph (6). In the primary anterior teeth (incisors and canines). Primary anterior teeth have one simple root canal and rarely have lateral or accessory canals. If possible. A child with systemic disease might necessitate different treatment than a healthy one. In a well-controlled histologic study of primary teeth with deep carious lesions. 9). Resorption is initiated on the primary root’s lingual surface. JOE — Volume 34. and any implications related to treatment must be consid- Figure 1. During this time. Such calcified masses are always indicative of advanced pulpal degeneration extending into the root canals (14). size. defective or missing restorations. these variations are usually in the facial to lingual plane and cannot be visualized on radiographs (7. faulty restorations. Mild. a distinction between provoked and spontaneous pain should be ascertained. oversized S7 Diagnosis of Pulpal Status in Primary Teeth As with any dental procedure. Primary teeth with such calcified masses are candidates for only pulpectomy or extraction (Fig. Because of the thinness of the primary molar roots. At root length completion. chemical. In addition. Secondary dentin deposition contributes to this change in morphology (10. and the price is prohibitive (13). 11). resorption on the roots’ internal surfaces adjacent to the forming permanent tooth might open other communications with the periapical tissues. Misinterpretation of the follicle can easily lead to an erroneous diagnosis of periapical pathology. Redness. fluctuance. but this equipment has not been perfected. Added to this is the normal physiologic resorption process. bite-wing radiographs are often best to observe pathologic changes in posterior primary teeth. or an erupting permanent tooth. most roots have only 1 canal. Percussion sensitivity might be valuable to the diagnosis. Consequently. Continued physiologic. Silicone models of the pulps of 2 primary mandibular second molars. In addition. if internal resorption can be seen radiographically. 3). Like permanent teeth. 5). calcification changes in pulp chambers and root canals. Also. At this time. This causes the apical foramen to move coronally. a thorough medical history must be completed. Electric pulp tests are not valid in primary teeth (1). might significantly change the number.
They also pointed out that no well-established treatment guidelines exist concerning healing processes and complications in primary teeth. The treatment least likely to damage the permanent tooth should be chosen (1. Calcific obliteration of the canal was influenced by tooth displacement and amount of root resorption. 21). Crown fracture decreased canal obliteration. Borum and Andreasen (20) found that 53% of subjects developed pulpal necrosis. The factors found to influence development of pulp necrosis were age of the patient. ranging from 77% in teeth with the least to 28% in teeth with the most developed roots (28). Cvek (28) noted a significant increase in cervical root fractures in treated immature teeth compared with those with completed roots. Thus. will always be perforated and a candidate for extraction. Others have shown a tendency toward more extensive disturbances in the mineralization when injured primary teeth were retained (22). (25) reported development of periapical osteitis in 82% of gray discolorations within 1 month. Because of the less dense bone and shorter roots as compared with permanent teeth. The size of a pulpal exposure and the amount and color of hemorrhage have been reported as important factors in diagnosing the extent of inflammation under a carious lesion. Color change of the tooth alone without other findings is not a reliable indicator of pulpal health (26). In a study of 545 traumatized primary maxillary incisors. In immature teeth. canals indicative of cessation of root formation and pulpal necrosis. In a 4-year study. 15) or deep purple (15) colored hemorrhage is evidence of extensive inflammation. when diagnosis cannot be established. the frequency of fractures was dependent on the stage of root development. Although all carious exposures are accompanied by pulpal inflammation. July 2008 .Pulp Symposium Near universal agreement exists that avulsed primary incisors should not be replanted because of the possibility of danger to the permanent tooth bud (1). and concurrent crown fracture. Primary teeth with yellow discoloration frequently have radiographic signs of pulp canal calcification and have a low incidence of pulpal necrosis (20. Hemorrhage that cannot be controlled within 1–2 minutes by light pressure with a damp cotton pellet at an exposure site indicates more extensive treatment is necessary. formation of a partial or complete obliteration of the canal (18. bone fractures. Figure 2. root fractures. The same is true after removal of tissue when doing a pulpotomy. Conflicting data exist regarding treatment of primary injuries. A pulpectomy or extraction would then be indicated. Camp JOE — Volume 34. 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. prognosis for prolonged retention of the tooth Figure 3. 20). Number 7S. S8 Diagnosis of Pulpal Status in Permanent Immature Teeth In teeth with incomplete root formation. In addition to the aforementioned tests and observations when dealing with traumatic injuries to the primary teeth. 17). even if treatment is successful. Internal resorption (arrow). Calcified masses within the pulp (arrow). Schroder et al. as seen in this primary maxillary second molar. Diagnosis of pulp necrosis in primary incisors is primarily based on dark gray color change and radiographic evidence of periapical pathology or lack of root formation (1) (Fig. Excessive (2. 4). 5. and these teeth are candidates for pulpectomy or extraction. Injured primary teeth with dark gray discoloration are reported to have necrotic pulps in 50%– 82% of the cases. imbedded tooth fragments. Conversely. and after trauma. and 25% developed pulp canal obliteration. 14. Roughly half of traumatized primary teeth presenting for treatment develop transient or permanent discoloration. Thus. 23). or foreign bodies in soft tissues. which form away from the exposure site. Such injuries might heal normally without sequelae by formation of an amorphous diffuse calcification histologically resembling osteodentin. and histologic changes in the pulps of injured primary incisors present mixed findings. These colors vary from yellow to dark gray and usually become evident 1–3 weeks after trauma. the larger the exposure. and internal resorption (as in this primary mandibular first molar) are indicative of advanced degeneration. most injuries are displacements rather than fractures. radiographic. 23–25). other factors must be considered. Note the perforated root after extraction and the periodontal probe in the resorptive perforation. Studies have shown no relationship between treating injured primary teeth compared with extraction regarding disturbance of the permanent teeth (16. necrosis of the pulp occurred in teeth with no discoloration in approximately 25% of injured primary incisors (20. correct pulpal and periapical diagnosis is of paramount importance before proceeding with any endodontic treatment because of the devastating result of loss of vitality. Attempts to correlate discoloration to pathologic. it is justifiable to wait for further developments. Andreasen and Riis (27) have shown that pulp necrosis and periapical inflammation of 6 weeks’ duration did not lead to developmental disturbances of permanent teeth. Every attempt should be made to preserve the vitality of these immature teeth until maturation has occurred. It has been suggested that the proximity to the succedaneous tooth is an important factor when deciding on treatment for the injured primary tooth. the more likely it is to be widespread or necrotic. degree of displacement and loosening. Studies have shown that 1 in 3 children receive traumatic injuries to the primary dentition (16. 19). or result in pulpal necrosis. displacement of teeth.
on the other hand. The medical and dental histories are followed by a thorough clinical examination. defective or missing restorations. Consequently. 37). all treatments in this group of teeth are oriented toward vital procedures. This limitation is significant. Thermal testing with ice and ethyl chloride are of limited value diagnostically. irreversible pulpal inflammation or necrosis. Number 7S. 36. The potential for healing is greater with incomplete root development than in fully formed teeth. Electric and thermal tests were shown to be unreliable after traumatic injury to a tooth. The nature. this equipment has not been perfected for routine dental diagnosis and is cost-prohibitive for the practicing dentist. is usually associated with widespread. with possible periodontal breakdown as a result of increased mobility. Thus. The dental history and characteristics of associated pain might be helpful in determining pulpal status. and inability to un- Figure 5. including any infrapositioned or suprapositioned teeth. Presence of discolored crowns or a parulis might indicate pulpal necrosis. Laser Doppler flowmetry has been reported to be very reliable for diagnosing pulpal vitality (13. dental. whereas in vital ones the data were correct 74% of the time. Although numerous scientific studies have been reported on the treatment of permanent teeth with immature apices. Ice and ethyl chloride have consistently been reported to be inferior to carbon dioxide snow (29 –32) and dichlorodifluoromethane (DDM) (31. It has also been shown that blood pigment within a discolored tooth crown interferes with laser light transmission (38). Electric pulp tests and thermal tests are of limited value because of the varied responses as roots mature. History of any traumatic injury to the facial area should be explored in depth and recorded for future medical. Therefore. electric pulp tests are of little value during the period of root formation. Yanpiset et al. 39). and insurance purposes. Also. Any areas of redness. invalid data might be obtained as a result of the often unreliable responses from children because of fear. In addition. The alignment of the teeth. the tooth can still be treated with apexification. dental decay. In nonvital pulps. might provide valuable information. 35). length. the histologic study proved to be accurate in 95% of cases. If these more conservative procedures fail. degenerative. is greatly diminished. This significant difference in readings was observed at as early as 4 weeks. In a very detailed histologic and radiographic study of revitalization of dogs’ teeth after reimplantation. Dark gray discoloration of the crown of this permanent maxillary central incisor indicates pulpal necrosis. most diagnoses are made on observation of clinical symptoms and radiographic evidence of pathosis. Provoked pain caused by thermal. or mechanical irritants usually indicates pulpal inflammation of a lesser degree and is often reversible. (36) were able to make a correct diagnosis 84% of the time. because discoloration after trauma is frequent. The diagnosis begins with a thorough medical history and any implications related to the anticipated treatment. It is also possible to obtain a false-positive in teeth with liquefaction necrosis (33). Although the authors pointed out the validity of determining nonvital teeth. The dark gray discoloration of the crown of this primary maxillary central incisor is indicative of pulpal necrosis. Researchers have shown carbon dioxide snow to consistently give positive responses near 100% even with open apices (29 –32). or fractured or mobile teeth are noted. type. chemical. management problems. and distinction between provoked and spontaneous pain are recorded. JOE — Volume 34. Inconsistent results ranging from 11% in 6. tissue tenderness. fluctuance.Pulp Symposium derstand or communicate accurately. the literature is almost devoid in the area of diagnosis of pulpal status in this group of teeth. and no response might be elicited even after circulation has been restored (34. or conventional root canal treatment. legal.to 11-year-olds with completely open apices (29) to 79% in older children (31) have been reported. Loss of vitality before completion of root length will lead to a poorer crown-to-root ratio. July 2008 Diagnosis Dilemmas in Vital Pulp Therapy S9 . Figure 4. because the data are not reliable. they cautioned against relying solely on this test and would only initiate pulpal therapy after observing other signs of pathology. Spontaneous pain. extensive. swelling. Numerous studies (29 –32) have reported the unreliability of electric pulp tests in permanent teeth with open and developing apices. apical barrier techniques.
(B) 4-mm plug of MTA placed at the apex. Radiographic examination and interpretation are key elements in the diagnosis of pulpal pathology in teeth with developing apices. proximity of lesions to the pulp. In posterior teeth. displaced teeth. radiographs are essential to determine the presence of fractured bone and roots. (A) Preoperative radiograph of permanent maxillary left central incisor. Good quality periapical radiographs of any involved teeth are used to assess root development and discover periapical rarefaction and root resorption. The pulp is necrotic. and imbedded foreign objects. After traumatic injury. Number 7S. and quality of any restorations. S10 Camp JOE — Volume 34. and the apex is open. bite-wing radiographs are also necessary to detect caries. (D) Two-and-a-half–year follow-up showing covering of MTA with cementum and healing of a periapical lesion. previous pulpal treatments. July 2008 . (C) Remainder of canal restored with bonded composite resin. Figure 6.Pulp Symposium Thermal tests with heat in permanent teeth with developing apices are of limited value because of inconsistent responses (32) and are rarely performed. Apical barrier with MTA and strengthening of the thin root with bonded composite.
loss of pulpal sensibility. and a permanent external seal is placed. Mass E. healing is unlikely. Lundgren T. JOE — Volume 34. producing thickening of the canal walls and apical closure. Fuks AB. Yellow discoloration is usually indicative of pulp space calcification. On dental trauma in children and adolescents: incidence. MTA produced significantly more dentinal bridging in a shorter time with significantly less inflammation and less pulpal necrosis (47– 49). Philadelphia: WB Saunders. Ireland RL. Reid J. If doubtful. Hibbard E. tenderness to percussion. McDonald RE. Management of deep caries of pulpally involved teeth in children. 16. Transient coronal discoloration has been reported (42) in 4% of teeth after luxation injuries as a result of vascular damage and hemorrhage immediately after injury. 9. Endod Dent Traumatol 1999.8:41. 6C). 5. negative electric pulp test. Sarkar et al. and cost. The development of bonded composite techniques now allows strengthening of these weak roots to levels of intact. or periapical rarefaction (42). Benzer D. allowing continued root development. Stirrups D. Bevelander G. Transient apical breakdown apparently is linked to the repair process in the pulp and periapical tissues and returns to normal when healing is complete (42). Ireland RL. Once considered taboo. Borum M. 6). and pulpotomy procedures in permanent teeth is being replaced with composite resins (45. The use of MTA as an apical barrier has become the standard for treatment of the open apex pulpless tooth (Fig. The canals are not instrumented. 7th ed. J Dent Child 1995. Epidemiology of traumatic dental injuries to primary and permanent teeth in a Danish population sample. (50) studied the interactions of MTA. In: Cohen S. OK). Morphology of the root canals of the primary molar teeth. 1925. 44:678 – 82. eds. July 2008 Diagnosis Dilemmas in Vital Pulp Therapy S11 . Stem cell research holds great hope for the future. Caldwell RC. After clotting. 6. mobility. ciprofloxacin. 17. time. MO: Mosby. vital pulp exposure. particularly when the apical foramen is wide open. Orban BJ.62:342–5. a synthetic tissue fluid. In: McDonald RE. Flores MT. In: Andreasen JO. Andreasen JO. Strang R. 1988. Forrest SP. Fuks AB. 3rd ed. vital pulpal treatment of symptomatic permanent teeth with MTA has been reported (5. 1957. McDonald RE. Pediatric endodontics: endodontic treatment for the primary and young. Dietz W. Dental hemogram. ed. allowing further development of teeth and bone or possibly the formation of new teeth to replace those ravaged by decay or lost to traumatic injuries. Partial pulpotomy: another treatment option for cariously exposed permanent molars. it was speculated that pulpal healing depends on the bacterial status. Revascularization of teeth with necrotic infected canals has been reported by using combinations of antibiotics (57. Evans D. which produces the radiolucency. permanent dentition. et al.28:1626. Apical barrier techniques with MTA now allow timely completion of apexification and have eliminated the use of calcium hydroxide. and dentin of extracted teeth. determination of bacterial status could not be ascertained on the basis of coronal discoloration. References 1. Oxford. and endodontic files are inserted through the apices to stimulate bleeding to produce a blood clot at the level of the CEJ. 1967. Bone loss. 15. Universal agreement exists that immature teeth have the greatest potential to heal after trauma or caries. biocompatibility. 18. Int J Oral Surg 1972. treatment. cementum. Zilberman U. et al. Philadelphia: WB Saunders.Pulp Symposium Discoloration of a tooth crown after trauma is a common sequela and one of the foremost diagnostic indicators (40 – 42). MO: Mosby. In: Pinkham JR. Dentistry for the child and adolescent. 14. Secondary dentin formation in deciduous teeth. St Louis. The canals are accessed and disinfected with copious irrigation of sodium hypochlorite. Diagnosis. 19. MO: Mosby. 9th ed. In: Finn SB.1:235–9. 4th ed. Transient apical breakdown occurs after displacement injuries and might lead to misdiagnosis (42. To avoid mistakes. St Louis. Textbook and color atlas of traumatic injuries to the teeth. vol 3. Swed Dent J 2000. J Am Dent Assoc 1943. 4th ed. J Dent Child 1957. Bull Tokyo Dent Coll 1967. progressive root resorption. Tulsa. pulpal inflammation. 5). Clinical pedodontics. The sealing ability. and incidence of pulpal necrosis when compared with calcium hydroxide and glass ionomer cement (46). Pulp capping with resin composites in monkeys produced the lowest incidence of bacterial microleakage. 46) and mineral trioxide aggregate (MTA) (ProRoot. Guthrie TJ. Studies on morphological change in the alveolar region of the jaw bone with development of the permanent tooth from the standpoint of clinical anatomy. A comparison of laser Doppler flowmetry with other methods of assessing the vitality of traumatized anterior teeth. 51. 1999. risk. This group of teeth also has the greatest chance of misdiagnosis and mistreatment. Cheraskin E. The anatomy of the root canals of the teeth of the deciduous dentition and of the first permanent molars. eds. Hargreaves K. Camp JH. The treatment of primary and young permanent teeth has changed dramatically in recent years as new materials have been developed and researched. Holan G. In these cases. do not start treatment. By stimulating the body’s intrinsic capacities. When compared with calcium hydroxide. The use of calcium hydroxide (for decades the standard for pulp protection). Andersson L. 2006:822– 82. 1968. 58). Avery DR. and a gray color usually signifies pulpal necrosis (40) (Fig. 12. 2. Pulp calcifications in traumatized primary incisors: a morphologic and inductive analysis study. They concluded that calcium from the MTA reacted with phosphate in tissue fluid. Starkey PE. with the aim of healing impaired dental tissues including dentin. The clot is then revascularized. 3. 10. St Louis. producing hydroxyapatite. 4. and cold response up to 4 months—was shown to subsequently regain the original color and normal pulpal responses (43). The development of transient periapical radiolucency—together with coronal discoloration. 43). The tooth is re-entered. and dentinogenic activity of the material occur because of these physiochemical reactions. Robertson A. 2007. Andreasen F. Morphology and incidence in secondary dentin in human teeth. MTA is placed over the blood clot. and pulpless teeth in children. Hoyer I. Dentsply Tulsa Dental. and arrested root development compared with other adjacent teeth (44). Tube like mineralizations in the dental pulp of traumatized primary incisors. pulp capping. radiographically detectible bone loss.15:284 –90.14:279 – 84. 52) to be successful. Morphology of the primary teeth. Byrd DL. UK: Blackwell Munksgaard. New York: William Wood & Co. In this group of teeth. Current therapy in dentistry. with attachment of cementoblasts to the material (49).140(Suppl):1–52. In: Goldman HM. Eur J Oral Sci 1997. Andreasen JO. Kamijo Y. Endod Dent Traumatol 1998. Avery DR. and periodontal tissues. Loss of pulpal vitality in open apex teeth in the past led to protracted treatment and often ended in early tooth loss caused by fracture of weak roots. Finn SB. eds: Pathways of the pulp. Keep the patient under close observation and continue to reassess the diagnostic criteria until a definitive diagnosis can be established. Pediatric dentistry: infancy through adolescence. With bacterial infection. Noren JG. MTA has been shown to be cementoconductive. Holan G. 8. 13.105:196 –206. eds. Pinkham JR. Andreasen JO. Glendor U. Ravn JJ. eds. and minocycline is placed in the canals and left for 1 month. MO: CV Mosby Co. fully formed roots and has virtually ended root fractures (53–56) (Fig. clinical signs of periradicular infection including swelling. we will be able to regenerate tissues. A paste of metronidazole. St Louis. Number 7S. Mitchell DF. Zurcher E. Treatment of deep caries. or parulis formation. J Dent Res 1965. Injuries to the primary dentition.24:250. treatment must not be undertaken on the basis of negative responses to pulp testing. Stronger roots with greatly improved prognosis for permanent retention are now possible. Radiographic and symptomatic assessment is currently the principal diagnostic criterion. ed. Oral histology and embryology.30:1079. 7. pulp. except as a temporary canal disinfectant. 11. J Am Dent Assoc 1941. The following factors are key in making the diagnostic determination: symptoms of irreversible pulpitis or apical periodontitis. eventually heals with new bone.
Karibe H. 49. Revascularization of immature permanent teeth with apical periodontitis: new technique protocol? J Endod 2004. Bakland LK.46:443. Resistance to fracture of endodontically treated premolars restored with new generation dentin bonding systems. Schmitt D.54:401–22. Ontario. 28. Influence of splints and temporary crowns upon electric and thermal pulp-testing procedures. J Endod 2005.9:238 – 42. Karni S. Cox CF.19:289 –91. Ehrmann EH. Rotstein I. 40.73:166 –227. Endod Top 2003. 50. 34. Croll TP. Bhaskar SN. Int Endod J 1994. Endod Dent Traumatol 1992. Trope M. Fulling HJ. 48.127:1491– 4. Boston D. Wennberg E.77:1006 –13. Jacobsen I. Scand J Dent Res 1976.2:9 –19.88:306 –12. Sigurdsson A. Strengthening immature teeth during and after apexification. Kohno H. 31.45:199 –202. Lawley GR. Rickoff B.34:61–70. Influence of maturation status and tooth type of permanent teeth upon electrometric and thermal pulp testing procedures.24:256 –9. Abedi HR. 27. Rappaport HM. Holan G. Katebzadeh N. Dalton BC. Identification of hierarchical factors to guide clinical decision making for successful long-term pulp capping. 33. Fuss Z. Dent Traumatol 2001.1:95– 8. Pulp testers and pulp testing with particular reference to the use of dry ice. 35. Caicedo R. Study on thermal pulp testing of immature permanent teeth. Traumatically injured primary incisors: a clinical and histological study. Mejare I. 53. 56. Yanpiset K. Quintessence Int 2003. Aust Dent J 1977. Swed Dent J 1977. Sarkar NK. Selliseth N. Klein H. J Endod 2004.Pulp Symposium 20. Shigaku Odontol 1989. Partial pulpotomy in young permanent teeth with deep carious lesions. Scand J Dent Res 1980. Suzuki S.31:97–100. 24.23:326 –30. Andreasen JO. Kariyawasam SP. 55. Eur Orthodont Soc Trans 1970. Trope M. S12 Camp JOE — Volume 34. Endodontics. 23. Cvek M. The significance of traumatized primary incisors on the development and eruption of permanent teeth. Endod Dent Traumatol 1986. Heithersay GS. Using mineral trioxide aggregate as a pulp-capping material. J Am Dent Assoc 1994. 54. In: Ingle JI. Bader S.84:286 –90. Dental vitality tests and pulp status. Prognosis of luxated non-vital maxillary incisors treated with calcium hydroxide and filled with gutta-percha: a retrospective clinical study. 51. Hafez AA. Ohide Y.186:54 – 8. 58. Quantitative assessment of dentin bridge formation following pulp-capping with mineral trioxide aggregate (MTA). Cox CF. Iwaya SI. Vongsavan N.22:272–9. Andreasen F. Endodontic considerations in dental trauma. Hill FJ. 45. Moiseyeva R.27:281– 4. Bakland LK. Kubota M. Lee J. Murray PE. Multifaceted use of Pro Root MTA root canal repair material. 36. Kolodrubetz D. Pediatr Dent 2001. Br Dent J 1999. McMillan P. Somerman MJ. Reinforcement effect of a resin glass ionomer in the restoration of immature roots in vitro. Transient apical breakdown following tooth luxation. Pulp responses to electric pulp stimulator in the developing permanent anterior dentition. Thomson TS. 32. Criteria for diagnosis of pulpal necrosis in traumatized permanent incisors. Ikawa M. Moller H. Mackie IC. Odontol Tidskr 1965. 57. J Dent Child 1987. Evaluation of ultrasonically placed MTA and fracture resistance intracanal composite resin in a model of apexification. Number 7S.29:407–12. Endod Dent Traumatol 1993. Int J Oral Surg 1978. Kirkwood KL. Traumatized primary incisors: follow-up program based on frequency of periapical osteitis related to tooth color. Andreasen JO.7:178 – 87. 26. 37.8:45–55. Quintessence Int 1993. Cohenca N. Bakland LK.17:63–70. 25.5:12–25. Pediatr Dent 1996. Sequelae of trauma to primary maxillary incisors: I— complications in the primary dentition. Dent Traumatol 2002. Development of clinical and radiographic signs associated with dark discolored primary incisors following traumatic injuries: a prospective controlled study. J Endod 1986.30:196 –200. Trope M. Canada: BC Decker Inc. Trope M. Pitt-Ford TR.86:409 –11.125:823–31. J Am Dent Assoc 1996. Andreasen JO.12:301–5.20:276 – 87. 44. Andreasen JO. Dent Traumatol 2004. Goldberg F. Andreasen JO. Dent Traumatol 2003. Healing and sensitivity to pain in young replanted human teeth: an experimental clinical and histologic study. Pascon EA.84:291– 6. Banchs F. Tooth discoloration and resolution following a luxation injury: Significance of blood pigment in dentin to laser Doppler flowmetry readings. Roitman M. Holan G. Riis I. July 2008 . 42. J Endod 1998. Borum MK. Revascularization of an immature permanent tooth with apical periodontitis and sinus tract. 22. Walker WA. 46.30:167–72.24:278. Berry JE. The effect of traumatic injuries to primary teeth on their permanent successors: II—a clinical and radiographic follow-up study of 213 teeth. Ohman A. Fulling HJ. 30. Dent Traumatol 2001.18:70 –2. Physiochemical basis of the biologic properties of mineral trioxide aggregate.79:284 –94. Kawashima I. Ritwik R. Langeland K. 21. Granath LE. The diagnosis value of coronal dark-gray discoloration in primary teeth following traumatic injuries. eds. Transient apical breakdown and its relation to color and sensibility changes. Assessment of reliability of electrical and thermal pulp testing agents. Scand J Dent Res 1976. Efficacy of laser Doppler flowmetry for the diagnosis of revascularization of reimplanted immature dog teeth. Influence of pulp necrosis and periapical inflammation of primary teeth and their permanent successors: combined macroscopic and histological study in monkeys. Picca M. Hamilton. Endod Dent Traumatol 1998. Trowbridge H. J Am Dent Assoc 1973. Scand J Dent Res 1971.24:669 –76. Junn DJ.17:185–7. et al. J Dent Child 1978. Bakland LK. 5th ed. 38. A clinical guide to the endodontic treatment of nonvital immature permanent teeth. 47. J Endod 2003. Smith AJ. 41. Manfre S. Hernandez R.18:224 –7. 39. Cvek M. Ravn JJ. Re-evaluating pulpal protection: calcium hydroxide liners vs cohesive hybridization. Bender IB. Sigurdsson A. Kaplan A. Pulpal diagnosis. Fuks AB. 29.14:31– 44. 2002: 795– 843. J Endod 1998. Schröder U. Schindler WG. 43. Cementoblasts maintain expression of osteocalcin in the presence of mineral trioxide aggregate. Bogen G. Torabinejad M. Torabinejad M. 52. Hirsch RS.
The rationale for this approach is that most young pulps can heal as long as the coronal restoration does not allow leakage of additional inflammatory stimulants or microorganisms. the better its repair potential. The difference in success rates is explained by the status of the pulp at the time of the procedure (Fig. Volume 30. Conflict of Interest: Martin Trope. Although our diagnostic ability to differentiate a vital from a necrotic pulp is good. For apical periodontitis to be present. Cox et al. July 2008 Regenerative Potential of Dental Pulp S13 . with a carious exposure the area and depth of inflammation are very unpredictable.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists.edu. regeneration. Issue 3. Hence. that the younger the pulp. vital The Pulp’s Regenerative Potential The Unexposed Pulp The inflamed pulp unexposed by caries or trauma always has the potential to be repaired. 1). This article is being published concurrently in Pediatric Dentistry. and pulp capping at the superficial exposure site is popular. reports no financial interests or potential conflicts of interest. the vital (noninfected) pulp ensures no apical periodontitis. and as such. DMD. whereas vital pulp therapy on the cariously exposed tooth is not nearly as successful (4). E-mail address: martin_trope@dentistry. May/June 2008. 2) (5. Thus. whereas capping the inflamed pulp results in lower and less predictable success (Fig. due to the material not sealing adequately.001 Approaches to Treatment of Carious Exposure in the Immature Tooth Pediatric Dentistry Because the young vital pulp has such good potential for repair. it is also important to understand its value in a fully formed tooth. Therefore. pulp capping. Philadelphia. our improved understanding of pulpal inflammation and repair and improved dental materials and technologies make vital pulp therapy a viable alternative to root canal treatment. 0099-2399/$0 . Key Words Pulp. (J Endod 2008. and the potential to regenerate an injured or necrotic pulp would be the best root filling possible. Another extremely important factor in the success of treating a vital exposure is the coronal seal after the pulp capping/pulpotomy (8). This is considered much more important than the material used on the vital pulp. maintaining the vital pulp prevents apical periodontitis. however. Capping the healthy pulp gives very high success rates. Suite 402.1016/j. Endodontics Pulpal inflammation is usually superficial and is unlikely to extend past the canal orifices. in fact.2008. and more failures (necrotic pulps) would result. However. DMD. 6. and the healing potential is good if a healthy pulp is treated. it is considered reasonable to perform an indirect or direct pulp cap on a carious exposure as long as a good coronal restoration can be placed (9). The articles are identical. From private practice. Address requests for reprints to Martin Trope. PA 19102. differentiating between reversibly and irreversibly inflamed pulp remains an educated guess at best (2). When the root canal has JOE — Volume 34. the optimal approach is to perform a full pulpotomy (thus removing the coronally inflamed pulp) and treating the presumably healthy pulp at the canal orifices. the root canal must contain a necrotic infected pulp (1). 7). Thus.04. Number 7S. doi:10. We do know. has been considered extremely limited.34:S13-S17) The Importance of Vital Pulp Although it is easy to understand the value of a vital pulp when the tooth is immature and underdeveloped. Pennsylvania. Philadelphia. DMD Abstract The regenerative potential of dental pulp.Pulp Symposium Regenerative Potential of Dental Pulp Martin Trope. and that what was previously interpreted as toxicity was. Therefore. 1601 Walnut St. revascularization. it is very likely that we would be capping an inflamed pulp. This article explores our knowledge in this regard and the future potential of saving or even regenerating the pulp as a routine dental procedure.unc.joen. Vital therapy (ie. with different approaches endorsed by different dental specialties. The Exposed Pulp Treatment of the exposed pulp remains quite controversial. On the other hand. Endodontic disease is apical periodontitis. (8) showed that the pulp can withstand the toxicity of most dental materials. partial or full pulpotomy) on traumatically exposed pulps is very successful (3). it is considered essential that a well-sealed coronal seal be placed over the vital pulp therapy. the biologic rationale for endodontics is the prevention or treatment of apical periodontitis. particularly in mature teeth. Either citation can be used when citing this article.
metronidazole. Francisco Banchs). (10) demonstrated that in extracted dog teeth. containing a scaffold for new tissue to grow and to be largely resistant to further bacterial penetration. The immature avulsed tooth has an open apex. With currently available technologies it could be possible to effectively disinfect an infected pulp. the materials and instruments available 40 –50 years ago were probably not sufficient to create an environment similar to the avulsed tooth. and a partial pulpotomy is performed on the remaining healthy pulp with calcium hydroxide (Courtesy Dr. The antibacterial effectiveness of the triantibiotic paste reported by Hoshino et al. 6. It has been experimentally shown that the apical portion of a pulp might remain vital and proliferate coronally after reimplantation. we are unsure of which factors in the blood clot are important.25% sodium hypochlorite and the use of a mixture of ciprofloxacin. then more traditional treatment methods can be initiated. Skoglund et al. Our case (Fig. short root. However. The ischemically necrotic pulp that is unique to an avulsion injury acts as a scaffold into which the new tissue grows. It is important to understand the biologic features permitting revascularization in young avulsed teeth. they can be incorporated into a synthetic scaffold that will be easier to for clinicians to manipulate compared with a blood clot. leaving a necrotic but uninfected pulp. Revascularization of the pulp space in a necrotic. mixed as described in Fig. and at the 24-month recall it was obvious that the root walls were thick. Clinical and radiographic evidence of healing was observed as early as 22 days. artificially place a scaffold. Only about 1 mm of superficial pulp is inflamed. July 2008 . Figure 1. indicating that it might be possible to replicate the unique circumstances of an avulsed tooth to revascularize the pulp in infected necrotic immature roots (11–13). 7). If no signs of regeneration are present after 3 months. so that we might attempt to reproduce these unique conditions when the pulp space is infected. The speed with which the tissue completely revascularizes the pulp space is important because bacteria from the outside are continually attempting to enter the pulp space. The canal was disinfected without mechanical instrumentation but with copious irrigation with 5. and the development of the root below the restoration was similar to the adjacent and contralateral teeth. Carious exposure caused by caries. and the presence of vital pulpal tissue greatly slows or prevents the bacterial penetration into this tissue compartment. When these factors are isolated. infected tooth with apical periodontitis was attempted by Nygaard-Ostby and Hjortdal (15) in the 1960s but was mostly unsuccessful. a full pulpectomy can be performed (Fig. ie. S14 Trope JOE — Volume 34. our group demonstrated in dogs that the potential for revascularization does exist (Fig. and intact but necrotic pulp tissue. (17) was confirmed by our group in a dog model with infected immature roots (18). and the Figure 2. At this point. The procedure described in this section can be attempted in most cases. and minocycline (17). replacing the necrotized coronal portion of the pulp (11–13). the race between proliferation of new tissue and infection of the pulp space favors the new tissue. A blood clot was produced to the level of the cementoenamel junction to provide a scaffold for the ingrowth of new tissue followed by a double seal of mineral trioxide aggregate in the cervical area and a bonded resin coronal restoration above it. It has been shown that under certain conditions revascularization can be achieved in young teeth that have been traumatically avulsed. A recent case report by Banchs and Trope (16) has reproduced results in cases reported by others. the new tissue has easy access to the root canal system and a relatively short distance for proliferation to reach the coronal pulp horns. and then effectively seal the access cavity to resist subsequent infection. Thus. In addition. The large radiolucency had disappeared within 2 months.Pulp Symposium fact that the crown is usually intact (rather than carious or with an access cavity) slows bacterial penetration because their only access to the pulp is through cracks (14) or enamel defects. developed thick dentinal walls and the apices are closed. 5) described the treatment of an immature second lower right premolar with radiographic and clinical signs of apical periodontitis with the presence of a sinus tract. pulpal revascularization started immediately after reimplantation and was completed after approximately 45 days (Fig. Therefore. Histologic section of a pulp after a traumatic exposure 24 hours previously. Number 7S. 4). and that the blood clot was essential as a scaffold (19). a canal that is free of bacteria. The underlying inflamed pulp is removed. Revascularization of Infected Pulp Space Pulp Revascularization Revascularization of an immature necrotic tooth has many potential advantages. 3).
July 2008 Regenerative Potential of Dental Pulp S15 . Number 7S. When the root canal has developed thick dentinal walls and the apices are closed. The teeth were extracted and immediately replanted. JOE — Volume 34.Pulp Symposium Figure 3. a full pulpectomy can be done (Courtesy Dr. Figure 4. Francisco Banchs). During the course of 45 days the blood supply moves into the pulp space. In this case a full pulpotomy was performed (thus removing the coronally inflamed pulp) and treating the presumably healthy pulp at the canal orifices. Revascularization of immature dog teeth during period of 45 days.
July 2008 . (17)). Number 7S. Immature tooth with a necrotic infected canal with apical periodontitis. Reproduced with permission from Banchs F. At 7 months the patient is asymptomatic. After 4 weeks the antibiotic is removed. S16 Trope JOE — Volume 34. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod 2004. and a blood clot is created in the canal space. The canal is disinfected with copious irrigation with sodium hypochlorite and triantibiotic paste. and the apex shows healing of the apical periodontitis and some closure of the apex.30:196-200. Composition and mixing instructions for the triantibiotic paste (adapted from Hoshino et al.Pulp Symposium Figure 5. The access is filled with a mineral trioxide aggregate base and bonded resin above it. Figure 6. Trope M.
Iwaya SI.1:172– 8.26: 541–5. Hicks R. Oral Surg 1972. J Endod 1978. Bergenholtz G. 4. Uematsu H. Int Endod J 1980. Cox CF. Revascularization of mouse tooth isografts and allografts using autoradiography and carbon-perfusion. Love RM. After treatment similar to that described in Fig. 20. Tronstad L.17: 185–7. Prosthet Dent 1987. 2. Trope M. but the canal walls are thicker as well. Ikawa M. Leuenberg A. Oral Surg Oral Med Oral Pathol 1978. radiography. Wallenius K. Revascularization of an immature permanent tooth with apical periodontitis and sinus tract. Winter GB. Tronstad L. Biocompatibility of surface-sealed dental materials against exposed pulps. Presently. Huws D. Clinical signs and symptoms in pulp disease. J Endod 2005. 3. 16. Number 7S. Liu Y. 19.20:75– 84. Rule DC. Some have used the cases shown as examples of pulp regeneration and the beginning of stem cell technology in endodontics. Andreasen JO. Reade PC. however. Caplan DJ.12:289 –93. 5. The healing of experimentally induced pulpitis.525– 8. There has been a great deal of discussion as to the correct terminology for what has been called pulp revascularization in this article.25:347–58. Teixeira F. J Endod 2008.30:196 –200. Ostro E. yet this is not the case for pulp. Oral Surg 1974.13:27–35. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod 2004. Guided tissue regeneration has been used in periodontics and has some merit. A clinical report on partial pulpotomy and capping with calcium hydroxide in permanent incisors with complicated crown fracture. However. Sonoyama W. Cleaton-Jones PE.33:680 –9. Pulp revascularization of replanted immature dog teeth after treatment with minocycline and doxycycline assessed by laser Doppler flowmetry. 8. Murrah V. Sato I. Pulp capping of carious exposures: treatment outcome after 5 and 10 years: a retrospective study. Skoglund A. 11. Windley W III. Br Dent J 1966. Kubota M. July 2008 Regenerative Potential of Dental Pulp S17 . Pulp revascularization of immature dog teeth with apical periodontitis. Trope M. Pulp reactions to exposure after experimental crown fractures or grinding in adult monkeys. Bergenholtz G. Noda T. Bacterial penetration of the root canal of intact incisor teeth after a simulated traumatic injury.57:1–9. On the basis of research in avulsed teeth and a recent study on infected teeth. 5. Root growth and apical repair subsequent to pulpal necrosis in children. Barthel CR. Dummer PM. In vitro antimicrobial susceptibility to combinations of drugs on bacteria from carious and endodontic lesions of human deciduous teeth. Levin L. Cvek M. Hoshino E. Kurihara-Ando N. Revascularization of an immature dog tooth with apical periodontitis. The root was artificially infected. Future research will need to be performed to stimulate pulp regeneration from the pluripotential cells in the periapical region (21). Hoshino E.38:115–9. 10.Pulp Symposium Figure 7. Endod Dent Traumatol 1996. 6. Hjortdal O. Micro-organisms from necrotic pulps of traumatized teeth. Mjor IA. Ritter AL. Mjor IA. Sigurdsson A. Ritter AV. A microradiographic study of vascular changes in replanted and autotransplanted teeth in young dogs. Arch Oral Biol 1981. we can only say with certainty that the pulp space has returned to a vital state.26. JOE — Volume 34. J Endod 2007. Sigurdsson A. revascularization has occurred. 21. Rosenkranz B. J Endod 2000.120:586 –90. Trope M. Barrett AP. 7. 14. Apexogenesis accomplishes a closed apex and thicker dentinal walls but by definition uses remaining vital root pulp to attain this goal. Odont Revy 1974. and histology. Dent Traumatol 2001. Yamaza T. 15. et al. 18. Yamauchi M. Keall HJ. Oral Microbiol Immunol 1993. Capping of the inflamed pulp. we must distinguish between revascularization and pulp regeneration. Characterization of the apical papilla and its residing stem cells from human immature permanent teeth: a pilot study. 13. Scand J Dent Res 1971:79:333– 48. Roulet JF. Teixeira F.8:391–9. 12. producing apical periodontitis. In-vitro antibacterial susceptibility of bacteria taken from infected root dentine to a mixture of ciprofloxacin. Cvek M. 9. J Endod 1982.29:125–30. Tissue formation in the root canal following pulp removal. it is more likely that the tissue in the pulp space is similar to a periodontal ligament than to pulp tissue (19). guided tissue regeneration in periodontics assumes regeneration of periodontal structures. In the present cases.34:477– 83. et al. Banchs F.4:232–7.6:439 – 43. It appears that there is approximately a 30% chance of pulp tissue reentering the pulp space (20). Tronstad L.34:166 –71. Nygaard-Ostby B.8:172– 6. Thibodeau B. Sato T. 17. References 1. Disinfection of immature teeth with a triple antibiotic paste. which is not the case here. Trope M. It is clearly not apexification because not only the apex is closed. metronidazole and minocycline. Int Endod J 1996. Dent Traumatol 2004. Austin JC.
primary teeth. and differentiation of progenitor cells can give rise to a new generation of reparative dentinforming cells (odontoblast-like cells). the odontoblasts might survive.34:S18-S24) he aim of vital pulp therapy is to treat reversible pulpal injuries in both permanent and primary teeth. Volume 30. Indirect pulp treatment is recommended as the most appropriate procedure for treating primary teeth with deep caries and reversible pulp inflammation. contrary to what was believed in the past. a new generation of odontoblast-like cells might differentiate and form tubular tertiary dentin (reparative dentinogenesis) (3. the amputated pulp can be repaired by itself or after application of capping materials (8 –10). Hadassah School of Dental Medicine.1016/j. It must be emphasized that under clinical conditions. restorative procedures. and mineral trioxide aggregate and ferric sulfate have been considered appropriate alternatives to formocresol for pulpotomies in primary teeth with exposed pulps. Address requests for reprints to Dr Fuks at fuks@cc. mineral trioxide aggregate. the dentinogenic potential of pulp cells can be expressed. reports no financial interests or potential conflicts of interest. Fuks. 3 different physiopathologic conditions might be observed at the dentin-pulp border: 1. pulp therapy Professor Emeritus. It is impossible to distinguish these processes at the in vivo level. migration. aiming at regeneration of the dentin-pulp complex. reparative dentin. we are able to assess the biologic validity of the various vital pulp treatments. 3. maintaining pulp vitality and function (1). Advances in biomedical research open avenues for the design of new methods of dental treatment. The use of a high-speed handpiece or laser might result in an exposure of a “normal” pulp that would otherwise not be exposed. provided that this diagnosis is based on a good history. The articles are identical. or fibrodentin formation. 13). reconstituting the lost continuum at the pulp-dentin border (12. formocresol.Pulp Symposium Vital Pulp Therapy with New Materials for Primary Teeth: New Directions and Treatment Perspectives Anna B. the matrix formed at the pulp-dentin interface often comprises reactionary dentin. Issue 3. Vital pulp therapy aims to treat reversible pulpal injury in cases in which dentin and pulp are affected by caries. and that the tooth has been sealed with a leakage-free restoration. In this light. Israel. 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). With severe dentinal injuries without pulp exposure as in rapidly progressing carious lesions or in severe tissue damage caused by cavity preparation. 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). Proliferation. Pulp exposure caused by caries shows very limited potential for pulp recovery as a result of bacterial infection of the pulp for a substantial period of time. Formocresol has been a popular pulpotomy medicament in the primary dentition and is still the most universally taught pulp treatment for primary teeth. Conflict of Interest: Anna B. T Key Words Ferric sulfate. Controlled clinical studies have been critically reviewed. and several alternatives have been proposed. in primary teeth it is important to preserve the tooth until its natural exfoliation time. As part of the wound healing process in the repairing pulp. Concerns have been raised over the use of formocresol in humans. 0099-2399/$0 . In addition to these. odontoblasts are destroyed subjacent to the affected dentin (5. or trauma. Either citation can be used when citing this article. Reactionary dentin shows many similarities to the primary and secondary dentin and can effectively oppose exogenous destructive stimuli to protect the pulp (4). and the odontoblastic layer is stimulated to form a tertiary dentin matrix beneath the injury (reactionary dentin). Department of Pediatric Dentistry. July 2008 . Whenever the dentin-pulp complex is affected by injury. the caries removal method has not been described. doi:10. thus preserving arch integrity (2). In most of the studies reviewed. Fuks. (J Endod 2008. 2. 7). In the case of mild injuries as in noncavitated enamel caries or slowly progressing dentinal caries. which compromises the defense reaction (11). and the process might also be indistinguishable from a biochemical and molecular point of view. 6). Hebrew University. New approaches have been based on the understanding of the molecular and cellular mechanisms regulating dentinogenesis during dental tissue repair and their potential for clinical exploitation (1). In an appropriate metabolic state of the dentin-pulp complex. In the case of pulp exposure.031 Indirect Pulp Treatment After this brief review of the cellular changes during tooth development and how they are mimicked during tissue repair. a proper clinical and radiographic examination. This article is being published concurrently in Pediatric Dentistry. May/June 2008.il. CD Abstract Vital pulp therapy aims to treat reversible pulpal injury and includes 2 therapeutic approaches: (1) indirect pulp treatment for deep dentinal cavities and (2) direct pulp capping or pulpotomy in cases of pulp exposure. Number 7S. CD.joen.huji. provided that the diagnosis is based on a good history and proper clinical and S18 Fuks JOE — Volume 34.2008. can also be an acceptable procedure for primary teeth with reversible pulp inflammation. Jerusalem. ac. IPT.02.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists.
Presently. a failure of treatment would not imply the need for a space maintainer after extraction. however. we can recommend IPT as the most appropriate treatment for symptomfree primary teeth with deep caries. osteogenic protein (50). (65) reported that MTA was superior to FC. 39). and C if it scored 59% or less. These authors claimed that MTA induces less undesirable responses and might be a suitable replacement for FC. blood samples were taken before (control) and after treatment to observe the mutagenic potential of FC on lymphocytes cultures. On the basis of the information available. and “strong but not sufficient evidence” for leukemia. This issue will be discussed in greater detail further in this symposium.” ranging from chronic inflammation to necrosis (35). He concluded that extrapolation of these research results to pediatric dentistry suggests an inconsequential risk of carcinogenesis associated with formaldehyde use in pediatric pulp therapy. No correlation between FC pulpotomies and cancer has ever been demonstrated.to 10-year-old children. an expert working group has determined that there is now sufficient evidence that formaldehyde causes nasopharyngeal cancer in humans. preserving arch integrity (2). ferric sulfate (FS) (51–56). which meant that it had to be excluded. and sodium hypochlorite (60). All articles were graded according to the aforementioned criteria and classified as A if the article met 90% or more of the criteria. FC and can be used as alternatives to pulpotomies in primary teeth. Fuks and Papagiannoulis (63) assessed the relevant articles that have appeared after the aforementioned reviews by using the clinically based criteria listed by Curzon and Toumba (64). no conclusion could be reached as to the optimum treatment or technique for pulpally involved primary teeth. B1 if an article scored from 75%– 89%. Milnes (33) published an extensive and detailed review of the more recent research on the metabolism. Following Cochrane’s criticism regarding the paucity of appropriately designed. 57–59). The tooth must be asymptomatic. This treatment. Formocresol (FC) has been a popular pulpotomy medicament in the primary dentition for the past 70 years since its introduction by Sweet in 1932. however. There has been a significant amount of discussion in the dental literature about the appropriateness and safety of using aldehyde-based products in pediatric dentistry (29). The pulp dressing materials and techniques proposed include: electrosurgery (36. the Cochrane review found that evidence is lacking to conclude which is the most appropriate technique for pulpotomies in primary teeth (61). Peng et al. and the histologic response of the primary pulp is “capricious. the success rate is not particularly high in primary teeth. laser (38. Nevertheless. not only randomized ones. and the sieving of these articles was conducted by examining the article title and assessing its relevance (62). Although a considerable number of clinical trials and laboratory animal studies have been published on this subject. and it is still considered the most universally taught and preferred pulp treatment for primary teeth (22–24). FC was mutagenic for one patient. and several others have begun to contribute to the literature (32). FC is no longer used in some countries. statistically assessed investigations and the lack of longterm outcomes. In these children. leakage-free restoration can be placed. Pulpotomy Pulpotomy is still the most common treatment for cariously exposed pulps in symptom-free primary molars. On the basis of the biologic changes previously described and the growing evidence of the success of IPT in primary teeth. DPC of a carious pulp exposure in a primary tooth is not recommended but can be used with success on immature permanent teeth. the MEDLINE search used generated a total of 358 citations. pharmacokinetics. The aim of this treatment is to preserve the radicular pulp. In a recent article. July 2008 S19 . The International Agency for Research on Cancer classified formaldehyde as carcinogenic for humans in June 2004. as it would in younger children. Direct Pulp Capping DPC is carried out when a healthy pulp has been inadvertently exposed during an operative procedure. and with the exception of 3 articles. a rare cancer in developed countries. freeze-dried bone (48). mineral trioxide aggregate (MTA) (24.” Several articles reported the success of this technique in primary teeth (15–19). avoiding pain and swelling. leaving the profession to look for other alternatives to FC (31). (14) concluded that “in deep lesions. B2 if it scored between 60%–74%. mainly as a result of its toxicity and potential carcinogenicity (25–32).Pulp Symposium radiographic examination. Even with different weights attributed to the evaluated articles. Ricketts et al. calcium hydroxide (CH) (45– 47). In a meta-analysis to compare the clinical and radiographic effects of MTA with FC. Number 7S. and the exposure site must be pinpoint in diameter and free of oral contaminants. Treatment failure might result in internal resorption or acute dentoalveolar abscess (20). provided that a proper. bone morphogenetic protein (49). and ultimately to retain the tooth. The Cochrane review assessment is extremely rigorous. and the tooth has been sealed with a leakage-free restoration (2). A calcium hydroxide medicament is placed over the exposure site to stimulate dentin formation and thus “heal” the wound and maintain the pulp’s vitality (20). In a recent systematic review on complete or ultraconservative removal of decayed tissue. In a case-control study in which FC pulpotomies were performed in 5. (62) published an evidence-based assessment of FC versus FS by using a different sieving system including all suitable clinical trials. They concluded that both materials were likely to produce similar clinical/radiographic success. limited evidence for cancer of the nasal cavity and paranasal sinuses. 37). Presently. if not better than. No statistically significant differences could be observed in the cultured lymphocytes. DPC should still be looked on with some reservations in primary teeth. there are several pulp dressing medicaments that have been proposed to maintain radicular pulp vitality that are equal to. Caicedo et al. many studies have been reported. several studies have reported that the clinical success of FC pulpotomies decreases with time. DPC is indicated for small mechanical or traumatic exposures when conditions for a favorable response are optimal. and carcinogenicity of formaldehyde and concluded that formaldehyde is not a potent human carcinogen under conditions of low exposure. leading the authors to raise doubts about the desirability of using this technique in children (34). In this review. mainly as a result of safety concerns. Concerns have been raised over the use of FC in humans. could be recommended for exposed pulps in older children 1 or 2 years before normal exfoliation. Evidence-Based Analysis of Pulpotomy Literature Loh et al. Even in these cases. (21) demonstrated good pulp response in primary teeth after DPC or pulpotomy with MTA and concluded that MTA might be a favorable material for pulp capping and pulpotomy in primary teeth. glutaraldehyde (GT) (40 – 44). Vital Pulp Therapy with New Materials for Primary Teeth JOE — Volume 34. none of the articles evaluated could meet the criteria and were excluded. partial caries removal is preferable to complete caries removal to reduce the risk of carious exposure.
Only asymptomatic molars without clinical and/or radiographic evidence of pulp degeneration were included. Duplicate publications of the same study were excluded. Four children (12 molars) dropped out. Only restorable molars without clinical and/or radiographic evidence of pulp Studies Comparing MTA With FC Cuisia et al. Molars. white MTA. This search generated a total of 358 citations. (2005) Holan et al. (2004) Farsi et al. MTA N (%) 29 (97) 19 (100) 30 (94) 38 (100) 32 (97) 24 (100) Success (x-ray). formocresol. clinical trial compared gray MTA. clinical trials. Each child had at least 3 molars with severe carious involvement and received pulpotomies with all 3 medicaments. formocresol. both types of MTA formed thick dentin bridges. as described by Fuks and Papagiannoulis (63). but the randomization method was not reported. they are regarded as observational studies of evidence (67– 69). (2004)72 This randomized. MTA. whereas the radiographic success was 77% for FC and 93% for MTA. Language bias can also occur because researchers whose native language is not English are more likely to publish nonsignificant results in non-English journals and significant results in English journals (70). Jabbarifar et al. (1991) Fuks et al. including publication bias and the variable quality of the primary studies. and all the teeth were restored with SSCs. can threaten the validity of metaanalysis (70). With these points in mind. the clinical success rate was 93% for FC and 97% for MTA. but there was no mention of the use of a rubber dam. FS N (%) 28 (97) 41 (93) 20 (84) 54 (74) 77 (92) 42 (86) 30 (81) Follow-up (mo) 12 35 24 36 42–48 24 18 S20 Fuks JOE — Volume 34. FC N (%) 26 (96) 31 (84) 21 (88) 58 (97) 78 (97) 46 (96) 30 (91) Success (clinical). FC (N) 27 37 24 60 80 48 33 Molars. FC N (%) 28 (93) 18 (90) 29 (91) 35 (97) 24 (83) 23 (100) Success (clinical). In the histologic study. (2005) Naik and Hegde (2005) FC. clinical trial compared MTA with FC. were not included. and CH with FC and are presented in Tables 1–3. Articles Comparing Directly FS and FC Direct comparison articles: FC FS Fei et al. clinical trial compared MTA with FC in 64 molars assigned to 2 groups by the toss of a coin. Articles Directly Comparing MTA and FC Direct comparison articles: MTA FC Cuisia et al. Number 7S. and outcome assessment after 12 months was done by 2 “blinded” pediatric dentists. MTA (N) 30 19 32 38 33 24 Success (clinical). The number of pediatric dentists who performed the treatments was not specified. Usually the reviewer identifies the relevant studies from the literature and decides whether to include or exclude them. with the addition of the relevant studies published after that date. Most databases date only from 1965. Deery (66) concluded that pulpotomies performed with either FS or FC were likely to produce similar results. ferric sulfate. but the gray MTA appeared to be better than white MTA and FC as a pulp dressing. FC N (%) 22 (81) 27 (73) 19 (80) 47 (78) 75 (94) 43 (90) 28 (85) Success (x-ray). (2004) Jabbarifar et al. FC N (%) 23 (77) 18 (90) 29 (91) 31 (86) 24 (83) 23 (100) Success (x-ray). and another 6 teeth (4 white MTA and 2 FC) failed as a result of abscesses. (2001)71 This randomized. An additional 15 carious teeth planned for serial extractions after 6 months were selected for the histologic part of the study. rubber dam isolation was not reported. The articles assessed will be limited to the comparisons of FS. July 2008 . particularly on CH or FC pulpotomies. FC (N) 30 20 32 36 29 23 Molars. FS (N) 29 55 24 73 84 49 37 Success (clinical). and FC in 72 molars of 24 children. (2001) Agamy et al. The remaining 53 teeth appeared to be clinically and radiographically successful. One of the aims of evidence-based dentistry is to reach an evidence-based conclusion and then translate it into a clinical decision that would result in a better treatment outcome. The results were assessed by 2 pediatric uncalibrated dental residents at 6-month follow-up. Outcome assessment of 64 molars remaining at 12 months was done by 2 “blinded” pediatric dentists. FS. Only restorable molars without clinical and/or radiographic evidence of pulp degeneration were included. Farsi et al. crown. Agamy et al. Although meta-analysis generally pools data from randomized. FS N (%) 29 (100) 51 (93) 21 (88) 66 (90) 81 (96) 49 (100) 33 (89) Success (x-ray). Clinical and radiographic success for MTA was 94% and for FC was 91%. Molars. (2005)59 This randomized. (1997) Aktoren and Gencay (2000) Papagiannoulis (2002) Ibrevic and Al-Jame (2003) Huth et al. clinical trials. Therefore. 1 (gray MTA) exfoliated normally. All pulpotomies were performed by the same pediatric dentist. Problems. because it presented the closest to normal pulp architecture. the strength of conclusions drawn from a meta-analysis might only be comparable to that drawn from observational studies. For this reason articles that could have been relevant. The number of molars treated at the baseline and the number of dropouts were not reported. (2005) Markovic et al. and of the remaining 60 teeth in 20 patients. (2005) FC. MTA N (%) 28 (93) 19 (100) 30 (94) 38 (100) 32 (97) 24 (100) Follow-up (mo) 6 12 12 24 74 6 In another meta-analysis that included clinical trials and randomized. this article will consist of critically assessing the randomized and nonrandomized human clinical trials that resulted from a MEDLINE search. which are open to various forms of bias. Another limitation of meta-analyses is that they all search for relevant articles in electronic databases and are limited to the English language. (2004)57 This randomized. clinical trial compared MTA with FC in 120 molars of 100 children assigned to 2 groups by the toss of a coin.Pulp Symposium TABLE 1. Pulpotomies were performed in 60 molars by 1 pediatric dentist using a local anesthetic and restored with a stainless steel TABLE 2.
TABLE 3. Articles Directly Comparing CH and FC Direct comparison articles: FC CH
Waterhouse et al. (2000) Huth et al. (2005) Markovic et al. (2005)
FC, formocresol; CH, calcium hydroxide.
Molars, FC (N)
44 48 33
Molars, CH (N)
35 38 34
Success (clinical), FC N (%)
37 (84) 46 (96) 30 (91)
Success (clinical), CH N (%)
27 (77) 33 (87) 28 (82)
Success (x-ray), FC N (%)
37 (84) 43 (90) 28 (85)
Success (x-ray), CH N (%)
27 (77) 25 (66) 26 (76)
To exfoliation 24 18
degeneration were included. The number of pediatric dentists who performed the treatments was not specified, rubber dam isolation was not reported, and all the teeth were restored with SSCs. At 24 months, 46 molars (38%) were lost, leaving 74 molars for evaluation. All the MTAtreated molars were successful clinically and radiographically (100%). For the FC, clinical and radiographic success was 97% and 86%, respectively.
the pulpotomies under a local anesthetic and with a rubber dam, but outcome assessors were not reported. Molars with pulp canal obliteration (PCO) were not considered failures. The dropout rate was 4% (4/96 molars) after 6 –34 months. Clinical success for FC was 84% and for FS was 93%; radiographic success was 80% for FC and 93% for FS. No statistical difference was observed between the 2 groups.
Holan et al. (2005)24 This randomized, clinical trial compared MTA with FC in 64 molars of 35 children assigned to 2 groups by the toss of a coin. The number of operators was not specified, and in 56 molars SSCs were placed, 1 molar received a composite restoration, and the other 7 teeth were restored with amalgam. Clinical outcomes were assessed by 1 pediatric dentist without “blinding.” Radiographs were assessed by 3 “blinded” pediatric dentists using a standardized evaluation form for calibration (complete agreement for all cases). Internal resorption was considered a failure only when it reached the bone. Arrested internal resorption, calcific metamorphosis, and pulp canal obliteration were not considered failures. At 74 months, 2 molars (3%) were lost, leaving 62 molars for evaluation. Clinical and radiographic success was 97% for MTA and 83% for FC, respectively. Naik and Hegde (2005)58 This randomized, clinical trial compared MTA with FC in 50 molars assigned randomly (method not specified) to 2 groups. The inclusion criterion was “asymptomatic deep carious lesion with no frank exposure.” Pulpotomies were performed by a postgraduate dentist under local anesthesia and rubber dam. It was not clear whether preoperative radiographs were taken and SSCs were placed 24 hours later. Three teeth were lost to follow-up (2 FC and 1 MTA), and all the remaining teeth were clinically and radiographically successful at the 6-month follow-up.
Aktoren and Gencay (2000)73 This randomized, clinical trial compared FS, FC, and GT. Only asymptomatic and restorable molars without clinical and radiographic signs of pulp degeneration were included. Clinicians performing the pulpotomies and outcome assessors were not described. At 24 months, clinical success rates for 72 molars were reported to be 88% for both FC and FS, and radiographic success was 80% for FC and 84% for FS. Papagiannoulis (2002)74 This randomized, clinical trial compared FS with FC in 133 molars in 90 children assigned to 2 groups by a toss of a coin. Only asymptomatic and restorable molars without clinical and radiographic signs of pulp degeneration were included. Pulpotomies were performed by 3 pediatric dentists; most molars were restored with SSCs, and a few received composite resin restorations. Outcomes were assessed by a separate “blinded” pediatric dentist. Molars with PCO or nonprogressive internal resorption were not considered failures. Clinical success was 97% for FC and 90% for FS, and radiographic success was 78% for FC and 74% for FS. Ibrevic and Al-Jame (2003)54 This randomized, clinical trial compared FS with full-strength FC in 194 molars in 70 patients allocated alternately to 2 groups. Only restorable molars without clinical and radiographic signs of pulp degeneration were included. Pulpotomies were performed by 1 pediatric dentist, and most molars received SSCs; a few molars were restored with amalgam. Clinical outcomes were assessed by the operator, but radiographic outcomes were assessed by both the operator and another “blinded” evaluator. Calibration was not reported, but both assessors reached consensus on radiographic outcomes. Ten patients (30 molars) dropped out after 42 months. Clinical success rates were 97% in the FC group and 96% in the FS group. The radiographic success rate was 94% in the FC group and 92% in the FS group. No statistical differences were found between the radiographic assessments of both pulpotomy agents. Huth et al. (2005)47 This randomized, clinical trial compared FS, FC, CH, and laser in 107 children. A power calculation estimated the numbers of molars required to achieve statistical significance. Randomization was done by casting a concealed lot from a box of 4 50 lots, such that 200 molars were allocated to 4 groups. Only asymptomatic restorable molars without clinical and radiographic signs of pulp degeneration were included. The molars received SSCs or composite resin restorations. Two pediatric dentists performed the pulpotomies under local or general anesthesia and rubber dam, and 2 other “blinded” experienced dentists perVital Pulp Therapy with New Materials for Primary Teeth
Studies Comparing FS With FC
Fei et al. (1991)51 This randomized, clinical trial compared FS wth FC in 83 molars in 62 children assigned by a table of random numbers to 2 groups. Only restorable molars without clinical or radiographic signs of pulpal degeneration were included. Teeth with pulpal hemorrhage persisting after 2 applications of FS or FC were eliminated. A pediatric dentistry postgraduate student performed all pulpotomies, and 2 pediatric dentists were “blinded” and calibrated before radiographic assessment. At 12 months, 27 molars were lost, leaving 56 molars for assessment. Clinical success for FC was 96% and for FS was 100%; radiographic success was 81% for FC and 97% for FS. Fuks et al. (1997)52 This randomized, clinical trial compared FS with FC in 96 molars in 72 children assigned to 2 groups by a toss of a coin. Only asymptomatic and restorable molars without clinical and radiographic signs of pulp degeneration were included. Three pediatric dentists performed
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formed outcome assessments. Intraexaminer and interexaminer reproducibility was optimal (K 1.0). The dropout rate was 8% (16/ 191 molars), and the remaining participants were examined after 24 months. Clinical success rate was 96% for FC and 100% for FS, and radiographic success was 90% for FC and 86% for FS. radiographically successful. In the control group, 85% and 78% achieved clinical and radiographic success, respectively. The success rate of the Nd:YAG laser was significantly higher than that of the FC pulpotomy. The permanent successors of the laser-treated teeth erupted without any complications.
Markovic et al. (2005)56 This randomized, clinical trial compared FS, FC, and CH in 104 molars in 104 children assigned randomly to 3 groups. Vital cariousexposed molars with no radiographic signs of pulpal degeneration were included. Pulpotomies were performed by 3 pediatric dentists, and outcomes were assessed by a separate evaluator. The intraexaminer agreement was moderate (K 0.70). The number of molars at baseline and the number of dropouts were not reported. The clinical success rate at 18 months for FC was 91%, for FS was 89%, and for CH was 82%. The radiographic success was 85% for FC, 82% for FS, and 76% for the CH group. These differences, however, were not statistically significant.
Study Comparing Sodium Hypochlorite With FS
Vargas et al. (2006)60 This prospective randomized, clinical study compared the effectiveness of 5% sodium hypochlorite (NaOC1) with that of FS as a pulpotomy medicament in decayed primary molars. Twenty-three healthy patients between 4 and 9 years old with at least 2 primary molars needing a pulpotomy were included in the study. The teeth were clinically and radiographically examined, and the signs/symptoms were recorded at 0, 6, and 12 months. Six-month results were based on the first 32 teeth in the NaOC1 group and 28 teeth in the FS group. Twelve-month results were based on 13 teeth in the FS group and 14 in the NaOC1 group. At 6 months, 100% clinical success was found in both the FS and NaOC1 groups. Radiographic success for FS was 68%, with internal resorption being the most common finding. The NaOC1 showed 91% radiographic success. At 12 months, FS had 85% clinical success and 62% radiographic success. NaOC1 had 100% clinical success and 79% radiographic success. The authors concluded that preliminary evidence showed that NaOC1 can be used successfully as a pulpotomy medicament.
Studies Comparing CH With FC
Three articles compared directly CH with FC. Two of them have been summarized previously (47, 56).
Waterhouse et al. (2000)75 This randomized, clinical trial compared FC and CH in 84 molars in 52 children assigned to 2 groups by the toss of a coin. Only healthy children with restorable molars without clinical and radiographic signs of pulp degeneration were included. Pulpotomies were performed by clinicians under rubber dam or cotton roll isolation; SSCs were placed “where indicated” (indications not described), and other molars were restored with amalgam, glass ionomer, or compomer. Outcomes were assessed by a separate pediatric dentist, “blinded” and calibrated in a parallel study (77% interexaminer agreement). At 22 months, 5 molars in 3 patients dropped out, leaving 79 molars in 49 children. Clinical and radiographic success was 84% for FC and 77% for CH.
From this review of the randomized, clinical trials, one can observe that all the studies comparing MTA with FC showed that MTA presented better results, even though in some of them there was no statistical difference as a result of the small number of teeth tested. FS was also better than FC in some studies and similar to FC in others, whereas the 3 studies with CH showed inferior outcomes. It should be emphasized, however, that in most of the studies the method of caries removal has not been described. The use of a high-speed handpiece or laser might result in an exposure of a “normal” pulp that would otherwise not be exposed and not need a pulpotomy or that could be alternatively treated by IPT. As previously mentioned, one of the aims of evidence-based dentistry is to reach an evidence-based conclusion and then translate it into a clinical decision that would result in a better treatment outcome. It should be kept in mind, however, that improving patient care requires the consideration of other factors including the cost and technique sensitivity of the new medicament. From the studies previously presented, MTA showed better results in all cases and should be recommended as an alternative to FC. One of the drawbacks of this material, however, is its high cost, and its use in pediatric dentistry practice can become almost prohibitive in some circumstances. Hence, FS can still be considered a valid and inexpensive solution for pulpotomies in primary teeth (2). A recent preliminary evaluation of sodium hypochlorite showed promising results when compared with FS. The follow-up time, however, is only 1 year. Longer follow-up and more clinical studies are needed to confirm these results.
Studies Comparing Laser With FC
Saltzman et al. (2005)39 This randomized single-blind, split-mouth clinical trial compared a diode laser pulpotomy with MTA with a conventional FC/zinc oxide– eugenol (ZOE) pulpotomy. A total of 26 pairs of teeth from 16 patients between 3– 8 years old were selected on the basis of clinical and radiographic criteria. All teeth were followed up clinically and radiographically for 15 months. A total of 7 laser-MTA–treated teeth were radiographic failures, as opposed to 3 FC/ZOE-treated teeth at 15.7 months; however, these results were not statistically significant. The authors suggested that an improved success rate among a larger patient sample and a longer follow-up period would be required for the laser-MTA pulpotomy to be considered a suitable alternative to conventional FC pulpotomy. Liu JF (2006)76 This clinical study compared the effects of Nd:YAG laser pulpotomy with FC on human primary teeth. Patients without any medically compromised disease were selected from the patient population at a hospital-based dental clinic in Taiwan. Primary teeth that required pulpotomy “because of carious pulp exposure” were selected for this study. Fifty children with an average age of 5 years, 3 months (range, 4 –7 years) participated in the study group, and a total of 68 primary molars were treated with the Nd:YAG laser. Forty-four children participated in the control group, and 69 primary molars were treated with diluted FC. Follow-up time was between 6 – 64 months. In the Nd:YAG laser group, clinical success was achieved in 66 of 68 teeth (97%), and 94% were
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Vital Pulp Therapy with New Materials for Primary Teeth
Davey Smith G. A study of mineral trioxide aggregate pulpotomies in primary molars (abstract). 76. The challenge of meta-analysis: discussion. compared with formocresol. Number 7S. Jabbarifar SE. 69.188:32– 6. Whitworth JN. J Dent Res 2000. J Res Med Sci 2004. Effects of Nd:YAG laser pulpotomy on human primary molars. Liu JF. J Clin Epidemiol 1955. Khadeni DD. and contraindications for meta-analysis. Accessed February 27. 68.26:401–9.79:543. Eur J Paediatr Dent 2002.Pulp Symposium 67. Clinical studies on ferric sulphate as a pulpotomy medicament in primary teeth.evidence-based-medicine. Br Med J 1997. Egger M.7:135– 48. Nunn JH.23:168. An illustrated guide to the methods of meta-analysis. 74. What is meta-analysis? Available at: http://www. result in greater clinical/radiographic success? Pediatr Dent 2004. Dummet CJR. Schneider P. Ghaseni DD. 71. 72. Papagiannoulis L. Johns DR. 70. Musselman R. Pediatr Dent 2001. S24 Fuks JOE — Volume 34. 75. Br Dent J 2000. July 2008 . 2008. sulphate. Phillips AN. J Eval Clin Pract 2001. Aktoren O. 73. Gencay K. indication.6:55– 8. Meta-analysis: principles and procedures. An investigation of the relative efficacy of Buckley’s formocresol and calcium hydroxide in primary molars vital pulp therapy. A two-year clinical-radiographic follow-up of the pulpotomies in primary molars (abstract). Waterhouse PJ.315:1533–7.32:404 –7.uk. Success rates of formocresol pulpotomy vs mineral trioxide aggregate in human primary molar tooth. Sutton AJ.3:126 –32. Cuisia ZE.48:5– 8. J Endod 2006. Norbert V.co. Abrams KR.
the basic principle of vital pulpal treatment can be broken down into 2 broad phases. There are long-term prognostic advantages of this treatment outcome over apexification treatment. Mineral trioxide aggregate (MTA) currently is the optimum material for use in vital pulp therapy. Address requests for reprints to Dr David Witherspoon at dewspoon@ntendo. Issue 3. In the medium-term clinical assessment. Number 7S. the primary goal when treating immature permanent teeth should be to maintain pulp vitality so that apexogenesis can occur (5– 8). MS.Pulp Symposium Vital Pulp Therapy with New Materials: New Directions and Treatment Perspectives—Permanent Teeth David E. and its composition appears to have greater structural integrity (3). an alternative material. BDS. including free crystalline silica. induce mineralization. Historically. free magnesium oxide. Compared with the traditional material of calcium hydroxide. it has superior long-term sealing ability and stimulates a higher quality and greater amount of reparative dentin. sealed from the oral environment. 0099-2399/$0 . To date. The ideal material for vital pulp treatment should be able to resist long-term bacterial leakage and stimulate the remaining pulp tissue to return to a healthy state. (J Endod 2008. This article is being published concurrently in Pediatric Dentistry. MS Abstract Pulp necrosis in immature teeth subsequent to caries has a major impact on long-term tooth retention. 10) eloquently established the role of bacteria in pulpal health and necrosis. Either citation can be used when citing this article. The aim of vital pulp therapy is to maintain pulp viability by eliminating bacteria from the dentin-pulp complex and to establish an environment in which apexogenesis can occur. it has demonstrated a high success rate. The principal procedures aimed at maintaining pulpal vitality include direct pulp caps and pulpotomies. with some Ca(OH)2 also being formed.1016/j. BDS. MTA has resisted leakage predictably and repeatedly. May/June 2008. The classic study by Kakehashi et al. promoting the formation of dentin. 25). the best method appears to be the ability to control pulpal hemorrhage by using sodium hypochlorite. The initial phase involves removing the diseased and bacterially contaminated tissue. MTA is a good substitute for calcium hydroxide in vital pulp procedures. has acted as a Workshop Coordinator for the annual session of the American Association of Endodontists. pulpal demise was inevitable.6% insoluble residue.joen. Thus. Hydration of the powder results in the formation of a finely crystalline gel of the hydrated forms of the components. Volume 30. The early data for MTA suggest that it is the optimum material for fulfilling these goals when vital pulp therapy is the treatment of choice. These include the ability of the material to kill bacteria. Ultimately. Witherspoon. abnormal root development will impact the long-term prognosis for tooth retention (1– 4). In a germ-free environment. MTA has been shown to have an antibacterial effect on some of the facultative bacteria and no effect on strict anaerobic bacteria (23). By removing the affected coronal pulp tissue and leaving the unaffected radicular pulp tissue in situ. potassium. has become available for use in pulpal procedures. It has a compressive strength equal to intermediate restorative material (IRM) and Super-EBA IRM but less than that of amalgam. A complicating factor in treating immature teeth is the difficulty predicting the degree of pulpal damage.com. MTA’s ability to resist the future penetration of microorganisms appears to be high. doi:10. The ability of the clinician to manage the health of the remaining pulpal tissue during the procedure is paramount. and calcium sulfate dihydrate. Other trace constituents might include calcium oxide. Conflict of Interest: David E. tricalcium aluminate.34: S25-S28) Key Words Apexogenesis. It can result in irreversible pulpal damage. (9. Witherspoon. This limited antibacterial effect is less than that demonstrated by Ca(OH)2 pastes. Plano. eventually causing necrosis of the pulpal tissues and associated arrested development of the tooth root. Direct pulp caps and pulpotomies in teeth with incomplete root formation promote normal development of the root complex. the material of choice has been calcium hydroxide (Ca(OH)2) (14 –20). This solidifies to a hard structure in less than 3 hours (22). July 2008 Vital Pulp Therapy with New Materials S25 . Thus. mineral trioxide aggregate.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. Currently. bismuth oxide. The tooth structure formed is of a great quantity. In the presence of bacteria. a number of materials (11–13) have been advocated to induce normal root development. Several properties are necessary when choosing a material to be used in vital pulp treatment. D MTA’s Physical and Chemical Properties MTA is composed of tricalcium silicate. pulpotomy Private practice. and sodium sulfate compounds (21). This fundamental premise is integral to the success of all vital pulp procedures.2008. and establish a tight bacterial seal. MTA might also contain up to 0. normal root development can take place. The second phase involves establishing an environment that will prevent any further and future bacterial contamination. mineral trioxide aggregate (MTA). MTA frequently performs better JOE — Volume 34. Thus. Most recently. The articles are identical.030 ental caries is one of the greatest challenges to the integrity of the developing tooth. The result is that the fully developed tooth is more resistant to vertical root fractures (4). direct pulp cap. Texas. In in vitro leakage studies (24. dicalcium silicate.02. the pulp demonstrated the ability to heal and deposit additional dentin material.
of the 15 teeth in younger patients that were not fully formed at the time of treatment. Calcific metamorphosis was evident radiographically in 2 teeth treated with Ca(OH)2 and in 4 teeth treated with MTA (56). In the second study.25%– 6. the treatment consisted of caries removal with the aid of an operating microscope and extensive use of caries detector dye. The recall period ranged from 6 –53 months. During that time. 41– 43. 47). the patient is anesthetized with a standard local anesthetic protocol. no symptoms. After 6 months. Several human clinical studies with MTA for direct pulp capping and pulpotomies have recently been published. 39 – 45). the pulps were capped with MTA. Tulsa. The net result is that vital pulp therapy with MTA produces negligible pulpal necrosis (34. with an average recall period of 21 months. MTA 93%). The remaining affected tissue is removed by using a coarse. 33). July 2008 . with an average recall period of 3. In the case of a pulpotomy. high-speed diamond bur with copious irrigation. Exposed pulp tissue was removed with a diamond bur. The patients’ ages ranged from 7–15 years. When comparing MTA and Ca(OH)2 pulpotomies within the same patient at the 12-month recall time frame. 39). MTA’s leakage patterns are similar (31. In a prospective clinical trial comparing success rates of partial pulpotomies with treated cariously exposed permanent molars by using Ca(OH)2 or MTA. The single tooth that required nonsurgical root canal treatment had completed normal root development before requiring nonsurgical root canal treatment. OK) and has been advocated for use in vital pulp therapy (34 –38).00% NaOCl applied for up to 10 minutes. In addition. The key factor in deciding whether to complete a pulpotomy as opposed to a pulpectomy was the ability to control pulpal hemorrhage. Although 6 of 28 teeth did not respond to vitality testing at the final followup. and the pulps were free of inflammation. Fifty-one teeth in 34 patients were available for recall. with evidence of continued root growth and no reported symptoms (53). and the teeth were temporized with unbonded composite Photocore (Kuraray Co Ltd. The gross caries can be removed with either a sharp spoon excavator or a large. there was no statistically significant difference in the success rate between each group (Ca(OH)2 91%. with a normal radiographic appearance.6 months. It develops more complete dentin bridges and demonstrates an improved ability to maintain pulp tissue integrity (34. MTA also appears to induce the formation of a dentin bridge at a faster rate than Ca(OH)2 (48). Forty-nine of the 53 teeth were available for recall at the 1-year time frame. Technique With the vital pulp therapy technique. in animal studies. 36. The teeth were restored with amalgam or stainless steel crowns. with an average of 34. 53 teeth with carious exposures that had been diagnosed with reversible pulpitis and normal periradicular tissue were treated with MTA pulp caps. Pulpal bleeding was controlled with 5. The use of gray MTA for partial pulpotomy in cariously exposed young permanent first molars diagnosed with reversible pulpitis and normal periradicular tissue has resulted in a very high success rate. In cases in which pulpal hemostasis could be achieved with NaOCl. Histologic examination of these teeth showed an apparent continuous dentin bridge formation in both teeth. with an average age of 10 years (57). 32). Furthermore. which ranges from 93%–98% (53. The patients’ ages ranged from 7. At the 24-month recall period. a 93% clinical and radiographic success rate was reported at the 24-month recall period. the pulp is removed to a level where adequate hemostasis can be achieved. Osaka. Mineralization MTA has demonstrated the ability to induce hard tissue formation in pulpal tissues when used as either a direct pulp capping or pulpotomy material (34. whereas none of the teeth treated with MTA failed (0 of 15 teeth). After hemostasis was achieved. the cavity is flushed with NaOCl to decrease the bacterial load. with an average age of 10 years. In all cases. Number 7S.2–13. Japan) and a moistened cotton pellet placed directly over the MTA. slow-speed tungsten carbide bur. a success rate of 92% was reported (58). a pulpotomy was completed. the presence of blood has little impact on the degree of leakage (29. Histologic evaluation in animal and human studies has shown that MTA stimulates reparative dentin formation.4 – 45. Hemostasis is achieved by irrigating with 6% sodium hypochlorite (59) for up to 10 minutes. The process by which MTA acts to induce dentin bridge formation is not known. Both of these studies have reported a high rate of success. 22 of 28 teeth showed no signs of clinical or radiographic failure and responded within normal limits to pulp vitality tests. A total of 40 patients between 7 and 45 years old were treated. In a case series outcomes report that used MTA pulpotomies to treat cariously exposed immature permanent teeth (first or second molars) that had been diagnosed with irreversible pulpitis. 54). the teeth were removed as part of planned orthodontic treatment.8 –13. round. It is commercially available as ProRoot MTA (Dentsply Tulsa Dental. In 1 case report (52) partial pulpotomies were conducted on 2 cases of dens evaginatus. All the teeth showed signs of vitality and absence of periapical radiolucency. with thick dentinal bridging. Care should be taken to avoid the application of pressure to the JOE — Volume 34. permanent.1 years. 2– 4 mm of gray MTA was placed against the fresh wound and then covered with a layer of glass ionomer cement. minimal inflammation. a rubber dam is used to isolate the tooth being treated. In 1 study (54). The teeth were restored with a bonded composite 5–10 days later.8 months (55). and the follow-up period was from 25. The study used a similar protocol to direct S26 Witherspoon Pulpotomy The human clinical data available on MTA pulpotomies in cariously exposed permanent teeth have reported high success rates. The affected enamel is removed by using a high-speed bur with copious irrigation.Pulp Symposium than amalgam IRM or Super EBA (26 –30). It has been theorized (49) that the tricalcium oxide in MTA reacts with tissue fluids to form Ca(OH)2. Briefly. and a normal response to cold testing. The patients ranged from 6. and the teeth were asymptomatic. The maximum period of observation was 9 years.3 years old. MTA promotes rapid cell growth in vitro (46). MTA consistently induces the formation of dentin at a greater rate with a superior structural integrity. all subsequently demonstrated continued normal apexogenesis to complete root formation (54). Compared with Ca(OH)2.94 years. pulp cap 30 young. 2 of the 15 teeth in the Ca(OH)2 group were considered failures. Clinical Outcomes The initial response reported in case reports has been very positive (50 –52). resulting in hard tissue formation in a similar manner to Ca(OH)2. 98% of the cases presented a favorable outcome. Compared with composite resins placed under ideal conditions. As the pulp is approached. and after hemostasis. and nominal hyperemia. Direct Pulp Capping The clinical data available on MTA pulp capping of cariously exposed permanent teeth are limited to 2 studies. the radiographic appearance was within normal limits. which ranged from 93%–100%. cariously exposed asymptomatic teeth with MTA.
(D) Recall at 3. Monsef M. Otoboni Filho JA. 20. 21. Number 7S. therefore. May KN Jr. Prognosis of luxated nonvital maxillary incisors treated with calcium hydroxide and filled with gutta-percha: a retrospective clinical study.2:43–7. 2. 12. 24. J South Calif Dent Assoc 1966.32:197–203. Currently. Figure 1. Dent Clin North Am 1984. Torabinejad M. Once the MTA is in place. J Endod 2002. Kontakiotis EG. Direct pulp capping treatment: a long-term follow-up.28:5–7. Kiba H. Criteria for standardizing and increasing credibility of direct pulp capping studies. McDonald F. Endod Dent Traumatol 1992.16:1393– 8. bonded. Horsted-Bindslev P. Conclusion The major difficulty in treating permanent immature teeth is the ability to predictably diagnose the state of pulpal health and.23:329 – 40.99:472–5. Preventive endodontics: vital pulp therapy. Langer M. Bernabe PF. Yamamoto H. Bernabe PF. JOE — Volume 34. Yaari A. Adamo HL. J Am Dent Assoc 1978. Fischer EJ. Schroder U. Treatment of teeth with open apices using mineral trioxide aggregate.12:315–20. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. 14. Arch Oral Biol 1971. 38 (quiz). Torabinejad M. de Mello W. Dycal. pulp. Nery MJ.97:607–12.33:30 – 4. de Souza V. 27. Granath LE.34:449 –51. a layer of MTA should be placed and mixed according to the manufacturer’s recommendations over the exposed pulpal tissue. 18.9:427–36. Yamazaki M. Endod Dent Traumatol 1986. Rabie G. Capping the inflamed pulp under different clinical conditions. J Endod 1995. 22. Wu MK. Shabahang S. Noren JG. a small amount of flowable compomer (or an equivalent light-cured resin or glass ionomer liner) should be applied to cover the MTA material. J Endod 1995. Andreasen FM. The tooth responds within normal limits to pulp tests. Levin L. 3.Pulp Symposium References 1. thus. Quintessence Int 2002. Webber RT. 19. Pract Periodontics Aesthet Dent 1997. Nery MJ. Hong CU.21:349 –53. Material safety data sheet: ProRoot MTA root canal repair material. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003. J Endod 1998. Buruiana R. Schertzer L. Leakage evaluation of root end filling materials using endotoxin. A comparison of MTA. and Super-EBA as a root-end filling material. J Endod 1993.20:340 –9. 2002:1–2. J Endod 2001. Robertson A. Rastegar AF. Chandler NP. July 2008 Vital Pulp Therapy with New Materials S27 . Roy CO. Am J Dent 1998. Katebzadeh N. Pract Periodontics Aesthet Dent 2000. Stanley HR. Tang HM. 23. it has demonstrated a high success rate. Andreasen JO. Int Endod J 1999.28: 669 –97.21:109 –12. Tulsa-Dental. Torabinejad M. Love RM. The remainder of the cavity can then be etched. Miller CH. J Endod 1998. Strengthening immature teeth during and after apexification. 17. J Oral Sci 2000. Having achieved hemostasis. Holland R. The current data available on the use of MTA in vital pulp therapy indicate that it is the optimum material and better than the traditionally used material Ca(OH)2. J Endod 1998. Torabinejad M. Martell B. Fitzgerald RJ. Bacterial leakage of mineral trioxide aggregate as compared with zinc-free amalgam.11(special issue):S17–34. 30. de Mello W. Torabinejad M. Gerrets TF.Nov:663–73. Otoboni Filho JA. 6. Massler M. Dalton BC. Kettering JD. and restored (Fig. Kakehashi S. The current tests available to the clinician make it difficult to accurately predict the degree of pulpal degeneration before commencing treatment. Sela J. Stanley HR. Therefore. Vilkinis V. Pitt Ford TR. 31. Stanley HR. Evaluation of healing following experimental pulpotomy of intact human teeth and capping with calcium hydroxide.21:403– 6. Kettering JD. Electrical and dye leakage comparison of three root-end restorative materials. Kettering JD. Nakanuma K. a good substitute for Ca(OH)2 in vital pulp procedures. 13. Schroder U. Torabinejad M. and amalgam as root-end filling materials using a bacterial microleakage model.24:557– 60. Int J Paediatr Dent 2000. Direct capping of human pulps with a dentin bonding system or with calcium hydroxide cement. Strengthening of immature teeth during long-term endodontic therapy. Antibacterial effects of some root end filling materials.27:7– 8. 25. Fitzgerald RJ. Trope M. Wesselink PR. Cvek M. 7. 26. 28.10:191–9. Holland R. (A) Preoperative radiograph of a symptomatic cariously exposed mandibular second premolar. (B) Postoperative radiograph showing an MTA pulpotomy completed and restored with bonded composite resin.96:591– 600. Apexogenesis versus apexification. 22 (quiz).24:176 –9. Effect of an acid environment on leakage of root-end filling materials. Pitt Ford TR. Sealing ability of a mineral trioxide aggregate for repair of lateral root perforations. In clinical outcomes evaluation. 1). Long-term seal provided by some root-end filling materials. Tronstad L. Swift EJ Jr. Arens DE. 29. J Endod 1995. Sidlauskas A. The thickness of the material should be approximately 2 mm. Dentsply. de Souza V. Hayakawa T. Permeability of the hard tissue bridge formed after pulpotomy with calcium hydroxide: a histologic study.24:256 –9. Odontol Revy 1972. Kakehashi S. J Esthet Restor Dent 2002. McDougal R.42:69 –74. Lee SJ. 16. Bacterial leakage of mineral trioxide aggregate as a root-end filling material. Jeansonne BG. Physical and chemical properties of a new root-end filling material. Ulmansky M. the ability of predicting it to heal. intermediate restorative material. Response of pulpotomy wounds in normal human teeth to successively applied Ledermix and Calxyl. 9. (C) Recall at 2. Pulpal reactions to two experimental bonding systems for pulp capping procedures. Tulsa.4 years showing the tooth continuing to respond within normal limits to pulp tests. Stringfellow H.7:185–91. Stanley HR. Haskell EW. 11.23:211–20.8:45–55. 8. the clinician’s ability to assess the health of the remaining pulpal tissue during the procedure is paramount. composite. Trope M. or MPC: histological study in dog teeth. Odontol Revy 1972.7 years showing continued root formation (apexogenesis). Healing process after pulpotomy and covering with calcium hydroxide.14:349 –57. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Effects of dental trauma on the pulp. Oral Surg Oral Med Oral Pathol 1965.19:541– 4. OK: Dentsply. Dent Clin North Am 1967. 5. Hong CU. Pitt Ford TR. MTA is. 4. It has a greater long-term sealing ability and stimulates a high quality and a great amount of reparative dentin. Rev Fac Odontol Aracatuba 1978. Trope M. Super-EBA. Scanning electron microscopy of hard tissue barrier following experimental pulpotomy of intact human teeth and capping with calcium hydroxide. the best method appears to be the ability to control pulpal hemorrhage with NaOCl. J Am Dent Assoc 1979. Boylan RJ. Long-term prognosis of crownfractured permanent incisors: the effect of stage of root development and associated luxation injury. Chellemi J. 15. 10.
J Endod 1998. Peikoff MD. Opperman LA. Torabinejad M. 36.24:278.22:328 –33. Microleakage of root-end filling materials. J Endod 1999. Int Endod J 2003. Identification of hard tissue after experimental pulp capping using dentin sialoprotein (DSP) as a marker. 54.29:646 –50. Dominguez MS. Iwamoto CE. A comparative study of white and grey mineral trioxide aggregate as pulp capping agents in dog’s teeth. Lee J. Shabahang S.29:324 –33. 47. Bakland L. Eur Arch Paediatr Dent 2007. Torabinejad M. Comparison of mineral trioxide aggregate and calcium hydroxide as pulpotomy agents in young permanent teeth (apexogenesis). Akimoto N. 58. 45. Clinical and histological evaluation of white ProRoot MTA in direct pulp capping.17:163– 6. 39. Chivian N. Farsi N. Vital pulp therapy with mineral trioxide aggregate. Torabinejad M. 40. J Endod 2001. Eghbal MJ. Number 7S. Mineral trioxide aggregate (MTA) and calcium hydroxide as pulp-capping agents in human teeth: a preliminary report.139:305–15.12:109 –13.28:399 – 404. Adachi E. Aeinehchi M. 37. Balto K. Maturogenesis of a cariously exposed immature permanent tooth using MTA for direct pulp capping: a case report. Bogen G. Pitt Ford TR. Kariyawasam SP.25:161– 6.19:85–90. July 2008 . Witherspoon DE. S28 Witherspoon JOE — Volume 34. Mineral trioxide aggregate pulpotomies: a case series outcomes assessment. Pantelidou O. Alvanou A. Chen NN.Pulp Symposium 32. Harris GZ. Mitchell PJ. Prophylactic treatment of dens evaginatus using mineral trioxide aggregate. Hafez AA. Bakland LK. Fogel HM. Biomaterials 1999. Barrieshi-Nusair KM. Holland R. Ghanbariha M.35:245–54. Higa RK. 41. Management of traumatically injured pulps in immature teeth using MTA. 42. Pediatr Dent 2006. Dent Traumatol 2005. McMillan P. Bernabe PF. Owais AI. Faraco IM Jr. Reaction of rat connective tissue to implanted dentin tubes filled with mineral trioxide aggregate or calcium hydroxide. 53. Cohenca N.21:150 – 4. de Souza V.21:240 –3. 51. Int Endod J 2002. Romberg EE. Tziafas D. Otsuki M. Abedi HR. 35. Junn DJ. 38. 55.23:326 –30. et al.32:731–5. Parirokh M. 43. Al Mushayt A. Holland R. Belibasakis G. Torabainejad M. J Endod 1994. An in vivo evaluation of hemorrhage control using sodium hypochlorite and direct capping with a one. Pameijer CH.31:72– 6. Qudeimat MA. Chacko V. 33:261–72.127:1491– 4. A prospective clinical study of mineral trioxide aggregate for partial pulpotomy in cariously exposed permanent teeth. 33. J Am Dent Assoc 2006. 46. Clinical applications of mineral trioxide aggregate.27:456 – 8. Gutmann JL. Barnes D. Qudeimat MA. Bogen G. J Clin Pediatr Dent 2006. Papadimitriou S. Quantitative assessment of dentin bridge formation following pulp-capping with mineral trioxide aggregate (MTA) (abstract). Saffar AS. Nery MJ. Avery DR. Barrieshi-Nusair KM. Response of the pulp of dogs to capping with mineral trioxide aggregate or a calcium hydroxide cement. The dentinogenic effect of mineral trioxide aggregate (MTA) in short-term capping experiments. Histological and scanning electron microscopy assessment of various vital pulp-therapy materials. Dezan Junior E. Quintessence Int 2002. Tarim B. Patel R. Witherspoon DE. 50. Calcium hydroxide vs mineral trioxide aggregates for partial pulpotomy of permanent molars with deep caries. 52. et al.36:225–31. Murata SS. McKendry DJ.30:203–9. J Endod 1999. Schmitt D. Pitt Ford TR. Bakland LK. de Souza V. Jefferies S. Cox CF.137:610 – 8. Clinical assessment of mineral trioxide aggregate (MTA) as direct pulp capping in young permanent teeth. Otoboni Filho JA. Iqbal M. Human pulpal response to mineral trioxide aggregate (MTA): a histologic study. Am J Dent 2006. Holland R.or two-component adhesive system in exposed nonhuman primate pulps. Asgary S. Wright K. J Endod 2001. 59. Kariyawasam SP.20:159 – 63. 49. Using mineral trioxide aggregate as a pulp-capping material. Kurikose S. J Calif Dent Assoc 2000. 48. J Endod 2006. 57. Dent Traumatol 2006.28:855– 8. Alamoudi N. Koh ET. Ford TR. 56. Multifaceted use of ProRoot MTA root canal repair material. 34. J Endod 2003. Pitt Ford TR. J Am Dent Assoc 1996. Eslami B.25:197–205. J Am Dent Assoc 2008. Torabinejad M. Torabinejad M. Pediatr Dent 2001. Braz Dent J 2001. Small JC. Dent Traumatol 2005. Osteoblast biocompatibility of mineral trioxide aggregate. J Clin Pediatr Dent 2006. Torabinejad M. McDonald F. El-Meligy OA.27:540 –2. J Endod 2003. Lim J. Dye leakage of four root end filling materials: effects of blood contamination. Li D.20:167–73. Karabucak B. 44. Healing process of dog dental pulp after pulpotomy and pulp covering with mineral trioxide aggregate or Portland cement. Andelin WE. Dent Traumatol 2001.8:99 –104. Direct pulp capping with mineral trioxide aggregate: an observational study.
tertiary dentin From the Department of Cariology and Endodontics. The articles are identical. or in particular the randomization? The level of evidence is the short answer to that question. A less invasive modified stepwise excavation approach is described. In Denmark and Sweden a randomized clinical multi-center trial is currently taking place. the RCT should be carried out in a number of trial centers. Within the concept of maintaining pulp vitality. and Cavitec formulations of calcium hydroxide (2). May/June 2008. 3. but it cannot be said which approach is best. 5. focusing on changing an active lesion into an arrested lesion even without performing an excavation close to the pulp. Number 7S. Expert opinion is allocated to the lowest level of evidence. University of Copenhagen. The perceived effect might in reality differ between the 2 studies. Partial caries removal appeared preferable in deep lesions to reduce the risk of carious exposure of the pulp. This article is being published concurrently in Pediatric Dentistry. which is that of confounding variables.035 The Latest Systematic Reviews from the Cochrane Collaboration Regarding Caries Treatment and the Pulp The Cochrane Collaboration carries out systematic reviews of high-quality clinical studies. A more extended answer deals with the largest problem in studies that are nonrandomized. is a Grant Recipient from the Danish Agency for Science Technology and Innovation. Faculty of Health Sciences. the following points were addressed in the review (1): 1. Recent systematic reviews are presented. At the top of the hierarchy is the systematic review of high-quality RCTs. adequate allocation sequences: for example. The distribution of prognostic factors might differ between the 2 studies. and the main message is that optimal randomized clinical studies are lacking. July 2008 Indirect Pulp Therapy and Stepwise Excavation S29 . Dycal.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. pulp. stepwise excavation. Either citation can be used when citing this article. Conflict of Interest: Lars Bjørndal. prognostic factors are equally distributed between the 2 interventions that are going to be compared.02. Issue 3. randomized clinical trial. PhD Abstract Various treatment concepts have been suggested to solve the deep carious lesion dilemma. The following is a list of factors that characterize a high-quality RCT: 1. 2. There is a great deal of difference between RCTs and observational studies. Why is RCT so important. School of Dentistry. 0099-2399/$0 . ku. dentin. in fact.joen. follow-up examination is done by an investigator(s) who is blinded as to the patient’s group assignment. No pulpal symptoms were found. treating the very same stage of diseases? With regard to caries. treatment modalities that included indirect pulp treatment (IPT) showed no differences in symptoms at 12 months among studies using Life. Key Words Caries. Volume 30.Pulp Symposium Indirect Pulp Therapy and Stepwise Excavation Lars Bjørndal. the presence of well-defined inclusion and exclusion criteria. with the next level being observational studies. JOE — Volume 34. adequate allocation concealment: the randomization is carried out with a central independent unit. Many factors cannot be controlled for if a simple comparison is made between 2 studies in which the same treatment has been provided. Guidelines for treatment are presented. The recent reviews of caries and pulp treatments all indicate the lack of RCTs (1. we cannot exclude the psychological phenomenon that investigators tend to see what they want to see.1016/j. and they are not all high-quality RCTs. DDS. the randomization of patients to control or experimental groups is generated by a computer. This trial is investigating the effects of stepwise excavation over 2 visits versus 1 complete excavation of deep caries in permanent teeth. how deep are the lesions? Finally. doi:10. 6. but this does not mean that the thousands of clinical studies that have been carried out with a non-RCT design do not indicate relevance.34:S29-S33) Introducing Thoughts about Level of Evidence in Clinical Research A demanding trend in clinical research is to perform a randomized clinical trial (RCT) to compare 2 interventions. PhD. Observational studies on indirect pulp treatment and stepwise excavation demonstrate that these treatments avoid pulp exposures. DDS. 2). Their conclusions are based on very few studies. ideally. 7. Are the 2 studies. the number of treatments needed to show a difference between control and experimental groups is calculated. Denmark. 2. 3.dk. The Cochrane Collaboration has found fewer than 10 studies that could be compared. the Caries and Pulp (CAP) trial. (J Endod 2008. Partial caries removal in symptomless primary or permanent teeth reduces the risk of pulpal exposure. indirect pulp treatment.2008. In relation to partial caries removal. but they simply do not have the highest level of evidence. 4. Copenhagen. Address requests for reprints to Dr Bjørndal at lb@odont.
Various excavation methods have been proposed. Carious tissue was removed. primary teeth were treated. is still based on indirect diagnostic procedures. For some practitioners. this approach provides one more chance to maintain the pulp’s integrity. This judgment was made in one case in which only half of the dentin was demineralized. and diagnoses such as asymptomatic pulpitis or chronic pulpitis have been made. Thus. and a 1-mm layer of calcium hydroxide was placed followed by a temporary restoration. who emphasized that a thin soft layer of dentin should remain on the pulpal wall. This stepwise excavation method has been a very common and widespread approach within the Nordic countries. (7). Number 7S. The majority of dentists selected lesions that penetrated to within three fourths of the entire dentin thickness or more as evaluated on x-rays. It is stated that all undermining enamel is removed to gain more easy access to the carious dentin along the enamel-dentin junction. means that if you apply additional pressure to the dentin with the excavator. The differences between the 2 methods mentioned above are that the IPT procedure involves almost complete removal of the affected dentin. July 2008 . What did these early clinical articles prescribe in terms of clinical procedure? One of the earliest articles describing a step-by-step approach is by Sowden (12). At the pulpal wall approximately 1 mm of carious dentin was left behind. For example. (14) provided details of the excavation procedures. the pulp will be exposed. The problem in comparing these studies is confounding factors. The authors did not describe in detail what was meant by a thin layer. For reasons discussed earlier. and there is a great deal of variation among them. general dentists were asked to judge the penetration depth of caries lesions that would pose a risk for pulpal exposure (4). An important point after treatment of such cases must be the maintenance of pulp sensibility. the clinical diagnosis of the pulp is centered on subjective symptomatic factors. we discussed the understanding of caries. the treatments are guided toward either invasive pulp therapy or procedures aiming to maintain the pulp integrity. and that the treatment of deep caries lesions has been placed in what one could call “no mans land. A more rigorous approach was addressed in the article by Magnusson and Sundell (11). I will return to this later. A Brief Historical Focus on Excavations Methods in Asymptomatic Deep Caries Lesions Many pulps have probably been exposed through the years on the basis of the concept that deep caries lesions are always associated with inflammation. because each represents its own decade. such as IPT (10) and the two-stage excavation procedure or stepwise excavation (11). Eidelman et al. ie. with confirmed pulpal sensibility but with no objective signs of apical pathology or subjective symptoms before start of the treatment. It has not been possible to devise an overall applied classification system on this issue. This point has in many studies been defined as a lesion in which one would expect a pulpal exposure if all caries was removed. Law and Lewis (13) accessed all areas of carious dentin and placed calcium hydroxide and an amalgam restoration. whereas the other 2 studies did not re-enter the lesion. (10). a stepwise excavation approach was used with lesions defined as deep. the stepwise excavation technique involves reentry at varying intervals. The Biologic Dilemma On the first day of this symposium. Another aspect is that we do not have any reliable or accurate clinical diagnostic device for monitoring the degree of pulpal inflammation. but in reality the term has not led to consensus. but studies that did not re-enter reported no adverse consequences. the deep carious lesion might also be a potential reversible pulpitis case. Re-entry and final excavation were then made after 2–3 weeks. However. A deep caries lesion is present when the penetration depth is in the range of three fourths of the entire thickness of the dentin or more when evaluated on an x-ray. because the finding of “no clinical symptoms” could be the result of a silently developing pulp necrosis. The diagnostic data should be collected from the following 3 areas: (i) the patient’s description of subjective symptoms. and (iii) paraclinical examinations (radiographs for exclusion of apical pathosis). because we do not always know in what direction the pulpal inflammation will turn. In 2 of the studies. and no follow-up examination was done after treatment was completed. One of the studies treated less progressed lesions. Re-entry was made after 6 months. Even though the absence of clinical symptoms is not a sign of absence of pulp pathology. and the final excavation was performed. which might be important when trying to compare the 2 interventions. the tooth will be managed with an invasive pulp treatment (9). Attempts to divide degrees of pulp pathology seem ambitious. Among the 4 included studies on which the above conclusions are based. Residual caries. but rather they represent our best clinical judgment. How Deep Is a “Deep” Caries Lesion? The definition of deep caries lesions points toward the potential exposure of the pulp (3). When do clinicians expect that a potential pulp exposure is close? In a practice-based observational study. S30 Bjørndal JOE — Volume 34. Within the latter diagnosticdichotomy. as described in detail by Reit et al. whereas for others the use of reversible and irreversible pulpitis is applied (9). There is insufficient evidence to show whether it is necessary to re-enter and excavate further in the stepwise excavation technique. Magnusson and Sundell (11) placed a zinc oxide– eugenol cement temporary restoration and performed the final excavation after 4 – 6 weeks. They most likely excavated as close as possible to the pulp.” with different schools of opinions as classically given by Tomes (5) and Black (6). One problem has been the definition of the penetration depth of the deep caries lesion. In 1962. leaving a thin layer of residual caries. until the opposite is proved. depending on the results from our clinical as well as paraclinical diagnostic procedures. in the study by Magnusson and Sundell (11). leaving a thin layer of demineralized dentin. which in the future might bring these conclusions further up the hierarchy of evidence. Re-entry is not attempted. The tooth was re-entered after 1 year.Pulp Symposium 4. In recent articles and reviews the expression “partial excavation” (1) has emerged to refer to various treatment modalities. The case selection for a given treatment. the words irreversible and reversible cannot solely be interpreted as the gold standard expression for the actual state of the pulp. as defined by Kerhove et al. (ii) pulp sensibility testing. We need high-quality RCTs to compare IPT and stepwise excavation. we cannot make detailed comparisons among these older studies. indicating that this definition varies substantially among practitioners. the lesions differed between deep lesions and those extending to half the thickness of the dentin. whether or not we want to avoid an exposure of the pulp. We might try to divide a few clinical stages of vital pulp problems. Let us adopt the same clinical concern for potential exposures as did the majority of these general practitioners. No final excavation was performed within the first visit. Let us add some comments. In contrast. The Dentist Must Handle the Biologic Dilemma! The clinical use of the irreversible pulpitis diagnosis as well as symptomatic pulpitis is essentially the same. symptomatic or nonsymptomatic pulpitis (8). because it can mean anything from almost no excavation to excavation very close to the pulp.
and drier demineralized dentin. (16) also reported that the IPT technique produces clinical success. Endodontic Topics 2002. evidenced by a darker demineralized dentin (c. yellowish demineralized dentin becomes a darker. the Cochrane review indicated that variation in base materials did not produce any differences (2). harder. Gruythuysen et al. The active. resembling a slowly progressing lesion. Reprinted with permission from Blackwell Munksgaard from Bjørndal L. 19). 20). Thus. 18% of respondents would partially remove caries in a deep lesion in which one would expect that complete caries removal would lead to pulpal exposure (24). 1) (18. Observational Data about Indirect Pulp Treatment In a retrospective study AL-Zayer et al. b) followed by a calcium hydroxide– containing base material and a provisional restoration. (15) found that IPT in primary posterior teeth is a successful technique and should be considered as an alternative pulp therapy. (17) concluded that IPT in primary teeth arrests the progression of the underlying caries. eventually reaching the residual level close to the dentin-pulp interface. Diagrams demonstrating the less invasive stepwise excavation procedure. I interpret this technique as the IPT with no re-entry.Pulp Symposium Note that it is also difficult to determine whether there are any differences between the classic IPT and the first excavation step as performed in the study by Magnusson and Sundell (11). The primary aim of the Is A Two-step Excavation Necessary? As shown from a recent survey. July 2008 Indirect Pulp Therapy and Stepwise Excavation S31 . d). regardless of the material used as a liner. Red zones indicate plaque. Number 7S. During the treatment interval the retained demineralized dentin has clinically changed into signs of slow lesion progress. Use the Knowledge from Caries Pathology to Design an Excavation Approach The optimal focus on avoiding a pulpal exposure and using caries pathology might be demonstrated by the concept of a less invasive or modified stepwise excavation (Fig. Marchi et al. first excavation is to change the caries environment and not to remove as much carious dentin. A closed lesion environment before and after first excavation (a. Recently. soft. the potential risk of creating pulpal exposures following either IPT or during the first step of stepwise excavation might very well be the same. Microbiologic and clinical studies have shown that it is possible to decrease the number of bacteria and arrest the caries process during a treatment interval (19. This aspect of using our knowledge of caries pathology as an integrated part of caries removal is also reinforced in a new textbook chapter (23). After final excavation (e) the permanent restoration is made (f). More detailed microbiologic observations also indicate that during a treatment interval the flora becomes a type associated with slow lesion progress in root caries (21). Whether the presence of such flora can remain “inactive” beneath a permanent restoration in a deep cavity needs further investigation. Also. (27) JOE — Volume 34. Concerning the more detailed treatment procedures. These findings have gained additional support (22). Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatment outcome. In the United States IPT Figure 1.2:10 –23.
Miyashita H. Oper Dent 1991. Consequently. because it is easier to remove the remaining dry carious dentin. we are forced to make a choice on the basis of indirect diagnostic methods. Thylstrup A. Deep lesion considered likely to result in pulp exposure if treated by a single and terminal excavation. the following presents the stepwise excavation technique (27): 1. follow-up examinations are required with regard to pulp sensibility and apical conditions. The CAP trial is being performed as a multi-center RCT. Otherwise. this would favor a second visit. 5. Petersson K. In: Bergenholtz G. Textbook of endodontology. Reit C. The placement of high-quality temporary and final restorative materials must be stressed. The main concern is that when excavating to a level close to the pulp. The control and prevention of further pulpal and periapical damage in relation to the restored tooth will. London: John Churchill. Worthington HV. Complete or ultraconservative removal of decayed tissue in unfilled teeth. Pulp management for caries in adults: maintaining pulp vitality. and the results are about to be analyzed (25). it is not easy to change a clinical habit from one of removing all carious dentin to one of leaving caries permanently. Finish the peripheral excavation of the cavity followed by a central excavation removing the outermost necrotic and infected demineralized dentin. Heys RJ. 4. July 2008 . 4. In addition. Hørsted-Bindslev P. Fitzgerald M. A High-quality RCT Concerning Deep Caries Treatment: The Caries and Pulp (CAP) Trial The aim of the CAP trial has been to investigate the beneficial and harmful effects of stepwise excavation of symptomatic and asymptomatic permanent teeth during 2 visits versus complete excavation of deep caries in 1 visit. 3. 6.5– 4. Reit C. Remember the second aim. Chicago: Medico-Dental Publishing Co. It Is Not Just a Matter of Selecting a Proper Clinical Treatment Concept We do not yet have noninvasive tools for the measurement of the severity of pulpal inflammation. Therefore. because failures are most often associated with inadequate restorations (4). The final step of stepwise excavation is 2-fold: (1) to assess the tooth’s reaction and (2) to remove the slowly progressing lesion in slightly infected discolored demineralized dentin before carrying out the final restoration. However. The clinician’s intention is to avoid a pulpal exposure on the basis of the best possible indications. The technical procedures in filling teeth. except for the less invasive first step. or test cavity. Kidd EAM. Black GV. include proper oral hygiene procedures for the removal of cariogenic biofilms. Because readers are alS32 References 1. the changes in dentin appearance during the excavation provide the clinician with information regarding the changes in caries activity. It is difficult to state which treatment approach is better. a number of pulpal complications might arise. 5. 2003:9 –18. vol II. The final excavation is often less invasive than expected. ranging between 6 and 8 months. 3. Number 7S. This is also true in cases in which the changes in color of the carious dentin are not as clear. Bjørndal JOE — Volume 34. The understanding of clinical treatment concepts also includes knowledge of its limitations. it might stimulate obliteration of the root canals. the discussion of reversible or irreversible development of pulpitis is controversial in relation to the actual state of the pulp. which is to remove the slowly progressing caries in slightly infected discolored demineralized dentin before carrying out the final restoration. different schools of thought exist. Clinical Guidelines Based on an Observational Study and a High-quality RCT Observational studies from dental practice environments have demonstrated the effectiveness of treating deep carious lesions by using a less invasive or modified stepwise excavation. Tomes J. A clinical histological evaluation of conservative pulpal therapy in human teeth. Innes N. which tend to accumulate where the problem began—in the areas of the restored tooth surfaces. 8. thereby reducing the risk of pulp exposure. in order that a provisional restoration can be properly placed. ready familiar with the guidelines of the IPT. because no highquality RCTs have yet been performed to give us the answer. and the status of inclusion has recently been reported. Molven O.5 years) has demonstrated a high success rate (92%). Select a provisional restorative material on the basis of the length of the treatment interval. follow-up examinations are mandatory for the evaluation of pulp sensibility and the possible presence of apical pathosis (28). as a result of the altered dentinal changes gained during the treatment interval. 2. 6. Diagnosis of pulpal and periapical disease. In reality. Qualtrough A. No history of pretreatment symptoms such as spontaneous pain and provoked pulpal pain. A work on operative dentistry in two volumes. which means that the enrollment of patients has been discontinued. Recognize that the procedure appears very similar to the IPT.Pulp Symposium has been carried out for years. 2. A practice-based study on stepwise excavation of deep carious lesions in permanent teeth: a 1-year follow-up study. When treating the deep carious lesion. Because of the possibility of asymptomatic development of irreversible pulp degeneration over time. Clinically. a 2-step excavation procedure will add to the cost of the treatment. besides a sufficient restoration. mild to moderate pain on thermal stimulation is accepted.3:CD003808.26:122– 8. Pretreatment radiographs that rule out apical pathosis. A system of dental surgery. Plasschaert A. Ricketts DNJ. Cochrane Database Syst Rev 2007. making future endodontic treatment more difficult. 1859:336. 2nd ed. Preliminary data on the outcome pulp exposure favor the use of stepwise excavation. but it has not been proved. Long-term recall (3. whereas we in the Scandinavian countries traditionally have applied a stepwise excavation approach. Evaluated by x-ray. Do not excavate as closely as possible during the first step. Positive pulp sensibility tested by an electric pulp tester. The final excavation is safer. Future high-quality RCTs might reduce this problem. thermal stimulation. the clinician will not promote local changes in the cariogenic environment. 7. eds. as indicated within the various stepwise excavation approaches.2:CD004484. indicating that the method can be carried out in clinical practice (26). If the operator leaves infected dentin. It is important to say that such a hypothesis is relevant. Oxford: Blackwell Munksgaard. Thus.16:101–12. Community Dent Oral Epidemiol 1998. However. 1908. the dentinal lesion involves three fourths or more of the dentin thickness. This requires the clinician to decide before reaching the pulp whether to perform a stepwise excavation approach before all carious dentin has been removed. 7. A Two-step Approach Might Be the First Way of Changing Clinical Habits The vast majority of respondents to the aforementioned survey selected an invasive approach in relation to the deep caries case because they presumably did not believe in leaving carious dentin behind (24). One way to accomplish this would be to experience the strategy of “changing the local caries environment” by performing a 2-step procedure next time a deep caries lesion presents in your practice. Clarkson J. Cochrane Database Syst Rev 2006. Bjørndal L.
Bjørndal L. Essential endodontology: prevention and treatment of apical periodontitis.31:68 –71. Chicago: Quintessence Publishing Co. 26. Oxford: Blackwell Munksgaard. In: Fejerskov O. Gruythuysen RJM.23:187–8. J Pedod 1978.Pulp Symposium 8. Clinical and microbiological effect of calcium hydroxide protection in indirect pulp capping in primary teeth. Indirect pulp treatment in primary and permanent teeth with deep carious lesions. In: Mjör IA. Am J Dent 2006.31:411–7. 28. Changes in the cultivable flora in deep carious lesions following a stepwise excavation procedure. Oral Surg Oral Med Oral Path 1961. Oxford: Blackwell Sci. J Dent Child 1956. Indirect pulp treatment of primary posterior teeth: a retrospective study. Klein AI. Vena D. Markvart M. Kidd EAM.19:382– 6. Dentin and pulp reactions to caries and operative treatment: biological variables affecting treatment outcome. 24. Caries removal and the pulpodentinal complex. Eidelman E. Bjørndal L: Behanding af profunde carieslæsioner med gradvis ekskavering. Herman SC. Koulourides T. Trope M. Law DB. Magnusson BO. 20. Feigal RJ. 2002:55–75. 2003:81. Clinical endodontics. Franzon R. Oen KT. The CAP-1 randomized trial: stepwise excavation versus one excavation . 12. J Child Dent 1965.41:270. July 2008 Indirect Pulp Therapy and Stepwise Excavation S33 . J Clin Pediat Dent 2006. Caries Res 2007. 21. A preliminary report on the recalcification of carious dentin. Finn SB. Straffon LH. 14. Pinto AS. McDonald RE. ed. Remineralization of carious dentin treated with calcium hydroxide. 23. Stuttgard: Thieme. Fejerskov O. Bjørndal L. Bjørndal L. Nör JE. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Sigurdsson A. Kerkhove BC. van Strijp AJP. The effect of calcium hydroxide on deep carious dentin. Al-Zayer MA.41:269. 1998:157–78. J Int Assoc Dent Child 1977. de Araujo FB. Caries Res 1997. Thompson VP.55:197–203. J Dent Child 1967. de Araújo FB. JOE — Volume 34. Pediatr Dent 2003. 13. Endodontic Topics 2002. Gen Dent 2007. 18. et al.8:36 – 40. 10. 22. Paddick JS. Pulp-dentin biology in restorative dentistry. Mjör IA. Bjørndal L.2:99–105. Ltd.34:192–201. Treatment of profound caries to prevent pulpal damage. Welch KB.2:10 –23. Clinical manifestation and diagnosis. Caries Res 2000. 25. Marchi JJ. Number 7S. Straffon LH. Pitt Ford TR.71:2467–72.status of inclusion. Fröner AM. 16.103:498 –506. Massler M. Bruun G. Sundell SO. et al. eds. Gunawan MIM. Phenotypic and genotypic selection of microbiota surviving under dental restorations. Kidd EAM.32:218 –25. Thylstrup A. En praksis baseret undersøgelse (English summary). Dental caries: characteristics of lesions and pulpal reactions. Attitudes and expectations of treating deep caries: a PEARL network survey. Brailsford SR. 2008: 367– 83. Beighton D. In: Ørstavik D. Bjørndal L. 2nd ed. 27. 15. Lewis TM. et al. 17.34:502– 8. Ramdas M. Indirect pulp capping in the primary dentition: a 4 year follow-up study. Dental caries: the disease and its clinical management. Kidd EAM. 9. 2nd ed. 19. Beighton D. eds. Larsen T. Jr. Bjørndal L. Stepwise excavation of deep carious lesions in primary molars. Tandlægebladet 1999.14:1130 –7. A clinical and television densitometric evaluation of the indirect pulp capping technique. Larsen T. Appl Environ Microbiol 2005. 11. Caries Res 2007. Tronstad L. Sowden JR.25:29 –36.
Coll.Pulp Symposium Indirect Pulp Capping and Primary Teeth: Is the Primary Tooth Pulpotomy Out of Date? James A.5 mm of the pulp and the reparative dentin was involved.25– 0. Volume 30. Second. doi:10. It fixes or denatures the vital pulp so it is no longer pulp tissue in addition to its bactericidal properties. The AAPD guidelines further state that there is only one other choice for vital pulp therapy in primary teeth where caries approach the pulp. Conflict of Interest: James A. MS. The guidelines state the objective of a pulpotomy is to keep the remaining pulp healthy without adverse clinical signs or symptoms or radiographic evidence of internal or external root resorption. but is pulpotomy indicated for a carious pulp exposure? For deep caries with possible radiographic exposures that are asymptomatic. July 2008 . but especially those with reversible pulpitis compared with FP. What is the histologic and clinical research that can help dentists determine which teeth with deep caries are vital and.2008. Issue 3. pulp exposure. University of Maryland Dental School.3 mm of the pulp.34:S34-S39) Key Words Indirect pulp therapy. The difference occurs when the caries removal process results in a pulp exposure. no significant pathologic changes were evident in permanent teeth. IPT or pulpotomy? The purpose of this article was to review the dental literature and new research in vital pulp therapy to determine the following: (1) Is a pulpotomy indicated for a true carious pulp exposure? (2) Is there a diagnostic method to reliably identify teeth that are candidates for vital pulp therapy? (3) Is primary tooth pulpotomy out of date. IPT is clearly not indicated when the pulp is exposed by caries. candidates for pulpotomy? Reeves and Stanley (3) found that as long as the advancing edge of the carious lesion was 1. Address requests for reprints to Dr Coll at www. which is the better choice of treatment.033 he guidelines of the American Academy of Pediatric Dentistry (AAPD) on pulp therapy for primary and young permanent teeth states that a pulpotomy is a procedure in which the coronal pulp is amputated. DMD. thus. Baltimore. however. MS Abstract Formocresol pulpotomy (FP) in the United States is most frequently used to treat asymptomatic caries near the pulp in primary teeth. the radicular pulp might be preserved through minimal inflammatory insult by using a hemostatic agent such as ferric sulfate to form a clot barrier to preserve the deeper remaining pulp tissue. This article is being published concurrently in Pediatric Dentistry. according to Rodd (2). but research shows the majority of such teeth are nonvital or questionable for treatment with vital pulp therapy. and the tooth is restored to prevent microleakage. 0099-2399/$0 . a pulpotomy is then undertaken. Regarding the effect of pulp exposures on the pulp’s capacity to repair.joen. Maryland.1016/j.net. The third pulpotomy mechanism encourages the radicular pulp to heal and form a dentin bridge by using calcium hydroxide or mineral trioxide aggregate (MTA). Indirect pulp therapy (IPT) is also indicated and has a significantly higher long-term success. because the direct pulp cap in a primary tooth is contraindicated for carious exposures (1). First. then significant pathologic changes were noted. and should indirect pulp therapy replace pulpotomy? (J Endod 2008. For deep caries in primary teeth. it was questionable S34 Coll JOE — Volume 34. and should IPT replace pulpotomy? T Is Pulpotomy Indicated for Carious Exposures? A primary tooth pulpotomy should be performed on a tooth judged to have a vital pulp (1). is a paid consultant to the Maryland State Dental Board in the review of dental charts of pediatric patients. Pulpotomy is thought to be indicated for primary teeth with carious pulp exposures. The objectives of treatment are the same as for a pulpotomy (1). Coll. Shovelton (4) examined permanent teeth and showed that as caries approximated 0. Number 7S. After the coronal pulp is amputated. IPT has a significantly higher success in treating all primary first molars. May/June 2008. The articles are identical. Lin and Langland (5) showed that that when no pulp exposure occurred from caries. dmd1@comcast. The purpose of this article was to review the dental literature and new research in vital pulp therapy to determine the following: (1) Is a pulpotomy indicated for a true carious pulp exposure? (2) Is there a diagnostic method to reliably identify teeth that are candidates for vital pulp therapy? (3) Is primary tooth pulpotomy out of date. This choice is indirect pulp therapy (IPT). such as by using formocresol. After a carious exposure. IPT is a procedure in which the caries closest to the pulp is left in place and covered with a biocompatible material.1 mm from the pulp. Once the caries approached within 0. IPT purposely avoids an exposure by leaving the deepest decay in place. DMD.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. Either citation can be used when citing this article. pulpotomy From the Department of Pediatric Dentistry. and the remaining radicular pulp tissue is treated with a medicament or electrocautery to preserve the pulp’s health (1). hyperemia and pulpitis were seen. the remaining radicular pulp can be rendered inert. the pulp’s repair capacity was excellent. the indications for IPT and pulpotomy are identical for reversible pulpitis or a normal pulp when the pulp is judged to be vital from clinical and radiographic criteria (1). this leaves behind vital radicular pulp tissue that has the potential for healing and repair in 3 general ways.02.
soft dentin over the pulp. No clinical or radiographic sign of irreversible pulpitis. They also found that in teeth with a history of pain. Number 7S. Pain stopped from day glass ionomer placed. (8) tested stepwise caries removal versus conventional in 127 permanent teeth with a patient mean age of 10.Pulp Symposium Figure 1. Teeth without pulp exposures and no total necrosis likely as a result of trauma were histologically diagnosed as treatable with vital pulp therapy in 23 of 26 cases (88%). (f) Tooth 16 months after treatment without signs of pain or irreversible pulpitis clinically or on the radiograph. After 8 –24 months. (e) View of IPT with a glass ionomer base. 8). the lesion’s periphery is made cariesfree. and all the caries is removed. except in the midcoronal region. Rodd (2) stated that carious primary and permanent teeth showed similar neural changes when mounting a pulpal defense to deep caries. (9) studied severely decayed primary incisors with no pulp pathology in nonrestorable teeth from 20.to 42-month-old children. Bjorndal et al. 16 of 24 (67%) of the incisors judged to be nontreatable (total necrosis) or questionable (chronic partial pulpitis) for treatment with vital pulp S35 JOE — Volume 34. and unpredictable. thus increasing the risk of pulpal inflammatory breakdown (6). After fixation. (d) Two months after caries control. The lesion is then re-entered. July 2008 Indirect Pulp Capping and Primary Teeth . Many of these permanent tooth findings likely apply to primary teeth. Then. the pulp chamber would have an area of necrosis often extending into the radicular pulp. (b) Preoperative radiograph. Eidelman et al.2 years. Others have stated that the dentist risks displacing infected dentin chips into the pulp when performing total excavation of deep carious lesions. caries was removed with a slow-speed round bur. (c) View immediately after glass ionomer placement. Caries excavation is a 2-appointment procedure. Leskell et al. Example of using glass ionomer caries control to diagnose reversible pulpitis or food impaction in a mandibular first primary molar with a history of pain to chewing sweets and solid foods for 2–3 weeks. Stepwise caries removal in permanent teeth thought to have radiographic pulp exposures has been proposed as a method to minimize pulp exposures and preserve vitality (7. while the center of the caries is partially removed to leave moist. Initially. (7) found no pulp exposures on re-entry in 31 permanent teeth by using stepwise caries removal. calcium hydroxide and a temporary filling are placed for 6 –12 months. A sharp explorer was used to evaluate total caries removal and check for a pulp exposure. and showed a similar degree of vasodilatation and new vessel formation with caries progression. (a) Preoperative view. stepwise removal resulted in approximately 18% pulp exposure versus 40% for conventional caries removal. Rodd found that primary and permanent teeth have similar vascularity. By contrast.
Teeth with a carious pulp exposure have a low likelihood of being totally vital (9) and are. 14). the following conclusions can be made on using glass ionomer caries control: 1. A group of primary molars had GICC after minimal caries excavation for a mean time of 3. Dentists might think they can obtain a 90% level of pulpotomy success in such a case. leaving only 33% that were unquestionably vital. Loyola-Rodriquez et al. Radiographs and examinations excluded teeth with apical pathosis. Germany). Yet Are Candidates for Vital Pulp Therapy? Identifying those teeth with deep caries that are vital and treatable with vital pulp therapy leads to this article’s second purpose. From these histologic and clinical findings. 2000 (21) Casas et al.001) in the subsequent vital pulp therapy success (98%) versus the non-GICC group’s vital pulp therapy success (75%). This procedure takes less than 5 minutes and can be done at the initial examination visit of a child presenting with multiple open carious lesions. A glass ionomer temporary filling is then placed by using a material such as Fuji IX (GC America Inc. (13) showed in vitro that all glass ionomer liners had good antibacterial activity against Streptococcus sobrinus and S. The GICC group showed a significant increase (P . Stepwise caries removal will result in fewer pulp exposures than total caries removal performed in 1 visit (7.Pulp Symposium therapy had a carious pulp exposure. Another group of primary molars had no GICC. 2004 (11) Smith et al. nonpainful decay by using a slow-speed no. Another recently completed study reported on GICC’s diagnostic success in deeply cavitated carious lesions (16). The pulp’s repair capacity is excellent when the carious lesion remains 1 mm or more away from the pulp (3). IL). however. symptomless teeth with apparent radiographic exposures or near Coll JOE — Volume 34. The GICC intermediate therapeutic temporary restoration had to have remained intact without displacement for 1– 4 months. 4 or 6 round bur or spoon excavation. 2004 (22) Eidelman et al. From these microbiologic and clinical studies. Both groups had IPT or formocresol pulpotomy and were restored with an immediate steel crown the day of treatment and were followed for a mean time of more than 3 years. (26) calculated MTA success at 91%. 1). temporary restoration by using glass ionomer caries control (GICC) for 1–3 months before starting pulp therapy has been shown to be an excellent method of diagnosing the pulp’s vitality. TABLE 1. 2001 (23) Jabbarifar et al. They also reported a “drying out” effect of the moist caries on re-entry after GICC similar to that reported by Bjorndal et al. the second dentin samples showed that total bacterial counts decreased significantly (P . Regarding the effect of glass ionomer on the subsequent vital pulp therapy. Peng et al. (7) after 6 –7 months of stepwise caries removal. poor candidates for vital pulpotomy. (14) published an in vivo study of 32 primary molars with open deep carious lesions. 2002 (18) Huth et al. but the intermediate therapeutic temporary restoration should not be in occlusion. 4. the pain was diagnosed as reversible. (12) studied dentin samples in 40 primary molars before and after ART excavation. There was a subgroup of 18 teeth that presented with pain and/or a questionable diagnosis of their vitality. or a resin-modified glass ionomer. 2. however. carious dentin samples were taken. Voco Ionofil Molar AC (Voco Gmbh. Scanning electron microscopy inspection of dentin samples in the same time frames showed dentin reorganization and narrower dentin tubules. For the other 11. 2). Treating primary teeth with deeply cavitated carious lesions after minimal excavation with glass ionomer caries control for 1–3 months initially before instituting pulp therapy causes the bacteria to significantly decrease within the lesion (13. which was to describe a new method to reliably diagnose these teeth. In vital. Is There a Diagnostic Method to Identify Teeth with Deep Caries That Are Symptomless or Questionable. No anesthesia is used to perform minimal caries excavation with spoon excavators or slow-speed round burs and is a form of alternative restorative treatment (ART) (10) or stepwise caries removal (7). Numerous studies have reported on the biologic effects of a glass ionomer temporary filling. performing a pulpotomy likely increases the chance of displacing infected dentin chips into the pulp and impairing the pulp’s repair capacity (5. All received GICC initially for 1– 4 months to diagnose the tooth’s vitality. The total bacterial count and mutans streptococci were significantly reduced from the excavation process alone. The GICC produced the correct diagnosis for all the teeth in that 7 molars returned with signs of irreversible pulpitis and were extracted. The authors believed the results suggested that sealing the cavitated lesion with glass ionomer contributes to remineralization. After 30 and 60 days of temporization. and all were treated with vital pulp therapy successfully. no matter what form or type of pulpotomy procedure is used (1. would equal a 30% chance of a cariously exposed tooth having a successful pulpotomy. (15) reported on 32 permanent teeth after minimal caries excavation and temporization for longer time periods. Only the outer carious layer needs to be removed to accomplish this result.05). Cuxhaven. 2005 (19) Rolling and Thylstrup 1975 (20) Vij et al. (11) reported that GICC temporization for 1–3 months increased success of the subsequent vital pulp therapy from 79% to 92%. if the tooth has been asymptomatic and shows no signs of irreversible pulpitis clinically or on a new radiograph. MN). mutans associated with their fluoride release. and then minimal caries excavation was performed folS36 lowed by a resin-modified glass ionomer temporary filling. vital pulp therapy can be instituted by using IPT or pulpotomy (Fig. Alsip. thus.5 months. GICC is indicated in cavitated carious lesions to diagnose their vitality in teeth with signs and symptoms of reversible pulpitis or a symptomless tooth thought to have no pulpitis before instituting any pulp therapy (11). 2004 (24) Holan et al. 3. Number 7S. For teeth without carious pulp exposures. The simple mathematics of 33% (chance of finding a vital pulp) 90% (chance of pulpotomy success). Oliveira et al. counting internal resorption. Primary tooth pulpotomy requires a vital radicular pulp. and all bacterial strains had similar trends in both time periods. Initially. 2005 (25) Pulpotomy Formocresol 1/5 formocresol Formocresol Formocresol Ferric sulfate Ferric sulfate MTA MTA MTA Success (%) 92 85 70 70 74–80 67 100 94 91 Time (mo) 6–12 24 36 40 19 36 13 12 38 NOTE. The technique involves minimally removing the superficial. 6). Bonecker et al. the following conclusions can be drawn: 1. July 2008 . however. St Paul. All Types of Pulpotomy Usually Show Decreased Success over Time References Dean et al. Ketac Molar (3M ESPE. therapeutic. Vij et al. had a success rate of 67%. They concluded that total caries removal did not seem essential to stop caries progression. 8). Wambier et al. Internal root resorption was not always considered failure. Initially placing an intermediate. After 1–3 months of GICC. or the tooth was successfully diagnosed with irreversible pulpitis after 1–3 months of GICC. Diagnostic success was based on the vital pulp therapy success. Teeth temporized with zinc oxide– eugenol. A matrix band does not have to be used.
immediate restoration did not alter IPT’s success when steel crowns were compared with composite fillings and glass ionomers (11. and most had immediate steel crowns placed after pulpotomy. and 1% some other type of pulpotomy (electrocautery. 30). From a statistical standpoint. or time periods (Table 2. July 2008 Indirect Pulp Capping and Primary Teeth S37 . Most of these MTA pulpotomy studies were performed on teeth with symptomless radiographic exposures. Even using dental students of vastly different abilities and likely different techniques. treating them with caries control will likely stop caries progression (15). Vij et al. They Figure 2. exposures. with the possible exception of the 1 long-term MTA study (25). 17). 30). 20. Yet these reports generally are of shorter duration (only one 24 months (25)) and have small sample sizes ( 38 teeth) from which to draw strong conclusions. signifying the toxic concerns regarding formocresol do not seem to be a concern for most schools or practicing dentists. 2. Coll JA. dental schools as a method to treat deep asymptomatic caries. from calcium hydroxide (28 –30). 11. medicament. †Combined success of both groups. 18% ferric sulfate. whereas the other 24% taught ferric sulfate. Success rates of formocresol pulpotomy and indirest pulp therapy in the treatment of deep dentinal caries in primary teeth. Number 7S. most pediatric dentists believe it is best to enter the pulp and do a formocresol pulpotomy. 14). Is the Primary Tooth Pulpotomy out of Date for Treatment of Deep Caries and Should IPT Replace Pulpotomy? Knowing the pulpal diagnosis of primary teeth with deep caries by using GICC should greatly improve the chance of any vital pulp therapy. (11) studied IPT and pulpotomy success treating molars with reversible pulpitis pain. and the affected dentin likely remineralizes similar to dentin after stepwise excavation (7. Milnes (33) in 2006 disputed the cancer concern by stating that the amount of formocresol in a pulpotomy was likely such a small amount that formocresol pulpotomy was a low-exposure condition. IPT Studies Show Success Rates of 90% or Greater over Time with Differing Techniques and Medicaments IPT medicaments Nirschl and Avery 1983 (28) Al-Zayer et al. 1 child showed a 6-fold increase in white blood cell chromosomal abnormalities. Of the 689 pediatric dentists. 27). glass ionomer (11.S. Shelton P. 2000 (17) Calcium hydroxide Calcium hydroxide — Glass ionomer Glass ionomer Success (%) 94 95 90† 94 93 Time (mo) 6 14 (median) 24 40 50 Sample (N) 33 187 48 108 55 *Adhesive resin alone without a liner or calcium hydroxide liner and adhesive resin. etc). Falster et al. In addition. The type of final. as shown in Table 2. Pediatr Dent 2000. which had been TABLE 2. 17. A recent meta-analysis of MTA versus formocresol pulpotomy studies suggested that MTA was superior to formocresol as a result of its lower failure rate (26).* 2002 (30) Vij et al.Pulp Symposium used in other pulpotomy studies (17. MTA. dental schools and 689 of the board-certified pediatric dentists. JOE — Volume 34. and most dentists practice the way they were taught. Figure 2). even though long-term formocresol pulpotomy success is significantly lower than IPT (11.22:278 – 86. Kuwabara A. Even when no medicament was placed for IPT and the composite filling was bonded to the remaining decay and decay-free dentin. The 2005 survey (31) also had a clinical scenario question regarding deep caries removal in a primary second molar in a 5-year-old. (30) reported success greater than 90%. IPT usually shows success rates of 90% or greater no matter the technique. The MTA pulpotomy appears to have a higher long-term success rate ( 90%) than other pulpotomy types (23–25). 81% used diluted or full-strength formocresol. The International Agency for Research on Cancer stated in a 2004 press release that formaldehyde causes nasopharyngeal cancer (32). How are pulpotomy and IPT being taught and practiced in the United States? Dunston and Coll (31) in 2005 surveyed 48 of the 56 pediatric program directors in the U. 2003 (29) Falster et al. GICC for 1–3 months changes the character of the dentin so that it is drier and harder. (34) found that when studying the white blood cells after formocresol pulpotomy in 20 children. as reported by Al-Zayer et al. Using GICC as a diagnostic tool for 1–3 months in teeth with symptomless radiographic exposures or ones with pain and questionable vitality will diagnose those that can be treated successfully with vital pulp therapy 98% of the time (16). to none (30). 3.to 3-year follow-up grouping. 22) (Table 1. Seventy percent of the program directors and more than 80% of the pediatric dentists reported that a pulpotomy was the treatment of choice over IPT. There have been various medicaments used for IPT. Zazar et al. Long-term success rates of formocresol pulpotomy and IPT were statistically different starting in the 2. Other factors need to be considered when choosing IPT or pulpotomy for deep caries in primary teeth. did not significantly decrease IPT’s success below 95%. The immediate crown should have minimized microleakage and increased pulpotomy success compared with a large amalgam (27). all of which did not significantly change IPT’s success rates. They found that 76% of the dental schools taught either diluted or full-strength formocresol pulpotomy. (29). IPT’s long-term success (3– 4 years) surpasses all other pulpotomy studies. but further studies were needed to verify this. Formocresol remains the overwhelming choice for pulpotomy. This leads to the article’s third purpose: Is IPT or pulpotomy the best choice for vital pulp therapy for deeply cavitated carious lesions? Most pulpotomy success decreases over time from 90% or more initially (6 –12 months) to 70% or less after 3 years or more (11. 20.S. they believed formocresol was not mutagenic. 2004 (11) Farooqet al. Figure 2). Reproduced with permission from Forooq NS. It appears that IPT is not emphasized in U.
it also showed a significantly lowered success for formocresol pulpotomy in primary first molars. Finally. The following conclusions on choosing IPT or pulpotomy can be drawn from these studies: 1.29:228 –34. Int Dent J 1968. A pain in the pulp: innervation inflammation and management of the compromised primary tooth pulp—synopses. 18. 3. Guedes-Pinto AC.18:392– 405.22:278 – 86. is potentially less painful. Pediatr Dent 2001. Kenny DJ. Khademi A. Lin L. 31:423– 8. 13.22:59 – 65. Newsl Aust N Z Soc Paediatr Dent 2005. Oral Surg 1966. 30). J Dent 2003. IPT has been shown to have a significantly higher success rate for teeth with reversible pulpitis compared with formocresol pulpotomy (11). Another concern in the choice of using IPT or pulpotomy is the early exfoliation of pulpotomized teeth. Effectiveness of 4 pulpotomy techniques: randomized controlled trial. dos Santos FA. whereas the IPT requires no pulpal entry and. Ridell K. 4. Maltz M. Pediatr Dent 2007. Int J Paediatr Dent 2002. 20. Bjorndal L. Toi C. 24. because profound anesthesia is always needed for a pulpotomy. and the carious dentin that had been left behind cultured. on the basis of published dental insurance reimbursement for the 2 procedures (35. Pediatr Dent 2004. has fewer potential side effects. 17. Stay out of the pulp by using IPT for a higher long-term chance of success compared with formocresol and ferric sulfate pulpotomy. A 3-year clinical follow-up study of pulpotomized primary molars treated with formocresol technique. 2007. IPT or pulpotomy can be performed. higher success longterm. 19.31:411–7. Smith NL. They also found that there was significantly (P . When the data of Holan et al. Fontanella V. 2. 4. 36).6:304 –7. Lindquist R. and does not exhibit early exfoliation as pulpotomy does (11. Jabbarifar SE. which might result in less utilization. whereas IPT-treated teeth exfoliate normally (11. 20. IPT is less expensive. 14. Garcia-Godoy F. (15) studied 32 permanent teeth judged by radiographs to have a pulp exposure. Paschos E. Cvek M. Crit Rev Oral Biol Med 2004. MD: University of Maryland Pediatric Dental Department. Endod Dent Traumatol 1996. and additional research is needed to see whether MTA pulpotomy performs as well as IPT. Campbell A.26:214 –20. Holan G. 12. 17). Mutans streptococci and lactobaccili in carious dentin before and after atraumatic restorative treatment. what are the concerns of leaving this decay after a 1-visit IPT? Aponte et al. Simionato MRL.26:44 – 8. In 28 of 30 teeth (93%). Pediatr Dent 2006. 10. Judd PL. 15. Pediatr Dent 1994. Cleaton-Jones P. Shelton P. 22. the choice of IPT or pulpotomy is up to the treating dentist. however. 4.04) than the 53% in 19 primary first molars treated with formocresol pulpotomy.32:3–5. Huth KC. Michaeli Y. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals.14:1372–5. 5. Stanley HR. Thylstrup A.15:99 –114. Most U. Coll JA. 29 months). Do not treat carious exposures in primary teeth with pulpotomy or direct pulp caps. 9. 36). July 2008 .04) low success (61%) when first primary molars were treated with formocresol pulpotomy compared with the 92% success with IPT in these molars. 7.51:292–316.12:192– 6. More than 35% of formocresol pulpotomies exfoliate significantly earlier ( 6 months) than nonpulpotomized teeth.23:15– 8. Baltimore. Pediatr Dent 2000. Ultrastructural and microbiological analysis of the dentin layers affected by caries lesions in primary molars treated by minimal intervention. From the present review of the literature and research. better exfoliation pattern. Fuks AB. Success rates of formocresol pulpotomy and indirest pulp therapy in the treatment of deep dentinal caries in primary teeth.16:346 –9. Pediatr Dent 2004. Ulmansky M. Forooq NS. Leskell E. IPT success was 85%.83:47–53. Clinical guideline on pediatric restorative dentistry: reference manual 200607. the residual carious dentin was sterile. Coll JA. Oral Surg 1981. Oliveira et al. Growth inhibition of glass ionomer cements on mutans streptococci. Reeves R. Wambier DS. and better success treating reversible pulpitis than pulpotomy. Larsen T. pulpotomies cost more than 2. Light and electron microscopic study of teeth with carious pulp exposures. Shovelton DS.84:1144 – 8. after 10 years in vivo. Rodd H. Thylstrup A. Loyola-Rodriquez JP. 6. The relationship of bacterial penetration and pulpal pathosis in carious teeth. Rolling I. 16. the 10-year prospective study by Mertz-Fairhurst et al. In the United States. (38) conclusively showed that in 85 teeth after obvious occlusal caries was successfully sealed from microleakage. Ghasemi D. et al. 3. Eidelman E. Number 7S. 17. Clinical guidelines on pulp therapy for primary and young permanent teeth: reference manual 2006-07. IPT shows higher long-term success rates than any pulpotomy other than possibly MTA (Tables 1 and 2). IPT has been shown to have a lower cost. Scand J Dent Res 1975. Ferric sulfate pulpotomy in primary molars: a retrospective study. J Dent Res 2005. Consider pulpectomy or extraction because S38 Coll JOE — Volume 34. Pediatr Dent 2006. Shelton P. Spangberg L. (27) were tested with 2 analysis. Bonecker M. References 1. Conclusions Controversy persists as to the best way to perform vital pulp therapy.22:192–9. Casas MJ. After 6 – 46 months (mean. The pulpotomy could be more painful. Pulp exposure after stepwise vs direct complete excavation of deep carious lesions in young posterior permanent teeth. Histopathology of the pain in primary incisors with deep dentinal caries. Dean JA. From digitized radiographs taken 6 –7 months after partial caries removal followed by temporary fillings. Majare I. Nunn ME. Mineral trioxide aggregate vs formocresol in pulpotomized primary molars: a preliminary report. Pediatr Dent 1992. Langeland K. AAPD. of the high chance of irreversible pulpitis and failure of vital pulp therapy after a carious pulp exposure. Caries Res 1997. 11. Farooq NS. Clin Oral Investig 2006. the amalgam and calcium hydroxide were removed. Use glass ionomer caries control for deep cavitated lesions to diagnose the status of the pulp with or without history of pain to attain the highest success for vital pulp therapy.Pulp Symposium reported that in 20 first primary molars with such pain. The monitoring of deep caries lesions after incomplete caries removal: results after 14-18 months. Jacqer RG. 3. Thesis: diagnostic success of the glass ionomer sedative filling determining pulpal vitality in primary molars with deep caries. Bergenholtz G. 2. Hajek-Al-Khatar N. 8. there was no progress of the caries in permanent teeth. For deep caries approaching the pulp. Seale NS. Sanders BJ. Fulkerson BT. Mack RB. (37) reported performing indirect pulp capping with calcium hydroxide followed by amalgam restorations in 30 primary molars. Carminatti G. Caries control and other variables associated with success of primary molar vital pulp therapy. A study of deep carious dentin. In addition. When performing IPT and leaving residual decayed dentin. 35. most dental insurers do not cover IPT for primary teeth.28:136 – 43. there was mineralized improvement in the carious dentin over time.12:177–82. therefore. Success rate of formocresol pulpotomy vs mineral trioxide aggregate in human primary molar tooth. pediatric dentists currently choose to use formocresol pulpotomy over IPT (31). Coll JA. 21. Oliveira EF. J Res Med Sci 2004. MTA pulpotomy has not been shown to be effective in treating teeth with reversible pulpitis. Pediatr Dent 2000. Eidelman E. Comparison of electrosurgical and formocresol pulpotomy procedures in children. Formocresol and ferric sulfate pulpotomy have a significantly lower long-term success for treatment of deep caries compared with IPT (11. 23. 2. which was significantly better (P . Johnston DH.S.3 times more than IPT.28:144 – 8. American Academy of Pediatric Dentistry. Long-term outcomes of primary molar ferric sulfate pulpotomy and root canal therapy. 17. the following conclusions can be made: 1. Controversies in endodontics. For a tooth with deep caries 1 mm away from the pulp.10:134 –9. Kuwabara A. Vij R.
International Agency for Research on Cancer. J Am Dent Assoc 1998. Ye L. J Dent 2003. 32. Al-Zayer MA. Keltz N. J Can Dent Assoc 2006. Zazar PA. Rosenblatt A.htm. Accessed November 23. Rueggeberg FA. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006. Welch KB. Takahashi CS. J Dent Child 1983. Zhou X. Pediatr Dent 2002. 30. Peng L. Holan G.30:42– 48. Mertz-Fairhurst EJ. 29. Dunston B. June 15. 27:129 –36. 2007. Pediatr Dent 2008.iarc. Evaluation of the formocresol vs mineral trioxide aggregate primary molar pulpotomy: a meta-analysis. 36.asp. Costa Jr LA. Adair SM. Hartsook JT. Available at: http://www.fr/ENG/Press_Releases/archives/pr153a. Pediatr Dent 2005. 35. IARC classifies formaldehyde as carcinogenic to humans. Indirect pulp treatment: In vivo outcomes of an adhesive resin system vs calcium hydroxide for protection of the dentin-pulp complex. Creighton International dental fee schedule for Pennsylvania. Pediatr Dent 2003. 34. 38.com/ FeeSchedule/FeeScheduleDownload. Coll JA. J Dent Child 1966. 31. Accessed November 23.dentalbenefitsplus.Pulp Symposium 25. 2008. Aponte AJ. Available at: http:// www. Crowley MC. World Health Organization. Falster CA. Persuasive evidence that formocresol use in pediatric dentistry is safe. A survey of primary tooth pulp therapy as taught in US dental schools and practiced by diplomates of the American Board of Pediatric Dentistry. Fuks AB. JOE — Volume 34. Indirect pulp capping verified. 28.25:29 –36. Pediatr Dent 2002. Accessed February 27. Feigal RJ. Curtis JW. Ergle JW.50:25–30.33:164 – 6. 153.129:55– 66. Press release no. Avery DR. 37. Eidelman E. Takeuchi PL. Indirect pulp treatment of primary posterior teeth: a retrospective study. Straffon LH. Long-term evaluation of pulpotomy in primary molars using mineral trioxide aggregate of formocresol. Number 7S.com/care/jump.nationalinsurancestore.31:479 – 85. 2004. 27. Nor JE. Araujo FB. Available at: http://www. Dental Benefits Plus fee schedule.html. Nirschl RF.102:e40 – 4. Evaluation of a new pulp capping agent in indirect pulp therapy. 26. Milnes AR. Fuks AB. Straffon LH. 33. Ultraconservative and cariostatic sealed restorations: results at year 10.24:241– 8.24:212– 6. 2007.72:247– 8. Holan G. Success of formocresol pulpotomy in primary molars restored with steel crowns vs amalgam. Formocresol mutagenicity following primary tooth pulp therapy: an in vivo study. Tan H. July 2008 Indirect Pulp Capping and Primary Teeth S39 .
DDS. through a thorough review of the relevant literature. In 2002–2003.” which. some of which have shown efficacy equivalent to formocresol.4 mg/day from food. The World Health Organization (WHO) (2) has estimated that daily consumption of formaldehyde approximates 1.2008. (J Endod 2008. Conflict of Interest: Alan R. numerous investigations for alternatives to formocresol. This article is being published concurrently in Pediatric Dentistry. formocresol. 4 cotton pellet that has been squeezed dry. Key Words Carcinogens.02– 0. human cells are physiologically equipped to manage this exposure through multiple pathways for oxidation of formaldehyde to formate and incorporation into biologic macromolecules via tetrahydrofolate-depen- S40 Milnes JOE — Volume 34. May/June 2008. Department of Health and Human Services.10 mg.S.5–14 mg/day (mean.Pulp Symposium Is Formocresol Obsolete? A Fresh Look at the Evidence Concerning Safety Issues Alan R. devitalization approach of formocresol pulpotomy or primary tooth pulpectomy. and the U. PhD. biologic approach to pediatric pulp therapy is preferable to the absolutist.55 mg of formaldehyde per day (1). Formaldehyde is found in the air we breathe. The purpose of this review was to examine more recent research about formaldehyde metabolism.4 ppm of formaldehyde (6). doi:10.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. Canada. As a result. and 0.008 Pharmacokinetics of Formaldehyde Humans produce endogenous formaldehyde as part of normal cellular metabolism. This commentary will demonstrate. Milnes. Formaldehyde. in turn. Importantly however.8 mg/day). although daily intake from food is difficult to evaluate. assuming a 1:5 dilution of formocresol placed on a no. 7. oxidative demethylation. there are no estimates of pediatric exposure. Assuming a contribution of 9. Environmental Protection Agency. Health Canada (5) found formaldehyde levels of 2– 81 ppb in homes in Prince Edward Island and Ottawa. however.03. which resulted in erroneous conclusions. In unpopulated areas. pharmacokinetics. formaldehyde. Address requests for reprints to Dr Milnes at angelmanguel@shaw. Number 7S. and consequently. that the “evidence” for banning this medicament because of safety concerns has been either misinterpreted or replaced by better science. Second-hand cigarette smoke might contain up to 0. The National Institute for Occupational Safety and Health (7) in the United States has stated that formaldehyde is immediately dangerous to health and life at concentrations of 20 parts per million (ppm) and higher. T Ubiquity of Formaldehyde Daily formaldehyde exposure is a fact of life. DDS. and purine and pyrimidine metabolism have all been shown to produce formaldehyde (9). The articles are identical. which are summarized in Table 1. is a hazardous substance and is considered a probable human carcinogen by the International Agency for Research on Cancer. however. These results indicated that formaldehyde is probably not a potent human carcinogen under low exposure conditions. Owen et al (3) estimated that North Americans eating a typical North American diet ingest 11 mg/day. the Agency for Toxic Substances and Disease Registry in the U. Health Canada. The human body is physiologically equipped to handle formaldehyde through multiple conversion pathways. is used for the biosynthesis of macromolecules including DNA and RNA. toxicity Private practice in Kelowna. formocresol use in pediatric pulp therapy is obsolete. July 2008 . although it is likely that children are exposed to lower amounts because of lesser food intake. Amino acid metabolism. Canada. Reevaluation of earlier research that examined potential health risks associated with formaldehyde exposure has shown that this research was based on flawed assumptions. The estimated formaldehyde dose associated with 1 pulpotomy procedure. it is highly unlikely that the elimination of the microgram quantities of formaldehyde associated with formocresol pulpotomy will have a significant impact on a child’s daily exposure. have been completed. 1 mg/day from inhalation. Milnes. Volume 30. Given the environmental ubiquity of formaldehyde and the recognized daily intake by humans.joen.34:S40-S46) he suggestion has been made recently that formocresol use in pediatric dentistry is unwarranted because of safety concerns. There have also been instances of high concentrations of formaldehyde in the air inside homes. Either citation can be used when citing this article.1016/j. Humans inhale and ingest formaldehyde daily. At present. and the food we eat (1). Issue 3. 0099-2399/$0 . however. Extrapolation of these research results to pediatric dentistry suggests an inconsequential risk associated with formaldehyde use in pediatric pulp therapy. chemistry. an adult takes in 10. and produce formaldehyde during cellular metabolism. British Columbia. outdoor air contains approximately 0. the water we drink.2 parts per billion (ppb) formaldehyde. reports no financial interests or potential conflicts of interest. Hileman (8) has shown that endogenous levels of metabolically produced formaldehyde range from approximately 3–12 ng/g tissue. pulpotomy. PhD Abstract Concern has been expressed about the safety of formocresol use in pediatric dentistry. and research into alternatives is not only welcome but absolutely essential.15 mg/day from water. The resultant single carbon atom released during metabolism is deposited in the “1-carbon pool. is approximately 0. and carcinogenicity. There can be no doubt that a reparative. air concentrations range between 10 and 20 ppb. There are other numerous sources of formaldehyde exposure. In populated areas with truck and automobile traffic. a primary component in formocresol.S.ca.
Formate might be converted to a soluble sodium salt via alternative pathways and excreted in the urine. the liver converts formaldehyde to carbon dioxide at a rate of 22 mg/min (3. Ingested formaldehyde is readily absorbed by the gastrointestinal tract and exhibits little subacute toxicity after oral exposure (17). and other amino acids that are incorporated into RNA. false. and proteins during macromolecular synthesis. These studies have been widely quoted as evidence that formaldehyde is distributed to distant sites. methylene cross-links (28. in turn. thymidine. which is further oxidized to carbon dioxide and water by the action of formyltetrahydrofolate synthetase (13).4 ppm for 2 hours) and in unexposed controls. and lungs. In dogs. 50. inhalation. Exogenous formaldehyde has a biologic half-life of 1–1. and 173. Heck et al (16) used gas chromatography and mass spectrometry to measure blood formaldehyde concentrations in Fischer 344 rats exposed to a very high formaldehyde concentration (14. In dermal studies. kidney. Hence. Casanova et al (18) reported that the formaldehyde concentrations in the blood after prolonged exposure to a high concentration of inhaled formaldehyde (6 ppm for 6 hours per day. 1-carbon biosynthetic pathways. In an unrelated study. Casanova-Schmitz et al (34) sampled the venous blood of rats after injecting either [14C]formaldehyde or [14C]formate into the tail vein. 15). and nasal respiratory mucosa (12). The half-life of formaldehyde molecules in monkey blood is about 1. These results excluded the possibility that the labeling of macromolecules is due to formation of protein adducts by formaldehyde. S41 JOE — Volume 34. 14C. which.1 mmol/L. Heck et al (16) exposed 6 human volunteers for 40 minutes to 1. in a second slower reaction involving recruitment of a second amino group. In humans. were very small (1% of the total administered dose) (21. with the relative proportion depending on the route of administration (25. and monkeys showed that formaldehyde labeled with radioactive carbon (14C) was apparently distributed among the muscle.Pulp Symposium TABLE 1. but it is not distributed throughout the body because it is so rapidly metabolized (16). the conversion of formate to carbon dioxide and water results in a biologic half-life for formate of about 80 –90 minutes (13).5 minutes after intravenous infusion (20).0 mg/L. In rat and monkey tissues. Myers et al (32) and Pashley et al (33) concluded that [14C]formaldehyde is absorbed systemically from pulpotomy sites. formaldehyde was absorbed less readily by monkeys than by rats or guinea pigs (19). A concurrent rise in formic acid levels occurs. and dermal exposure. Experiments in humans. and humans was 2. 29). metabolism of formaldehyde and its elimination by pathways other than DPX formation overwhelmingly predominate (30). and not covalent binding. In rhesus monkeys. Formate is the principal oxidative product of formaldehyde. 0. The profiles of radioactivity in the blood after these injections were similar. The investigators in these studies. did not determine whether the labeling of tissues occurred by metabolic incorporation of the [14C] moiety of the labeled formaldehyde into macromolecules after the labeled formaldehyde molecule had been metabolized or by covalent binding (formation of protein adducts) by radiolabeled formaldehyde molecules. formaldehyde’s metabolism after administration via the pulp chamber is also rapid. whereas both [14C]formaldehyde and [14C]formate are precursors for macromolecular synthesis by the 1-carbon pool. Number 7S. however. 31–33). Results from dental pulp studies involving rats. July 2008 Is Formocresol Obsolete? .5. Sources of Human Formaldehyde Exposure (4) Atmospheric formation: photochemical oxidation of organic compounds Internal combustion engine exhaust Fertilizer production Hydrogen sulfide scavenger: oil operations Household products: Dishwashing liquid Antiseptics and disinfectants Carpet cleaners Carpets Preservatives and embalming solutions Cosmetics (maximum concentration. and the majority of conversion reportedly occurs within 2 hours after administration (21). Exogenous formaldehyde is taken up into the human body via ingestion. is used for the biosynthesis of purines. The single carbon atom released during metabolism of formaldehyde and formate is deposited in the “1 carbon atom” pool.3% v/v): Fingernail hardeners (maximum concentration. Human experiments have also provided compelling evidence that inhaled formaldehyde has virtually no impact on blood concentrations of formaldehyde. indicating formaldehyde’s metabolism (20). forming unstable hydroxymethyl protein adducts (DNA-protein cross-links [DPX]) and. heart.5 minutes (22) and is quickly cleared from human plasma. They showed that the blood concentrations of the 2 groups were virtually identical. respectively) than in unexposed workers (17 mg/L) (27). Formaldehyde also reacts covalently with amino and sulfhydryl groups in target tissues and with DNA.9 ppm formaldehyde (a concentration that is considered slightly irritating to the nasal and conjunctival membranes). and rats have shown no significant differences in formaldehyde concentration in the blood before and immediately after exposure by inhalation. and glutathione-dependent and glutathione-independent dehydrogenases are important enzymes in the metabolism of formaldehyde in hepatocytes (10). In rats. and expired air. but the concentrations before exposure were not significantly different from those measured immediately after exposure. The quantities of radiolabeled chemical detected. regardless of whether [14C]formaldehyde or [14C]formate was the source of 14 C. spleen. dogs. oral mucosa (11). DNA. however. mitochondrial aldehyde dehydrogenase. 26). monkeys. In mice and rats. Cytosolic alcohol dehydrogenase.15 g/g (mean standard error) or approximately 0. 23. liver. Higher urine concentrations of formic acid were found in 3 of 6 workers occupationally exposed to unspecified concentrations of formaldehyde in air (30. They verified that labeling of proteins and target tissues was due to metabolic incorporation of the radiolabeled metabolite of formaldehyde.70 0. Inhaled formaldehyde appears to be readily absorbed by the upper respiratory tract. in fact. 5% v/v) Paper products Adhesives Tire and rubber manufacturing Latex paints Resin production: Phenolic-formaldehyde resin Urea-formaldehyde resin Pentaerythritol resin Permanent press fabrics Manufactured wood products Forest and brush fires Tobacco products dent. 24). feces. The average formaldehyde concentration in the blood of rats.0. monkeys. because only [14C]formaldehyde is capable of forming protein adducts. however. it appears that the claims of systemic distribution in dental publications have been overstated and are. 5 days per week for 4 weeks) had no significant effect on the formaldehyde concentration in blood relative to preexposure levels. the metabolites of formaldehyde are eliminated in urine. or it might be incorporated into the 1-carbon pool for use in biosynthesis (14.
these authors found that formocresol did not produce detectable DNA damage and should not be considered genotoxic. cultured human fibroblasts. In addition. Those published articles. Last. micronuclei and chromosomal aberrations (42). which presumably would allow for deeper tissue fixation by the formaldehyde component of formocresol (35. (2) lack of detectable protein adducts or DPX in the bone marrow of glutathione-depleted (metabolically inhibited) rats exposed to [3H]formaldehyde and [14C]formaldehyde at concentrations as high as 10 ppm (22. July 2008 . Cresol has poor solubility. it has been assumed that it does not enter systemic circulation (35). a by-product of tricresol oxidation (38). 36).5–15 ppm for 6 hours per day for 5 days failed to detect either chromosomal aberrations or SCEs at any of the formaldehyde concentrations. represent the same study. Cresol is highly lipophilic. and excreted as hippuric acid. which are used in endodontic procedures. Dental studies have not supported the contention that formaldehyde. It has also been proposed that formaldehyde could induce the development of DPX at distant sites. and has been shown to completely destroy cellular integrity. intraoperatively. however. and the allowable daily intake. Peripheral venous samples were collected from each child immediately before and 24 hours after the pulpotomy. DPX are unlikely to occur. no mutagenesis occurred in cultured human lymphocytes below a formaldehyde threshold of 5 g/mL in the culture medium (56). and postoperatively from 30 children. conjugated with glycine in the liver. is mutagenic. (3) lack of detectable DPX in the bone marrow of rhesus monkeys exposed to [14C]formaldehyde at concentrations as high as 6 ppm (46). as used in dentistry. 47). as a result of formaldehyde exposure. and a series of formocresol dilutions similar to clinical doses. is 5 mg/kg (39. Zarzar et al (57) performed formocresol pulpotomy on 20 children by using Buckley’s original formula (19% formaldehyde and 35% cresol in a solution of 15% glycerin and water). Although Kerns et al (51) discussed the formaldehyde’s mutagenic potential in their animal model. including sister chromatid exchanges (SCEs). It also occurs naturally in many plants. whereas root canal sealer remains in the root canal and forms part of the final restoration. Benzyl alcohol. not mutation (55). Blood samples were examined for formaldehyde and cresol content by using gas chromatography and mass spectrometry detection. 40). no human studies have been published that have examined plasma concentration after exposure to cresol. It has no carcinogenic or mutagenic potential. They have regularly cited 2 studies as evidence of the genotoxic and mutagenic effects of formaldehyde (50. With a mouse lymphoma cell line. and because of this. with the potential for further release of formaldehyde. were associated with cytotoxicity. Furthermore. For several reasons. cresol. Cytogenetic studies (54) of lymphocytes from rodents after formaldehyde inhalation with exposures ranging from 0. have demonstrated cytotoxicity (60). Number 7S. however. Casas et al (49) have been critical of formocresol use in pediatric dentistry. in fact. 59) reported 2 studies that assessed the mutagenic potential of formocresol as well as several other chemicals commonly used in dentistry. Genotoxicity. contact of formocresol with vital pulp tissue during pulpotomy is restricted to only a few minutes. Ribeiro et al (58. they did not report results pertaining to mutagenicity. DPX have been shown to occur only at the site of initial contact in the nasal mucosa of rats and in the upper respiratory tract of monkeys exposed to formaldehyde (45. The authors observed chromosomal aberrations in 1 (5%) of the 20 patients but were unable to determine whether formocresol or other variables accounted for this finding. has received little attention in the debate about formocresol safety or in investigations of formocresol efficacy. however. Neither formaldehyde nor cresol was detected in any blood sample. No data exist regarding cresol metabolism or elimination in humans or other mammals. In vitro experiments with a Chinese hamster cell line (43) found that DPX and SCE. and Cytotoxicity Exposure of cells to formaldehyde leads to the formation of DPX (41). Also. No statistically significant differences were found between the 2 groups in terms of chromosomal aberrations. high as 15 ppm (41) or of mice receiving intraperitoneal injections of formaldehyde at doses as high as 25 mg/kg (48). At ambient concentrations consistent with environmental exposures. Mutagenicity. 46). A recent clinical study in Colorado has reexamined the issue of systemic distribution of formocresol (37). and lymphocytes were collected from each blood sample for cell culture and cytogenetic analysis. Quievryn and Zhitkovitch (53) have shown that DPX do not persist in tissues for more than a few hours and undergo either spontaneous hydrolysis or active repair by proteolytic degradation of cross-linked proteins. including raspberries and tea. these investigations are not comparable to formocresol pulp studies. chromatid breaks. Levels of formaldehyde-induced DPX are considered to represent a good molecular dosimeter of formaldehyde exposure at sites of contact and are frequently used for risk modeling and prediction of formaldehyde carcinogenicity for different species (44 – 46).Pulp Symposium Pharmacokinetics of Cresol The second active ingredient in formocresol. Laboratory investigations of root canal sealers containing formaldehyde. and is an essential ingredient in many essential oils (39). and deletions (43). with the first article reporting interim results of nasal tumor development in rodents (50) and the second (3 years later) (51) reporting the final results for the same study. Benzyl alcohol is present as a bacteriostatic preservative in many multidose intravenous drugs and solutions (39). The authors attributed their negative results to formaldehyde’s pharmacokinetics. was detected in microgram quantities in a dose-response fashion in blood samples collected after placement of formocresol-containing pellets. Moreover. and there is virtually no information about environmental sources of cresol to which humans might be exposed. Benzyl alcohol is oxidized rapidly to benzoic acid. A larger quantity of formaldehyde is released from root canal sealers than during pediatric formocresol pulpotomy because of the large quantity of sealer used. 51). The outcomes of these studies have included the following: (1) lack of detectable protein adducts or DPX in the bone marrow of normal rats exposed to formaldehyde labeled with radioactive hydrogen (3H) or carbon (14C) at concentrations as high as 15 ppm (34). or chromatid gaps. each of whom received comprehensive dental treatment including at least 1 pulpotomy under general anesthesia. and (4) failure of formaldehyde to induce chromosomal aberrations in the bone marrow of rats exposed to airborne concentrations as S42 Milnes JOE — Volume 34. however. This calls into question the role of DPX in formaldehydeinduced carcinogenesis. but no convincing evidence has been obtained from in vivo experimental studies. The most common types of DNA damage induced by formaldehyde are clastogenic lesions. More recent research by Heck and Casanova (52) has revealed that the development of DPX in the nasal tissues of rats and the upper respiratory tracts of primates is associated only with exposure to high doses of formaldehyde. Blood samples were drawn preoperatively. as established by WHO. Zarzar et al concluded that formocresol is not mutagenic. as was stated by Casas et al.
Some clarification of the press release is required. July 2008 Is Formocresol Obsolete? . have recognized that significant anatomic and physiologic differences between humans and other animal models have confounded extrapolation of animal data to humans (29. The model developed by CIIT overcomes problems associated with the standard risk assessment methods cited by the USEPA and the IARC.75 ppm) (62). mechanistic. 69 –71). The resultant toxic effects at these initial contact sites include ulceration. Hence. the International Agency for Research on Cancer (IARC) (65. and peer reviewers. integrating toxicologic. Leukemia was not observed in any of 7 long-term inhalation bioassays in rodents. however. ematically evaluate the cancer risks associated with formaldehyde inhalation (71). the CIIT researchers published a thorough evaluation of potential cancer risk from formaldehyde.S. Number 7S. Health Canada has stated that it considers the CIIT dose-response model (71) “to provide the most defensible estimates of cancer risk. the IARC reclassification was based primarily on the results of a single National Cancer Institute (NCI) study (44) among workers in formaldehyde industries. Those opposed to formocresol use in pediatric dentistry have cited the work of Swenberg et al (50) and Kerns et al (51) to support their argument about carcinogenicity. The Organization for Economic Cooperation and Development has stated. The CIIT researchers also developed a biologically motivated computational model. The improved understanding garnered from this research allowed the researchers to improve the accuracy of computergenerated predictions of the uptake and absorption of formaldehyde in each animal model. CIIT suggested that cancer risk is negligible until formaldehyde exposure reaches the levels associated with cytotoxicity (in the range of 600 –1000 ppb). in fact. 5 days per week for 24 months. Finally. under any circumstances. formaldehyde was classified as a “probable human carcinogen” by Health Canada (63. the argument that the microgram quantities of formaldehyde applied to pediatric pulp tissue for a few minutes will induce distant-site genotoxicity is not supported by the available evidence. these regulators (Health Canada. 64). replaced the inaccurate default assumptions that had been used by the regulatory authorities.S. hyperplasia.S. Department of Health and Human Services. These high-dose responses. however. the experimental conditions that resulted in nasal cancers in rodents in no way resemble the conditions associated with a 5-minute exposure to microgram quantities of formaldehyde. These 2 studies are. and DPX data. for formaldehyde the answer to this question is yes. however. More importantly. the IARC classification serves as a hazard identification. 71). On the basis of these investigations (55.Pulp Symposium In summary. That study included many workers at several plants. were more than 1000 times the typical human environmental exposure and 8 times the U. The formaldehyde concentrations that resulted in cancer. the Agency for Toxic Substances and Disease Registry (ATSDR) (62. and it was not observed in 3 drinking water S43 Carcinogenicity It is indisputable that cancer develops in experimental animals after inhalation of air with high concentrations of formaldehyde. 2005). cell proliferation data. on the basis that it encompasses more of the available biological data. We believe that the CIIT modeling effort represents the best available application of mechanistic and dosimetric science on the dose-response for portal of entry cancers due to formaldehyde exposure” (74). The IARC classification is not an assessment of risk but merely an attempt to answer the question of whether. A 2004 IARC press release (66) reclassified formaldehyde from a “probable” to a “known” human carcinogen and has been cited as evidence that formaldehyde should be eliminated from pediatric dentistry (49). with Swenberg et al reporting interim results after 18 months and Kerns et al reporting final results for the same study after 30 months. the author requested clarification from the head of the IARC Monographs Programme regarding a threshold dosage for carcinogenicity of formaldehyde. or readers will be left with the impression that the IARC classification is definitive and binding. These new experimental data. This is because. Although they lacked sufficient evidence to demonstrate the development of cancer in exposed humans. occupational exposure limit (0. that “taking into account the extensive information on its mode of action. 66). Clearly. the NCI has agreed to update the study. 67) in the U. formaldehyde is not likely to be a potent carcinogen to humans under low exposure conditions” (73). Dr Vincent Cogliano responded “the evaluations at IARC Monograph meetings concern only whether an agent can increase the risk of cancer at some dose. Researchers at the Chemical Industry Institute for Toxicology Centers for Health Research (CIIT) (70. according to a large body of undisputed evidence. “The dose response value in the EPA Integrated Risk Information System (for formaldehyde) is based on a 1987 study and no longer represents the best available science in the peer-reviewed literature. 71) developed dynamic 3-dimensional airflow models that accurately depicted both airflow and regional deposition of formaldehyde on mucosal surfaces of rodents. on the basis of combined rodent and primate data from the computer-generated nasal cavity airflow models. Pediatric pulp therapy with formocresol as recommended would be considered a “low exposure condition. direct contact between the formaldehyde and susceptible tissues. This group of researchers showed that nasal squamous cell carcinoma developed in Fischer 344 rats exposed to formaldehyde gas at concentrations of 6 ppm and higher for 6 hours per day. and humans. DPX’s development has been demonstrated only after prolonged exposure to formaldehyde at specific contact sites such as the nasopharynx. August 5. we did not discuss a possible threshold” (personal communication. These cancers occur as a result of long-term. In fact. as experienced by a child undergoing formocresol pulpotomy. however. ATSDR. monkeys. and squamous metaplasia and “are considered to contribute to the subsequent development of cancer” (61). Clearly. with input from the USEPA. 71). confounding variables might have affected the results. Moreover. Thus. on the basis of the CIIT research models. The resulting estimates of cancer risk are many orders of magnitude lower than the 1987 and 1991 USEPA estimates (55. Health Canada. are unlikely to occur at sites distant from the point of initial formaldehyde contact (such as the bone marrow). and the U. and USEPA) and advisory agency (IARC) predicted the cancer risk posed by low-dose exposure by extrapolating from the laboratory animal data previously cited. Environmental Protection Agency (USEPA) (68). they are not representative of human experience. We do not undertake dose-response analyses. This model allowed them to math- JOE — Volume 34. Various researchers. the same study. and dosimetric data (55). derived from sophisticated mathematical models. but only a small number of people working at a single plant were found to have a rare form of cancer. thereby offering considerable improvement over default” (72). The possibility that inhaled or ingested formaldehyde might induce cancers at sites distant from the respiratory or gastrointestinal tracts has been investigated in numerous long-term toxicity studies performed in rodents (61). a substance could produce cancer in humans. Recognizing these uncertainties. Therefore. the first step in a multilevel risk assessment process. Until recently. Those who have argued against the continued use of formocresol in pediatric dentistry on the basis that “formaldehyde causes cancer” have failed to recognize this very important distinction.” The USEPA Office of Air Quality Planning and Standards has stated. consequently. formaldehyde is not delivered to these distant sites.
or topically applied formaldehyde to distant sites. numerous randomized controlled trials examining both IPT and MTA have since been published. When used judiciously. one from the NCI (44) and the other from the National Institute of Occupational Safety and Health (77). however. Doi et al (82) found that the prevalence of immunoglobulin E sensitization to formaldehyde was very low among Japanese children. Antibiotics are used in dentistry at least as often as formocresol. in this case leukemia. however. a 1:5 dilution of Buckley’s formocresol is recommended. or immune sensitization associated with the proper use of formocresol in pediatric pulp therapy can be considered inconsequential. is genotoxic or immunotoxic or poses a cancer risk to children who undergo one or more formocresol pulpotomy procedures. a study of British chemical workers. The reader is referred to articles in this issue by Fuks and Coll for more detail about these promising alternatives. No data exist to verify the actual amount of formocresol delivered to the pulp during the performance of a formocresol pulpotomy. These chemicals are used in pediatric dentistry without warnings to parents and patients of the associated risks. and the data are unreliable because of a lack of critical detail and questionable histopathologic conclusions. especially given that the effects of the 2 formulations are equivalent (83). the researchers in each instance failed to use recognized epidemiologic criteria to evaluate the hypothesis that formaldehyde exposure leads to cancer.S. The dilution should be performed in the local pharmacy to ensure accuracy. did not support a strong causal relation between formaldehyde exposure and leukemia. and each year numerous children and adults are injured or die as a result of allergic or anaphylactic reactions to antibiotics (85). Therefore. The results of 2 large American studies. formocresol is a safe medicament.5 g/L. there are multiple pathways for detoxification. bonding agents.Pulp Symposium studies in which rodents were exposed to doses as high as 1. mutagenesis. in which Wistar rats were exposed to doses as high as 1. pediatric dentists who wish to continue to use formocresol should apply the lowest dose S44 Milnes JOE — Volume 34. A Canadian study (81) of urea formaldehyde foam insulation from products in the homes of asthmatic subjects found that long-term exposure had no effect on immunologic parameters. Where Do We Go From Here? On the basis of the evidence presented in this review. Results from a yet to be published study in Colorado of systemic formocresol distribution in children receiving at least 1 pulpotomy while under general anesthesia determined that the mean dose of formocresol within a cotton pellet was 0. yet irrefutable evidence (87) exists showing that radiation exposure can induce the development of cancers. regardless of whether they had asthma. Diagnostic radiation is an indispensable component of every dental office. Until a superior alternative is developed or there is definitive evidence substantiating a cancer risk. if a 1:5 dilution had been used. furthermore. That study. Hence. is regarded by the Cancer Assessment Committee of the U. and solvents used in adhesive dentistry all demonstrate cytotoxicity in vitro (86). and a suspected causative agent. judiciously used. there is no reason to discontinue its use. Importantly. More recent evidence supports the work of Rolling and Thulin (80). it is highly unlikely that formocresol. the mean milligram dose per pellet would have been 0.9 –5 g/L. Number 7S. Moreover. The facts are that formaldehyde occurs naturally throughout the body. showed no causal relationship between formaldehyde and leukemia. so perhaps it is time for the formocresol product manufacturers to develop and market a 1:5 dilution of this medicament to replace the “fullstrength” formulations now available. ingested. and such evidence is needed before definitive conclusions can be reached. Definitive data to support this hypothesis are lacking. Rolling and Thulin (80) found no increase in either immune response or allergic reactions in 128 children who had undergone formocresol pulpotomy. in this case formaldehyde — was weak (standardized mortality ratio. there is an acceptance that an allergic reaction is both a possibility and a risk in the treatment of dental infection.86). because most of the formocresol will remain in the cotton pellet. Singling out one chemical such as formocresol for elimination from practice protocols in the face of a complete lack of human experimental data identifying a clear risk is intellectual tomfoolery. The actual dose that interacts with the pulp tissue is probably much smaller in both cases. yet there has been no call for the elimination of antibiotics from dental practice. efforts are needed to disseminate information about dose delivered to both the profession and the public. Immune Sensitization Despite evidence from dogs that formocresol can produce antigenic activity in dental pulp tissue (79). evidence from both experimental investigations and epidemiologic research does not support the hypothesis that inhaled or ingested formaldehyde might induce distant-site toxicity. however. On the basis of the evidence presented in this review. Leukemia was observed in a single drinking water study (75). Peroxides for dental bleaching. Evidence from epidemiology investigations of industrial workers with exposure to formaldehyde provides weak and inconsistent evidence that such exposure is associated with leukemia. Considering these facts. To that end. It is important to put this discussion into a broader perspective. In addition. sponsored by the Medical Research Council Environmental Epidemiology Unit in the United Kingdom (78) and involving the highest chronic formaldehyde exposures and highest peak exposures of all 3 investigations. In keeping with accepted therapeutic principles. The strength of association—the extent to which a collective body of data indicates a positive association between a disease.0026 mg. possible for the shortest time possible to obtain the desired effect. they found no clinical relevance of formaldehydespecific immunoglobulin E. the suggestion that formocresol “sensitizes” children has not been supported. These investigations have shown that both IPT and MTA have clinical and radiographic results that are equivalent to or better than those produced by formocresol over time. Recent research (83) has indicated that a minority of pediatric dentists use diluted formocresol because it is not available commercially. Determining the actual doses delivered to the pulp represents an important area for further investigation. This study used full-strength formocresol. July 2008 . Nevertheless. In fact. yet they form an important part of every dentist’s restorative armamentarium. Evidence continues to accumulate that supports the successful application of indirect pulp treatment (IPT) procedures to primary teeth as well as the use of mineral trioxide aggregate (MTA) in pulpotomy procedures. the risk of cancer. 0. the negative findings provide convincing evidence that exposure of children to the formaldehyde component of formocresol during a pulpotomy is insignificant and inconsequential. A Cochrane systematic review by Nadin et al (84) in 2003 suggested that the paucity of randomized controlled trials in pediatric pulp therapy made it virtually impossible to make recommendations regarding pulpotomy procedures.013 mg (37). and only microgram quantities of formaldehyde are applied to pulp tissues during pulpotomy procedures for mere minutes. Food and Drug Administration (76) as questionable. The abundant negative evidence mentioned previously is undisputed and strongly suggests that there is no delivery of inhaled. Presumably.
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Integrated risk information system. et al. et al.5:699 –730. Glenny A.69:18333– 4. Cancer Res 1983. J Pediatr Surg 2007.pdf.21:1573– 80.23:473– 87. Kerns WD. US Department of Labor. Scand J Dent Res 1976. initial assessment profile. 78.gc. Priority substances list assessment report: formaldehyde.oecd. Allergy 2003. monkey. Pinkerton LE. Screening information data set. WHO. De Lima PL.hc-sc. Conolly RB. Gross EA. Nadin G. Available at: www.epa. Huang TH.ec.html. 1987. Rolling I. Hein M. Accessed March 13.15:767–71. Accessed March 13. Accessed March 13. Clark RH.ca/ewh-semt/alt_formats/hecs-sesc/pdf/ pubs/contaminants/psl2-lsp2/formaldehyde/formaldehyde_e. Mortality among a cohort of garment workers exposed to formaldehyde: an update. IRIS database for risk assessment. Al-Hiyasat A. Accessed March 13. Formocresol mutagenicity following primary tooth pulp therapy: An in vivo study. Erexson GL. Phelps MC. Allergy Clin Immunol 1987. J Natl Cancer Inst 2003. Agency for Toxic Substances and Disease Registry. Oral Surg Oral Med Oral Pathol 1978.79:797– 810. Heck H. 61. Yeung C. Morgan KT. Scolastici C. 72.osha. Toxicol Lett 1984. 64. Ribeiro DA. 2006. 86.82:279 –96.84:345–7. Number 7S.21:241– 6. 2006.gov/SLTC/formaldehyde. Schlosser PM. Human respiratory tract cancer risks of inhaled formaldehyde: dose response predictions derived from biologically motivated computational modeling of a combined rodent and human dataset. Pulp treatment for extensive decay in primary teeth. 60. 52. Palmer KT. Organization for Economic Development and Cooperation. Formaldehyde. Kao CT. Pumphreys RS. Harris EC. 2004. 71. Lilly PD.ca/substances/ese/eng/psap/final/ formaldehyde. Day JH. IARC classifies formaldehyde as carcinogenic to humans: press release no. Carcinogenicity of formaldehyde in rats and mice after long-term inhalation exposure. Hsu TZ. Safety and health topics: formaldehyde. 2007. 58. Zhitkovich A. 87. Review of radiation risks from computed tomography: essentials for the pediatric surgeon.cdc. Ontario. 63. and sanitizers. 77. Existing substances evaluation: assessment report—formaldehyde. 68. 80. J Dent 2003.257:116 –28.64:100 –10. Suppl 7. IARC Monogr Eval Carcinog Risks Hum 1996. Lewis RD. Maffei F. Accessed March 13.Pulp Symposium 51. Cochrane Database Syst Rev 2003.42:603–7. Antibody formation to dog pulp tissue altered by formocresol within the root canal. Root canal sealers induce cytotoxicity and necrosis. Cytogenetic analysis of lymphocytes from rats following formaldehyde inhalation. Extended follow-up of a cohort of British chemical workers exposed to formaldehyde.iarc. Formaldehyde: hazard characterization and dose-response assessment for carcinogenicity by the route of inhalation: position paper. Formaldehyde: an experimental multipotential carcinogen. and eugenol in children with pulpotomized primary teeth. 62.62:217–375. Toxicol Sci 2001. Kimbell JS. Donofrio DJ. Benchmark dose risk assessment for formaldehyde using airflow modeling in a single-compartment: DNAprotein cross-link dosimetry model to estimate human equivalent doses. Occup Environ Med 2004.160:86 –100.31:479 – 85. Risk Anal 2003.fr/ENG/Press_Releases/archives/pr153a. Pross HF. Health and Welfare Canada. Environment Canada and Health Canada. Available at: www. 65. Loss of DNA-protein crosslinks from formaldehyde exposed cells occurs through spontaneous hydrolysis and an active repair process linked to proteosome function. Thulin H. Genotoxicity of antimicrobial endodontic compounds by single cell gel (comet) assay in Chinese hamster ovary (CHO) cells. Toxicol Ind Health 1989. Canada: Department of National Health and Welfare. Doi S.30:593– 6. Sheats JB. Lees RE. 57.43:4382–92. 85. Rosenblatt A. Indirect food additives. April 7. 69.gov/iris. Kligerman AD. Janszen DB. paramonochlorophenol. Toxicological profile for formaldehyde: US Department of Health and Human Services. Conolly RB. Fatal anaphylaxis in the UK. S46 Milnes JOE — Volume 34. Public Health Service. Takahashi CS. Soffritti M. Accessed March 13. Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. Seale NS. Chemical Industry Institute for Technology. Concentration of formocresol used by pediatric dentists in primary tooth pulpotomy. 66. Casanova M. 79. IARC. and calcium hydroxide on mammalian cells by comet assay. Novartis Found Symp 2004. J Endod 2004.html. Available at: www. Janszen D. NC: CIIT. McWhorter AG. J Material Sci Mater Med 2004. Goel B.1:CD003220. Kimbell JS. Suzuki S.pdf. Marques ME. U. 54. Accessed March 13. production aids. 2006. and human nasal passages. Kreiger RA. adjuvants. Ding SJ. 67. Formaldehyde-induced cytotoxicity and sister-chromatid exchanges in human lymphocyte cultures. Allergy tests against formaldehyde.120:51–5. Ribeiro DA. Carcinogenesis 2000. Washington. Salvadori DM.
has research interests with Newcastle University through an internal fund and also supervises several graduate students at Newcastle University. In the middle of the last century there were many debates on the merits of different medicaments. The School of Dental Sciences. In 1874. Conflict of Interest: Paula Jane Waterhouse.019 History: Where were we? A perspective from the United Kingdom (UK) on formocresol preparations Recent advances in primary tooth pulp biology Formocresol: Saint or sinner? Treatment Evidence-based practice The current UK guidelines. The technique appeared to be unpopular until Buckley’s method of treating putrescent pulps was published in 1904. PhD. History: Where Were We? Debate centered on clinical technique is not a product of modern medicine. By the late 1920s. 7).1016/j. July 2008 New Age Pulp Therapy S47 . and several variations of formocresol existed. pulp amputation was followed by application of Buckley’s formocresol solution (1). It is suggested that such a move should be made not just because of concerns relating to the possible toxicity of formaldehyde but to reflect a more contemporary. During the 1700s and early 1800s.03. United Kingdom. gold or lead? Would you also prefer to cauterize the exposed tissue with a red-hot iron wire before placing the foil? From the mid-1800s to the early 1900s. In general. This is welcomed and should be regarded as a positive activity that will benefit ultimately those for whom we provide dental care. Discussion at meetings and within peer-reviewed and non–peer-reviewed publications has stimulated both specialist pediatric dentists and general dentists. These thoughts will be presented within the following sections: ● ● ● ● ● ● ● T From the Department of Paediatric Dentistry. even at a relatively early time in medical and surgical knowledge. not only on both sides of the Atlantic but worldwide. and cocaine to be superior to Buckley’s solution in pulp amputation procedures. This article is being published concurrently in Pediatric Dentistry.j. During this period of innovation and discovery. continue to use formaldehyde-containing medicaments in endodontic therapy? This counterpoint will provide my personal thoughts on an undoubtedly controversial topic.uk. pulp therapy. calcium compounds. The articles are identical. Framlington Place. May/June 2008. BDS. One year later. Should we. metal foils were used to cap exposed pulp tissue (1). the use of medicaments in pulp therapies emerged and involved wide-ranging substances such as asbestos fibers. 0099-2399/$0 . Volume 30.joen.2008. Either citation can be used when citing this article. (J Endod 2008. doi:10. Newcastle University. thymol. Interestingly. suggesting the use of equal parts of tricresol and formalini (an aqueous solution of formaldehyde gas equivalent to 38% w/w formaldehyde). biologic approach to pulp therapy in the primary dentition. BDS. and an additional application of formocresolized zinc JOE — Volume 34. clinicians from Europe favored Gysi’s Triopaste with paraformaldehyde. E-mail address: p. The defining time for pulpotomy for the extensively carious primary tooth was the work published during a period of 25 years by Sweet (6.ac. Issue 3. and others based on eugenol.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. PhD Abstract This article outlines the counterpoint delivered in the debate “Is Formocresol Obsolete?” It addresses the opinion supporting the need to move away from formaldehydecontaining preparations in the dental care of children. She is also a Council Member of the British Society of Paediatric Dentistry. In 1908. and it was here that Boennecken (5) suggested his preparation of 40% formalin. to consider their stance over this issue. which would one use. Newcastle University.Pulp Symposium “New Age” Pulp Therapy: Personal Thoughts on a Hot Debate Paula Jane Waterhouse. the use of a mummifying paste with a preparation including solid formaldehyde was advocated (4). cork. primary teeth. pulpotomy he debate over the use of formocresol solution and other formaldehyde-containing preparations in children’s dentistry continues. beeswax.34:S47-S50) Key Words Formocresol. School of Dental Sciences. Newcastle upon Tyne. During this time.waterhouse@ncl. the International Dental Congress was devoted to the pulp and its treatment. The varying treatments for the tooth pulp during the last 3 centuries illustrate this clearly. there was disagreement between clinicians from Europe and the United States of America (USA) on treatment criteria and medicaments. and in the USA. NE2 4BW UK. pulverized glass. the first recorded use of a formaldehyde-containing medicament was published. Newcastle upon Tyne. as providers of healthcare in the 21st century. Number 7S. it is documented that there was great debate between those who believed a pulp was capable of healing and those who did not (2). Address requests for reprints to Dr Paula Jane Waterhouse. Nitzel applied a tricresolformalin tanning agent to 8000 exposed pulps (3). multiple applications of Buckley’s formocresol were reduced to 2.
esis in relation to caries insult. formaldehyde will react directly with proteins and nucleic acids. There appear to be no data published related to the possible levels of formaldehyde vapor and indeed cresol vapor in the dental working environment. during my own undergraduate days. and Substance P is increased in painful caries cases. . The UK Perspective on Formocresol Preparations In the UK. It is classed as a medicament. Fewer findings appear to be available for cresol. Despite this. But what happens once it has contacted a tissue? This has been investigated mainly in rats (which are obligate nasal breathers). and the degree and potential effect of accumulative formaldehyde exposure to dental professionals are unknown. 9). and recent research has evaluated neuropeptide-containing nerve fibers. but in its diluted form it is considered unstable and should be diluted just before use. which is impractical. It was reported that the formocresol addition to zinc oxide– eugenol cement could be omitted (10). In addition to this.5 mg per cubic meter. Buckley’s formocresol solution (38% w/w formaldehyde) and other formocresol preparations are not available for purchase on the general market. is toxic and corrosive. July 2008 . As clinicians. In light of these contemporary findings. Both the permanent and primary dentitions show similar increases in innervation density with caries progression. in part. By virtue of the formaldehyde and cresol moieties. there appears to have been confusion within pharmacy services when preparing the medicament in its dilute form (1). Nerves that express substance P have provided insight into pulp nerve function. In Annex 2 of the report the toxicologic profile of formaldehyde is discussed. In the UK in 2005. Once within tissues. with responses predominantly in the region of the pulp horns. This is inarguably a small amount of formaldehyde. 15 mL. These have an obvious pain receptive role. In particular. the HSE’s Working Group on Action to Control Chemicals (WATCH) published findings from an Advisory Committee on Toxic Substances (ACTS) related to the carcinogenicity of formaldehyde (17). In the late 1990s and early this century fewer and fewer hospital pharmacists were willing to prepare Buckley’s formocresol solution. tricresol. but whether that amount might cause problems should be explored further. thus the final product contains 1/13 the concentration of formaldehyde (gas). The apparent confusion over its formulation might make comparison of studies problematic. It appears that the primary tooth pulp has good potential for tissue repair and healing. The amount of vapor exposure (ppm) to a child undergoing a formocresol pulpotomy is unknown. In Newcastle. we all know from our own experience and from the reported literature that a pulpotomy performed with a 5-minute application of a 20% dilution of Buckley’s formocresol has a good prognosis. We should be directing our research energies toward compiling a sound evidence base for therapies that favor pulp regeneration.Pulp Symposium oxide– eugenol cement was suggested. a volatile organic compound. irrespective of whether the radicular pulp is viable. but it does not have a medicine license. Studies have shown that within a tooth the nerve fibers are predominantly nociceptive. even in its diluted form. and in Annex 3 the carcinogenicity of formaldehyde is presented by a summary of the human epidemiologic data mainly relied on by the International Agency for Research into Cancer (IARC) Working Group in reaching its conclusion relating to formaldehyde exposure and cancer (18). 19 mL. since 1979 the following formulation has been used: formaldehyde solution BP (formalin). glycerol. we as a collective professional body should be re-evaluating our approaches to pulp therapy in the primary dentition as our colleagues within adult restorative dentistry have already begun to do. despite few published data. Since then. tricresol is said to decrease the solubility and diffusion properties of formaldehyde. Number 7S. Buckley’s original formula appears to have contained 50% of a 38% solution of formaldehyde (equivalent to 19% formaldehyde). 35 mL. but it too is a known irritant and corrosive substance in its own right (16). . However. but also have difficulty in determining a shelf-life for the product” (1). Compounding this problem. It has been suggested that these later developments were driven by the impetus from concerns regarding the safety of formocresol (1). even under strict criteria for success (11). This contains 19% of a 38% solution of formaldehyde (equivalent to 7% formaldehyde) and is then diluted to a 1:5. in a recent British survey of 184 specialists in pediatric dentistry. tricresol has been shown to increase the permeability of cell Recent Advances in Primary Tooth Biology Dental pulp is a richly innervated tissue. primary tooth pulps present a more pronounced and widespread inflammatory reaction compared with permanent teeth and might have been instrumental in continuing with the amputation procedures (14). which formulation should be used to produce a 1:5 dilution? This is reinforced by the Extra Pharmacopoeia stating that “. the solution has tissue fixative and antimicrobial properties and will fix and devitalize an irreversibly inflamed radicular pulp. This response is refuted by more recent immunohistochemical work that demonstrates equality between dentitions for the degree of vasodilation and angiogenS48 Waterhouse JOE — Volume 34. I believe that in the UK the move away from Buckley’s formocresol has. To put this into the context of formocresol. there is often confusion about the terminology and strength of formaldehyde” (1). thus reducing movement out of the root canal (19). The UK’s Health and Safety Executive (HSE) presently rates exposure limits for formaldehyde for both long-term and short-term periods in the workplace to be 2 ppm or 2. Further uncertainty related to shelf life was raised. Full-strength Buckley’s formocresol solution is considered to have a shelf life of approximately 2 months if stored in brown glass bottles. but uptake into skin is poor. How many pulpotomies with formocresol would a child receive in 1 visit? How many pulpotomies with formocresol might a pediatric dentist undertake during the course of 1 day? According to data sheets and a large base of published evidence for animal and human studies. “Laboratories making up these solutions have not only a certain reticence in handling these relatively toxic materials. the use of pharmacydiluted Buckley’s formocresol was effective. It is prepared from its raw constituents in hospital-based pharmacy departments. Formocresol: Saint or Sinner? Despite formocresol’s undoubted clinical record of success and its position as the gold standard medicament in both vital and nonvital pulp therapy techniques in the primary dentition. been driven by increasing difficulties in obtaining the medicament and the increasing reticence of pharmacy staff to prepare the formulation (1. the technique for a single visit. 5-minute application formocresol pulpotomy was developed by using an as effective but weaker strength solution (8. Formaldehyde will pass into tissues such as mucous membranes rapidly. Formaldehyde is a known and accepted direct-acting irritant. and water to 100 mL. Although primary teeth contain more immune cells in both intact and carious states. formaldehyde. 12). 54% expressed concern over the safety of formocresol (15). they appear to localize in a manner similar to permanent teeth (12). particularly local to the point of contact. but they also play a primary role in immunoregulation and healing (13). I was taught that in response to caries. I agree with other pediatric dentists in that the overall amount of formaldehyde in a working solution is small.
Indirect Pulp Therapy. To present the alternatives that are presently clinically viable as succinctly as possible. When formaldehyde was given to rats in drinking water. In many instances does this relate to our present understanding of primary pulp biology and pathophysiology? If one considers a carious exposure in a permanent tooth. these need further investigation with models that replicate the nasal and oral breathing patterns of humans. Since the IARC findings. mo.2% 1 y (white) (36) 77. in addition. . preservation. years. Overview of Some Alternatives to Formocresol for Vital Pulp Therapy Material IPT Ferric sulphate MTA Calcium hydroxide Lasers formaldehyde in humans. July 2008 New Age Pulp Therapy S49 . Repeat dose inhalational studies with rodents and monkeys demonstrated that length of exposure and the concentration of formaldehyde vapor (ppm) are related to the degree of histopathologic change observed. Evidence-based Practice Considering all the options we have. The carcinogenic potential of formaldehyde is less evident in other rodents. By extrapolation. and mild dysplasia) when compared with nonexposed controls (21). irrespective of whether formocresol is carcinogenic. According to press reports. With all the techniques/medicaments listed in Table 1 excluding indirect pulp therapy (IPT). It is generally accepted that formaldehyde is genotoxic in vitro. formaldehyde can enter a rapid metabolic pathway. or is oxidized to carbon dioxide and exhaled (21–23).4 y (34) 92% 4 y (35) 100% 1 y (gray). the treatment of the extensively carious primary tooth can be divided into devitalization. would be missed the most and. particularly in relation to nasopharyngeal cancer. If the techniques are used on healthy or reversibly inflamed pulp tissue.Pulp Symposium membranes by disrupting cell membranes’ lipid components (20). Nasal tumors in rats are thought to arise by a combination of severe chronic local irritation and local genotoxicity. IPT of symptom-free but extensively carious teeth shows great promise but should only be undertaken on teeth without signs of pulpal degeneration. MTA. 10 people had difficulty breathing and required emergency room treatment (26). care must be taken in assessing the status of the radicular pulp after coronal amputation.5 mo (11) 100% 90 days (37) Human Clinical Studies Yes Yes Yes Yes Yes Tested Against Formocresol Yes Yes Yes Yes Effect (Animal Studies) Preservation and remineralization Preservation Preservation Preservation and remineralization Preservation IPT. inducing mutations and DNA damage in bacteria and in humans. The levels that produced no observed adverse effect for long-term inhalation studies with rodents were in the range of 1–2 ppm (21. 39).1% at 22. many different regulatory authorities have assessed the data published before 2004 (22. Treatment Applying formocresol to the radicular pulp of a cariously exposed tooth will render the pulp in its most part nonvital. With respect to humans. and rodent cells (27–31). On the basis of the classification system of Ranly (33). These alternative techniques for vital pulp therapy might not provide such good success rates if used when radicular pulps are irreversibly inflamed. 23). Results from human and animal in vivo studies showed that findings indicate that formaldehyde acts as a mutagen at the site of contact (17). In such a situation other than pulpectomy. Formaldehyde has been shown to be an experimental animal carcinogen in rats. In 2005. If we wish to move away from such preparations. The latter two are where we can move away from formocresol and reflect a more modern. the Cochrane Systematic Review of pulp treatment for the exten- Clinical Success % 94% during period of mean 3.1 ppm in some humans. However. or enters normal metabolic pathways. Recent UK-based publications are beginning to reflect this approach for the primary dentition. Not withstanding this. Workers chronically exposed to mean levels of 0. The HSE interpretation of the data from the studies considered is that they justify “increased concern” for the carcinogenic potential of TABLE 1. but no signs of systemic toxicity were reported (22. biologic approach to treatment. for teeth exhibiting hyperalgesia or those without local analgesia where in the past one would have used a paraformaldehyde preparation such as Miller’s paste to devitalize the tooth over time. but that the data fall short of providing conclusive evidence. then a high degree of success has been recorded. Doubts were raised concerning inconsistencies in some prominent new studies (17). 84. there is not an equivalently successful pulpotomy medicament as formocresol solution (38. Alternatively. the techniques are tabulated by using a single example of related clinical research (Table 1). The WATCH group suggest that formaldehyde is toxic at the site of initial contact. what might the combined effect of formaldehyde and cresol be? Would the added local toxicity of cresol aid the local genotoxicity of formaldehyde? Are the levels of these substances so low in the air around a dental chair that this does not constitute a risk? Clearly. the HSE has appraised the epidemiologic studies considered within the IARC report and stated that “sufficient evidence” exists that formaldehyde has caused nasopharyngeal cancer in humans (32). it is certainly an area worthy of further study. it should be appreciated that much effort is directed at preserving the pulp. a dental clinic in California was evacuated after spillage of a 1-ounce bottle of Buckley’s formocresol solution and was closed for the rest of the day. In the context of formocresol vapor in a dental setting. . Number 7S. studies have shown that concentrations of 3 ppm formaldehyde gas can saturate detoxification pathways in nasal epithelial cells. Formaldehyde is an irritant to the eyes and respiratory tract in amounts as low as 0. Disrupting cell membranes might potentiate further local toxic effects. ranging from slight hyperplasia to squamous cell metaplasia of ciliated and non-ciliated respiratory epithelium. producing nasal tumors at high levels of exposure (time and concentrations) (31). Mineral Trioxide Aggregate. if removed completely. what works best? Unfortunately. goblet cell hyperplasia. JOE — Volume 34. I concur that it is in this area where formocresol. and remineralization. It is clearly stated by WATCH.2–2 ppm formaldehyde exhibited mild nasal epithelial lesions (loss of cilia. “. monkeys. a combination of these circumstances in humans would be of concern in relation to cancer” (17). Formaldehyde’s acute toxic effects are considered real and can occur in humans from both the vapor and solution (25). y. converting ultimately to formate that is excreted in urine as formic acid. thus allowing “free” formaldehyde to cause damage locally (24). months. then treatment of such teeth needs further research and development. 23). a 2-year study showed local effects on gastric tissue. 25).
Nadin G. Substance P exposure in human tooth pulp in relation to caries and pain experience. 153. Int J Paediatr Dentistry 2006.13:246 –50. Ranly DM. 7. Al-Jame Q. et al.unep. Br Dent J 1909. 9. July 2008 . 10.html. Bennette B.ch/irptc/sids/OECDSIDS/FORMALDEHYDE. 6. iarc. 23. Corpron RE. Pulp changes in deciduous teeth associated with deep carious dentine. 5. Elliott RD. 15.7:39 – 42. Macleod HD.html.30:1348 –9. Monographs on the evaluation of carcinogenic risks to humans: volume 62—wood dust and formaldehyde. Kopel HM.fr/pageroot/PRELEASES/pr153a. 2-butoxyethanol and 1-tert-butoxypropan-2-ol. Actual spill intrudes on medical center drill. Nunn JH. HCN-DECOS (Health Council of the Netherlands-Dutch Expert Committee on Occupational Standards) 2003.ox. Caries control and other variables associated with success of primary molar vital pulp therapy. Tran X. International Agency for Research on Cancer. Burkes J. Toxicol Appl Pharmacol 1987.29:915–25. Mutat Res 1976. 4. Han SS. J Dent Child 1966. Formaldehyde: health-based recommended occupational exposure limit. Accessed June 10. 17. A recent meta-analysis of formocresol versus ferric sulfate found ferric sulfate to be as effective as formocresol (41). Switzerland. This should include studies to increase our awareness of the possible formaldehyde and cresol vapor exposure in the clinical environment. Loh A. Committee paper 2005/6.70:231– 40. Pediatr Dent 1994. DNA synthesis and ribosomal RNA transcription in monkey kidney cells treated by formaldehyde. formaldehyde. discussing IPT. Effects of varying concentration of formocresol on RNA synthesis of connective tissues in sponge implants. 31. 36. 8. Working Group on Action to Control Chemicals. J Endod 1975.uk/ aboutus/hsc/iacs/acts/watch/130105/p6. Boennecken H. This is an acknowledgment that the debate is far from over.40:3398 – 401. Casanova M. 30.6:129 –32.ac. Available at: http://www. Accessed June 3. S50 Waterhouse JOE — Volume 34. Eur J Oral Sc 2000. Goel BR. Clinical evaluation of pulpotomies using dilute formocresol. Formocresol vital pulpotomy on the permanent dentition. Rodd HD. PediatDent 2004. IARC classifies formaldehyde as carcinogenic to humans. 1999.chem. Number 7S. J Dent 1979. 21. 3. J Canad Dent Assoc 1980. 2007.89:105–21. The Hague. 11. Whitworth JM.17:1150 –3. Biomaterials 1985. Gleny AM. Pulp healing. Schwartz EA.188:32– 6. Formaldehyde induced DNA-protein crosslinks in Escherichia coli. Smeaton I. Survival.2:115–27. O’Hoy P. Han SS. Thilly WG. Toxicological profile for formaldehyde. Is there life after Buckley’s Formocresol? part 1: a narrative review of the literature. Evaluation of the carbon dioxide laser on vital human primary pulp tissue. Monographs on the evaluation of carcinogenic risks to humans: volume 88: 2006. Some biochemical considerations of fixation in endodontics. 39. Cancer Res 1980. Orstavik D. Summary In light of the findings presented. From the review it was demonstrated that formocresol. Coll JA. 2007.Pulp Symposium sively decayed primary tooth showed a paucity of acceptable related clinical research but did draw conclusions.26:214 –20. Evidence-based assessment: evaluation of formocresol versus ferric sulphate primary molar pulpotomy. Available at: http://publicsafety. J Am Dent Assoc 1930. International Agency for Research on Cancer. WHO. Pulpotomy therapy in primary teeth: new modalities for old rationales. J Dent Child 1996.com/article/article. 2004. Department of Health and Human Services. atsdr. Available at: http://www.cdc. Roberts MW.21:327–31. The update reflects a shift in treatment modalities away from formocresol. SIDS Initial Assessment Report: 2002.33:381– 6.28:97–107.33:381– 6. Eur J Paediatr Dent 2003. Publication number 2003/020SH. Available at: http://physchem. Pediatr Dent 1999. 27. despite including only 3 prospective randomized controlled trials (40). J Col Dent Assoc 1955. 13. Hunter ML.17:199 –206. Beaver HA.116:417–22. 22. I would recommend that pediatric dentists should be engaged in further good quality research and debate relating to vital and nonvital pulp therapy for the primary dentition. and pulpectomy (12). 38. Mutagenicity of endodontic sealers. Formaldehyde is mutagenic for cultured human cells. Cochrane Database Syst Rev 2003. 2007. Yeung CA. Available at: http://www. 16. Agamy HA. The formocresol pulpotomy: the past. Geneva. Pulp treatment for extensive decay in primary teeth. However.gov. 1995. 34.gov. Patchett CL. Holgslo JK. Ranly DM. At the beginning of this 21st century. Sweet CAJ. Procedure for treatment of exposed and pulpless deciduous teeth. 14. there might be difficulties obtaining ethical approval for such work in certain countries.html. Int J Paediatr Dent 2006. June 2004. Heck HAD. J Dent Child 1975. 18. Vij R. Int J Paediatr Dentistry 2003. a 1:5 dilution of Buckley’s formocresol solution remains listed as a medicament within the guidelines. we have greater understanding of the pulp biology.42:360 –3.26:302–9. References 1. Geneva.4:28 –32. San Jose Mercury News 2005. The preparation of mummifying paste. Ibricevic H. Moreno G.46:570 – 8. Br Dent J 2000. International Agency for Research on Cancer.36:11– 6. we should reflect this in our approach to clinical management and aim to preserve what pulp we can. Rodd HD. Bakry NS. Switzerland: WHO. Avery DR. Available at: http://www. J Pedod 1978. In some instances. 19. Waterhouse PJ. Pediatr Dent 2004. Farooq NS. Treatment of vital primary teeth with pulpal involvelment. 25. Nunn JH. WATCH (2005). Physical and Theoretical Chemistry Laboratory.26:401–9. Waterhouse PJ. Pediatr Dent 2004. ferric sulfate. Acknowledgments Grateful thanks to Professor Helen Rodd and Dr. Goldmacher VS. Straffon LH.jsp?id 2460&siteSection 3. Boissonade FM. Swenberg JA. Patchett CL. Immunocytochemical investigation of immune cells within human primary and permanent tooth pulp. Zander HA. 2007. Hunter B.18:403–9. Br J Dent Sci 1908. An investigation of the relative efficacy of Buckley’s Formocresol and calcium hydroxide in primary molar vital pulp therapy. Southam JC. The effect of zinc oxide-eugenol cement on a formocresolised pulp. 40. electrosurgical pulpotomy. Int J Paediatr Dent 2006. The Current UK Guidelines The British Society of Paediatric Dentistry has produced a range of clinical guidelines. Press release no. J Dent Res 1949. This in itself might lead to a natural reduction in the use of formocresol and herald a new age of pulp therapy.1:CD003220. however. 20. The development of formocresol as a medicament for primary molar pulpotomy procedures. 26. Gralla EJ. Vital pulpotomy in the primary dentition: attitudes and practices of Specialists in Paediatric Dentistry practising in the United Kingdom. Mounir MMF. 24. Ferric sulphate and formocresol in pulpotomy of primary molars: long tern follow-up study. desensitizing pulpotomy. Rayner J. 28. Waterhouse PJ. 37. 35. 2007. Coppey J. Srinivasan V. Sabes WR. the present. Lazzari EM.51:02– 4. Further studies on the metabolic incorporation and covalent bonding of inhaled [3H] – and [14C] formaldehyde in Fischer-344 rats: effects of glutathione depletion. 41. Phillips C.toxprofiles/tp111. Pavkov KL. Oxford University. Accessed August 14. The carcinogenicity of formaldehyde. Gilroy J. Mutat Res 1983. Mitchell RI. Morawa AP. and zinc oxide– eugenol pulpectomy all performed equally well.108:476 – 84. Sweet CAJ. Agency for Toxic Substances and Disease Registry.1:233–7. Vidya Srinivasan for allowing use of their research and clinical materials. Srinivasan V.pdf. 29. 12. pathophysiology.16:2–9.63:51–3. 32. Nocentini S. Shelton P.hse. and the future.16:117–27. Accessed August 20.uk/MSDS/CR/cresol. and its powers of healing. 33. Comparison of mineral trioxide aggregate and formocresol pulp capping agents in pulpotomized primary teeth. Boissonade FM. Pulp amputation. Mutat Res 1980. Wilkins FJ. Glass RL. Organisation for Economic Cooperation and Development. Induction of squamous cell carcinomas of the rat nasal cavity by inhalational exposure to formaldehyde vapor. Straffon LH. 2006. 2.pdf. Kerns WD. vital pulpotomy. Accessed June 10. Oral Surg Oral Med Oral Pathol 1970. Accessed August 15. ‘s Gravenmade EJ. Is there life after Buckley’s Formocresol? part 2: evelopment of a protocol for the management of extensive caries in the primary molar.
is a Grant Recipient from the National Institutes of Health and is the Editor-in-Chief of the Journal of Endodontics. even after treatment. Unfortunately. DDS. China. Michael Henry. metronidazole. and medications) and knowledge from the trauma and tissue engineering fields that can be applied to regeneration of a functional pulp-dentin complex.* Todd Geisler. The purpose of this review was to summarize these findings and illustrate a path forward for the development and evaluation of regenerative endodontic therapies. T Regenerative Endodontic Procedures Several groups recently have published preclinical research or case reports that offer a biologically based alternative to conventional endodontic treatment of these complex clinical cases. developed by Hoshino and colleagues and consisting of ciprofloxacin. In general.032 reatment of the young permanent tooth with a necrotic root canal system and an incompletely developed root is fraught with difficulty. Taken together. Yan Wang. increased dentinal wall thickness. DDS. these teeth have an elevated risk for fracture (6).1016/j.edu. but the thin dentinal walls increase the risk of a subsequent fracture. and apical closure when treating cases of necrotic immature permanent teeth.2008.* and Yan Wang. This article is being published concurrently in Pediatric Dentistry. May/June 2008. An alternative approach is to provide treatment under conditions where continued dentin formation is promoted. these studies provide a strong foundation level of knowledge from the trauma literature that permits subsequent research to focus on developing clinical methods for regeneration of a functional pulp-dentin complex. School of Stomatology. Several reports document that under conditions where at least some pulp tissue appears vital. (J Endod 2008. Not only is the root canal system often difficult to fully debride. Hargreaves. is a Grant Recipient from the AAE Foundation. with approximately 75% of the root canal systems having no cultivable microorganisms present (19). Shandong University. E-mail address: Hargreaves@uthscsa.34: S51-S56) Key Words Endodontics. DDS. PhD. acceptable endodontic results have been achieved through apexification procedures with use of long-term calcium hydroxide. reports no financial interests or potential conflicts of interest. is effective for disinfection of the infected necrotic tooth. described as either continued root development (maturogenesis) or apical closure (apexogenesis) (7). Number 7S. In a recent preclinical study on dogs. In addition. where the following precepts have been established: 1. there is continued need to develop biologically based treatment regimens that offer the potential for continued hard tissue formation of the young permanent tooth with a necrotic root canal system and an incompletely developed root. DDS. Address requests for reprints to Dr K.02. in many clinical cases the dental pulp has already undergone tissue necrosis before specialist consultation. MTA has been shown to produce good sealing effects under these conditions (1. 0099-2399/$0 . The articles are identical. PhD. doi:10.joen. a pulp cap treatment permits continued dentin formation. University of Texas Health Science Center. 7703 Floyd Curl Dr. is a Grant Recipient from the National Institutes of Health. PhD. University of Texas Health Science Center. bonded composite resins have been reported to increase fracture resistance under some (3. JOE — Volume 34. Historically.* Michael Henry. 2). and minocycline. Instrumentation with NaOCl irrigation is not sufficient to reliably create the conditions necessary for revascularization of the infected necrotic tooth (13). Concerns have been raised. Revascularization occurs most predictably in teeth with open apices (9 –12). In addition. Thus. Mail Code 7982. recent case reports indicate that biologically based endodontic therapies can result in continued root development. Placement of Ca(OH)2 in root canal systems prevents revascularization coronal to the location of the Ca(OH)2 (14). regeneration. Hargreaves. 4) but not all experimental conditions (5). Either citation can be used when citing this article. DDS. and †Department of Endodontics. revascularization. 3. This triple antibiotic mixture has high efficacy. however. Jinan. July 2008 Regeneration Potential of the Young Permanent Tooth S51 . 4. Issue 3. San Antonio. setting the conditions for subsequent revascularization (15–19). The use of the “3 mix-MP” triple antibiotic paste. DDS. TX 78229-3900. these studies have evolved from the trauma literature. instruments. PhD. pulp biology. DDS. 2. PhD. Volume 30.Pulp Symposium Regeneration Potential of the Young Permanent Tooth: What Does the Future Hold? Kenneth M. tissue engineering From the *Department of Endodontics. materials. there has been a tremendous increase in our clinical “tools” (ie. DDS. that long-term calcium hydroxide therapy might alter the mechanical properties of dentin. PhD† Abstract During the last 10 –15 years. Conflicts of Interest: Kenneth M. conventional endodontic therapy is not expected to result in continued dentin formation in these circumstances.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists. Recent treatment strategies include 1-step creation of an artificial apical barrier by using mineral trioxide aggregate (MTA) with or without an apical matrix followed by compaction of obturating material and placement of a coronal restoration. Todd Geisler. Texas. Hargreaves. M. Although these findings and an emphasis for continued research on vital pulp therapy are important (8). San Antonio. the intracanal delivery of a 20-mg/mL solution of these 3 antibiotics via a Lentulo spiral resulted in a greater than 99% reduction in mean colony-forming unit (CFU) levels. Moreover.
Therefore. the precise cell source(s) supporting the continued root development of the cases described in Table 1 are unknown. and extensive reviews on dental applications are available for the interested reader (25. fosters continued root development for immature teeth. however. the critical importance of subjecting these initial findings to prospective randomized clinical trials to generate objective measures of treatment efficacy and the potential liability for adverse events. using the term revascularization for regenerative endodontic procedures has been questioned (20). 56. JOE — Volume 34. and medications and applies many principles from the fields of trauma research and tissue engineering (25–28). this review will focus on the concept of regenerating a functional pulp-dentin complex and will restrict the use of the term revascularization to trauma studies. Second. because many of the reported cases treated with Ca(OH)2 display intracanal calcifications that appear to impede the continued thickening of the dentinal walls of these immature teeth (20). whereas all of the studies used NaOCl as an irrigant. 43). Key features of these published cases (20. Taken together. indeed. We now recognize. 52–57). current research in regenerative endodontics uses greatly improved materials. Here we briefly review 3 major components of tissue engineering from the concept of developing regenerative endodontic treatment regimens. and several (33–37). bone. these are critical areas for future research. Connective tissue was demonstrated to grow as much as several millimeters into the apical portion of the root canal system in teeth with necrotic pulpal diagnoses (23). 65). other investigators (30) have suggested that the use of Ca(OH)2 might kill any remaining pulpal cells. or possibly disrupt the apical papilla (30) and its resident stem cells (42. and under appropriate conditions. but not all (38). Thus. however. however. 26. the goal from an endodontic perspective is to regenerate a pulp-dentin complex that restores functional properties of this tissue. Controversies exist among several of these studies. 29 –32) are summarized in Table 1. it is possible that the radiographic presentation of increased dentinal wall thickness might be due to ingrowth of cementum. given the level of materials. instruments. chondrogenic. The second component of tissue engineering is a physical scaffold. and an appropriate scaffold might selectively bind and localize cells (66). This lack of outcome is not surprising. Clearly. Sixth. the phenotype varies in cells located in the apical versus coronal dentin. including stem or progenitor cells known to be present in dental pulp tissue (39 – 41). 58 – 61).Pulp Symposium Although the trauma literature has used the term revascularization to describe this treatment’s outcome. a delivery method must be developed that permits controlled application of a known amount of cells into the apical region of the root canal system. and this is likely to aid future studies characterizing the conditions necessary for mesenchymal cells of multiple origins to differentiate into the odontoblast phenotype. and an appropriate scaffold is needed to promote cell growth and differentiation. that the radiographic finding of continued dentinal wall thickness does not address the cellular nature of this calcified material. It should be appreciated. 50). cells from dental pulp. contain growth factors (67). however. Outcome differences between these 2 medicaments might reveal an important aspect of regenerative methods. Thus. these recent case studies support the hypothesis that the immature necrotic permanent tooth might be particularly responsive to biologically based endodontic therapies. and undergo biodegradation Hargreaves et al. Instead. or a dentin-like material (23. 63). Application of Tissue Engineering Concepts to Regenerative Endodontics The field of tissue engineering has literally exploded during the last decade. several recent case reports have been published describing regenerative endodontic procedures applied to cases of necrotic immature permanent teeth. it is important to realize that the immature permanent tooth in general has a very wide apical opening that likely is conducive to tissue ingrowth. In part on the basis of this expanding base of tools and knowledge. In addition. To date. which is critical for continued root development. the discovery of fluoride emerged from the keen observations of a practicing clinician. none of the cases used instrumentation of the root canal walls. permitting 3-dimensional ingrowth of tissue. It is known that extracellular matrix molecules control the differentiation of stem cells (64. and histologic analysis failed to reveal regeneration of a functional pulp-dentin complex. instruments. studies suggest that younger ages have greater healing capacity or stem cell regenerative potential. and autogenous to avoid tissue rejection or introduction of foreign pathogens (25). The clinical challenge will be to find a reliable cell source capable of differentiating into odontoblasts. these and other case reports (51) should be viewed as generating a strong impetus for developing future prospective clinical trials. The results were variable. Moreover. these cases might serve as an important clinical model to evaluate the application of tissue engineering concepts to the regeneration of a functional pulp-dentin complex. It is possible that: residual pulp cells might have remained vital in some of the cases. or adipogenic phenotypes. and prevents or resolves apical periodontitis. First. This diversity in cellular response is not surprising. these patients are young (8 –13 years old). cells from the apical papilla underwent proliferation. It should be appreciated that research on regeneration of a pulpdentin complex has a long history. For example. Third. the apical papilla. Although basic research has applied nearly all of the tools of molecular biology for engineering of dental tissues. 50. even among odontoblasts. Not only do these treatments provide an important alternative in a clinical situation with an otherwise poor prognosis. depending on their exposure to different cocktails of growth factors and morphogens (49. Number 7S. and possibly other tissues can form odontoblast-like cells (49. The first component of tissue engineering is a cell source. we will adopt a different perspective: What concepts of tissue engineering are most likely to be available to clinicians when treating their patients with regenerative endodontic techniques? We have used this rather practical perspective to shape our review of this field and to suggest a path forward for developing and evaluating regenerative endodontics. and medications and the knowledge base available at the time. convenient for harvesting. although structurally weak. Largely on the basis of preclinical studies. Odontoblasts are of mesenchymal origin. There are several common factors observed in these cases. or bleeding-induced angiogenesis might have recruited stem/ progenitor cells from apical tissues including the apical papilla. 44 – 48). July 2008 . given that human dental pulp cells can develop odontogenic/osteogenic. Tissues are 3-dimensional structures. during the last 30 –50 years. both Ca(OH)2 paste and combinations of multiple antibiotics have been used in these patients. including transfections and knockout animals. 24. Nygaard-Østby and others have reported a series of preclinical studies and case studies on patients attempting to regenerate pulp-like tissue in teeth with either vital or nonvital diagnoses (21–24). Fifth. Indeed. Recent molecular studies have identified many of the genes selectively expressed in odontoblasts (62. because measuring only 1 or 2 characteristics of a cell might not be sufficient to conclusively determine whether the resulting cell is a true odontoblast. nearly all of these studies report continued thickening of the dentinal walls and subsequent apical closure. but equally important. Fourth. the formation of a blood clot might serve as a protein scaffold. however. One advantage of case reports is that they are based on outcomes observed in actual patients and therefore might have great value in stimulating the S52 development of subsequent treatment methods.
glass ionomer cement. thickening dentinal walls.5% NaOCl. Deep irrigation with 10 mL 5. Interappointment medicament: Ca(OH)2 paste. 1 month: Irrigate with 2. 20 ● JOE — Volume 34. Irrigate with 2. 30 ● ● 20 10 Female (Partial) pulpal necrosis Chronic periradicular abscess ● ● ● ● ● ● ● 3 months: Found hard tissue at Ca(OH)2 site. Cavit. 15 months: Positive response to electrical pulp test.5% NaOCl. No instrumentation. Applied Ca(OH)2 paste. MTA. thickening dentinal walls in apical half of root canal system. bonded composite resin. 9 days: Rubber dam and access.5% NaOCl. 6 weeks later: Broach probed vital tissue in canal. wet pellet.25% NaOCl and 0. ● Outcome Sixth appointment: Vital tissue observed 5 mm apical to canal orifice. Number 7S. 2 weeks later: Composite restoration. Tooth left open between first and second appointments to permit drainage. 18 months: Restore with amalgam. Bleeding initiated with endo explorer. 7 months: Apical closure.Pulp Symposium TABLE 1. No instrumentation. Cavit. Interappointment medicament: metronidazole and ciprofloxacin. First appointment: Rubber dam and access. Caviton/IRM. Asymptomatic. calcified coronal one third root canal system. 1 month: Replace Ca(OH)2. Stopped bleeding 3 mm from cementoenamel junction. 20 ● ● 20 10 Female (Partial) pulpal necrosis Chronic periradicular periodontitis ● ● ● ● ● ● 1 month: Found hard tissue at mid-root. no instrumentation. 11 months: Thickening of dentinal walls. No instrumentation. 3 months: Replace Ca(OH)2 11 months: Remove IRM and replace with amalgam. 35 months: Continued thickening of dentinal walls and apical closure. Irrigate with 20 mL 2. Formocresol pulpotomy. 11–54 months: Gradual apical closure. age (y) sex 29 13 Female Preoperative pulpal diagnosis Necrosis Preoperative periradicular diagnosis Chronic apical abscess ● Treatment1 5 weekly visits.5% NaOCl. Positive response to pulpal cold test. First appointment: Rubber dam and access. Reference no. 7 months: Restore with Caiton/Ketac Silver. and ciprofloxacin (Lentulo spiral). 20 29 10 Male Necrosis Acute periradicular abscess ● ● ● ● 2 months: Found hard tissue at Ca(OH)2 site. 1 month: Irrigate 20 mL 5.12% chlorhexidine. minocycline. Irrigate with 2. Key Features of Case Reports of Regenerative Endodontic Treatment Applied to Necrotic Immature Permanent Teeth Tooth Patient Patient no. 2 weeks later: Repeat. Interappointment medicament: Ca(OH)2 paste. July 2008 Regeneration Potential of the Young Permanent Tooth S53 . First appointment: Rubber dam and access. No instrumentation. Interappointment medicament: Ca(OH)2 paste. irrigation with 5% NaOCl and 3% H2O2. 2 months later and every 2–3 months for 11 months: Replace Ca(OH)2. Asymptomatic. 29 ● ● ● 29 11 Male Necrosis Chronic apical abscess ● ● ● ● 26 days: Vital tissue present 15 mm into canal system. 6 –24 months: Gradual apical closure with thickening of dentinal walls. 30 months: Apical closure with thickening of dentinal walls.35% NaOCl. 2 months: Replace Ca(OH)2. Interappointment medicament: Ca(OH)2 paste. Interappointment medicament: metronidazole.
Interappointment medicament: metronidazole. JOE — Volume 34. Disinfect tooth surface with Betadine. First appointment: Consultation. No instrumentation.12% chlorhexidine. MTA. Remove cotton pellet 1 hour later and place bonded composite.5% NaOCl. Gradual apical development and closure. (Continued) Tooth Patient Patient no.25% NaOCl and 10 mL sterile water. 32 ● IRM. S54 Hargreaves et al. 5– 60 months: Gradual development of root length. minocycline. Incision for drainage. Cavit. 20 ● ● ● 8 8 Male Necrosis Chronic periradicular abscess ● ● ● 8 months: Asymptomatic. No instrumentation. Interappointment medicament: Ca(OH)2 paste. 11 weeks: Irrigate with 10 mL 1. Diffuse radiopacities noted in root canal system. wet cotton pellet. Apical closure with thickening dentinal walls. 5 months: Repeat. Rubber dam and access. thickening of dentinal walls.Pulp Symposium TABLE 1. and ciprofloxacin. ● ● Outcome 5 weeks: Hard tissue found at mid-root. Fourth appointment: Remove Cavit and place bonded composite. Rubber dam and access. minocycline. 2 weeks and 5 weeks: Repeat. MTA. Diffuse radiopacities noted in root canal system. induce bleeding with endo explorer. Cavit. Interappointment medicament: metronidazole.25% NaOCl. IRM. Reference no. age (y) sex 29 9 Male Preoperative pulpal diagnosis Necrosis Preoperative periradicular diagnosis Chronic periradicular periodontitis ● ● Treatment1 Tooth left open for drainage at an emergency clinic. Second appointment: Rubber dam and access.25% NaOCl and 0. No response to pulp test (CO2 ice). mineral trioxide aggregate. 31 ● ● 8 9 Male Necrotic Acute apical abscess ● ● ● ● ● 3 months: Asymptomatic. 6 –12 months: Asymptomatic. Induce bleeding with endodontic file inserted beyond the apex. apical closure. Third appointment: Irrigate with 5. Place MTA over blood clot with moist cotton pellet. 15 minutes allowed for blood clot to reach cementoenamel junction. Irrigate 40 mL 2. Deep irrigation with 10 mL 5. No instrumentation. Number 7S. July 2008 . Irrigate copiously with 1. and ciprofloxacin (Lentulo spiral). No response to pulp test (CO2 ice). 36 months: Restore with amalgam to calcified bridge. intermediate restorative material. Cotton pellet placed 3 mm below cementoenamel junction for 15-minute control location of a blood clot.25% NaOCl. Trauma 2 years previously treated with Cvek pulpotomy procedure.
Replantation of 400 avulsed permanent incisors: 2—factors related to pulpal healing. References 1.24:256 –9. if natural tooth development takes several years to occur. Apical plug technique using mineral trioxide aggregate: results from a case series. Hoshino E. Nord CE. Stuart CH. Giuliani V. To date. J Endod 2006. 9. 3. Int Endod J 1996. Thomas DD. whether root canal irrigation with EDTA would promote the development of odontoblast proliferation in a regenerative endodontic procedure. this statement is accurate. Cvek M. the path to the future should focus on translational research models that simulate likely clinical procedures. Andreasen FM. one approach would be to focus on methods permitting the delivery of known cells. Weisleder R. fairly easy to prepare in a dental setting. or dentin. July 2008 Regeneration Potential of the Young Permanent Tooth S55 . On the basis of current concepts.104:587– 8. however. James GA. Kurihara-Ando N. Beeson TJ. and a scaffold such as PRP into the apical 1–2 mm of a root canal system and then “backfilling” the root canal system with a solution of PRP and signaling molecules. Replantation of avulsed teeth with immature root development. Dalton BC. Andreasen JO. although of clear scientific importance in understanding cellular mechanisms. and minocycline. Beeson TJ. Wilkinson KL. We believe. Kirkpatrick TC. Odontol Revy 1971.28:386 –90. For example. 6. thus avoiding tissue rejection) (77). Similarly. From many perspectives. Both growth factors and other compounds are capable of stimulating cellular proliferation and directing cellular differentiation. recent case reports from multiple investigators support the feasibility of developing biologically based regenerative endodontic procedures designed to restore a functional pulp-dentin complex. ethylenediaminetetraacetic acid (EDTA) very effectively releases growth factors from human dentin (74). instruments. Strengthening immature teeth during and after apexification. no publications have evaluated PRP for scaffold generation in regenerative endodontic applications. Cornelissen R. et al. 7.33:480 –3. Johnson WT.27:1–10. Oral Surg Oral Med Oral Pathol 1985. In- JOE — Volume 34. Schwartz SA. we believe that research modeling clinical procedures designed to regenerate a functional pulp-dentin complex is likely to have the greatest impact. Beele H. metronidazole. Benitez CR. depending on the combination of signaling molecules such as dexamethasone (49).22:379 –95. degrades over time. The third component of tissue engineering to consider for regenerative endodontics is signaling molecules. or composite. the observed radiographic thickening of the dentinal walls might be due to production of cementum. Interestingly. Int Endod J 2007. Trope M. 15. A recent editorial has suggested that “little progress has been made” in the years since the Nygaard-Østby studies on the regrowth of dental pulp (8). the revascularization of root canal systems has been evaluated in human tooth slices after implantation into nude mice (who are immunocompromised. we believe that platelet-rich plasma (PRP) satisfies many of these criteria.11:59 – 68.Pulp Symposium over time (68). Borum MK. Walker WA III. 11.32:350 –3. because many growth factors are embedded into the dentin matrix during dentinogenesis. Kling M. there has been a tremendous increase in our clinical tools (ie. Endod Dent Traumatol 1995. One possible approach is to develop a model system resembling clinical application. Hollender L. and medications) and knowledge from the trauma and tissue engineering fields during the last decade. The sealing ability and retention characteristics of mineral trioxide aggregate in a model of apexification. 75) is likely to have major clinical application. the important question facing us is “what are the issues that must be addressed to develop a safe. including increased concentration of growth factors and removal of erythrocytes that would be expected to undergo necrosis shortly after clot formation.119:346 –52. Cvek M. It is not yet known. A Path to the Future Collectively. 2. It is likely that the cell source and the available signaling molecules play major roles in guiding the development of cells in the regenerating tissue. Interestingly. a scaffold is far more than a simple lattice to contain cells. and forms a 3-dimensional fibrin matrix (69 –72). then we are not convinced that the growth of artificial teeth with cells of allogenic or even xeongenic origin (42. Baccetti T. Similarly. As aforementioned. it is quite possible that knowledge gained from this clinical application will have value in developing regenerative endodontic procedures for the fully developed permanent tooth. Fracture resistance of simulated immature teeth filled with resilon. materials.29:776 – 8. Moreover. research focusing on the initiation of pulpal regeneration at the apex is likely to have major impact in developing other clinically useful procedures. gutta-percha. Sato I. 13. J Endod 2002. In short. Number 7S. In vitro antibacterial susceptibility of bacteria taken from infected root dentine to a mixture of ciprofloxacin. the question is no longer “can regenerative endodontic procedures be successful?” Instead. Endod Dent Traumatol 1992. PRP is autologous. Katebzadeh N. we do not believe that gene transfection is likely to have major application in clinical endodontic procedures. 8. Who cares about the dental pulp? Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007. Because most cells must be less than 1 mm away from a blood vessel to survive (76). Prognosis of luxated nonvital maxillary incisors treated with calcium hydroxide and filled with gutta-percha: a retrospective clinical study. stead. or chondrocytes. Cellular proliferation could then occur along the backfill scaffold. J Endod 1998. Laureys W.29:125–30. Thus. Although these case reports primarily involve treating the immature permanent tooth. Extracts of dentin promote growth. 5. Spangberg L. 4. 73). J Endod 2007. Rate and predictability of pulp revascularization in therapeutically reimplanted permanent incisors. Early reaction of intact human teeth to calcium hydroxide following experimental pulpotomy and its significance to the development of hard tissue barrier. For example. Schindler WG. Mejare I.8:45–55. because it permits rapid evaluation of conditions necessary to initiate tissue regeneration and could be extended in future research by evaluating conditions necessary to optimally disinfect necrotic root canal systems before tissue regeneration. This and other potential scaffolds require future research. and consistent method for regenerating a functional pulp-dentin complex in our patients?” In our opinion. it might be possible to evaluate the initiation of pulpal regeneration after various treatments by implanting the apical 5–10 mm of sectioned human roots into nude mice. Pagavino G. adipoyctes. Am J Orthod Dentofacial Orthop 2001. Goodrich JL. Antimicrobial effect of root canal debridement in teeth with immature root: a clinical and microbiologic study. bone. Odontol Revy 1976. From our perspective of focusing on practical clinical applications.40:478 – 84. Granath LE.2:83–9. however. 14. 62. that the last decade has produced a critical mass of knowledge and methods that are likely to result in the generation of biologically based endodontic therapies that will answer the challenge issued decades ago. Jacobsen HL. effective. 12. Cvek M. Hachmeister DR. For example. 10. Dermaut L. Other investigators have shown that dentin or application of a dentin extract rich in growth factors will promote formation of an odontoblast phenotype (50.60:420 –7. This approach has particular advantages. Revascularization after cryopreservation and autotransplantation of immature and mature apicoectomized teeth. however. the same cultures of human dental pulp cells can differentiate into cells resembling odontoblasts/osteoblasts. It is likely that intracanal delivery of known signaling molecules or the solubilization of endogenous signaling molecules will promote the formation of dentin in regenerative endodontic methods. Schroder U. Reinforcement of immature roots with a new resin filling material. Pace R. the case reports from Table 1 all include formation of a blood clot. rich in growth factors. The use of PRP as an alternative source for a fibrin clot might have several advantages. Pini Prato L. Maturogenesis: is it a new concept? J Endod 2003. signaling molecules. Endod Dent Traumatol 1986.
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Revitalization of pulpless open apex teeth in rhesus monkeys. 49. nonvital immature teeth (abstract).8:191–9. Murrah V. Honda M. 57. Ueda M. Ling J. Paakkonen V. 65.93:474 – 82. Trope M. Fitzimmons JS. 26. Andia I. J Dent Ed 2003. Miura M. Andia I.13:1219 –27. In vitro antimicrobial susceptibility to combinations of drugs on bacteria from carious and endodontic lesions of human deciduous teeth. The effect of calcium hydroxide on solubilization of bioactive dentine matrix components. Modino SA. J Bone Miner Res 2003. Trends Biotechnol 2006. J Dent Res 1980. Robey PG. 54. Vuoristo JT. Kubota M. J Bone Miner Res 2001. J Endod 1976. Regenerative endodontics: A review of current status and a call for action. Holland GR. Differentiation of pulpal cells and inductive influences of various matrices with reference to pulpal wound healing. Gronthos S. Acta Odontol Scand 1989. Nurden P. Ayukawa Y. 58. et al. Nagasaka T. Shi S. Odontoblasts induced from mesenchymal cells of murine dental papillae in three-dimensional cell culture. SHED: Stem cells from human exfoliated deciduous teeth. Dent Traumatol 2004. Tooth slice-based models for the study of human dental pulp angiogenesis.1:e79. Amler MH. Levin L. Skoglund A. Differentiation ability of rat postnatal dental pulp cells in vitro. J Endod 2005. Vancouver. Thibodeau B. Tissue Eng 2005.23:130 – 6.101:724 –9. 47. Pulpal changes in replanted and autotransplanted immature teeth of dogs. Number 7S. Finkelstein F. Graham L. Mao JJ. PLoS ONE 2006. Wei X. Dong Z. J Dent Res 2002.33:811– 4.41:117–27. Nakashima M.81:531–5. Yamada S. Yamamura T. et al. Orive G. Biomaterials 2005. Nevins AJ. D’Ippolito G. Kilts TM. Stanley HR.30:196 –200. Smith AJ. bone substitute (Bio-oss). 48. Shapiro IM. 67. Garcia-Godoy F. J Bone Miner Res 1999. Stenderup K. Akamine A. Shi S. Tissue formation in the root canal after total pulpectomy and partial root filling. Iwaku M. Sloan AJ. Trope M. Biological character of human adiposederived adult stem cells and influence of donor age on cell replication in culture. Banchs F. Nor JE. 43.20:75– 84. using collagen-calcium phosphate gel. Rattan SI.14:1115–22. Dent Traumatol 2007.8:172– 6. Autogenous injectable bone for regeneration with mesenchymal stem cells and platelet-rich plasma: tissueengineered bone regeneration. O’Driscoll SW.317:173– 85. 60.2:159 – 65. Thibodeau B. Sharpe PT. Expression of mineralization markers in dental pulp cells. Orthod Craniofac Res 2005. 66. Asgor Moral A. 41. 35. 23. Kikuchi H. Stem cells and the dental pulp: potential roles in dentine regeneration and repair. Xiao Y. Bartold PM. Age-related osteogenic potential of mesenchymal stromal stem cells from human vertebral bone marrow. Zhao M. et al. Smith AJ. 33. Fan MW. Ritter AL. Hoshino E. Murray PE. Oral Surg Oral Med Oral Pathol 1978. Induction of hard tissue into pulpless open-apex teeth using collagen-calcium phosphate gel. Gronthos S.73A:63–72. Ando-Kurihara N. 50. The chondrogenic potential of periosteum decreases with age. Saris DB. Teixeira F. Perivascular niche of postnatal mesenchymal stem cells in human bone marrow and dental pulp.50:320 – 8. The efficacy of mesenchymal stem cells to regenerate and repair dental structures.100:5807–12.321:391– 400. 17. Huang GT. In Vitro Cell Dev Bio 2007. Ritchie HH. 71. Sheppard PR. Andersson L. J Endod 2008. Feinberg SE. Caplan DJ.64(Special issue):530 – 40. Nor JE. Aghaloo TL. The contribution of platelet-derived growth factor. Cell Tissue Res 2004.8:54 –9. S56 Hargreaves et al. Tissue Eng 2004.31:711– 8. 27. Sato T.16:1120 –9.86:33–5. Zhang W. 42. Smith AJ. Nurden AT. Bluteau G.26:3207–14. Tronstad L. Kukita T. Vacatello M. Anitua E. 61. 73. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod 2004. 32. et al. Finkelstein F. Proc Natl Acad Sci U S A 2003.43:120 – 8. Hata K.50:255– 8. Logani A. Horsted P.33:703– 8. The role of the blood clot in endodontic therapy: An experimental histologic study. Naiki T. Terada S. Borden BG. Yamada Y. JOE — Volume 34. Scand J Dent Res 1971. 419:99 –113. Stem cell properties of human dental pulp stem cells. Liu Y. Trope M. 22. Sigurdsson A. Alliot-Licht B. Baba S. Chueh LH. 62. and tissue-engineered bone with respect to their mechanical properties and histological findings. and histology. Comparative gene expression profile analysis between native human odontoblasts and pulp tissue. Kota K.81:695–700.27:2865–73. Takahashi M. Stem cell-based composite tissue constructs for regenerative medicine. Seo BM. Smith AJ. Ricordi C. Pulp revascularization of replanted immature dog teeth after treatment with minocycline and doxycycline assessed by laser Doppler flowmetry. Interstitial pH and pO2 gradients in solid tumors in vivo: high-resolution measurements reveal a lack of correlation. Sigurdsson A. Shagramanova K. 63. Sterilization of infected rootcanal dentine by topical application of a mixture of ciprofloxacin. Sloan AJ. 39. Sanchez M. Laporta R. Laporta R. Liu L. 59. Kassem M. Uematsu H. 20. 25. Ehirchiou D. J Endod 2007. Biotechnol Bioeng 2005. Ueda M.4:76 – 81.23:281– 6. Evaluation of revascularization to induce apexification/apexogensis in infected.32:1066 –73. Liu Y. Iwaya SI. J Dent Res 1985. Sci China 2007. Test-tube teeth. Ito Y. Arch Oral Biol 2005. Role of tissue engineering in oral and maxillofacial reconstruction: findings of the 2005 AAOMS Research Summit. 36.47:41–52. Pulp revascularization of a necrotic infected immature permanent tooth: case report and review of the literature.
and current situation (pediatric or endodontic practitioner. Dallas. doi:10. Glickman. including dental discipline. agree.05.1016/j. age. a more detailed set of 20 questions about the same topics was presented to the audience for their opinion via an electronic ARS. with a significance level of P . 0099-2399/$0 . DDS. immature permanent tooth. pulp therapy. Sue Seale. (J Endod 2008. The purpose of this article was to present the results of the opinion surveys and report the current status of agreement of the 2 specialties concerning the 3 major areas of interest: pulp therapy for the cariously involved primary tooth. To that end. pediatric dentistry and endodontics. Comparisons of presymposium and postsymposium responses and between the 2 groups of attendees indicated that the pediatric dentistry and endodontic communities agree that formocresol will be replaced as a primary tooth pulpotomy agent.034 JOE — Volume 34. the planning committee sought to determine. that IPT in primary teeth holds hope as a replacement for pulpotomy. MSD. Results were analyzed with 2 tests. age group. The AAE and the AAPD are positioned to begin preparation of best practice guidelines that share common language and treatment recommendations for pulp therapies performed by both specialties. DDS. to hear and evaluate the best evidence surrounding the pulpal therapy treatments they commonly perform. Address requests for reprints to Dr Seale at sseale@bcd. pediatric or endodontic resident. if any. pulpotomy From the *Department of Pediatric Dentistry and †Department of Endodontics. both currently under investigation. The articles are identical. and current career position by using 2 analysis. indirect pulp treatment (IPT) for cariously involved immature permanent teeth. and innovative treatment options including pulpal revascularization and pulpal regeneration. specifically regarding reaching agreements on the evidence presented to support the treatments being discussed. Such an outcome would require both disciplines to agree with interpretation of the evidence presented concerning the shared treatments. both within each individual specialty and across the 2 specialties. MSD. the baseline opinions of the attendees concerning the various topics to be presented. and that IPT is an acceptable pulp therapy technique for cariously involved young permanent teeth. Presymposium and postsymposium tests were administered. Both groups believe that pulp revascularization and regeneration will be viable treatment modalities in the future. or academician). 2007.34:S57-S61) his symposium was intended to bring together 2 different disciplines. including medicament choice and opinions about formocresol as a primary tooth pulpotomy agent. indirect pulp treatment (IPT) for the cariously involved. the conference presentations had on attendees’ opinions. it was anticipated that there would be a diverse cross-section of opinions. Five questions addressed pulpal revascularization and the potential for stem cell research for pulpal regeneration. through a brief pretest administered before the first speaker.see front matter Copyright © 2008 American Academy of Pediatric Dentistry and American Association of Endodontists.* and Gerald N. DDS. After the last speaker. Conflict of Interest: N. Either citation can be used when citing this article. July 2008 Contemporary Perspectives on Vital Pulp Therapy S57 . Glickman. The same 3 demographic questions that were asked in the pretest were repeated. Therefore. Key Words Indirect pulp capping. and current career position. This article is being published concurrently in Pediatric Dentistry. Volume 30. T Methods An 8-question pretest was prepared and administered to attendees before the first presentation. MS† Abstract The purpose of this study was to determine the level of agreement between pediatric dentists and endodontists at a pulp therapy symposium conjointly sponsored by the American Association of Endodontists (AAE) and the American Academy of Pediatric Dentistry (AAPD) on November 2–3. The first 3 questions asked for demographic data. reports no financial interests or potential conflicts of interest. age group. and strongly disagree and queried about primary tooth pulpotomy and primary and permanent tooth IPT.Pulp Symposium Contemporary Perspectives on Vital Pulp Therapy: Views From the Endodontists and Pediatric Dentists N. Opinions on 3 areas were sought: pulp therapy for cariously involved primary teeth. MS. and an additional 5 questions asked about the same procedure in permanent teeth. tamhsc.05. Because this was the first such endeavor to bring these 2 specialties together. Five additional questions used a 5-point Likert scale with the choices of strongly agree. and respondent answers were compared between pediatric dentists and endodontists.edu. Baylor College of Dentistry. Texas A&M University Health Science Center. The planning committee also needed to determine what effect. Issue 3. Texas. Six questions addressed primary tooth pulpotomy. Gerald N. disagree. and innovative treatment options including pulpal revascularization and regeneration. neutral. DDS. Frequency tables of responses to the pretest questions were calculated for all respondents and compared by discipline. so that attendees’ responses could be identified by discipline. Additional questions used the Likert scale or allowed the attendees to choose a single best answer from a list of options and patient scenarios. May/June 2008. Four questions asked for opinions about indirect pulp capping (IPC)/stepwise excavation in primary teeth. that mineral trioxide is the first choice to take its place.02. One anticipated outcome of the symposium was to begin preparation for working together to produce best practice guidelines that share common language and treatment recommendations.2008. Sue Seale. Frequency tables of responses to the ARS questions were calculated for all respondents and compared by discipline (pediatric dentist or endodontist) by using 2 analysis. Number 7S. a more in-depth post-test was created and administered to the attendees via a real-time electronic audience response system (ARS). with a significance level of P .joen. reports no financial interests or potential conflicts of interests.
” pediatric dentists (5%) were significantly (P . Pulpotomy agents or treatment alternatives for cariously involved primary teeth were addressed in 2 post-symposium ARS questions. Therefore. 2 analyses were only performed on responses from pediatric dentists and endodontists.001) less likely than endodontists (15%) to agree or strongly agree. IPT in primary teeth was addressed in the pretest by asking attendees whether IPT was an acceptable substitute technique to replace pulpotomy to maintain vitality of cariously involved primary teeth. Again. The postsymposium ARS used 5 questions to further explore opinions of attendees concerning the subject of IPT in primary teeth. and the use of IPT as an alternative to pulpotomy for cariously involved primary teeth. the status of different pulpotomy agents for primary teeth and the level of evidence that supports them. The numbers of residents and nonspecialists were small.001) from pediatric dentists.001) 60% % of respondents who chose each treatment option Figure 1.” attendees were divided Fact that is a carcinogen contraindictes its use 37% 18% Endodon Ped Den IPC NaOCl pulpotomy MTA pulpotomy FeSO4 pulpotomy Formo pulpotomy 0% 0 1% 4% 20% 20% 40% 4% 2% 34% 30% 58% 47% Documented danger to patient 15% 5% Endodon Ped Den 0% 10% 20% 30% 40% % of respondents who agreed or strongly agreed (P<. 18% of pediatric dentists agreed or strongly agreed. 2).001. but because there is much controversy about its potential to be dangerous. with 80% agreeing or strongly agreeing compared with only 29% of endodontists. Pretest responses concerning the acceptability of formocresol as a contemporary technique for primary tooth pulpotomy were significantly more positive (P . when used as a primary tooth pulpotomy agent. primarily concerning formocresol’s safety. Figure 3. however. A second question asked attendees to respond to the statement “there is convincing evidence that IPT is as successful as a pulpotomy in primary teeth with reversible pulpitis. formocresol presents a documented danger to the patient.Pulp Symposium Results A total of 376 individuals provided responses. IPT was offered as a treatment option in cariously involved primary teeth in a question that asked attendees to choose from a list the best treatment for a reversibly inflamed primary molar with a large carious lesion encroaching on the pulp. 3). Comparison by specialty of responses to the question: Which is the best treatment choice for a reversibly inflamed primary molar with a large carious lesion encroaching on the pulp? S58 Seale and Glickman JOE — Volume 34. 21 pediatric dental residents. Comparison by specialty of responses to the statements: The fact that formocresol is a potential carcinogen should contraindicate its future usage in pediatric pulp therapy. compared with pediatric dentists (32%). One of the major areas addressed by the speakers was pulp treatment for the cariously involved primary tooth. They did this by choosing from a list that included an IPT or a pulpotomy with formocresol. When asked whether the fact that formocresol is a potential carcinogen should contraindicate its future usage in pediatric pulp therapy. MTA was the favorite pulpotomy agent. and when used as a primary tooth pulpotomy agent.” Seventy-four percent of pediatric dentists and 70% of endodontists agreed or strongly agreed. Three of the postseminar ARS questions revisited this issue. and 22 other. Number 7S. The second question dealt with choices of Calcium Hydroxide Chlorhexidine NaOCl Formocresol MTA FeSO4 0% 20% 40% 60% 80% 100% Endodon Ped Den % of respondents who chose each treatment option Figure 2. ferric sulfate.” Pediatric dentists and endodontists were unified in their opinions. presents documented danger to the patient. respectively. Attendees were asked their opinion about the statement “formocresol will be replaced as a primary tooth pulpotomy agent. Endodontists were significantly (P . July 2008 . mineral trioxide aggregate (MTA). When attendees were asked to respond to the statement “formocresol. When asked to respond to the statement “there is convincing evidence that primary teeth with reversible pulpitis should all be treated by step-wise excavation for 3 months and only receive a pulpotomy if exposure occurs on re-entry to remove remaining caries. these differences were significant (P . which is the recommended medicament for pulpotomies in primary teeth?” MTA was the overwhelming winner. choosing it 85% of the time. 1). 23 endodontic residents. with 78% and 76%. Issues covered included the controversy surrounding the use of formocresol as a pulpotomy agent in primary teeth and the level of evidence supporting either discontinuing its use or maintaining it as a viable pulpotomy agent. compared with 37% of endodontists. Only 15% of pediatric dentists and 3% of endodontists chose formocresol (Fig. “If cost were not an issue. agreeing or strongly agreeing. not because of its danger to patients. chosen most often by both pediatric dentists (30%) and endodontists (34%). 231 pediatric dentists. Fig. with pediatric dentists and endodontists in agreement. or sodium hypochlorite. Comparison by specialty of responses to the question: If cost were not an issue. Attendees were asked to give their opinions of the best treatment for a reversibly inflamed primary molar with a large carious lesion encroaching on the pulp. whereas 20% of pediatric dentists and 4% of endodontists chose formocresol. which is the recommended medicament for primary tooth pulpotomy? agents for pulpotomy and asked. and they were divided as follows: 79 endodontists.003) more likely at 47% to agree or strongly agree. Forty-seven percent of pediatric dentists and 58% of endodontists chose IPT (Fig.
“there is insufficient evidence to support its efficacy and success” (18%). Forty percent of pediatric dentists and 63% of endodontists agreed or strongly agreed. Additional post-symposium ARS questions asked attendees’ opinions of the stepwise.” Endodontists were significantly (P . Comparison by specialty of responses to the question: What is your main reason for not performing stepwise excavation in a permanent tooth with an open apex? JOE — Volume 34. compared with 59% of endodontists. re-entry to ensure dentin remineralization More evidence for IPC MTA pulp better evidence Inadeq reimbursement Questionable pt compliance 0% 6% 48% 61% 20% 6% 10% 27% 52% 20% 40% 60% 80% Endodon Ped Den Pulpotomy better Inadequate reimbursement 0% % of respondents who chose each option % of respondents who chose each option Figure 4. cariously involved young permanent teeth. and inadequate reimbursement by third party payers for the procedure (10%). more predictable outcome” (28%). The first asked for reactions to the statement “indirect pulp capping is an acceptable contemporary technique for maintaining the vitality of asymptomatic. including those with an open apex. and inadequate reimbursement by third party payers for the procedure (6%) (Fig. Number 7S.” Pediatric dentists were significantly (P . One question asked about agreement with “step-wise excavation as a practical treatment modality for IPT in young permanent teeth. compared with endodontists (69%). Endodontists expressed different preferences for their answers. and “I don’t believe IPT is successful in primary teeth” (20%) (Fig.” Pediatric dentists were overwhelmingly positive and significantly (P . and “I don’t believe IPT is successful in primary teeth” (9%). The same trend was true for pediatric dentists. Pediatric dentists chose in descending order: patient compliance for 2 appointments might be questionable (52%). patient recall to assess evidence of root maturation (31%).001) more likely at 94% to agree or strongly agree. knowing that if they removed the remaining decay. “there is insufficient evidence to support its efficacy and success” (19%).001) at 7% agreeing or strongly agreeing that symptoms of reversible pulpitis were a contraindication to IPT.02) more likely to agree or strongly agree at 31% than pediatric dentists at 26%. attendees were asked to choose from a list their strongest argument for performing stepwise caries excavation in a young permanent tooth. A scenario question asked what they would do for a 5-year-old child with a second primary molar in which they had removed nearly all of the decay. with their first choice being: MTA pulpotomy is supported by evidence to have a better outcome (61%). Responses from pediatric dentists included patient recall to assess symptoms and vitality (41%). The most frequently chosen answers in descending order by pediatric dentists were “pulpotomy is supported by evidence to have a better. “pulpotomy is supported by evidence to have a better. A second major area addressed by the speakers was management of the carious lesion encroaching on the pulp of an immature permanent tooth. Finally. 6). Endodontists had slightly different rankings of their choices. More than half of the pediatric dentists (55%) and 71% of endodontists would stop caries removal and do an IPT. The second pretest question asked for reactions to the statement “symptoms of reversible pulpitis are contraindications to IPT in young permanent teeth. patient compliance for 2 appointments might be questionable (27%).03) more likely to agree or strongly agree at 71%. “there is inadequate reimbursement by third party payers for the procedure” (32%). July 2008 Contemporary Perspectives on Vital Pulp Therapy S59 . When the endodontists’ pretest responses (31%) were compared with their ARS responses. 2-appointment version of IPT in permanent teeth. with “there is inadequate reimbursement by third party payers for the procedure” (35%). Another question asked attendees to choose from a list their main reason for not performing stepwise excavation in a permanent tooth with an open apex. Two pretest questions dealt with attendees’ opinions about IPT for these teeth. 5). more predictable outcome” (40%). there is more evidence to support the efficacy of the 1-step indirect pulp cap (18%). there is more evidence to support the efficacy of the one-step indirect pulp cap (6%). Comparison by specialty of responses to the statement: My main reason for not performing a pulpotomy in a primary tooth with reversible pulpitis. I don't believe IPC works in primary teeth Insufficient IPC evidence 20% 9% 18% 19% 28% 40% 35% 32% 10% 20% 30% 40% Endodon Ped Den significantly fewer (P . a pulp exposure would be imminent. with 8% ARS postsymposium 7% Endodon Ped Den 31% Presymposium 26% 0% 10% 20% 30% 40% % of respondents who agreed or strongly agreed Figure 5.001) agreed or strongly agreed (8%) that symptoms of reversible pulpitis were a contraindication to IPT. The post-symposium ARS used the exact same question to assess opinions after the presentations.Pulp Symposium in their opinions. compared with their pretest responses (26%) (Fig. and there was a significant difference in how the attendees responded to this question by the end of the conference. The final question about IPT in primary teeth in the postsymposium ARS asked attendees to choose from a list their main reason for not performing an IPT in a primary tooth with reversible pulpitis. Comparison by specialty of presymposium and postsymposium responses to statement: Symptoms of reversible pulpitis are contraindications to IPT in young permanent teeth with open apices. Figure 6. 4). significantly fewer (P . MTA pulpotomy is supported by evidence to have a better outcome (20%).
even though those studies that are available report positive outcomes in favor of MTA. In that respect. ARS questions asked for opinions about whether. Although the pretest question did not ask respondents to choose formocresol from among other pulpotomy agents. the vast majority of pediatric dentists initially viewed formocresol pulpotomy as an acceptable pulp treatment for cariously involved primary teeth. post-symposium ARS data indicated that pediatric dentists and endodontists are unified in their overwhelming favor of MTA as the pulpotomy agent of choice. When applying these data to the production of practice guidelines. The trend away from formocresol would place pediatric dentists more in agreement with endodontists. Pt recall/root maturation Pt recall for symptoms & vitality Re-entry for dentin remin 0% Endodon Ped Den Discussion Evidence of a merging level of agreement between pediatric dentists and endodontists concerning important issues addressed by the presenters was needed for the symposium planning committee’s goal to be met for the collaborative production of pulp therapy guidelines. unpredictability (18%). A major aspect of this technique is usage of disinfecting irrigants such as sodium hypochlorite and chlorhexidine followed by the placement of a special antibiotic mixture. and use of antibiotic paste within the canal (2%). with 74% agreeing or strongly agreeing compared with only 45% of endodontists. Pretest responses indicated significant differences in opinions between pediatric dentists and endodontists concerning the acceptability of most of the pulp therapy treatments under consideration. re-entry to ensure dentin remineralization (25%). Finally. A second option being examined to replace formocresol pulpotomy as the treatment of choice for cariously involved primary teeth is IPT.Pulp Symposium Low cost Tx/Access to care Payment for 2nd visit 3% 4% 6% 0% 41% 31% 25% 14% 25% 24% 10% 20% 30% 40% 50% point whether they believed the future use of stem cells for pulp regeneration in permanent teeth would be an acceptable treatment. from a public health perspective. Pediatric dentists were favorably inclined. they were in complete agreement with the endodontists. and 75% agreed that there is evidence that IPT is as successful as pulpotomy in primary teeth. payment to practitioner for a second appointment (6%). complex case selection criteria (13%). use of antibiotic paste within the canal (14%). Although this exciting concept is at its early stages of development. pediatric dentists gave the following responses in descending order: no major concerns at this time (34%). patient recall to assess symptoms and vitality (25%). who did not favor formocresol either pre. with 33% of pediatric dentists and 21% of endodontists choosing neutral as a response. Endodontists responded differently. and only 15% chose it as the recommended medicament for primary tooth pulpotomy. the future use of stem cells for pulp regeneration in permanent teeth would be an acceptable treatment. This question had the highest percentage of uncommitted responders.or post-symposium. only 20% chose formocresol as the best treatment for a primary tooth with reversible pulpitis. They did appear convinced. Respondents’ opinions expressed through the ARS indicated that the vast majority of pediatric dentists (87%) and endodontists (86%) agreed or strongly agreed that this will be a viable treatment modality for permanent teeth with apical periodontitis within the next 10 years. and provides low-cost treatment for patients needing access to care (3%) (Fig. it is probably most important that the 2 groups be together in their opinions about the need to find and endorse a replacement for formocresol. All of the endodontists (100%) and 96% of pediatric dentists agreed or strongly agreed. that it will be replaced because it is too controversial. Endodontists gave slightly different ordering to their choices: no major concerns at this time (32%). current evidence is based primarily on case reports (16%). Continuing with the issue of primary tooth pulp therapy and with respect to agents used for pulpotomy. Their responses to ARS questions about its documented danger to the patient and whether its potential as a carcinogen should contraindicate its use indicated that they do not believe the case that formocresol is dangerous has been made. 80% of the pediatric dentists favored its use at that point. When asked to choose from a list their major concerns about the procedures. Pretest data indicated poor acceptance by the pediatric dentistry respondents. In the post-symposium ARS questions. Endodontists started out more positively than pediatric dentists about the procedure for primary teeth and remained that way. This finding is interesting in light of the fact that there are few well-designed studies examining MTA as a primary tooth pulpotomy agent. There was a different trend apparent when pediatric dentists were asked to comment on the safety of formocresol. 7). and provides low-cost treatment for patients needing access to care (4%). listing in order: patient recall to assess evidence of root maturation (41%). only 5% of pediatric dentists and 18% of endodontists agreed. The gap between % of respondents who chose each option Figure 7. compared with pediatric dentists at 37%. unpredictability (26%). Their post-symposium ARS responses appeared to indicate a marked trend toward a more positive attitude about IPT for primary teeth. and complex case selection criteria (12%). but these results certainly appear to suggest that formocresol lost popularity. with less than one third agreeing that it was an acceptable substitute technique for pulpotomy. The greatest disagreement between the 2 groups came when asked whether general dentists should perform such procedures if properly educated and trained. however. the ARS asked for opinions from an ethical standS60 Seale and Glickman JOE — Volume 34. Comparing the large number of positive responses initially to formocresol with the ARS responses appears to indicate a changing attitude by pediatric dentists. More than half would stop caries excavation and perform an IPT rather than a pulpotomy. current evidence is based primarily on case reports (33%). Beginning with primary tooth pulpotomy agents and formocresol in particular. The way the questions were phrased does not allow direct comparisons between presymposium and postsymposium responses. Endodontists were more likely to agree or strongly agree at 64%. Comparison by specialty of responses to the question: Which of the following would be your strongest argument for performing stepwise caries excavation in young permanent teeth? (24%). and gene therapies. growth factors. as did the ARS questions. Regeneration of pulp tissue involves tissue engineering therapies by using stem cells. July 2008 . Root canal revascularization via blood clotting in necrotic young teeth has been reported in the literature through documented case reports. the American Association of Endodontists has made regenerative endodontics and revascularization high priority areas for further investigation. Number 7S.
The length of time involved in completing the 2 procedures might make them impractical for patients on some payment programs such as Medicaid. Almost all of the pediatric dentists (94%) opined that IPT was an acceptable technique for the “asymptomatic cariously involved young permanent tooth. This is also the issue where there has previously been the most divergence of opinion between the 2 groups concerning the appropriateness of IPT for these teeth. many cariously involved teeth in these young individuals have open apices and are simply not candidates for complete endodontic treatment. The issue where pediatric dentists and endodontists have the most potential to both be treating the same kinds of teeth is the management of cariously involved young permanent teeth with immature or open apices. and that IPT is an acceptable pulp therapy technique for cariously involved young permanent teeth with open apices. In addition. The procedure has not received wide exposure in the United States because most of the publications on its use and success have appeared in journals not widely read by the practicing community. however. Most pediatric dentists and endodontists. The post-symposium ARS question was worded exactly the same way as in the pretest. what do endodontists and pediatric dentists agree on? These survey data appear to indicate that the pediatric dentistry and endodontic communities alike agree that formocresol will be replaced as a primary tooth pulpotomy agent. Number 7S. It is this topic of the more conservative. that IPT in primary teeth holds hope as a replacement for pulpotomy. both the endodontists and pediatric dentists believe that pulp revascularization and regeneration will be potentially new exciting treatment modalities in the near future. By the end of the conference.Pulp Symposium them narrowed. The IPT procedure in permanent teeth presented at the symposium was the variant called stepwise excavation. The postsymposium ARS questions dealt mainly with the stepwise excavation version of IPT and appeared to indicate similar favorable agreement on its use in permanent teeth by both pediatric dentists and endodontists.” compared with only approximately two thirds of the endodontists. agreed to a pretest question concerning reversible symptoms of pulpitis contraindicating IPT. The pretest question responses bore out this divergence. They need to be treated with the more complex and lengthy procedure of vital pulpotomy to obtain root closure followed by complete root canal treatment. July 2008 Contemporary Perspectives on Vital Pulp Therapy S61 . that MTA is the overwhelming first choice to take its place. The variant involves 2 appointments and aims to eventually remove all affected dentin rather than leave a small amount in the tooth as is performed in the 1-appointment IPT. The issue of access to care mandates that the 2 groups be unified in agreeing that IPT is an evidence-based and appropriate pulp therapy modality for young permanent teeth with immature or open apices. Only 8% of endodontists and 7% of pediatric dentists agreed that symptoms of reversible pulpitis were a contraindication to IPT. Conclusions In summary. In fact. as pediatric dentists more frequently expressed positive opinions in their responses after the symposium. where their eligibility might vary during the time period required. however. their opinions about whether such symptoms were a contraindication to IPT changed dramatically. JOE — Volume 34. indicating agreement on this important diagnostic issue. Many children and young adults who have the highest risk for caries and lesions and who are candidates for IPT have either no payer sources or sources with limited participation by individuals who perform endodontic treatment (general dentists and endodontists). cost-effective treatment modality of IPT for cariously involved young permanent teeth that is the most important issue for which the 2 communities must reach agreement and formulate practice guidelines with common language and intent.