Pediatric Endodontics: Endodontic Treatment for the

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The Pulp-Dentin Complex in Primary and Young Permanent Teeth

Differences in Primary and Permanent Tooth MorphologyRoot FormationPrimary Root Canal AnatomyPrimary Anterior TeethPrimary Molars

Clinical Pulpal Diagnosis in ChildrenHistory and Characteristics of PainClinical ExaminationPalpation, Percussion, and MobilityPulp TestsRadiographic ExaminationRestorative Diagnosis: Pulpal Exposures and HemorrhageDiagnosis After Traumatic Injuries in ChildrenPulp Diagnosis and Treatment Planning After Trauma

Principles of Endodontic Treatment in ChildrenPulp Therapy for the Primary Dentition

Indirect Pulp Therapy in Primary TeethDirect Pulp Capping in Primary TeethPulpotomy in Primary TeethFormocresol Pulpotomy

Alternatives to Formocresol PulpotomyGlutaraldehyde PulpotomyFerric Sulfate Pulpotomy

Mineral Trioxide Aggregate PulpotomyElectrosurgical PulpotomyLaser Pulpotomy

Nonvital Pulp Therapy on Primary TeethPulpectomy in Primary TeethAccess Openings for PulpectomyRoot-Filling Materials for the Primary Root CanalsFollow-Up After Pulpectomy in the Primary Dentition

Pulpal Therapy for the Young Permanent DentitionIndirect Pulp Therapy: Avoiding Pulp ExposureManaging Pulp Exposure

PulpotomyThe Cvek Pulpotomy on Immature Permanent TeethPartial Pulpotomy on Asymptomatic Young Permanent

Posterior TeethPulpotomy on Symptomatic Young Permanent TeethFollow-Up After Pulp Capping and PulpotomyFormocresol Pulpotomy on Young Permanent Teeth

ApexogenesisApexification

Apexification TechniqueArtificial Apical Barrier TechniquesRestoration After Apexification

New Horizons for Pulp Regeneration

Pediatric Endodontics: Endodontic Treatment for the Primary and Young

Permanent DentitionPAULA J. WATERHOUSE | JOHN M. WHITWORTH

CHAPTER 24

CHAPTER OUTLINE

Despite the dental profession’s emphasis on prevention, threats to pulp survival, such as caries, restorative dental treatment, and traumatic injuries, have not been eliminated. As a conse-quence, children continue to lose teeth prematurely, and pro-cedures aimed at preventing and treating pulp disease in the primary and immature permanent dentitions remain an inte-gral part of contemporary dental practice.

Some may question why efforts to preserve pulpally involved primary teeth are important. These practitioners maintain that such efforts may present a risk to developing permanent

successors and, in any case, the primary teeth will be lost before long. Preservation of arch space is one of the principal objectives of pediatric dentistry. Premature loss of primary teeth may cause aberration of the arch length, resulting in mesial drift of the permanent teeth and consequent malocclu-sion. Whenever possible, the tooth with pulp involvement should be maintained within the dental arch in a functional and disease-free condition.

Other objectives of preserving the primary teeth are to safeguard aesthetics and mastication, prevent aberrant tongue

e2 PART III Expanded Clinical Topics

3. Primary teeth have narrower and longer roots com-pared to crown length and width in permanent teeth.

4. The facial and lingual cervical thirds of the crowns of anterior primary teeth are much more prominent than those of permanent teeth.

5. Primary teeth are markedly more constricted at the dentinoenamel junction (DEJ) than are permanent teeth.

6. The facial and lingual surfaces of primary molars converge occlusally; therefore, the occlusal surface is much narrower in the faciolingual dimension than the cervical width.

7. The roots of primary molars are comparatively more slender and longer than the roots of permanent molars.

8. The roots of primary molars flare out from the cervical area, and more at the apex, than do the roots of perma-nent molars.

9. The enamel is thinner (approximately 1 mm) on primary teeth than on permanent teeth, and has a more consistent depth.

10. The thickness of the dentin between the pulp chamber and enamel in primary teeth is less than in permanent teeth.

11. The pulp chambers in primary teeth are comparatively larger than those in permanent teeth.

12. The pulp horns, especially the mesial horns, are higher in primary molars than in permanent molars.

Root FormationAccording to Orban,205 development of the roots begins after enamel and dentin formation has reached the future cemen-toenamel junction (CEJ). The epithelial dental organ forms Hertwig’s epithelial root sheath, which initiates formation and molds the shape of the roots. Hertwig’s sheath takes the form of one or more epithelial tubes (depending on the number of roots of the tooth, one tube for each root). During root forma-tion, the apical foramen of each root has a wide opening limited by the epithelial diaphragm. The dentinal walls diverge api-cally, and the shape of the pulp canal is like a wide-open tube. Each root contains one canal at this time, and the number of canals is the same as the number of roots (Fig. 24-2, A). When root length is established, the sheath disappears, but dentin deposition continues internally within the roots.

Differentiation of a root into separate canals, as in the mesial root of the mandibular molars, occurs by continued deposition of dentin. This narrows the isthmus between the walls of the canals and continues until the formation of dentin islands in the root canal and eventual division of the root into separate canals. During the process, communications exist between the canals as an isthmus and then as fins connecting the canals (Fig. 24-2, B). (See Chapter 12 for a complete description of pulp and dentin formation.)

As growth proceeds, the root canal is narrowed by contin-ued deposition of dentin, and the pulp tissue is compressed. Additional deposition of dentin and cementum closes the apex of the tooth and creates the apical convergence of the root canals common to the completely formed tooth (Fig. 24-2, C).

Root length is not completed until 1 to 4 years after a tooth erupts into the oral cavity. In the primary dentition, root length is completed in a shorter period than in the permanent tooth because of the shorter length of the primary roots.

habits, aid in speech, and prevent the psychological effects that may be associated with tooth loss. Premature loss of the maxil-lary incisors before 3 years of age has been shown to cause speech impairment that may persist in later years.229

It is equally undesirable for children to suffer the unplanned loss of permanent teeth, and it should be noted that the prognosis for lifelong retention of an immature tooth with a short root and fragile dentinal walls is far worse than for a mature permanent tooth. Special treatments for the immature permanent tooth, therefore, focus on preserving vital pulp functions, at least until dental development is complete (see also Chapter 10).

This chapter attempts to provide a review of current thera-pies for the prevention and treatment of pulpal disease in primary and young permanent teeth. The biologic basis of these procedures is emphasized and supported with clinically relevant evidence to help clinicians preserve functional and disease-free teeth in children.

THE PULP-DENTIN COMPLEX IN PRIMARY AND YOUNG PERMANENT TEETHPulp therapies should be based on an understanding of dental tissues and their innate reaction patterns. Some fundamentals of tissue structure and behavior merit review, and the reader is encouraged to see Chapter 12.

DIFFERENCES IN PRIMARY AND PERMANENT TOOTH MORPHOLOGYSuccessful pulpal therapy in the primary dentition requires a thorough understanding of primary pulp morphology, root for-mation, and the special features associated with physiologic resorption of primary tooth roots. These factors are considered in the following sections.

According to Finn74 and Nelson and Ash,196 there are 12 basic differences between primary and permanent teeth (Fig. 24-1):

1. Primary teeth are smaller in all dimensions than cor-responding permanent teeth.

2. Primary crowns are wider in the mesial-to-distal dimen-sion compared with crown length than are permanent crowns.

FIG. 24-1 Cross section of a primary and permanent molar for compari-son. Divergence of the primary molar roots allows space for the developing permanent premolar.

CHAPTER 24 Pediatric Endodontics: Endodontic Treatment for the Primary and Young Permanent Dentition e3

FIG. 24-2 Faciolingual cross section of the mesial root of a mandibular primary molar. A, Formation of the root at the time the root length is completed; only one canal is present. B, Differentiation of the root into separate canals by the continued, but incomplete deposition of dentin in central areas. Small fins and branches are present between the two canals. C, Canals are completely divided; root resorption has begun.

A CB

The root-to-crown ratio of the primary teeth is greater than that of the permanent teeth. The primary roots are narrower than the permanent roots. The roots of the primary molars diverge more than those of the permanent teeth; this feature allows more room for the development of the crown of the succeeding premolar (see Fig. 24-1).194

The primary tooth is unique insofar as resorption of the roots begins soon after formation of the root length has been completed. At this time, the morphology of the root canals roughly corresponds to the form and shape of the external anatomy of the teeth. Root resorption and the deposition of additional dentin within the root canal system, however, sig-nificantly change the number, size, and shape of the root canals within the primary tooth. A more detailed description of how this affects the primary teeth is presented later in this section.

It should be noted that most variations within the root canals of primary and permanent teeth are in the faciolingual plane; dental radiographs do not visualize this plane but show the mesiodistal plane. Therefore, when reviewing clinical radiographs, many of the variations that may be present are not visible. Figures 24-3 and 24-4 show silicone models of root canals, and Figure 24-5 shows a reconstructed digital image to illustrate morphology not visible with plain radiographs. The increasing availability of three-dimensional imaging techniques, such as cone beam computed tomography,211 is bringing greater understanding of such anatomic features to practicing clinicians.

Primary Root Canal AnatomyTo treat the pulps of primary teeth successfully, the clinician must have a thorough knowledge of the anatomy of the primary root canal systems and the variations that exist within them.196

Understanding some of the variations in the primary root canal systems requires an understanding of root formation (see pre-vious discussion and Box 24-1).

Primary Anterior TeethThe morphology of root canals in primary anterior teeth resembles the form and shape of the roots of the teeth them-selves (see Figs. 24-3 and 24-4). The permanent tooth bud lies lingual and apical to the primary anterior tooth, so physiologic root resorption of primary incisors and canines begins on the lingual aspect of the apical third of the roots (see Fig. 24-3, A).

Maxillary IncisorsThe root canals of maxillary primary incisors are almost round in cross section but somewhat compressed in a faciolingual

BOX 24-1

Root Canal Anatomy Considerations in Primary Teeth

◆ After root-length completion, dentin deposition continues in the root canal.

◆ After root-length completion, dentin deposited in a root canal may change the number, size, and shape of the root canals.

◆ Often root canal variations are not visible on clinical radiographic images.

◆ In anterior teeth, one root canal is usually present, although mandibular incisors occasionally have two.

◆ In anterior teeth, accessory and lateral canals and apical ramifications are rare.


A

C

B

FIG. 24-3 Primary central incisors and silicone models of pulp canals. A, Facial surfaces. B, Beginning resorption of roots on apical third of lingual surfaces. C, Models. Pulp canals were injected with silicone, and the tooth structure decalcified away, leaving a model of the root canal systems. Note the division of the canal in the model on the left.

FIG. 24-4 Maxillary primary canine and silicone model of the root canal. A, Mesial surface. B, Model of the root canal.

A B

direction. Commonly these teeth have one canal without bifur-cations. Apical ramifications and accessory and lateral canals are rare but may occur (see Fig. 24-3).309

Mandibular IncisorsThe root canals of primary mandibular incisors are flattened on the mesial and distal surfaces and are sometimes grooved, progressing in an apical direction to an eventual division into two canals (facial and lingual). The presence of two canals is seen less than 10% of the time. Occasionally, lateral or acces-sory canals are observed.309

Maxillary and Mandibular CaninesThe root canals of primary maxillary and mandibular canines correspond to the exterior root shape: a rounded, triangular shape with the base toward the facial surface. Sometimes the lumen of the root canal is compressed in the mesiodistal dimension. The canines have the simplest root canal systems of all the primary teeth and offer few challenges during endodontic treatment. Bifurcation of the canal does not nor-mally occur. Lateral canals and accessory canals are rare (see Fig. 24-4).309


Primary MolarsOften, primary molars have the same number and position of roots as the corresponding permanent molars (see Fig. 24-5). Maxillary molars have three roots, two facial and one palatal; mandibular molars have two roots, mesial and distal. The roots of the primary molars are long and slender compared with crown length and width, and they diverge to allow for perma-nent tooth bud formation.

When full-length root formation has just been completed in the primary molars, only one root canal is present in each of the roots. The continued deposition of dentin internally may divide the root into two or more canals. During this process, communications exist between the canals and may remain in the fully developed primary tooth as isthmi or fins connecting the canals (see Fig. 24-2, B, and Fig. 24-5).

In primary teeth, the deposition of secondary dentin has been reported to occur after root-length completion.21,111,127 This may result in changes to the basic root canal morphology, producing variations and alterations in the number and size of the root canals. This deposition begins at about the time root resorption begins. Variations in form are more pronounced in teeth that show evidence of root resorption.111

The greatest variation in morphology of the root canals occurs in the mesial roots of maxillary and mandibular primary molars. This variation originates in the apical region as a thinning of the narrow isthmus between the facial and lingual extremities of the apical pulp canals. Subsequent deposition of secondary dentin may produce complete sepa-ration of the root canal into two or more individual canals. Many fine connecting branches or lateral fibrils form a con-necting network between the facial and lingual aspects of the root canals (see Fig. 24-5).

The variations found in the mesial roots of the primary molars are also found in the distal and lingual roots but to a lesser degree. Accessory canals, lateral canals, and apical

FIG. 24-5 Three-dimensional tomographic images of a maxillary second primary molar. A, Mesial view of primary molar with four root canals. Note the fins of pulp tissue between the distofacial and palatal canals. B, Same tooth from the distal view. Note the wide area of pulp tissue connection between the distofacial and palatal canals. (Courtesy Paul Dummer and Sue Bryant, Cardiff University, Wales, UK.)

BA

ramifications of the pulp are common in primary molars, occurring in 10% to 20%.111,309

In the primary molars, resorption usually begins on the inner surfaces of the roots next to the interradicular septum. The effects of resorption on canal anatomy and root canal filling on the primary teeth are discussed in detail later in this chapter.

Maxillary First Primary MolarThe maxillary first primary molar has two to four canals that correspond approximately to the exterior root form, with much variation. Usually, the palatal root is round and often longer than the two facial roots. Bifurcation of the mesiofacial root into two canals is common and occurs in approximately 75% of maxillary first primary molars.194,309

Fusion of the palatal and distofacial roots occurs in approxi-mately one third of maxillary first primary molars. In most of these teeth, two separate canals are present, with a very narrow isthmus connecting them. Islands of dentin may exist between the canals, with many connecting branches and fibrils.

Maxillary Second Primary MolarThe maxillary second primary molar has two to five canals roughly corresponding to the exterior root shape. The mesio-facial root usually bifurcates or contains two distinct canals. This occurs in approximately 85% to 95% of maxillary second primary molars.111,309

Fusion of the palatal and distofacial roots may occur. These fused roots may have a common canal, two distinct canals, or two canals with a narrow connecting isthmus of dentin islands between them and many connecting branches or fibrils.

Mandibular First Primary MolarThe mandibular first primary molar usually has three canals, again corresponding approximately to the external root


Provoked pain is usually triggered by a thermal or an osmotic stimulus (e.g., cold drinks, eating candy) and usually ceases when the stimulus is removed. This history is indicative of minor, reversible pulp inflammation. Provoked pain may sometimes be confused with that caused by interproximal impaction of food (Fig. 24-6), soreness associated with tooth exfoliation, or eruption of permanent teeth.

By contrast, spontaneous pain is not consistently associated with an external stimulus, may arise at any time of the day, or may wake the child from sleep. In both primary and young permanent teeth, spontaneous pain and provoked pain that continues long after the causative factor has been withdrawn are usually associated with extensive, irreversible pulpal inflammation that extends into the root canals.101 Primary teeth with a history of spontaneous toothache are unreliable candi-dates for vital pulp therapy and should not be considered for any form of treatment short of pulpectomy or extraction. The situation is quite different for immature permanent teeth. Because the consequences of losing vital pulp functions are so serious, immature permanent teeth with a similar pain history should always be considered for pulpotomy, apexogenesis, or even regenerative techniques in an effort to safeguard tooth development (see later sections on immature permanent teeth).

anatomy, but it may have two to four canals. It is reported that approximately 75% of the mesial roots contain two canals, whereas only 25% of the distal roots contain more than one canal.111,309

Mandibular Second Primary MolarThe mandibular second primary molar may have two to five canals, but it usually has three. The mesial root has two canals approximately 85% of the time, whereas the distal root con-tains more than one canal only 25% of the time.111,309

CLINICAL PULPAL DIAGNOSIS IN CHILDRENRestorative dental treatment should never commence without a working diagnosis and treatment plan. Chapter 1 provides a comprehensive account of diagnostic procedures, but certain points should be emphasized for examination of the child patient. As always, the diagnostic process should follow an orderly pattern, with attention to the medical and dental history, clinical examination, and special tests, including radiographs where appropriate. Parents or caregivers may be helpful in clarifying the case history and may need to be involved if any systemic condition is likely to influence clinical management. The medicolegal dimensions of careful history taking, diagnostic procedures, and case documentation should also be recognized.

Every effort should be made to establish a working pulp diagnosis before anesthetizing the suspect tooth and isolating it with a rubber dam. These conditions are rarely conducive to accurate history taking or diagnostic reliability, especially in young children. The opportunity should also be taken before treatment to discuss contingent alternatives that may become necessary as a result of an unexpected event, such as the expo-sure of a pulp during deep caries excavation.

Established tests to determine the extent of pulpal inflam-mation are crude at the best of times and may be of little or no value in young and anxious children and on primary or immature permanent teeth. The literature on pulp diagnosis in children is mostly outcome reports based on empiric treatment and anecdotal case reports. Assumptions about pulpal status before treatment have often been based on retrospective find-ings rather than histologic or microbiologic data to support the prerestorative diagnosis. Histologic investigation remains the only true method of determining the nature and extent of pulp inflammation, and any correlation with clinical signs and symptoms is limited.53,172,264

Although every effort should be made to discern the condi-tion of the pulp before treatment, exhaustive pulp provocation tests may not be helpful in children. From a clinical stand-point, the characteristics of the presenting pain are often criti-cal to the working diagnosis, especially when summated with additional information from the clinical and radiographic examination. Further evidence can be provided by clinical observations during the procedure, such as the nature, volume and ability to control hemorrhage from an exposed pulp. It should be recognized that pulp diagnosis in children is as much an art as a science.

History and Characteristics of PainThe character of any presenting pain is first identified in the history. Wherever possible, the distinction should be made between provoked and spontaneous pain.

FIG. 24-6 Bone loss (and pain) caused by food impaction in interproxi-mal space between primary molars. A, First and second mandibular primary molars with caries and marginal bone loss caused by food impaction. B, Healthy bone after restoration of teeth.

A

B


Klein139 showed responses ranging from 11% in 6- to 11-year-olds with completely open apices to 79% in older children with complete root formation.

Thermal tests may be more reliable than electrical methods for determining the presence of vital responsive tissue in immature permanent teeth, and carbon dioxide snow has been shown to be more effective than ice and ethyl chloride.86,87,89,139 Heat is unreliable as a diagnostic test in young children.87

Laser Doppler flowmetry has been reported to be reliable for diagnosing pulpal vitality in immature permanent teeth,66,256,306 but the equipment has not been perfected for clinical use66 and is cost prohibitive. It is also affected by blood pigmentation of the crown, or by the presence of large or full-coverage coronal restorations.

Radiographic ExaminationThe clinical examination should be supplemented where appropriate with high-quality radiographs. Interradicular (furcal) radiolucencies, a common finding in primary posterior teeth with pulpal pathoses, are best observed in bite wing radiographs. If the apical area cannot be clearly observed, a periapical view should be obtained. The integrity of the lamina dura of the affected tooth should be compared with that of adjacent or contralateral teeth.214

Current radiographs are essential in examining for caries, restoration integrity, previous endodontic treatments, and resorptive and periapical changes in primary and young per-manent teeth. In children, interpretation of radiographs is complicated by physiologic root resorption of primary teeth and incompletely formed roots of permanent teeth. If the clini-cian is not familiar with interpreting radiographs of children or does not have radiographs of good quality, these normal conditions can easily be misinterpreted as pathologic changes in need of treatment. In the case of immature permanent teeth, comparison of root formation with the contralateral tooth should always be considered.

The radiograph does not always demonstrate periapical pathosis, nor can the proximity of caries to the pulp always be accurately determined (see also Chapter 2). What may appear as an intact barrier of secondary or tertiary dentin overlying the pulp may actually be a perforated mass of irregularly min-eralized and/or carious dentin overlying a pulp with extensive inflammation.53

The presence of calcified masses within the pulp is an important diagnostic sign (Fig. 24-7). Mild, chronic irritation to the pulp stimulates tertiary reactionary dentin formation. When the irritation is acute and rapid in onset, the defense mechanism may not have a chance to lay down reactionary dentin. When the disease process reaches the pulp, the pulp may form calcified masses away from the exposure site. These calcified masses can be associated with degeneration of the coronal pulp and inflammation of the radicular pulp in primary teeth.53 In the absence of other clinical evidence, it is unclear whether this warrants invasive treatment in all cases. Certainly for immature permanent teeth, the presence of calcific meta-morphosis within the coronal pulp chamber would not in isolation warrant pulpectomy and root canal treatment.

Pathologic changes in the periapical tissues surrounding primary molars are most often apparent in the bifurcation or trifurcation areas rather than at the apices (as generally seen in permanent teeth) (see Fig. 24-7). Pathologic bone and root resorption indicates advanced pulpal degeneration that has

Clinicians faced with an apparently graphic pain history should not neglect to conduct a proper clinical examination because other conditions, such as papillitis caused by inter-proximal food impaction, can mimic pulpal pain.

Equally, the absence of pain should not encourage clinical complacency because varying degrees of pulp degeneration or even complete necrosis can be encountered without any report of pain. Consequently, children may present without any com-plaint, despite extensive carious lesions and a draining sinus tract. Those who have developed early childhood caries (e.g., nursing bottle caries) may have no experience of their teeth feeling any other way and thus no special pain history to report.214

Clinical ExaminationA careful extraoral and intraoral examination is of great impor-tance in identifying teeth with pulpal involvement. Signs such as tooth discoloration, gross caries, redness and swelling of the vestibulum, or a draining sinus tract may strongly suggest pulpal pathoses. In addition, attention should be paid to teeth with extensive fractured or missing restorations or restorations with recurrent caries. All may indicate involvement of the pulp through the relatively thin and porous dentin of the cavity floor.

Palpation, Percussion, and MobilityFluctuation, felt by palpating a swollen mucobuccal fold, may be the expression of an acute dentoalveolar abscess that may not be visualized yet externally. Bone destruction associated with a chronic dentoalveolar abscess may also be detected by palpation.

Although significant inflammatory bone loss can make primary teeth mobile, this is not a reliable, objective test of pulpal status. Teeth with varying degrees of pulpal inflamma-tion may have very little mobility, whereas mobility can be significant during phases of active physiologic root resorption in primary teeth with healthy pulps.

Comparing the mobility of a suspicious tooth with its con-tralateral equivalent can be especially helpful in clarifying such quandaries. If a significant difference in mobility is noted, this, along with other diagnostic information, may suggest pulpal inflammation or necrosis.

Sensitivity to percussion may reveal a painful tooth in which pulpal breakdown has resulted in acute periradicular periodon-titis. Exceptions include recently traumatized teeth. Care should be taken in percussing the teeth of children; Pinkham et al.214 recommend gentle use of a fingertip rather than the end of a dental mirror.

Pulp TestsStandard electrical and thermal pulp provocation tests are of limited value in the primary dentition and in young permanent teeth with incompletely developed apices.7 Although these tests may indicate the presence of some vital responsive tissue, they do not give reliable data on the extent of pulpal inflam-mation. Many children with perfectly normal teeth do not respond to the electrical pulp tester, even at the higher settings. In addition, young patients may give unreliable responses to such provocation tests because of apprehension, fear, or general management problems.

The unreliability of electrical pulp testing in immature per-manent teeth has been reported in several studies.86,87,89,139


misleading because under normal conditions, they show the mesiodistal plane of the tooth but give little information about the faciolingual dimension. Except for the maxillary central and lateral incisor, all other root canals of the permanent teeth are wider in the faciolingual plane than in the mesiodistal plane. The faciolingual aspect of the root canal is two to three times as wide as the mesiodistal width and is the last to become convergent apically as the root develops. Therefore, it is possible to have a dental radiograph showing an apically con-vergent root canal, whereas in the faciolingual plane, the root canal is divergent. Equally, canals that are apically diverging in the faciolingual view may be parallel or converging in the mesiodistal view. As mentioned, contemporary three-dimensional imaging techniques are beginning to improve understanding, both in the research laboratory (Fig. 24-9) and in the clinic.211

In summary, radiographs add to the diagnostic process by visualizing the presence or absence of the following:

1. Deep caries with possible or definite pulp involvement2. Deep restorations close to a pulp horn3. A successful or failing pulp cap, pulpotomy, or

pulpectomy4. Changes within the pulp, such as calcific barrier

formation, calcific metamorphosis, and pulp stones (denticles)

5. Pathologic root resorption, which may be internal (within the root canal) or external (affecting the root or the surrounding bone). Internal inflammatory resorption indicates inflammation of a vital pulp, whereas external inflammatory resorption demonstrates a nonvital pulp

spread into the periapical tissues. The pulpal tissue may remain vital even with such advanced degenerative changes. Periapical radiolucencies of primary anterior teeth, like those in perma-nent teeth, are usually at the apices.

Internal resorption occurs frequently in the primary denti-tion after pulpal involvement. It is always associated with extensive inflammation,101 and it usually occurs in the molar root canals adjacent to the bifurcation or trifurcation area. Because of the thinness of primary molar roots, once the inter-nal resorption becomes visible on radiographs, it has usually advanced to root perforation (Fig. 24-8). In some instances, however, the process is reversible and self-correcting, and the resorbed area becomes filled with mineralized tissue.105,208 If a perforation of the root occurs in a primary tooth because of internal resorption, all forms of pulp therapy are contraindi-cated. The treatment of choice is observation (if the area of the resorption is confined to the tooth) or extraction (if the process has reached the bone).105,208

In immature permanent teeth, it is often difficult to assess the extent of apical closure. Plain-film images are frequently

FIG. 24-7 Calcified mass in the pulp chamber. Internal and external root resorption has occurred. The calcified mass (arrow) is an attempt to block a massive carious lesion. Because of the root resorption, this tooth should be extracted. Note the bone loss in the bifurcation area.

FIG. 24-8 Pulpotomy failure. Note the internal resorption, which has per-forated the pulp chamber floor and resulted in a furcal radiolucency.

FIG. 24-9 Three-dimensional tomographic images of an immature max-illary canine. A, Faciolingual view. B, Mesiodistal view. Such imaging tech-niques are bringing new anatomic awareness to both the research laboratory and the clinic. (Courtesy Paul Dummer and Sue Bryant, Cardiff University, Wales, UK.)

A B


determining the extent of degeneration within the pulp. A white blood cell differential count (i.e., hemogram) was made for each of 53 teeth included in the study. A detailed history was obtained, including percussion, electrical pulp testing, thermal tests, mobility, and history of pain. The teeth were extracted and histologically examined. On correlation of the histologic findings with the hemogram and history, it was determined that percussion, electrical and thermal pulp tests, and mobility were unreliable in establishing the degree of pulpal inflammation. The hemogram did not give reliable evi-dence of pulpal degeneration, although teeth with advanced degeneration of the pulp involving the root canals did have an elevated neutrophil count. A consistent finding of the study, however, was advanced degeneration of pulpal tissue in teeth with a history of spontaneous toothache.

The outward clinical signs of inflammation represent a succession of cellular, vascular, and immunologic processes involving many endogenous mediators. Inflammatory media-tors (vascular mediated and cell released) and their role in pulpal inflammation have been the subject of much research. The relationship between the concentration of a known cell-released inflammatory mediator (prostaglandin E2 [PGE2]) in pulpal blood samples and treatment outcome after vital pulpotomy in extensively carious primary molars has been reported.297 Thirty-nine primary molars with no history of spontaneous pain had blood samples harvested from the radic-ular pulp stumps immediately after coronal pulp amputation. Enzyme immunoassay of the samples for PGE2 detected the inflammatory mediator in all samples. A wide range of concen-trations was detected, and it was shown that the concentration of PGE2 detected correlated positively with radiologic signs of failure after treatment. The authors tempered their findings by describing the dependence upon a single inflammatory media-tor to predict prognosis as oversimplistic and suggested the “trauma” of pulp amputation would stimulate prostaglandin production irrespective of the underlying inflammatory status of the tissue. Similarly, a rapid and low-cost, chairside diagnos-tic kit to assess the extent of pulp inflammation does not yet exist. Therefore, despite research in this area, clinicians still rely upon empiric clinical findings to diagnose the inflamma-tory status of the pulp.

Diagnosis After Traumatic Injuries in ChildrenThe details of trauma management are considered in Chapter 20. Injuries to the primary dentition are common, occurring in 1 in 3 children by the age of 5 years.9,94 Diagnosis after traumatic injuries requires consideration of other factors in addition to those previously discussed. The most frequent injury in the primary dentition is tooth displacement that occurs because the bone is less dense and the roots are shorter. Healing varies from normal without sequelae to canal calcifica-tion or pulpal necrosis. Canal calcification may vary from an amorphous material resembling osteodentin to partial or com-plete closure of the canal.115,234

Pulp Diagnosis and Treatment Planning After TraumaTreatment guidelines are almost nonexistent concerning healing and complications after trauma in primary teeth. The

with extensive inflammation, including resorption of the adjacent bone. External, replacement resorption usually follows trauma and is discussed more fully in Chapters 16 and 20.

6. Periapical and interradicular radiolucencies of bone. In primary molar teeth, any radiolucency associated with a nonvital tooth is usually located in the furcation area, not at the apices. This is because of the presence of acces-sory canals on the pulpal floor area. A bite wing film is frequently a useful diagnostic aid, particularly in maxil-lary molars where the developing premolar obscures the furca in a periapical radiograph.

7. The degree of root formation in young permanent teethIt is important to emphasize once again that the clinician

should be familiar with the normal factors that complicate interpretation of radiographs in children: larger bone marrow spaces, superimposition of developing tooth buds, normal resorption patterns of the teeth, and immature root apices.214

Restorative Diagnosis: Pulpal Exposures and HemorrhageIt has been reported that the size of the exposure, the appear-ance of the pulp, and the color and amount of hemorrhage are important factors in diagnosing the extent of inflammation in a pulp exposed by caries. The presence of excessive53,214,264 or deep purple214 hemorrhage from an exposed or amputated pulp is evidence of extensive inflammation in both primary and young permanent teeth. A true carious exposure is always accompanied by pulpal inflammation (see Chapter 13),53,264 and even a pinpoint carious exposure can be associated with pulpal inflammation ranging from minimal to extensive or even complete necrosis. However, massive exposure in primary teeth is always associated with widespread inflammation or necrosis and makes the tooth a poor candidate for any form of vital pulp therapy. As discussed previously, this rule does not apply for young permanent teeth with incomplete root devel-opment, where the premature loss of vital pulp functions is so catastrophic that every effort should be made to safeguard tooth development (see later section on the management of pulpal exposure in immature permanent teeth).

Sometimes a final working diagnosis can be reached only by direct evaluation of the pulp tissue, and a decision about treatment is made accordingly. For example, if a pulpotomy is planned in a primary molar, the bleeding from the amputation site should be normal, and hemostasis should be evident after 2 to 3 minutes of light pressure with a moistened cotton pellet. Significant bleeding beyond this point indicates inflammation of the radicular pulp, and a more radical treatment, such as pulpectomy or extraction, should be considered. Conversely, if a pulp polyp is present and bleeding stops normally after coronal pulp amputation, a pulpotomy may be performed instead of a more radical procedure.214

In the case of an immature permanent tooth, persistent hemorrhage after several minutes of sodium hypochlorite application is an indication of serious pulp inflammation, and a tooth initially scheduled for a direct mineral trioxide aggre-gate (MTA) pulp cap may be a better candidate for a pulpot-omy, apexification, or pulp regeneration (see later section on immature permanent teeth).

Guthrie et al.101 attempted to use the first drop of hemor-rhage from an exposed pulp site as a diagnostic aid for


this diminishes the potential for pulpectomy and root canal treatment, should this become necessary, but as new opportu-nities open for regenerative therapies, traditional approaches to the root canal treatment of pulpless immature teeth may be coming into question.

PULP THERAPY FOR THE PRIMARY DENTITION

Indirect Pulp Therapy in Primary TeethIndirect pulp treatment (IPT) in the primary dentition is con-sidered a contemporary, effective approach to the management of a deep carious lesion in the absence of signs or symptoms of irreversible pulp pathosis.249 It involves the removal of caries to leave a layer of stained dentin at the cavity floor in areas where its removal would result in exposure of pulp tissue. A decision to use this treatment is derived from a thorough pain history, clinical and radiographic examination, direct evalua-tion of the cavity preparation, and a good knowledge of tooth anatomy and the caries process.11

The aims of IPT are to arrest the carious process, provide conditions conducive to the formation of reactionary dentin, and promote remineralization of the altered dentin remain-ing.235 This in turn is expected to promote pulpal healing and preserve the vitality of the pulp.

TechniqueThe clinical steps in IPT may be divided into stages involving partial caries removal, placement of an antibacterial agent, and restoration of the crown in a way that provides the optimum coronal seal.

Some studies of IPT in primary teeth have advocated a two-stage approach.67,284 After initial partial caries removal without local anesthetic, the cavity was restored for 1 to 3 months, using a reinforced zinc oxide–eugenol (ZOE) cement or glass ionomer restoration. After this, further caries removal and definitive restoration were undertaken under local anes-thesia. It has been suggested that this approach may have a use in the very young or very anxious child, but it may be argued that a single-visit approach is more appropriate and successful.68 Thinner dentin in the primary tooth compared with the permanent tooth may result in a higher risk of pulp exposure if a primary tooth is reentered to remove residual caries.262

The following technique is based on a recommended approach235:

1. Local anesthetic2. Isolation with a rubber dam3. Removal of all caries at the enamel-dentin junction of

the cavity, ensuring caries-free walls4. Judicious removal of soft, deep carious dentin, using

large, round steel burs (#6 to #8). Hand excavators should be used only to remove caries at the dentino-enamel junction and should be angled outward at the DEJ, with care taken not to produce a pulp exposure.

5. Placement of an appropriate lining material, such as glass ionomer cement, hard-setting calcium hydroxide (Ca(OH)2). ZOE, or a directly bonded restoration

6. Definitive restoration providing the optimal coronal seal, such as an adhesive restoration or preformed metal (stainless steel) crown

literature is devoid of histologic or microbiologic studies in this area. In a study of 545 traumatized primary maxillary incisors, Borum and Andreasen27 found that 53% developed pulpal necrosis, and 25% developed canal obliteration. The age of the patient, degree of tooth displacement, concurrent crown frac-ture, and amount of root resorption were factors influencing pulpal necrosis and calcification. Teeth with a coronal fracture were less likely to suffer mineralized obliteration of the root canal than those that had been luxated.

In deciding on the appropriate treatment, the proximity of the primary tooth to the permanent successor is an important consideration. The treatment least likely to damage the perma-nent tooth should be chosen.7,27 Studies present conflicting data on the merits of treating or extracting traumatized primary teeth. Some have suggested no relationship,8,9 whereas others have shown more extensive developmental disturbances if the primary tooth is treated and preserved.250

Transient or permanent discoloration of the crown occurs in approximately 50% of traumatized primary incisors, varying from yellow to dark gray and usually becoming evident in 1 to 3 weeks. The yellow discolorations are frequently associated with canal calcification but are not commonly associated with pulp necrosis.27,114

Pulpal necrosis ranging from 50% to 82% has been reported in traumatized primary incisors with dark gray discoloration, compared to 25% in those with no discoloration.27,114,116,247 Croll et al.43 pointed out that color change in the absence of other clinical findings is unreliable. The diagnosis of pulpal necrosis is usually based on dark gray color and radiographic evidence of periapical pathology or cessation of root development.

In immature permanent teeth, discoloration of the crown is also one of the best diagnostic indicators after traumatic inju-ries.124,129 Yellow or brown-tinted discoloration usually indi-cates calcification of the pulp space; a gray color is usually associated with pulpal necrosis. A return to normal after tran-sient coronal discoloration6,38 and transient apical breakdown up to 4 months’ duration38 has also been reported.

PRINCIPLES OF ENDODONTIC TREATMENT IN CHILDRENEndodontic procedures are undertaken to preserve teeth in a comfortable, functional, and ideally disease-free condition. The following sections describe a range of clinical procedures that aim to achieve these goals in the primary and young per-manent dentitions, but they should not be seen merely as technical exercises. Readers should bear in mind that clinical management goes beyond the simple restorative procedure. The general care of anything from a preschool child requiring pulp therapy on a carious primary molar to an 8-year-old who has sustained trauma to an immature maxillary incisor requires special skills. In purely dental terms, the principle adopted is that the best root filling is a healthy pulp, and emphasis is given to methods of pulp preservation in both the primary and young permanent dentitions. Pulpotomy techniques for the partial preservation of pulp tissue are also presented as legitimate therapies—in primary teeth where young and well-perfused tissues combine with the relatively transient nature of the dentition to win success, and in young permanent teeth where therapies strive to maintain the well-perfused and resilient apical pulp, at least until root formation is complete. None of


permanent tooth. Primary teeth undergo dramatic physiologic and physical changes over a relatively short period. Clinicians should keep in mind that pulp tissue is not static in nature, and outcomes for the same procedure may differ, depending on the age of the patient. Furthermore, because of the aging process within dental pulp, the likelihood of successful pulp capping diminishes with age. This may be explained by the increase in intrapulpal fibrous and calcific deposits seen with aging, together with a reduction in both pulpal volume and pulp fibroblast proliferation.105

Direct pulp capping should not be performed on carious pulpal exposures in primary teeth. Guidelines developed by both the American Academy of Pediatric Dentistry (AAPD) and the British Society of Paediatric Dentistry (BSPD) recommend that direct pulp capping should be reserved only for small mechanical or traumatic exposures in primary teeth.54,235 Under these cir-cumstances, it is presumed that the conditions for a favorable pulpal response are optimal.

Pulpotomy in Primary TeethThe AAPD guidelines for pulp therapy for primary and young permanent teeth describe the pulpotomy procedure in primary teeth as the amputation of the affected or infected coronal portion of the dental pulp, preserving the vitality and function of all or part of the remaining radicular pulp.54 Evidence of successful pulp therapy includes the features listed in Box 24-2.

Complete amputation of the coronal pulp is the norm for pulpotomy procedures performed on the cariously exposed vital pulps of primary teeth. After this, and once hemostasis has been achieved, a decision is made on the wound dressing or technique to apply to the pulp stumps.

The following are some of the available options. The success of all procedures depends upon ensuring that the residual pulp tissue is correctly diagnosed as healthy or reversibly inflamed.

• Hemostasis and maintenance of vital tissue (e.g., ferric sulfate solution, electrosurgery, laser)

• Dentin bridge formation and maintenance of vital tissue (e.g., MTA)

• Superficial (partial) pulp tissue fixation and maintenance of vital tissue (e.g., dilute formocresol solution, gluta-raldehyde solution)

Many pharmacotherapeutic agents have been used for pulp therapy in the past. Formocresol has been the most popular agent, mainly because of its ease of use and good clinical success. Nonetheless, formocresol, and in particular one of its constituents, formaldehyde (FAD), has come under close

Unfortunately, the evidence currently is insufficient to promote a definitive choice for the lining material placed over the residual stained dentin.235 Studies show good success rates for resin-modified glass ionomer lining/restoration, self-etching adhesive systems, and Ca(OH)2 linings.35,36,142

Although additional prospective clinical evaluation of IPT is required, studies involving the primary dentition show good success rates (over 90% at 3 years).4,67,68,295 However, it has been suggested that a successful outcome is highly dependent upon obtaining the optimal coronal seal to eradicate the nutri-ent supply to residual cariogenic microorganisms. When intra-coronal amalgam restorations were compared with extracoronal preformed metal (stainless steel) crowns after IPT, failure was 7.7 times more likely with the amalgam restorations. Adhesive restorations also were reported to provide the optimal coronal seal after pulp therapy.103 Therefore, to secure the best possible outcome after IPT, or indeed after any pulp therapy for the primary tooth, definitive restoration should involve a bonded restoration and/or preformed metal (stainless steel) crown.

The Hall TechniqueThe Hall technique, an emerging method of managing dental caries in primary molars, is noteworthy in this section on indirect pulp therapy. The technique was introduced by Dr. Norna Hall, a primary care clinician in Scotland, who was overwhelmed by the number of children with dental caries. In Scotland, by the age of just 5 years, 55% of children had visible decay into dentin, and 16% had experienced tooth extraction. In response, this clinician decided to manage lesions in primary molars (that were symptom free and free of radiographic signs of periradicular pathology) by cementing a preformed metal (stainless steel) crown in place without local anesthesia, tooth preparation, or any attempt at caries removal. This is viewed in the United Kingdom as an undoubtedly novel approach to caries management and caught the attention of clinical aca-demics in Scotland. Audit data from Hall’s records indicate that her technique may have results similar to those for more con-ventional approaches in the primary care setting.126

Subsequently, a randomized, controlled clinical trial was undertaken comparing the Hall technique with conventional restorations in carious primary molars in primary care.125 Inter-estingly, the Hall technique was preferred to conventional res-torations by most children, guardians, and clinicians. After a review period of 2 years, in which the teeth managed using Hall preformed metal (stainless steel) crowns were compared with conventional restorations, the “Hall crowns” showed better treatment outcomes for both pulpal health and restora-tion longevity. In the United Kingdom, this has further stimu-lated an ongoing debate over whether restorative treatment provided by general clinicians in primary care is an effective way of managing caries in the primary dentition.70,179

Certainly this new and novel approach would appear to encompass present-day theory. Potentially cariogenic microor-ganisms require a very specific environment to start or progress a carious lesion. By sealing the lesion within the tooth, this removes the nutrient supply and stops or slows the lesion’s progress.168 Nevertheless, obtaining an effective and complete coronal seal should be of utmost concern.

Direct Pulp Capping in Primary TeethThe life span of the average primary tooth from initial develop-ment to exfoliation is significantly shorter than that of a

BOX 24-2

Evidence of Successful Pulp Therapy

◆ Vitality of most of the radicular pulp◆ No prolonged adverse clinical signs or symptoms (e.g.,

sensitivity, pain, or swelling)◆ No radiographic evidence of internal resorption reaching the

alveolar bone◆ No breakdown of periradicular tissue◆ No harm to permanent successor teeth◆ Pulp canal obliteration (abnormal calcification)—not considered a

failure


challenging, particularly in young children. The following points highlight the diagnostic aids available.

• An accurate pain history is helpful for determining the possible stage or extent of pulpal inflammation, but it may be difficult to elicit such information from a child.

• Radiographic findings can guide treatment decisions. Pretreatment radiographs are essential to assess the extent of the carious lesion and its proximity to the pulp horns or chamber. They also provide information about periradicular pathosis.

• Clinically, pulpal involvement can be assessed immedi-ately after caries removal by a very careful search for evidence of a pulp exposure.

Technique for Coronal Pulp AmputationRemoval of the coronal pulp tissue is a process common to whichever pulpotomy procedure is chosen for the cariously exposed vital primary tooth. After successful coronal amputa-tion and hemostasis (Fig. 24-10, A and B), the subsequent management of the radicular pulp stumps is defined by which pulpotomy technique the clinician chooses. For example, once hemostasis has been achieved, a wound dressing may be applied to the pulp wounds or, alternatively, the exposed tissue might be subjected to electrosurgery or laser application. Figure 24-10, C to H provides a schematic overview of the options and expected outcomes.

Stages of the Technique for Coronal Pulp Amputation1. After the initial diagnosis of probable vital pulpal involve-

ment, the primary tooth is anesthetized and isolated with a rubber dam.

2. All caries is removed, and the observation of bleeding from exposure sites indicates vital (if inflamed) coronal pulp tissue (Fig. 24-11, A and B).

3. The entire roof of the pulp chamber is removed using a high-speed non–end cutting bur and copious water spray.

4. All the coronal pulp is amputated with a slow-speed #6 or #8 round bur or spoon excavator. Care must be exercised to fully unroof the chamber and extirpate all filaments of the coronal pulp (Fig. 24-11, C and D). If any filaments remain in the pulp chamber, hemorrhage will be impossible to control.

5. The pulp chamber is thoroughly washed with sterile water or saline to remove all debris, and the site is dried by vacuum and sterile cotton pellets.

6. Hemorrhage is controlled by slightly moistened cotton pellets (wetted and blotted almost dry) placed against the stumps of the pulp at the openings of the root canals. Com-pletely dry cotton pellets should not be used; fibers of the cotton will be incorporated into the clot, and when the pellet is removed, hemorrhage will result. Dry cotton pellets are placed over the moist pellets, and pressure is exerted on the mass. Hemorrhage should be controlled in this manner within 3 minutes. It may be necessary to change the pellets to control all hemorrhage.

7. If bleeding persists, the clinician should carefully check that all tissues of the pulp were removed from the pulp chamber and that the amputation site is clean. If the bleeding persists from one of the canals, that canal can be reentered with a small round bur to amputate the suspected inflamed tissue; the canal then is rinsed again, and cotton pellet pressure is applied.

scrutiny because of reported concerns related to the systemic distribution of FAD and its potential for toxicity, allergenicity, carcinogenicity, and mutagenicity. Other medicaments (e.g., glutaraldehyde, Ca(OH)2, collagen, ferric sulfate, MTA) have been suggested as possible replacements. However, varying success rates and questions about the safety of these materials make it clear that additional research is required on the use of these and other pharmacotherapeutic agents.

Nonpharmacologic hemostatic techniques have been rec-ommended, including electrosurgery163,197,237,253,254 and laser therapy.62 Research involving human clinical trials on both these techniques is sparse; nevertheless, electrosurgical pulp-otomy currently is taught in several dental schools. Compre-hensive reviews of the techniques and agents used in vital pulp therapy and discussion of possible new modalities are available in the literature.223,262,296

Indications and Contraindications for PulpotomyPulpotomy is indicated for pulp exposure on primary teeth in which the inflammation or infection is judged to be confined to the coronal pulp.137,278 If inflammation has spread into the tissues within the root canals, the tooth should be considered a can-didate for pulpectomy and root canal filling or extraction. The contraindications to pulpotomy on a primary tooth are out-lined in Box 24-3.

TechniquePulpotomy is used for primary teeth with radicular pulp tissue judged to be free of inflammation and infection. Compromise on this principle leads to a diminished success rate. If inflamed vital (coronal) pulp tissue is amputated to leave residual healthy pulp tissue (radicular), the tissue remaining has the capacity to remain healthy if managed correctly. The overall success of vital pulp therapy in the primary dentition depends upon several factors:

• Effective control of infection• Complete removal of inflamed coronal pulp tissue• Appropriate wound dressing• An effective coronal seal during and after treatmentAn accurate diagnosis of pulp status is very important in

aiding appropriate pulpal management. However, this can be

BOX 24-3

Contraindications to Pulpotomy in a Primary Tooth

◆ History of spontaneous toothache (not caused by papillitis resulting from food impaction)

◆ Nonrestorable tooth where a postpulpotomy coronal seal would be inadequate

◆ Tooth near exfoliation; or, no bone overlies crown of the permanent successor tooth

◆ Evidence of periapical or furcal pathosis◆ Evidence of pathologic root resorption◆ Pulp that does not bleed (necrotic)◆ Inability to control radicular pulp hemorrhage after coronal pulp

amputation◆ Pulp with serous or purulent drainage◆ Presence of a sinus tract


• Permanent placement of MTA• Electrosurgical manipulation of the wound surfaces• Laser manipulation of the wound surfacesFigure 24-11, G shows the treated tooth restored with a

preformed metal crown.

Formocresol PulpotomyTechnique (See Fig. 24-10, C and D)1. After coronal pulp amputation and once hemostasis has

been achieved, a cotton pellet moistened with one-fifth dilu-tion formocresol solution (Box 24-4) is blotted to remove excess formocresol and then placed in direct contact with the pulp stumps for 5 minutes. Formocresol is caustic and creates a severe tissue burn if allowed to touch the gingiva.

2. When the pellet is removed, the tissue appears brown, and no hemorrhage should be evident.

3. If an area of the pulp was not in contact with the medica-tion, the procedure must be repeated for that tissue. Small cotton pellets for applying the medication usually work best because they allow closer approximation of the material to the pulp.

4. A cement base of ZOE is placed over the pulp stumps and allowed to set. The tooth may then be restored permanently.

5. The restoration of choice is a preformed metal (stainless steel) crown for primary molars. On anterior primary teeth, a composite tooth-colored restoration is the treatment of choice unless the tooth is so badly broken down that it requires a crown.The use of formocresol in dentistry remains controversial.

Formaldehyde, a volatile organic compound, is toxic and cor-rosive, especially at the point of contact. Formocresol’s other active constituent, cresol, is also an irritant and corrosive in nature.144

Local and Systemic Accumulation of FormaldehydeLocalized accumulation of formocresol or FAD has been demonstrated in pulp, dentin, periodontal ligament, and bone surrounding the apices of pulpotomized teeth.88,190

Although animal studies have identified radioisotope-labeled formocresol or FAD in major organs after systemic injection or multiple pulpotomies, researchers concluded that the doses of formocresol were far in excess of those used in normal clinical practice. Therefore, it has been suggested that the findings should not be extrapolated to clinical use in humans.187-189 More recently, a review of the safety of formo-cresol, including FAD metabolism, suggested that FAD is rapidly metabolized, so the findings of previous studies may have been identifying FAD metabolites systemically and not FAD itself.178 Notwithstanding this, the amount of formocresol

FIG. 24-10 Three different approaches to the radicular pulp after coronal pulp amputation during pulpotomy in an extensively carious primary molar. A, Primary molar with caries extending to the pulp. Note the inflammatory response in the coronal pulp. B, The tooth has undergone removal of the coronal pulp. The radicular pulp tissue is healthy and has stopped bleeding. C, A 1 : 5 dilute solution of formocresol may be applied to the pulp stumps for 5 minutes. This produces partial tissue fixation, which is greatest near the point of application. D, Intracoronal restoration: zinc oxide eugenol (ZOE) is placed directly over the pulp stumps, and an intracoronal restoration is placed. Vital radicular pulp may remain apically. E, A 15.5% ferric sulfate solution is applied to the pulp stumps for 15 seconds. This produces mechanical blockage of open capillaries by a protein-iron complex. F, Intracoronal restoration has been provided as in D. Healthy, vital pulp tissue remains in the root canals. G, Mineral trioxide aggregate (MTA) is placed directly over the radicular pulp stumps, and an intracoronal restoration is provided as before. H, The radicular pulp tissue remains vital beneath the MTA; a calcific bridge may form over time beneath the MTA.

C

A B

D

E

F

G

H

8. If hemostasis is not achieved within 2 to 3 minutes, the pulp tissue within the canals is probably inflamed, and the tooth is not a candidate for a pulpotomy. The clinician should then proceed with pulpectomy, or the tooth should be extracted.Once bleeding has stopped at the radicular pulp stumps,

the wounds are managed according to one of the following pulpotomy techniques (see Fig. 24-10):

• Application of dilute formocresol solution for 5 minutes• Application of 15.5% ferric sulfate solution for 15

seconds (Fig. 24-11, E and F)

BOX 24-4

Formulation of a One-Fifth Dilution of Formocresol Solution

Mix 1 part Buckley’s formocresol solution with:• 1 part distilled water• 3 parts glycerin


FIG. 24-11 Clinical stages of a vital pulpotomy using ferric sulfate solution. A, Extensive dental caries affecting a mandibular first primary molar. Note the proximity of the radiographic lesion to the mesial pulp horn. B, Caries removal, showing a carious pulpal exposure; bleeding is evident. C, Partial unroofing of the pulp chamber; note the bleeding coronal pulp before amputation. D, Roof of pulp chamber removed completely. E, A 15.5% solution of ferric sulfate is applied to the radicular pulp stumps with a dento-infuser tip supplied by the manufacturer. F, Hemostasis is evident at the radicular pulp stumps. G, Definitive restoration involves placement of zinc oxide eugenol, overlaid with glass ionomer intracoronally, followed by a preformed metal (stainless steel) crown. (Courtesy Vidya Srinivasan, Edinburgh Dental Institute, Scotland, UK.)

A

B

C

F

E

D

G


studies comparing dilute formocresol (see Box 24-4) with the undiluted solution (Table 24-1). Histochemical investigations comparing dilute and undiluted formocresol noted little difference between initial effects on pulp tissue fixation but earlier recovery of enzyme activity and improvement in the rate of recovery from the localized cytotoxic effects of formo-cresol with diluted formocresol.158,159,268 Clinical studies have shown diluted formocresol to be as successful as full-strength formocresol.81,82,180

There is enough evidence today to conclude that if formocresol is to be used at all, the one-fifth concentration should be preferred for pulpotomy procedures because it is as effective as and less damaging than the traditional preparation.

Formocresol and the Permanent SuccessorThe fear of damage to the succedaneous tooth has been offered as an argument against formocresol pulpotomy on primary teeth. Results from studies are inconsistent, ranging from the same incidence of enamel defects in treated and untreated contralateral teeth181,236 to an increase in defects and positional alterations of the underlying permanent tooth.177 It should be pointed out that studies of this nature are follow-up studies long after treatment, and the researchers had no knowledge of the existing status of the pulp before pulpotomy.

The effect of a formocresol pulpotomy upon the exfoliation time of primary molars is also equivocal; some studies found no consistent effect,181,290 and others reported early exfoliation.113,180

Unlike the tissue response to Ca(OH)2 or MTA, no dentin bridge should be anticipated after formocresol is applied to exposed pulp tissue (see Fig. 24-10, C and D). However, nar-rowing of the root canal through the continued deposition of dentin by the preserved radicular pulp may be observed in some cases (Fig. 24-12).

Criteria for SuccessFailure of a formocresol pulpotomy is usually detected on radiographs (see Fig. 24-8). The first signs of failure are often internal resorption of the root adjacent to the area where the formocresol was applied. This may be accompanied by external resorption, especially as the failure progresses. Sometimes, however, the internal resorption is self-corrected with deposi-tion of calcified tissue. In the primary molars, radiolucency develops in the bifurcation or trifurcation area. In the anterior teeth, a radiolucent area may develop at the apices or lateral to the roots. With more destruction, the tooth becomes exces-sively mobile; a sinus tract usually develops. It is rare for pain to occur with the failure of a formocresol pulpotomy. Conse-quently, unless patients receive follow-up checks after a formo-cresol pulpotomy, failure may go undetected. When the tooth

absorbed systemically by way of the pulpotomy route is small and may not contraindicate use of the drug.210

Formocresol as an AllergenThe results of studies investigating the allergenic risks of formocresol are equivocal. Studies have shown no evidence of an allergic response in nonpresensitized animals,258 and pre-sensitized animals showed only a weak allergic potential.292 However, demonstration of an immune response to formocresol-fixed, autologous tissue implanted in connective tissues or injected into root canals has been reported.24,293

Is Formocresol Carcinogenic?With respect to mutagenicity and carcinogenicity, it is generally accepted that FAD is genotoxic in vitro, inducing mutations and DNA damage in cells from a variety of organisms, includ-ing humans.96,200,207,272,302 The possible link between FAD and carcinogenesis has been investigated in the field of occupa-tional health medicine. In a review of several large longitudinal studies, the International Agency for Research on Cancer (IARC) reported that “sufficient evidence” exists that FAD had caused nasopharyngeal cancer in humans.32 This was sug-gested to be linked to a localized combination of irritation and genotoxicity of FAD, which repeat-dose inhalation studies using rodents has corroborated.209 In the dental context, the amount of FAD in a diluted solution of formocresol is small, but no data are available on the amounts of FAD vapor inhaled by patients or dental personnel during pulpotomy procedures and whether this may constitute a potential risk. Moreover, the often disregarded cresol ingredient itself may pose a genotoxic risk to mammalian cells.104 Formocresol solution used in pulpotomies in children has been reported as genotoxic after postpulpotomy harvested lymphocyte cultures displaying sig-nificantly increased chromosomal aberrations were compared with nonpulpotomized controls.160

Despite these concerns, the formocresol pulpotomy contin-ues to be one treatment choice available for primary teeth with vital, carious exposures of the pulp in which inflammation or degeneration is judged to be confined to the coronal pulp. The last reported worldwide survey of dental schools (in 1989)13 showed that most pediatric dentistry departments and pediat-ric dentists advocated the formocresol pulpotomy technique, and it may still be widely used in clinical practice. In the United Kingdom, since 2004, a general trend away from using formocresol has been noted, driven by several factors, such as difficulty obtaining the medicament, concerns related to its safety, and promising clinical results for newer, nonaldehyde techniques.296 However, the recent U.K. clinical guideline, Pulp Therapy for Primary Molars, still includes the formocresol pulpotomy as an option,235 as do the AAPD guidelines.54 Although formocresol pulpotomy is still taught in predoctoral pediatric dentistry programs in the United States,218 consensus is lacking on its use for vital pulp therapy in primary teeth.

The current formocresol pulpotomy technique is a modifi-cation of the technique reported by Sweet in 1930.271 The effect of formocresol on pulp tissue (i.e., the amount of tissue fixa-tion) is controlled by the quantity that diffuses into the tissue and depends on the duration of application, the concentration used, the method of application, or a combination of these factors.63,90,167,173

A one-fifth dilution formocresol solution has been widely advocated based on the outcomes of both in vitro and in vivo

TABLE 24-1

Formulation of Full-Strength Buckley’s Formocresol

Formaldehyde 19%

Tricresol 35%

Glycerin 15%

Water 31%


stratified squamous epithelium, which suggests the potential for cyst formation. In a subsequent study involving failed, pulpotomized primary molars, most specimens were diagnosed as furcation cysts.186 These findings emphasize the importance of periodic follow-up to endodontic treatment on primary teeth. Figure 24-13 shows a favorable long-term outcome after a formocresol pulpotomy in a mandibular primary molar.

ALTERNATIVES TO FORMOCRESOL PULPOTOMYA 2006 comprehensive review by Srinivasan et al.262 is sug-gested for readers requiring a more detailed look at the numer-ous alternative techniques available.

Glutaraldehyde PulpotomyGlutaraldehyde has been suggested as an alternative to formo-cresol as a tissue fixative for vital pulpotomy. Histologic studies showed that it produced rapid surface fixation of pulp tissue but with limited depth of penetration, so a larger amount of radicular pulp tissue remained vital.275,300 Fixed pulp tissue may be replaced with dense collagenous tissue over time.141 Studies have also demonstrated less systemic distribution than was thought to occur with formocresol.51,152,187,210,301

Glutaraldehyde has been shown to be rapidly metabolized with little toxic effect.112,130,135,187,227 It has also been demon-strated that although glutaraldehyde has antigenic action similar to that of formocresol, it is of a lower potential.224,226

FIG. 24-12 Narrowing of the apical region of the root canal after formo-cresol pulpotomy. Histologic section of a tooth showing deposition of new dentin along the walls of the apical region of the root canal.

FIG. 24-13 Five-year follow-up of a primary tooth treated by formocresol pulpotomy. A, Pretreatment radiograph showing deep caries on the lower right first and second primary molars. B, One-year posttreatment radiograph. C, Five-year follow-up radiograph. Note the eruption of the lower right first permanent molar and first bicuspid.

A

C

B

loosens and is eventually exfoliated, the parents and child may consider the circumstances normal.

The development of cystic lesions after pulp therapy in primary molars has been reported.29,243 An amorphous, eosino-philic material shown to contain phenolic groupings similar to those present in medicaments was found in the lesions. Myers et al.185 have observed furcal lesions in untreated, pulpally involved primary molars containing granulomatous tissue with


steel) crowns. In a study by Papagiannoulis,208 half of the teeth were restored with composite resin and the remaining half with preformed metal (stainless steel) crowns.

Prospective StudiesIn a study by Fei et al.,71 27 teeth were included in the formo-cresol group and 29 in the ferric sulfate group. Although the sample size was small, the recall rate was excellent, and in the 3- and 6-month intervals, no statistically significant difference was found between the two groups. However, at the end of this 1-year study, a statistically significant difference was seen in the success rate in favor of ferric sulfate (97% for ferric sulfate, 78% for formocresol). The most frequent evidence of failure in this short-term study in both groups was furcation radiolu-cency. In a study by Fuks,79 the sample consisted of 37 teeth in the formocresol group and 55 in the ferric sulfate group. The follow-up period ranged from 6 to 34 months, with a mean of 20.5 months. In this study, the sample size was bigger and the evaluation period much longer than in the previous one. The total success rate between the two groups over the total period of 34 months did not present any statistically significant difference; it was 92.7% for ferric sulfate and 83.8% for formo-cresol. Calcific metamorphosis and internal resorption were the most common radiographic findings. In this study, internal resorption that was stable and unchanged throughout the study was not recorded as failure.

In a later study by Ibricevic and Al-Jame,123 34 teeth were used in each group, and identical results were obtained 24 months after treatment for both ferric sulfate and formocresol: a 97% total success rate was recorded. In each group, only one tooth showed internal resorption and was therefore considered a failure.

The results of a larger comparative study208 were published in 2002. The sample comprised 133 pulpotomy-treated molars of 90 children from 3 to 10 years old, with a mean age of 6.2 years. Sixty teeth (45%) were treated with formocresol and 73 (55%) with ferric sulfate. The number of teeth restored with either a stainless steel crown or a composite resin material was almost equal within each group. After 36 months, the clinical success rate was 97.3% for formocresol and 90.3% for ferric sulfate, but the difference in success rate between the two groups was reported to be statistically insignificant. The radio-graphic success rate was 78.3% for formocresol and 74% for ferric sulfate, again with no statistically significant difference between them. This success rate seems to be the lowest recorded compared with the previously mentioned compara-tive studies. The study’s author believed that this finding could be due to three reasons: (1) the larger sample size, (2) the very good recall rate, which increased the possibility to observe and locate more failures; and (3) the very strict radiographic assess-ment. Internal resorption was the most common radiographic finding for both treatments, with no statistically significant difference between ferric sulfate and formocresol. However, most cases classified initially as failures because of internal resorption remained stable throughout the 36-month observa-tion period, and in two cases the respective areas were self-filled with reparative hard tissue. Based on this observation, the data were reevaluated, and only cases of internal resorption that were either extensive in size or progressing with time were considered as failures. After the reevaluation, the overall success rate became 78.7% for ferric sulfate and 85% for formocresol, with no statistically significant difference between

However, there are perceived problems with the use of gluta-raldehyde as a pulpotomy agent:

• Glutaraldehyde solutions are reported to be unstable.222

• Neither the optimum concentration nor optimal dura-tion of application of glutaraldehyde solution have been established conclusively.92,156,225

• Clinical studies reported increasing failure rates with increasing time after pulpotomy,83 with lower levels of clinical success than with formocresol.5

Despite its perceived enhanced safety compared with formo-cresol, glutaraldehyde has not gained favor over formocresol for pulpotomy in the primary dentition.13,72

Ferric Sulfate PulpotomyTechnique1. After completion of coronal pulp amputation and achieve-

ment of hemostasis with moist cotton pellets, a 15.5% solu-tion of ferric sulfate is applied to the radicular pulp stumps for 10 to 15 seconds.

2. The ferric sulfate may be applied using a cotton pellet or by allowing small droplets of the solution to drip from a bur-nisher tip onto the surface of the pulp tissue. One manu-facturer also supplies a special dento-infuser tip for this purpose (Astringident, Ultradent Products, Salt Lake City, Utah) (see Fig. 24-10, E, and Fig. 24-11, E).

3. Upon removal of the cotton pellet, the wounds appear brown, and no bleeding should be evident. If a small amount of residual bleeding occurs, one further application of ferric sulfate should be considered.

4. A cement base of ZOE is placed over the pulp stumps and allowed to set. The tooth may then be restored perma-nently as described for the formocresol pulpotomy (see Fig. 24-10, F).Ferric sulfate is well esablished as a hemostatic agent for

crown and bridge impressions.75 Its hemostatic action occurs by the reaction of blood with ferric and sulfate ions within the acidic pH of the solution. The agglutinated proteins form plugs that occlude the capillary orifices and prevent blood clot for-mation.153 Initially the use of ferric sulfate was recommended as a hemostatic agent during Ca(OH)2 pulpotomy on the grounds that it may prevent problems arising from clot forma-tion after coronal pulp amputation and minimize the chances for inflammation and internal resorption246; some consider these to be important factors contributing to the failure of pulpotomies using Ca(OH)2. The first documented use of ferric sulfate in this way was in primate teeth.145

The use of ferric sulfate itself as a hemostatic pulpotomy agent was investigated by researchers using animal models (rat40 and baboon79). Published clinical studies using ferric sulfate as a pulpotomy medicament have included both pro-spective comparative71,79,123,208 and retrospective28,261 designs.

In all the comparative studies, formocresol was included as the gold standard. The materials and methods used in all these studies are similar, which allows more meaningful comparison of their findings. Pulpotomies were performed in primary molars of healthy children who were selected on the basis of symptomless exposure of vital pulp by caries, absence of clini-cal or radiographic evidence of pulp degeneration, and possi-bility of proper restoration.

In all of the aforementioned ferric sulfate studies, the teeth were treated using the pulpotomy technique already outlined, and the teeth were restored with preformed metal (stainless


results.208 Others proposed that internal resorption should not be considered as pulpotomy failure and based this proposal on the fact that none of the teeth with internal resorption in their sample developed an osseous lesion.261 This proposal may be accepted only in cases of minimal or unchanged internal resorption; not for severe or progressive resorption. Internal resorption may indicate pulp inflammation that is expected at the amputation site after pulpotomy. However, if the inflam-mation can be restricted and confined to a very small part of the pulp while the remainder is healthy, the resorption process will cease or even self-heal by the apposition of hard tissue and therefore will not be a failure. In all the other cases, internal resorption indicates irreversible or extensive inflammation and should be considered a failure.

It can be seen from these studies and the results of a meta-analysis157 that for human carious primary molars with revers-ible coronal pulpitis, ferric sulfate and formocresol pulpotomies give similarly good clinical and radiographic results, with high tooth survival rates and no statistically significant differ-ences in success rates. These findings agreed with an earlier Cochrane Review of pulp treatment for extensive decay in primary teeth.192

Based on these studies, ferric sulfate can be used instead of formocresol for treatment periods up to 36 months.

Mineral Trioxide Aggregate PulpotomyTechnique1. After completion of coronal pulp amputation and achieve-

ment of hemostasis with moist cotton pellets, MTA powder is mixed with sterile water until the powder is adherent. Excess moisture is removed from the powder by placing a dry paper point into the mixture to act as a moisture wick.

2. The MTA may be applied to the pulp tissue using an excava-tor or retrograde amalgam carrier, ensuring enough material to completely cover the exposed pulp tissue to a depth of 3 to 4 mm (see Fig. 24-10, G).

3. The MTA mixture is gently packed over the pulp tissue using the blunt end of a large paper point and a broad-ended amalgam compactor. This layer of MTA is a permanent wound dressing.

4. A cement base of ZOE or glass ionomer cement is placed gently over the MTA and allowed to set. The MTA will take several hours to reach its optimum physical strength, so care must be taken to ensure an intact layer of MTA is in contact with the pulp tissue.

5. The tooth may then be restored permanently as described for the formocresol pulpotomy.MTA used as a pulp capping agent in monkey teeth showed

the pulp tissue responses to MTA to be superior to those pro-duced using Ca(OH)2.

215 Similar results were found when human intact third molars were used to compare the effect of pulp capping with MTA and Ca(OH)2.

1 MTA was found to maintain pulp integrity after pulp capping and pulpotomy in animal studies55,239 and to have a dentinogenic effect on the pulp expressed by the induction of dentin bridge formation (see Fig. 24-10, H) where it touches the pulp tissue.239,241,288

Clinical StudiesOne of the first preliminary studies published comparing MTA with formocresol in humans60 involved 45 pulpotomy-treated primary molars in 26 children with a mean age of 6 years, 5

them. The survival rate of the treated teeth after 6 months was 98% for both treatments and then 97% for ferric sulfate and 94% for formocresol after 1 year. These figures decreased with time for both groups, and the survival rate dropped to 81% for ferric sulfate and 78% for formocresol from 25 to 36 months.

Retrospective StudiesIn a retrospective study published in 2000 by Smith et al.,261 ferric sulfate pulpotomies performed over a period of 5 years by a private pediatric dentist were evaluated. The clinical success rate was very high: 99% up to 36 months and no further failures after 36 months. The radiographic success varied from 80% for the 4- to 12-month period, 74% for the 13- to 24-month period, 81% for the 25- to 36-month period, and 74% for the over 36-month period. The estimated tooth survival time was very high, starting with 99% up to 10 months and dropping to 80% after 43 months. The two most common radiographic findings in this study were calcific metamorpho-sis and internal resorption. The records in this study showed that 13 teeth that presented with internal resorption did not develop osseous lesions for the period of 43 months.

A second retrospective study, published 2 years later in 2002, reported results comparing different pulpotomy treat-ments; 83 formocresol pulpotomies, 45 ferric sulfate pulpoto-mies, and 74 pulpotomies treated with a combination of ferric sulfate and formocresol were selected from the records of chil-dren treated in a public clinic at different times and by different clinicians.28 The initial results showed that the total success rate was similar in the three groups, but after a 36-month follow-up, the success rate was better for formocresol than for ferric sulfate, and the combination of the two agents was the worst. The last finding is not surprising because the teeth were treated initially with ferric sulfate for hemostasis and then with formocresol, and they had a poor prognosis (i.e., hyperemic and/or symptomatic). As pointed out by the authors, this study had several shortcomings, the most serious being that the pulpotomies were performed by many clinicians of different levels of experience and expertise; the criteria for selection of cases were not strictly defined; and the radiographs were not always satisfactory, compromising accurate evaluation of the periradicular and furcal areas of the treated teeth.

The studies described demonstrate a higher success rate for both ferric sulfate and formocresol in those with shorter obser-vation times and smaller sample sizes. As the sample size increases and the observation period becomes longer, the success rate drops; this holds true for both ferric sulfate and formocresol pulpotomies. The most important finding is that no statistically significant differences in the success rates between ferric sulfate and formocresol existed, with the excep-tion of one short-term study71 in which a statistically signifi-cant difference was observed in favor of ferric sulfate at the 1-year period. In all the reviewed studies (prospective and retrospective), both ferric sulfate and formocresol treatments gave very good results with high tooth survival rates. More-over, the type of restoration (stainless steel crown or composite resin) was not reported to influence the success rate for either pulpotomy agent.208

Clinical OutcomeIn one study, the cases of internal resorption that remained unchanged throughout the 36-month observation period were not considered as failures in the final examination of the


6 months after treatment. Sixty pulpotomy-treated teeth in 20 children were reviewed; of these, one tooth (gray MTA) exfo-liated normally, and six teeth (four white MTA and two formocresol) failed because of abscesses. All the remaining 53 teeth showed success clinically and on radiographs. Pulp canal obliteration was found in 11 teeth treated with gray MTA and one treated with white MTA. The histologic evalua-tion demonstrated that both types of MTA induced thick dentin bridges, whereas in the formocresol group these were thin and poorly calcified. The pulpal architecture observed with the gray MTA was closer to normal than the white MTA, which presented a dense fibrotic pattern with isolated pulp calcification. These authors concluded that gray MTA was better than both white MTA and formocresol as a pulp dress-ing for pulpotomy-treated primary teeth. More recently, MTA pulpotomies were compared with Ca(OH)2

154,273 and ferric sulfate,56,65 with reported results showing that MTA is a suit-able pulpotomy agent.

The growing evidence from clinical studies and a systematic review257 allows MTA to be recommended as an effective pul-potomy agent in primary teeth.

MTA is commercially available in the United States as ProRoot MTA (DENTSPLY Tulsa Dental Specialties, Tulsa, OK). Angelus MTA (Angelus Indústria de Produtos Odon-tológicos, Londrina, Brazil) is also available in Latin America and Europe. ProRoot MTA is considered expensive, particu-larly because it is retailed in cartons containing a number of sealed 1-g packets. The composition of MTA is similar to that of cement used in the building industry, and such material should be kept dry during storage because contact with moist air leads to “air setting,” which affects the powder’s physical properties. The same could be applied to the “clinical grade” cement, and the manufacturer of ProRoot MTA recommends the 1-g sachet as single use, which would be expensive. The unused MTA remaining in a sachet may actually be stored for up to a further 4 weeks in a water-tight, air-tight container such as an Eppendorf tube (Eppendorf UK, Cambridge, Great Britain, UK), reducing its cost.265 It has been suggested that the MTA powder can be stored indefinitely if the corner of the packet is folded firmly and the packet is stored in a sealable plastic bag. Angelus MTA is presented in a sealable glass vial, with the recommendation that 1 g may provide up to seven treatments. Care must be taken not to contaminate the MTA powder when it is dispensed.

Electrosurgical PulpotomyTechniqueThe steps in the electrosurgical pulpotomy technique are basi-cally the same as those for the formocresol technique through the removal of the coronal pulp tissue.

1. Large sterile cotton pellets are placed in contact with the pulp, and pressure is applied to obtain hemostasis.

2. The Hyfrecator Plus 7-797 (Birtcher Medical Systems, El Paso, Texas) is set at 40% power (high at 12 W), and the 705-A dental electrode is used to deliver the electric arc. The cotton pellets are quickly removed, and the elec-trode is placed 1 to 2 mm above the pulpal stump.

3. The electric arc is allowed to bridge the gap to the pulpal stump for 1 second, followed by a cool-down period of 5 seconds. Heat and electrical transfer are minimized by

months. Clinical and radiographic follow-up ranged between 6 and 30 months, involving 18 children with 32 teeth. Internal resorption was seen in one molar treated with formocresol (17 months after treatment). None of the teeth from the MTA group presented any clinical or radiographic pathosis. Pulp canal obliteration was observed in 9 of 32 (28%) molars evaluated.

Preliminary results of a 3-year prospective follow-up study comparing MTA with formocresol were reported at a scientific congress.232 Pulpotomies were undertaken on 60 primary molars in 22 children aged 2 to 8 years, each needing at least two pulpotomies. Each child received at least one MTA and one formocresol pulpotomy, followed by application of a pre-formed metal (stainless steel) crown. Six months after treat-ment, seven teeth of the formocresol group and two of the MTA group presented abnormal radiographic findings, but these differences were not statistically significant.

More promising results were observed in a more extensive study by Holan et al.117 that included part of the material pre-sented by Eidelman et al.60 and a longer follow-up time. Holan and colleagues assessed the long-term success rate of pulpot-omy in primary molars with carious pulp exposure using MTA or formocresol as pulp dressing agents. Sixty-four primary molars of 35 children were treated by a conventional pulpotomy technique. After removal of the coronal pulp and hemostasis, the pulp stumps were covered with MTA in the experimental group. In the control group, formocresol was placed with a cotton pellet over the pulp stumps for 5 minutes and then removed; the pulp stumps were then covered with ZOE paste. Eight teeth from each group were restored with an amalgam restoration, and all others were covered with a pre-formed metal (stainless steel) crown. Thirty-three children with 62 teeth (29 treated with formocresol and 33 with MTA) were available for long-term clinical and radiographic evalua-tion. Follow-up ranged from 4 to 74 months, with a mean follow-up time of 38 months and with no difference between the groups. Twenty-nine teeth were followed until natural exfoliation (mean, 33 months). Failures were detected after a mean period of 16 months (range, 4 to 30 months). The success rate of pulpotomy was 97% for MTA (one failure) and 83% for formocresol (five failures). Eight teeth showed internal resorption. In four (two from each group), progress of the resorption process stopped, and the pulp tissue was replaced by a radiopaque calcified tissue. Pulp canal obliteration was observed in 55% (34 of 62) of the evaluated molars. This finding, which was not considered a failure, was detected in 58% (19 of 33) of the MTA and in 52% (15 of 29) of the formocresol group. The authors concluded that MTA showed a higher long-term clinical and radiographic success rate than formocresol as a dressing material following pulpotomy in primary molars and recommended it as a suitable replacement for formocresol.

The clinical, radiographic, and histologic effects of gray MTA, white MTA, and formocresol as pulp dressings in pulpotomy-treated primary teeth have been reported.102 This involved 24 children with a mean age of 6 years (range, 4 to 8 years), each with at least three primary molars requiring pulpotomy, for the clinical and radiographic part of the study. An additional 15 carious primary teeth planned for serial extractions were selected for the histologic part of the study. All the teeth were evaluated periodically for 12 months except those selected for histologic evaluation; these were extracted


observed for 12 to 27 months. All were clinically successful, and only one showed evidence of internal resorption at the 6-month follow-up visit. The authors observed complete cal-cification on radiographs after 9 months in approximately half of the treated teeth.

On the basis of these initial studies, the use of the carbon dioxide laser could be considered a viable alternative to formo-cresol. More randomized controlled human clinical trials are recommended.

In summary, the search for alternatives to the formocresol pulpotomy in cariously exposed vital primary teeth has yet to reveal an agent, instrument, or technique that has unequivocal long-term clinical success rates better than those of formocre-sol, although MTA is beginning to show evidence of excellent success rates in comparative studies.56,65,270 Until such an agent, instrument, or technique is found, ferric sulfate, MTA, or formocresol (one-fifth dilution) can be used with equal confi-dence in primary tooth pulpotomies.80,235,262

NONVITAL PULP THERAPY ON PRIMARY TEETH

Pulpectomy in Primary TeethThe anatomic and normal physiologic features of primary teeth can present challenges to the clinician wishing to undertake pulpectomy procedures. However, with knowledge of these features and how they may affect the clinical technique, pul-pectomy and root canal obturation of primary teeth with irre-versibly inflamed or necrotic pulp can be a clinically successful option.

In brief, these features are:• Root anatomy: Apical positions, lateral and accessory

canals• Root physiology: The effect of exfoliation upon root

anatomy and choice of root canal filling material• The permanent tooth bud: Its proximity to the primary

root apex

Effect of Resorption on Canal Anatomy and Apical ForaminaIn the newly completed roots of the primary teeth, the apical foramina are located near the anatomic apices of the roots. After the deposition of additional dentin and cementum, there are multiple apical ramifications of the pulp as it exits the root, just as in the mature permanent tooth.

The physiologic resorption of the roots of the primary incisors and canines starts on the lingual surfaces in the apical third because of the position of the permanent tooth bud. In primary molars, resorption usually begins on the inner surfaces of the roots near the interradicular septum (Box 24-5).

As resorption progresses, the apical foramen may not cor-respond to the anatomic apex of the root but be coronal to it. Subsequently, radiographic establishment of the root canal length may be challenging (Fig. 24-14). Resorption may extend through the roots and into the root canals, creating additional communications with the periapical tissues other than through the apical foramina or lateral and accessory canals. This has been shown to occur at all levels of the root.231 Because of these factors, use of an apex locator is not reliable to establish canal length.

keeping the electrode as far from the pulpal stump and tooth structure as possible while still allowing electric arcing.

4. If necessary, this procedure may be repeated up to a maximum of three times. The procedure is then repeated for the next pulpal stump.

5. When the procedure is properly performed, the pulpal stumps appear dry and completely blackened.

6. The chamber is filled with ZOE placed directly against the pulpal stumps. Research by Fishman76 has shown no difference between ZOE and Ca(OH)2 as the dressing. The tooth should then be restored with a preformed metal (stainless steel) crown.

Although electrocoagulation on the pulps of teeth was reported in 1957,150 it was a decade later that Mack162 became the first U.S. clinician to routinely perform electrosurgical pulpotomies. Oringer206 also strongly advocated this technique in his 1975 text on electrosurgery.

Electrosurgery is a nonpharmacologic, hemostatic pulpot-omy technique used directly on the radicular pulp stumps after coronal pulp amputation. Depending on the currents used and thus the heat generated, incision, coagulation, or electrofulgu-ration can occur. Electrosurgical pulpotomy carbonizes and denatures pulp tissue, producing a layer of coagulative necro-sis. This acts as a barrier between the lining material and healthy pulp tissue below.262

Several clinical studies237,254 have produced results compa-rable to those found with the use of formocresol. Conflicting results have been reported from histologic studies, ranging from results comparable to formocresol pulpotomy253 to patho-logic root resorption with periapical and furcal involvement.255 A retrospective human study in 1993163 showed a success rate of 99% for primary molars undergoing electrosurgical pulpoto-mies. Compared with a formocresol pulpotomy study of similar design, the success rate of the electrosurgery technique was shown to be significantly higher. A more recent study197 com-pared the use of two different base lining materials during electrosurgical pulpotomy. Success rates at 12 months were high for both groups, 98% and 96% for ZOE and zinc polycar-boxylate cements, respectively.

Laser PulpotomySeveral reports have appeared in the literature on the use of the carbon dioxide laser for performing vital pulpotomies on primary teeth.62,155 Elliott et al.62 compared the use of the laser with formocresol in caries-free, primary cuspid teeth that were scheduled for extraction in children between 6 and 10 years of age. Thirty teeth were included in the study. No significant differences were found between the formocresol and laser-treated groups. Areas of isolated internal resorption were iden-tified in one of the formocresol-treated teeth and two of the laser-treated teeth. These authors concluded that on the basis of symptomatic, clinical, and histologic findings, the carbon dioxide laser appeared to compare favorably with formocresol treatment. It was suggested that additional studies be con-ducted to establish the ideal applied laser energy to maximize optimum residual pulpal response and to explore the effects of laser pulpotomy upon pulps previously exposed by carious lesions.

Liu et al.155 reported the use of the laser on primary teeth with vital carious pulpal exposures. Thirty-three teeth, 21 primary molars and 12 primary canines, were treated and


BOX 24-5

Physiologic Root Resorption in Primary Teeth

Physiologic root resorption begins:• Soon after root-length completion• In primary incisors and canines, on the lingual aspect of the

apical third of the roots• In primary molars, on the inner surfaces of the roots next to

the inter-radicular septum

FIG. 24-14 Primary maxillary canine. A, Facial view: the apical foramen appears to be at the apex of the root. B, Physiologic root resorption has occurred at the palatal aspect of the root; the apical foramen is positioned more coronally and will not be coincident with the perceived radiographic apex of the tooth.

A B

Permanent Tooth BudThe effects of primary endodontic therapy on the developing permanent tooth bud should be of paramount concern to the clinician. Manipulation through the root apex of a primary tooth and overextension of root canal instruments and filling materials are to be avoided because the permanent tooth bud lies in close proximity. If radiographic signs of resorption are visible, the canal length is usually established by measurement of the diagnostic radiograph, ensuring that the working length of endodontic instruments is 2 or 3 mm short of the radio-graphic apex. Use of the long cone radiographic paralleling technique for maximal accuracy is recommended. Hemorrhage after pulp removal may indicate overextension into the periapi-cal tissues.

Anesthesia is usually necessary for pulp extirpation and cleaning of the canals but may be unnecessary when primary teeth are filled at a subsequent appointment. The response of the patient can sometimes be used as a guide to the proximity of the apex and as a check of the length of the canal. However, this can only be done in cooperative patients because the dis-comfort caused by placing the rubber dam clamp or by the approach of the instrument to the apex might create disruptive behavior in some children.

The material used to obturate root canals in primary teeth must be resorbable, so that as the tooth resorbs, it offers no resistance or deflection to the eruption of the permanent tooth. Permanent obturating materials, such as gutta-percha, are contra-indicated in root canal therapy for primary teeth that have per-manent successors.

PulpectomyPulpectomy and root canal filling procedures on primary teeth have been the subject of much controversy. Fear of damage to developing permanent tooth buds and a belief that the tortuous root canals of primary teeth could not be adequately negoti-ated, cleaned, shaped, and filled have led to the needless sac-rifice of many pulpally involved primary teeth. Much has been

written regarding potential damage to the developing perma-nent tooth bud from root canal fillings. The extraction of pul-pally involved primary teeth and placement of space maintainers is an alternative to pulpectomy. However, there is no better space maintainer than the primary tooth. If a space maintainer is placed but adequate monitoring and preventive care are not provided, further problems often occur.

For example, with a “band and loop” design of space main-tainer, loose bands and poor oral hygiene increase the risk of dental caries and gingival inflammation. Prolonged retention of the appliance may cause deflection of the erupting perma-nent tooth, and premature loss of the band can result in loss of space, particularly if the patient delays returning for treatment.

It has been reported that minor hypoplasia is increased in permanent successor teeth after root canal treatment of the primary precursors.119 Coll39 reported no such increased effect and concluded that defects result from the infection existing before the pulpectomy and not the procedure itself. It is note-worthy that these studies are retrospective, involving erupted permanent teeth; findings should be viewed with caution.

Economics has been advanced as an argument against end-odontic treatment of primary teeth, but it is not a reasonable argument when compared with the cost of space maintainers, including the required follow-up treatment. In fact, endodontic treatment is probably the less expensive alternative when the entire treatment sequence is considered.

The success of endodontic treatment on primary teeth is judged by the same criteria used for permanent teeth. The treated primary tooth must remain firmly attached and func-tion without pain or infection. Radiographic signs of furcal and periapical infection should be resolved with a normal peri-odontal attachment. The primary tooth should resorb normally and in no way interfere with the formation or eruption of the permanent tooth.

Success rates ranging from 75% to 100% have been reported.10,118,147,269,305 The usual modalities of evaluating root canal treatment in primary teeth have been clinical and radio-graphic. More comprehensive evaluation in this area is greatly needed.

Early reports of endodontic treatment on primary teeth usually involved devitalization with arsenic in vital teeth and the use of creosote, formocresol, or paraformaldehyde pastes in nonvital teeth. The canals were filled with a variety of materials, usually consisting of zinc oxide and numerous additives.59,93,131,263

Rabinowitch221 published the first well-documented scien-tific report on endodontic procedures on primary teeth in 1953. A 13-year study of 1363 cases of partially or totally


nonvital primary molars was reported. Only seven cases were failures; most patients were followed for 1 or 2 years clinically and with radiographs. Patients underwent multiple visits to achieve root canal fillings of ZOE and silver nitrate. Periapi-cally involved teeth required an average of 7.7 visits to com-plete treatment, and teeth with no periapical involvement required an average of 5.5 visits. Rabinowitch listed internal resorption and gross pathologic external resorption as contra-indications to primary root canal fillings.

Another well-documented study reported a success rate of 95% in vital and infected teeth using a filling material of thymol, cresol, iodoform, and zinc oxide.10 (See Bennett19 for a review of the techniques of partial and total pulpectomy.)

In a well-controlled clinical study of primary root canal treatments using Oxpara paste as the filling material,147 five preexisting factors were reported to render the prognosis less favorable:

1. Perforation of the furcation2. Excessive external resorption of roots3. Internal resorption4. Extensive bone loss5. Periodontal involvement of the furcationWhen teeth with these factors were eliminated, a clinical

success rate of 96% was achieved. When all symptoms of residual infection were resolved before filling of the canals, the success rate improved.

Contraindications to Primary Root Canal FillingsMany primary teeth with pulpal involvement that has spread beyond the coronal pulp are candidates for root canal fillings, whether they are vital or nonvital. Box 24-6 lists the categories of teeth that are not good candidates for pulpectomy.

Internal resorption usually begins just inside the root canals near the furcation area. Because of the thinness of the roots of the primary teeth, once internal resorption has become visible on radiographs, a perforation of the root by the resorption invariably has occurred (see Fig. 24-8). The short furcal surface area of the primary teeth leads to rapid communication between the inflammatory process and the oral cavity through the peri-odontal attachment. The end result is loss of the periodontal attachment of the tooth and, ultimately, further resorption and loss of the tooth. Mechanical or carious perforations of the floor of the pulp chamber fail for the same reasons. It has been shown that root length is the most reliable criterion of root

BOX 24-6

Contraindications to Pulpectomy in the Primary Dentition

◆ Unrestorable tooth◆ Internal resorption in the roots visible on radiographs◆ Teeth with mechanical or carious perforations of the floor of the

pulp chamber◆ Excessive pathologic root resorption involving more than a third

of the root◆ Excessive pathologic loss of bone support, with loss of the

normal periodontal attachment◆ Presence of a dentigerous or follicular cyst◆ Periapical or interradicular lesion involving the crypt of the

developing permanent successor

integrity; at least 4 mm of root length is necessary for the primary tooth to be treatable.231

Access Openings for PulpectomyAnterior Primary TeethAccess openings for endodontic treatment on primary or per-manent anterior teeth have traditionally been through the lingual surface. This continues to be the surface of choice, except for discolored maxillary primary incisors, for which a facial approach is recommended, followed by an acid-etched composite restoration to improve aesthetics (Fig. 24-15).164

Posterior Primary TeethAccess openings into the root canals of posterior primary teeth are essentially the same as for the permanent teeth. Important differences between the primary and permanent teeth are the length of the crowns, the bulbous shape of the crowns, and the very thin dentinal walls of the pulpal floors and roots. The depth necessary to penetrate into the pulpal chamber is much less than that in the permanent teeth. Likewise, the distance from the occlusal surface to the pulpal floor of the pulp chamber is much less than in permanent teeth. In primary molars, care must be taken not to overinstrument the relatively thin pulpal floor, owing to the high risk of perforation (Fig. 24-16).

When the roof of the pulp chamber is breached and the pulp chamber identified, the entire roof should be removed. Because the crowns of the primary teeth are more bulbous, less exten-sion toward the exterior of the tooth is necessary to uncover the openings of the root canals than in the permanent teeth.

TechniqueAs in permanent endodontic therapy, the main objective of the chemical and mechanical preparation of the primary tooth is debridement of the canals. Although an apical taper is desir-able, it is not necessary to have an exact shape to the canals because obturation is achieved using a resorbable paste. Figure 24-17 provides a schematic overview of the procedure.

Canal Preparation1. A preliminary working length is determined by measure-

ment of a radiograph taken with a paralleling technique.2. Local anesthesia is advisable.3. Placement of a rubber dam is mandatory.4. The working length is determined from a radiograph with

an endodontic file in the canal. The use of apex locators is often unreliable in primary teeth because root resorption may create lateral openings into the periodontal tissues at any level,231 causing unreliable readings.

5. To prevent overextension through the apical foramen, it is advisable to shorten the working length to 2 to 3 mm short of the radiographic length, especially in teeth showing signs of apical root resorption (see Fig. 24-17, B).

6. After establishment of the working length, the canal is cleaned and gently shaped (as described in Chapter 6). Because of the thin root walls, sonic and ultrasonic cleaning devices should not be used to prepare the canals. Also, the use of Gates-Glidden (GG) or Peeso drills (Pulpdent, Watertown, Massachusetts) is contraindicated because of the danger of perforation or stripping of the roots.

7. Flexible nickel-titanium (NiTi) instruments are recom-mended. Hand or rotary techniques are ideal for primary


A B

C

E

D

FIG. 24-15 Primary anterior root canal treatment using a facial approach. A, Discolored primary central incisor with a necrotic pulp. B, Tooth during root canal cleansing. C, Root canal filling with zinc oxide eugenol (ZOE) has been completed. ZOE was removed to the cervical line, and a Dycal liner was placed over the dentin. The tooth has been acid etched. D, Composite resin has been bonded over the facial surface to achieve aesthetics. E, Postrestorative radiograph showing completed procedures.

teeth. If stainless steel files are used, the instruments must be gently precurved to help negotiate the canals.

8. Care must be taken not to perforate the thin roots during cleaning and shaping procedures. The canals are enlarged several sizes past the first file that fits snugly in the canal, with a minimum size of 30 to 35.

Importance of Irrigation During TreatmentBecause many of the pulpal ramifications cannot be reached mechanically, copious irrigation during cleaning and shaping must be maintained (see Chapter 6). Debridement of the primary root canal is more often accomplished by chemical means than by mechanical means.124 This statement should not be misinterpreted as deemphasizing the importance of thor-ough debridement and disinfection of the canal. Initially, RC-Prep (Premier Dental Products, Norristown, Pennsylvania)

may be used as the canals are negotiated. It helps to emulsify pulp tissue and is an effective lubricant. Once a working length has been established, sodium hypochlorite (NaOCl) solution is used to dissolve organic debris; this can play an important part in removal of tissue from inaccessible areas of the root canal system (see Fig. 24-17, C).

The Nonvital Discolored Primary IncisorIf a primary incisor is intrinsically discolored after loss of pulp vitality, aesthetics may demand an improvement of the tooth’s color. Bleaching is not advised in the primary dentition. The anatomy of the maxillary primary incisors is such that access may be made successfully from the facial surface. The only variation to the opening is more extension to the incisal edge than with the normal lingual access to give as straight an approach as possible into the root canal.


• Be antiseptic• Fill the root canals easily• Adhere to the walls of the root canal• Not shrink• Be easily removed if necessary• Be radiopaque• Not discolor the tooth161

No material currently available meets all these criteria. The filling materials most commonly used for primary pulp fillings are ZOE paste, iodoform paste, and Ca(OH)2.

Zinc Oxide Eugenol PasteMost reports in the U.S. literature have advocated the use of ZOE as the filler, whereas other parts of the world have used pastes containing iodoform.118,143 The antibacterial activity of ZOE has been shown to be greater than that of an iodoform-containing paste (e.g., KRI paste, Pharmachemic AG, Zurich,

The root canal is filled with ZOE (see the following section); then the ZOE is carefully removed to near the cervical line. A liner of calcium hydroxide cement, such as Dycal or Life, is placed over the ZOE to serve as a barrier between the compos-ite resin and the root canal filling. The liner is extended over the darkly stained lingual dentin to serve as an opaquer. The access opening and entire facial surface are acid etched and restored with composite resin (see Fig. 24-15, C and D).

The Decision to ObturateAfter canal debridement, the canals are again copiously flushed with NaOCl and then dried with sterile premeasured paper points. If the canals are dry and no exudate is present, obtura-tion is performed in the same session. If the obturation cannot be done at the first appointment, a slurry paste of nonsetting Ca(OH)2 can be injected into the canals and the tooth restored with a well-sealing temporary restoration.

At a subsequent appointment, the rubber dam is placed and the canals reentered. As long as the patient is free of all signs and symptoms of inflammation, the canals are irrigated with NaOCl to remove the intracanal dressing and dried before obturation. If signs or symptoms of inflammation are present, the canals are recleaned and remedicated, and the canal obtura-tion delayed until a later time.

Root-Filling Materials for the Primary Root CanalsThe ideal root canal filling material for primary teeth should meet the following criteria:

• Resorb at a similar rate as the primary root• Be harmless to the periapical tissues and the permanent

tooth germ• Resorb readily if pressed beyond the apex

FIG. 24-16 Safe removal of the roof of a pulp chamber in a primary molar. A non–end cutting bur ensures that the relatively thin floor of the pulp chamber is not perforated inadvertently by rotary cutting instruments.

FIG. 24-17 Stages of pulpectomy and root canal filling in a mandibular second primary molar. A, Extensive approximal caries. Note the irreversible inflammation present in the coronal and radicular pulp. B, After caries removal and unroofing of the pulp chamber, the coronal pulp is amputated. Irreversibly inflamed tissue bleeds profusely. A premeasured hand file is placed approxi-mately 2 mm from the radiographic apex; the canals are gently cleaned with minimal shaping. C, Irrigation with sodium hypochlorite or chlorhexidine diglu-conate solution should be performed during the cleaning phase. D, If the root canals are not to be obturated at the same visit, they may be dressed with nonsetting calcium hydroxide; or, the canals can be left empty and the tooth restored with a small cotton pledget and an interim intracoronal restoration. E, At the subsequent visit, root canals can be obturated with a resorbable root-filling material, such as zinc oxide eugenol (ZOE). This can be applied using various methods; here, the ZOE is tamped down the canal by the piston action of a cotton pledget held in tweezers. F, After root canal filling, the tooth is restored internally before definitive coverage with a preformed metal (stain-less steel) crown.

A

D E F

B C


This technique is particularly easy to use for primary incisors but less practical for the narrow canals of primary molars.203

Regardless of the method used to fill the canals, care should be taken to prevent extrusion of the material into the periapical tissues. It is reported that a significantly greater failure rate occurs with overfilling of ZOE than with filling just to the apex or slightly underfilling.39,118 The adequacy of the obturation is checked by radiographs (see Fig. 24-15, E; also Fig. 24-18, A-C and Fig. 24-19, A-E).

In the event a small amount of the ZOE is inadvertently forced through the apical foramen, it is left alone (because the material is absorbable). It has been reported that defects on successor teeth have no relationship to length of the ZOE filling.39

When the canals have been satisfactorily obturated, a fast-setting temporary cement is placed in the pulp chamber to seal over the root canal filling. The tooth may then be restored permanently. In primary molars, it is advisable to place a pre-formed (stainless steel) crown as the permanent restoration to ensure good coronal seal and prevent possible fracture of the tooth (see Fig. 24-17, F).

If a primary tooth requires pulpectomy and the permanent successor tooth is absent, the primary root canals are filled with gutta-percha and sealer in an attempt to retain the primary tooth long term (Fig. 24-20).

Follow-Up After Pulpectomy in the Primary DentitionAs previously stated, the rate of success after primary pulpec-tomy is high. However, these teeth should be periodically recalled to check for success of the treatment and intercept any problem associated with a failure. It has been reported that pulpectomized primary teeth may show delayed exfolia-tion.39,265 One study39 described a 20% incidence of crossbites or palatal eruption of permanent incisors after pulpectomy on primary incisors. In the posterior teeth, extraction was required in 22% of cases because of ectopic eruption of the premolars or difficulty in exfoliation of the treated primary molar.39 After normal physiologic resorption of the roots reaches the pulp chamber, the large amount of ZOE present may impair the resorptive process and lead to prolonged retention of the crown. Treatment usually consists of simply removing the crown and allowing the permanent tooth to complete its eruption.

Retention of ZOE in the tissues is a common sequela to primary pulpectomy. One long-term study reported that after loss of the tooth, 50% of cases had retained ZOE. Teeth filled short of the apices had significantly less retained filling mate-rial, and in time, most showed complete absorption or reduc-ing amounts. Retention of filling material was not related to success and caused no pathosis.238 Therefore, no attempt is made to remove retained material from the tissues (see Fig. 24-18, A, and Fig. 24-19, C).

While resorbing normally without interference from the eruption of the permanent tooth, the primary tooth should remain asymptomatic, firm in the alveolus, and free of patho-sis. Traditionally, root canal treatments were considered successful when no pathologic resorption associated with bone rarefaction was present.91,118 If evidence of pathosis is detected, extraction and conventional space maintenance are recommended.

Switzerland), whereas ZOE’s cytotoxicity in direct and indirect contact with cells is equal to and less than (respectively) that of KRI paste. The filling material of choice in the United States is ZOE without a catalyst. The lack of a catalyst is necessary to allow adequate working time for filling the canals.

Iodoform PasteSeveral authors have reported the use of KRI paste, which is a mixture of iodoform, camphor, parachlorophenol, and menthol.176,230 It resorbs rapidly and has no undesirable effects on successor teeth when used as a pulp canal medicament in abscessed primary teeth. Furthermore, if KRI paste extrudes into the periapical tissue, it is rapidly replaced with normal tissue.118 Sometimes the material is also resorbed inside the root canal. A paste developed by Maisto has been used clini-cally for many years, and good results have been reported with its use.171,274 This paste has the same components as the KRI paste, with the addition of zinc oxide, thymol, and lanolin.

Calcium HydroxideSeveral clinical and histopathologic investigations of Ca(OH)2 and iodoform mixture (Vitapex, Neo Dental Chemical Prod-ucts, Tokyo) have been published.16,78,199 These authors found that this material is easy to apply, absorbs at a slightly faster rate than that of the roots, has no toxic effects on the perma-nent successor, and is radiopaque. For these reasons, Machida161 considers the calcium hydroxide–iodoform mixture a nearly ideal primary tooth root canal filling material. Another prepa-ration with similar composition, Endoflas, is available in the United States (Sanlor Laboratories, Cali, Colombia, South America). The results of root canal treatments using Endoflas were similar to those observed with KRI paste85 and ZOE.269

Obturation of the primary root canal is usually performed without a local anesthetic. This is preferable, if possible, so the patient’s response can be used to indicate proximity to the apical foramen. However, it sometimes is necessary to anesthe-tize the gingiva with a drop of anesthetic solution to place the rubber dam clamp without pain.

Obturation of the Root CanalThe chosen obturation technique depends upon the material used and the accessibility of the canal to relevant instruments.

If ZOE is used, it is mixed to a thick consistency and carried into the pulp chamber with a plastic instrument or on a Lentulo spiral. The material may be packed into the canals with plug-gers or a Lentulo spiral. A cotton pellet held in cotton pliers and acting as a piston within the pulp chamber is quite effec-tive in forcing the ZOE into the canals (see Fig. 24-17, E). The endodontic pressure syringe is also effective for placing the ZOE in root canals.20,98 However, in a study of apical seal and quality of filling evaluated on radiographs, no statistically sig-nificant differences were reported between the Lentulo spiral, pressure syringe, or plugger.50

When the root canal is filled with a resorbable paste, such as KRI, Maisto, or Endoflas, a Lentulo spiral mounted in a low-speed handpiece can be used to introduce the material into the canal. When the canal is completely filled, the material is compressed with a cotton pellet. Excessive material is rapidly resorbed.

Vitapex is packed in a convenient sterile syringe, and the paste is injected into the canal with a disposable plastic needle.

A

B

C

FIG. 24-18 Pulpectomy and root canal filling with zinc oxide eugenol (ZOE) paste in a primary maxillary central incisor. A, The root canal has been slightly overfilled, with extrusion of ZOE paste apically. B, The same patient showing newly erupted permanent inci-sors. Note that no enamel defects are present on the crown, despite overfill of the root canal of the predeces-sor. C, Radiograph almost 5 years after pulpectomy and root canal filling of predecessor. Note the normal apical development and almost total absorption of ZOE remnants.


A B

C

E

D

FIG. 24-19 Pulpectomy and root canal filling with zinc oxide eugenol (ZOE) in a maxillary second primary molar. A, Carious pulp exposure with a chronic abscess. Note the furcal and periapi-cal radiolucencies. B, Instruments in place, establishing the working length. C, Root canal filled with ZOE. Note the overfill and extrusion of ZOE. D, At 4 1

2 years after root canal treatment, the primary tooth is near exfoliation. E, One year later, the premolar is fully erupted, and all traces of ZOE have been resorbed.

Payne et al.212 claim that most clinicians are prepared to accept pulp-treated primary teeth that have a limited degree of radiolucency or pathologic root resorption in the absence of clinical signs and symptoms. This is contingent on the assur-ance that the parent will contact the clinician if an acute problem develops, and the patient will return for review in 6 months. These criteria seem to be more suitable for pediatric dental practices and have been adopted clinically by Fuks et al.,85 who consider such teeth to be “successfully treated.”

PULPAL THERAPY FOR THE YOUNG PERMANENT DENTITIONIt could be argued that mature permanent teeth can survive for a lifetime without the support of a vital pulp. For the immature permanent tooth, the future is less secure. Premature loss of a functioning pulp results in a fragile tooth with a compromised crown-to-root ratio, thin dentin walls, and a wide and often apically diverging root that presents significant endodontic and


Indirect Pulp Therapy: Avoiding Pulp ExposureThe pulps of young permanent teeth are at risk of breakdown after traumatic injuries (considered fully in Chapter 20), dental caries, and restorative dentistry. Good evidence indicates that residual dentin thickness is a key determinant of pulp survival after cavity preparation,183 and avoiding pulp exposure has been considered advantageous. The management of deep caries by partial or serial excavation has gained considerable support in recent years, reducing the risks of pulp exposure and harnessing the natural defenses of the pulp in laying down protective tertiary (reactionary) dentin.* In the case of serial excavation, the need for a secondary excavation has recently been brought into question,166 although the need for a tightly sealing coronal restoration to ensure that any residual caries is inactivated has been acknowledged.228 Researchers continue to investigate the role of antimicrobial treatments, including ozone fumigation,216 photoactivated disinfection (PAD), and antimicrobial resins in sterilizing deep layers of affected dentin286 and creating the conditions for arrest and remineral-ization. Considerable interest has also focused on the active up-regulation of reactionary dentinogenesis by applying bioac-tive agents, such as the transforming growth factor beta (TGF-β) family of molecules, to the depths of cavity preparations.285 Therapeutic approaches present a hopeful future for pulp pro-tection after deep caries, but significant challenges remain, not least in defining optimal agents and predictably delivering them to the pulp through the fluid-filled dentinal tubules of vital teeth.219 More basic and clinical research is needed before such agents can be widely adopted in practice.

However, a substantial body of evidence supports the view that complete excavation is not necessary for the successful management of deep caries200 and that indirect pulp therapy may be the most effective means of securing pulp health in asymptomatic teeth.

restorative challenges (Fig. 24-21). A central responsibility of all clinicians is therefore to safeguard pulp survival at least until dental development is complete.

The procedures described in this section have much in common with those for primary teeth and focus on preserving all or part of the pulp in a functional condition. In addition to aspects of pulp protection, indirect pulp therapy, direct pulp capping, and pulpotomy, attention is given to the root canal treatment and restoration of nonvital, immature permanent teeth. The emerging potential of pulp regeneration and bioroot engineering is also considered.

FIG. 24-20 Pulpectomy and root canal filling with gutta-percha in a retained mandibular primary second molar with no succedaneous permanent tooth. A, Carious exposure of the pulp. B, Because the permanent premolar is absent, the root canals were filled with gutta-percha and sealer rather than just zinc oxide eugenol.

A B

FIG. 24-21 Premature loss of vital pulp functions in an immature maxil-lary permanent incisor. Development is arrested, leaving a fragile tooth with a compromised crown-to-root ratio, thin dentin walls, and a wide-open root end; these factors present endodontic and restorative challenges.

*References 22, 23, 52, 99, 106, and 165.


of the previous authors of this chapter (Dr. Joe Camp) has advocated complete caries excavation and direct capping of the exposure in the immature teeth of children (Fig. 24-22). Teeth with percussion sensitivity, swelling, or other obvious signs of pulpal necrosis are not considered good candidates, and the pulp tissue exposed during caries excavation must appear vital with no signs of degeneration or suppuration. In this proce-dure, the tooth is anesthetized and isolated with a rubber dam. All decay is removed with round carbide burs and copious water spray. No further pulpal tissue is removed except that occurring with the caries removal. The often profuse bleeding that occurs is controlled by rinsing the pulp with NaOCl, which is not only antimicrobial but appears to have no adverse effects on pulpal healing, odontoblastic cell formation, or den-tinal bridging.2,42 The solution may be left in contact with the exposed pulp tissue for 10 to 15 minutes; it is refreshed with new solution every 3 to 4 minutes. Care must be taken in aspirating the excess NaOCl to prevent further hemorrhage; the aspirator tip is placed lateral to, and never directly above, the crown. Once hemorrhage has been controlled, the tooth structure is cleansed with cotton pellets moistened with NaOCl, again avoiding further pulp hemorrhage.

The exposed pulp is then covered with a 0.5- to 1-mm thickness of MTA, which is gently teased against the exposed

Managing Pulp ExposureEven when treated with the greatest clinical judgment and restorative skill, pulps are sometimes exposed during deep caries excavation. A 2007 survey showed that 62% of clinicians would remove all caries when presented with a case in which one would expect pulp exposure, whereas only 18% would partially excavate caries, and 21% would initiate root canal treatment.204 In a comparable study among Brazilian public health dentists, 71% favored direct, complete caries excavation over more conservative approaches, although dentists graduat-ing after the year 2000 were more likely to embrace conserva-tive approaches.299 Direct pulp capping has generally not enjoyed predictable success in cariously exposed teeth. One study showed a 44.5% failure at 5 years and a disappointing 79.7% failure at 10 years.17 A more recent systematic review points to success of 73% at 3 years for permanent teeth, but longer term outcomes appear variable and uncertain.3

Although much of the evidence is relatively short term and involves previously uninflamed pulps, calcium silicate cements, such as MTA, are developing a profile for promoting reparative tertiary dentin bridge formation after direct pulp capping.148,193

In a radically different approach to the management of deep caries in immature permanent teeth where pulp diagnosis may be uncertain and the stakes for pulp preservation are high, one

FIG. 24-22 Direct pulp capping in a symptomatic young permanent mandibular molar with an open apex. A, Extensive carious exposure in an immature molar with a history of spontaneous pain. B, After complete caries excavation and hemostasis, the pulp is overlaid with mineral trioxide aggregate and the tooth sealed with com-posite resin. C, Three-year recall shows completed root formation. Note the lack of mineralization in the pulp chamber and canals.

A

B C


with MTA; 93% were successful at 24 months, with contin-ued root development. In the second report, Bogen et al.25 described a series of 53 teeth diagnosed at the outset with deep caries and reversible pulpitis but with no periapical involvement. Caries was completely eliminated with the help of a caries-detector dye and magnification (Fig. 24-23, A and B), often resulting in multiple, large pulp exposures. Hemo-stasis was secured by bathing the pulp with 5.25% to 6% NaOCl for 1 to 10 minutes (Fig. 24-23, B to D). One pulp that continued to bleed after this time was considered unsuit-able for direct capping. After application of 1.5 to 3 mm of gray or white MTA (Fig. 24-23, E) and permanent bonded restorations at 5 to 10 days, the teeth were reviewed for 1 to 9 years (mean, 3.94 years). The recall rate was 92.5%, and 97.96% of the teeth were found to have favorable outcomes

pulp tissue with a damp cotton pellet. Wisps of cotton are wet with sterile water and placed over the MTA so it is completely covered. The tooth is then provisionally sealed with a tempo-rary cement, such as Cavit, to allow hardening of the MTA.

The patient is seen again within 12 to 48 hours, and the tooth is anesthetized and isolated with a rubber dam. After removal of the Cavit and cotton, the MTA is examined to ensure that it has set hard, and the tooth is restored with a bonded composite restoration. If the MTA has failed to harden, Camp advocated washing out the uncured material and repeating the procedure after removing pulp tissue to the canal orifice level. This approach has received further support from two studies. In a study by Farsi et al.,69 30 asymptom-atic permanent molars were reviewed clinically and radio-graphically after caries excavation and direct pulp capping

FIG. 24-23 Radiographic and clinical sequence of mineral trioxide aggregate (MTA) direct pulp capping of a mandibular right molar in a 9-year-old female. A, Pretreatment radiograph showing initial deep caries and immature apices. B to D, Five-minute application of 5.25% sodium hypochlorite hemostasis on two 1.5- to 2-mm exposures. E, Radiograph of molar with MTA, water-moistened cotton pellet, and unbonded Clearfil Photocore (Kuraray Medical, Okayama, Japan) provisional restoration after initial visit. F, Radiograph taken at the 5.5-year recall appointment shows permanent restoration and evidence of complete root formation. The tooth showed a normal response to cold testing. (From Bogen G, Kim JS, Bakland LK: Direct pulp capping with mineral trioxide aggregate: an observational study, J Am Dent Assoc 139:305, 2008.)

A B

C D

FE


resected at a deeper level to preserve a vital apical pulp stump (see the section on apexogenesis).

Hemostasis was obtained with saline, and a pulp cap of calcium hydroxide was overlaid with a sealing coronal restoration. Cvek reported success in an impressive 94% to 96% of cases (Fig. 24-24). More recent reports suggest that histologic tissue responses may be more favorable in response to calcium silicate cements, such as MTA, than to Ca(OH)2.

133,191,193,215 Thus MTA is recommended as the pulp-capping agent of choice in cases that do not extend deeply into the roots, where subsequent retrieval may present a consider-able challenge. Preference should be given to white MTA prod-ucts in an effort to minimize the risk of unsightly tooth staining, although this possibility cannot be ruled out.18

The question, then, is whether such techniques can be applied to posterior teeth, especially those with symptomatic cariously affected pulps. The answer historically has been no, except as a short-term, pain-relieving exercise. Studies involv-ing cavity preparations into teeth that left areas of impacted food, debris, and bacteria in contact with pulp tissue resulted in inflammation extending from 1 to 9 mm into the pulp, with abscess and pus formation.47,108 The extent of inflammation in a cariously exposed pulp is difficult to judge. Pulpotomy may consequently be less predictable in preserving vital pulp func-tions after a carious pulp exposure compared to a traumatic pulp exposure.

Partial Pulpotomy on Asymptomatic Young Permanent Posterior TeethA technique called partial pulpotomy for the management of vital carious pulp exposure on young permanent molars has been reported by several researchers.169,172,175,202 This approach has usually been reserved for teeth with little or no history of pain and in the absence of radiographic signs, percussion sensitivity, swelling, or mobility.

The procedure usually involves removal of 1 to 3 mm of pulp tissue suspected to be inflamed, beneath the exposure site, in order to reach underlying healthy tissue. After hemo-stasis, the exposure site traditionally has been covered with Ca(OH)2 and the tooth sealed with ZOE and a permanent restoration. Mejàre and Cvek175 followed 31 initially symptom-free teeth for a mean of 56 months (range, 24 to 140 months) and found a healing rate of 93.5%. Mass et al.169 reported a 91.4% success rate in 35 cases followed for 12 to 48 months. Exposures exceeding 2 mm in diameter and those in which bleeding could not be controlled within 1 to 2 minutes were excluded from this study.

The use of MTA as the capping agent has met with success in the hands of the authors and others,201,244 although long-term success has also been reported after the use of more tra-ditional materials in properly selected cases.170

Pulpotomy on Symptomatic Young Permanent TeethAlthough some success has been reported,175 vital pulp therapy in permanent teeth with a history of pain has generally been contraindicated. However, reports do support this pulp-preserving approach, even for symptomatic teeth (see Chapter 26 for more details).244 In the study by Mejàre and Cvek,175 of the six teeth with temporary pain, widened periodontal

on the basis of radiographic appearances, subjective symp-toms, and cold testing (Fig. 24-23, F). Of the 15 teeth that were immature at the time of treatment, 100% went on to complete root formation.

At the time of writing, a conservative general consensus probably holds with partial or serial caries excavation, avoiding pulp exposure and attempting to create an environment that will up-regulate reactionary tertiary dentin responses.22,228,280 However, evidence is growing that in correctly chosen cases with no indication of irreversible pulpitis or periapical change and when radical caries excavation is followed by confirmation of hemostasis, direct capping with calcium silicate cements, such as MTA, can achieve remarkable levels of success in teeth with incomplete apices.

Because the loss of vital pulp functions is so devastating in teeth with immature apices, it seems advisable to attempt con-servative pulp-preserving procedures in deeply carious perma-nent teeth. If these procedures fail, apexification or regenerative techniques can always be considered.

PULPOTOMYThe pulpotomy procedure involves removing only part of the pulp, eliminating tissue that has inflammatory or degenerative changes and leaving intact the underlying healthy pulp tissue.12 The healthy tissue is then covered with a wound dressing agent in an effort to promote healing at the amputation site and to promote the survival of the underlying pulp tissue. Tradition-ally, the term pulpotomy has implied removal of pulp tissue to the cervical line. However, the depth to which tissue is removed is determined by clinical judgment of how deeply the pulp is affected. Superficial amputation (partial pulpotomy) may allow better visualization of the working area but risks leaving damaged tissue that may go on to break down. In multirooted teeth, the procedure may be simplified by removing tissue to the orifices of the root canals (complete or pulp-chamber pulpotomy).

The Cvek Pulpotomy on Immature Permanent TeethPulpotomy is an established technique for preserving vital pulp functions in immature teeth that have been subject to pulp-exposing trauma. A full account of the Cvek pulpotomy is provided in Chapter 20 (see Fig. 20-11). Briefly, studies have shown that inflammation is confined to the surface 2 to 3 mm of the pulp when it is traumatically exposed and left untreated for up to 168 hours.47,108,109 In experimental animals, the results were the same whether the crowns were fractured or ground off.47 Direct invasion of vital pulp tissue by bacteria did not occur, although the pulps were left exposed to saliva.

In a classic report, Cvek45 described a pulpotomy technique in which only the superficial 2 to 3 mm of hyperplastic inflamed tissue was removed with a water-cooled, high-speed diamond bur97 to place the wound in a healthy site. Hemostasis was then secured before capping with an appropriate material. If hemostasis could not be secured after several minutes of saline-moistened cotton pellet application, the preparation was checked carefully for residual superficial tags of bleeding tissue that had not been fully removed, or questions were asked about the condition of the underlying pulp. Persistent bleeding from an inflamed pulp usually indicates that the tissue should be


treated by full coronal pulpotomy, hemostasis for 1 minute with 6% NaOCl, and wound dressing with MTA. Follow-up of 6 to 53 months (mean, 19.7 months) revealed that 79% had healed, 16% were healing, and only 5% had evidence of per-sistent disease. More research is needed, but the MTA pul-potomy seems to be gaining an evidence base as a reliable technique for preserving vital pulp functions in both asymp-tomatic and symptomatic teeth in children.

This body of evidence suggests that young teeth, with their rich vascular supply, are good candidates for conservative pulp-preserving treatments. Again, the stakes are high, and efforts to secure vital pulp functions are to be commended. Outcomes are probably more predictable in asymptomatic cases than symptomatic, and care should be taken preoperatively to dis-tinguish between cases with symptoms of reversible and irre-versible pulpitis. However, the correlation of clinical symptoms with histologic state is poor.57

Follow-Up After Pulp Capping and PulpotomyPatients undergoing pulp capping and pulpotomy procedures should be seen periodically for 2 to 4 years to determine

ligament space, and/or condensing osteitis that were managed by Ca(OH)2 pulpotomy, 66.7% healed. A study by Calişkan30 undertook a similar Ca(OH)2 pulpotomy procedure on 26 per-manent vital molars with carious pulp exposures and apical periodontitis. Observation between 16 and 72 months revealed that 24 (92.3%) were free of clinical symptoms, responded to sensibility testing, and showed evidence of hard tissue barrier formation, resolution of periapical involvement, and the absence of intraradicular pathosis radiographically.

Partial pulpotomy was also found to be successful in a ran-domized, controlled trial220 that compared Ca(OH)2 and MTA pulpotomies in the permanent molars (n = 64) of children. Mean follow-up was 34.8 months (range, 25.5 to 45.6 months), and success was comparably favorable in both the Ca(OH)2 (91%) and MTA (93%) groups.

A full coronal pulpotomy may be more predictable in the symptomatic case in which the depth of pulp inflammation is difficult to predict. Follow-up of MTA pulpotomies in 15 children with immature molars revealed no clinical or radio-graphic failures at 12 months, although four pulps had under-gone calcific metamorphosis.61 In a 2006 clinical report, Witherspoon et al.304 described a series of 23 irreversibly pul-pitic anterior and posterior teeth in children and adolescents,

C

BA

FIG. 24-24 Follow-up of a Cvek pulpotomy. A, Pretreatment radiograph of a right maxillary central incisor after traumatic pulp exposure. B, Four months after Cvek pulpotomy and application of a calcium hydroxide dressing, formation of a dentin bridge can be seen. C, Three-year recall shows continued root formation. In this case, the dentin bridge has not thickened. There is no evi-dence of uncontrolled mineralization in the pulp space.


for a retentive post. Nevertheless, calcific obliteration, internal resorption, and pulp necrosis are potential sequelae of pulp-capping and pulpotomy procedures, and the clinician should screen for these problems during recall appointments. Although unlikely, they are possible, and the patient should be clearly informed.

Formocresol Pulpotomy on Young Permanent TeethBecause of the historical track record of formocresol pulpot-omy in primary teeth, interest developed in this technique for the management of young permanent teeth. Reports have dem-onstrated the potential for continued apical development after formocresol pulpotomy in young permanent teeth,73,184,240,294 although the high incidence of internal resorption82,213 adds to broader concerns about the use of formocresol in pediatric endodontics.

In most circumstances, the formocresol pulpotomy has been performed as an emergency treatment, with reports showing that teeth may remain symptom free after 3 years.282 However, alternatives to the formocresol pulpotomy are pre-ferred, and renewed interest has been shown in the potential of pulpotomy with materials such as MTA as a short- and long-term treatment strategy for damaged pulps.259

APEXOGENESISApexogenesis is a treatment designed to preserve vital pulp tissue in the apical part of a root canal so that formation of the root apex may be completed (Fig. 24-26).107

The clinical procedure is essentially a deep pulpotomy undertaken to preserve the formative capacity of the radicular pulp in immature teeth that have deep pulpal inflammation.

success. Although normal sensibility tests (e.g., electrical and thermal sensitivity tests) are reliable after pulp capping, they are not usually helpful in the pulpotomy-treated tooth. Because histologic success cannot be determined, clinical success is judged by the absence of any clinical or radiographic signs of pathosis and the presence of continued root development in teeth with incompletely formed roots.

Controversy exists as to whether the pulp should be reen-tered after the completion of root development in the pulpotomy-treated tooth. Langeland et al.146 believe that pulp capping and pulpotomy procedures invariably lead to progres-sive calcification of the root canals. They advocated that, after successful root development, pulpectomy and root canal treat-ment should be performed before canals became obliterated, and difficult to manage endodontically if they did become infected. However, it has been the experience of the authors and others48,84,109 that with good case selection, a gentle tech-nique in removing infected tissue and dentin chips, and care in avoiding the compaction of pulp dressing into underlying pulp tissue, calcification of the pulp is an infrequent sequela of pulpotomy (see Fig. 24-24, C, and Fig. 24-25). The routine use of microscopy has also transformed the management of many cases that might in the past have been considered untreatable. The prophylactic root canal treatment of teeth after successful pulpotomy is therefore difficult to justify.

In a follow-up study of clinically successful pulpotomies,45 researchers removed the pulps 1 to 5 years later for restorative reasons and found the tissue to be histologically normal.48 They concluded that the changes observed do not present suf-ficient histologic evidence to support routine pulpectomy after pulpotomy in accidentally fractured teeth with pulp exposures. Thus, routine reentry to remove the pulp and place a root canal filling after completion of root development is contraindicated unless dictated by restorative considerations, such as the need

FIG. 24-25 Deep pulpotomy for apexogenesis. A, Immature maxillary central incisor 10 weeks after traumatic pulp exposure and a deep pulpotomy dressed with calcium hydroxide. Note the early formation of a dentin bridge. B, At three-year recall—the dentin bridge has thickened, and root formation is complete; the tooth remained asymptomatic and required no further treatment at that time. Note the absence of uncontrolled mineralization in the apical pulp space.

BA


Examples include carious exposures and some trauma cases in which treatment of the exposed pulp is delayed and it becomes necessary to extend farther into the canal to reach healthy tissue.

Deep resection of pulp tissue is usually undertaken in single-rooted anterior teeth with a small endodontic spoon excavator or round, abrasive diamond bur (see Fig. 24-25). In posterior teeth, the use of endodontic files or reamers may be necessary if tissue is to be amputated within the canals. Exten-sion of the amputation site into the root canals is undertaken only when there is little confidence that more superficial pulp capping or pulpotomy will be successful and when there is a desperate desire to preserve pulp functions in teeth with wide-open, blunderbuss apices (Fig. 24-27).

Bleeding is usually controlled with saline-soaked cotton pellets or NaOCl. If hemostasis cannot be secured by conven-tional means, this may indicate that even the deep pulp is inflamed and treatment will be compromised. Despite the risks, it is legitimate to attempt pulp-preserving treatment after controlling the hemorrhage with hemostatic chemicals such as aluminum chloride or ferric sulfate.

The pulp wound is then covered with a dressing material before the crown is securely restored. It is challenging to deter-mine the status of pulp tissue deep in the root canal, and its capacity for survival is difficult to predict. Radiographic and clinical follow-up is mandatory, and if there is no evidence of

FIG. 24-26 Schematic representation of apexogenesis. Apexogenesis is a treatment designed to preserve at least the apical portion of pulp tissue in a healthy condition so that root formation can be completed. A, After a deep pulpotomy and hemostasis, the radicular pulp is dressed and a sealing coronal restoration is applied. B, Success is evidenced by continued root development (length and wall thickness) and formation of a calcific barrier in response to the wound dressing.

Healthypulp

tissue

Continued rootformation: lengthand wall thickness

Reparativebridge formationWound

dressing

Sealingcoronal

restoration

A B

FIG. 24-27 Apexogenesis after deep calcium hydroxide pulpotomy on a mandibular permanent molar. A, Pretreatment radiograph showing extensive caries, incomplete root development, and possible periapical pathosis. The tooth was asymptomatic. B, One year after deep pulpotomy (which extended several millimeters into the canals), hemostasis, and restoration. Root formation is progressing, and the periapical tissues appear healthy. C, Two years later, root formation is complete.

B

CA


and the intrinsic difficulties of sealing a fragile, incompletely formed apex with traditional materials. A more predictable and less traumatic approach was desirable.

Until recently, the most widely accepted technique has involved cleaning and filling the canal with a temporary paste, most commonly Ca(OH)2, which was replaced at intervals over several months to stimulate the formation of an apical calcified barrier (see Fig. 24-28, A and B, and Fig. 24-29).266

Diagnosis of pulpal necrosis in a tooth with an incompletely formed apex is often difficult; the electronic pulp tester rarely provides meaningful data, and thermal tests often give equivo-cal or false results in young children and traumatized teeth. The presence of acute or chronic pain, percussion sensitivity, mobility, coronal discoloration, or a discharging sinus may be helpful guides, whereas radiographic diagnosis can be compli-cated by the normal radiolucencies appearing at the apices of developing teeth. Comparison of root formation with contra-lateral teeth should always be considered.

If any doubt persists, it is usually wise to adopt a watch and wait approach before entering the immature tooth endodonti-cally. Only when convincing evidence indicates pulp break-down should the tooth be entered, and in the interim, exposed dentin should be covered to reduce the risks of microbial entry to a potentially compromised pulp.

The extent of apical closure may be difficult to ascertain with plain radiographs. Three-dimensional imaging offers new opportunities to understand the complexity of root ends, which may have different conformations in mesiodistal and faciolingual dimensions (see Fig. 24-9). In practical terms, the precise limit of apical opening that can be filled by conven-tional means is unclear.

continued root formation and calcific barrier formation in response to the dressing, apexification or a regenerative tech-nique may be considered.

Because of the depth at which this procedure is performed, preference has usually been given to the use of Ca(OH)2 rather than MTA because, in the event of failure, this may facilitate reentry to the root canal to perform apexification or pulp regeneration. Also, if apexogenesis is successful and root-end formation is complete, the tooth could be reentered if desired for conventional root canal treatment. It is unclear whether these concerns hold true in an era of microscopy and contem-porary microinstrumentation.

Calcium hydroxide powder has usually been preferred over hard-setting products, carried into the canal with an amalgam carrier or gun system used for MTA application. Small incre-ments of Ca(OH)2 powder are carefully teased against the entire surface of the pulp stump with a rounded-end, plastic instrument, ideally with microscope control. Care must be taken not to pack the Ca(OH)2 into the pulp tissue because this causes greater inflammation and increases the chances of failure. Even if pulpotomy is successful, there is an increased risk that the remaining pulp tissue will mineralize around impacted particles of Ca(OH)2.

287

Commercial nonsetting calcium hydroxide pastes may also be spun or injected to flow lightly over the pulp stump. Care must be taken to avoid trapping air bubbles when such prod-ucts are applied, and it is recommended that they be overlaid with a hard-setting calcium hydroxide or glass ionomer cement44 before meticulous cleaning of the cavity walls and restoration with a bonded composite resin restoration. Although little has been published on this topic, MTA probably represents a viable alternative to calcium hydroxide, provided the challenges in its retrieval are recognized.

APEXIFICATIONApexification, or root-end closure, is the process in which a nonvital, immature, permanent tooth that has lost the capacity for further root development is induced to form a calcified barrier at the root terminus (Fig. 24-28). This barrier forms a matrix against which root canal filling or restorative material can be compacted with length control.

Unlike the pulp capping, pulpotomy, and apexogenesis pro-cedures described previously, apexification at best results in closure of the root end and cannot be expected to cause further root development in terms of length or wall thickness. Apexi-fication thus is regarded as a treatment of last resort in imma-ture teeth that have lost pulp vitality. The growing body of recent evidence on pulp regeneration, even in infected, nonvi-tal immature teeth, may also relegate this approach to the history archives in the years to come.120

For now, root-end closure techniques, both those involving the generation of a biologic calcific barrier and those involving artificial root-end closure with a material such as MTA, still have a place in practice and should be considered.

Before the introduction of conservative apical closure tech-niques, the usual approach to this problem was surgical. Although this could be successful, psychological and patient-management issues in patients who were usually young children offered many contraindications. Local dental consid-erations presented a further disincentive, including a reduction in the crown-to-root ratio if root-end reduction was required,

FIG. 24-28 Schematic representation of apexification. Apexification is a treatment performed to develop a hard barrier at an open root end. A, Imma-ture permanent tooth with a nonvital pulp. B, Traditional approach: a “calcified barrier” forms at the root end after repeated dressing over many months with calcium hydroxide. The canal is subsequently filled with gutta-percha and sealer before coronal restoration. C, Artificial apical barrier technique: a 4- to 5-mm plug of mineral trioxide aggregate is placed at the root end. The canal space is subsequently restored with dual-curing composite resin, often accompanied by a fiber post to provide mechanical support.

4-5 mm MTAapical barrier

Composite rootreinforcement,often incorporatinga fiber post

Immature tooth withnecrotic pulp

Traditionalapproach

Apical barriertechnique

Complete but porouscalcific barrier aftermonths of Ca(OH)2treatment

Gutta-perchaand sealer

Compositecoronal seal

C

A

B


have advocated mixing Ca(OH)2 with CMCP or Cresanol, whereas reports from other parts of the world44,174 showed the same success using distilled water or physiologic saline as the vehicle. The addition of 1 : 8 barium sulfate to Ca(OH)2 enhanced radiopacity with no apparent adverse effects on apexification.298 Comparable outcomes have been noted in humans and animals with tricalcium phosphate,41,140,233 colla-gen calcium phosphate,198 osteogenic protein-1,252 bone growth factors,281 and a number of other materials.298

The most important factors in achieving apexification seem to be thorough debridement of the root canal to remove all necrotic pulp tissue and microbial infection, and sealing of the tooth to prevent the ingress of bacteria and substrate.64

Many materials have been reported to stimulate apexifica-tion successfully. The use of nonsetting Ca(OH)2 was first reported by Kaiser in 1964.134 The technique was popularized by the work of Frank.77 Since that time, Ca(OH)2 alone or in combination with other drugs was the most widely accepted material for promoting apexification, until the development of MTA and the potential for rapid, artificial barrier formation.

For historical perspective, Ca(OH)2 powder has been mixed with camphorated mono-chlorophenol (CMCP), metacresyl acetate, Cresanol (i.e., a mixture of CMCP and metacresyl acetate), physiologic saline, Ringer’s solution, distilled water, and local anesthetic solution. All have been reported to stimu-late apexification. Most reports in the U.S. literature31,103,267

A B

C

FIG. 24-29 Apexification with calcium hydroxide (Ca(OH)2). A, Maxillary central incisor after several months of Ca(OH)2 medication. B, After removal of the Ca(OH)2, a calcific barrier is apparent. C, Tooth after root filling with thermoplastic gutta-percha and sealer. Note the extrusion of the filling material through porosi-ties in the calcific barrier. The root canal filling is dense; nevertheless, how the gutta-percha and sealer have added to the structural integrity and reinforcement of this fragile tooth is open to question.


proprietary paste syringe. There is little evidence to commend any commercial Ca(OH)2 paste over another in this applica-tion. The tooth is then sealed coronally, and the patient is recalled at 3-month intervals so that the clinician can wash out the Ca(OH)2 paste and inspect clinically (with the aid of gutta-percha or paper points or by direct visual inspection through the microscope) and radiographically for the devel-opment of a calcified barrier (see Fig. 24-29, B). Treatment typically extends over 9 to 24 months, with obvious demands on patient and parent compliance. The reduced mechanical properties of root dentin and consequential risks of cervical root fracture after exposure to Ca(OH)2 for 5 weeks or longer are also recognized.46,307

Histologic studies consistently report the absence of Hert-wig’s epithelial root sheath, and normal root formation should never be anticipated. Instead, differentiation of adjacent con-nective tissue cells into specialized cells appears to occur, and calcified tissue is deposited adjacent to the filling material. The calcified material that forms over the apical foramen was his-tologically identified as an osteoid (i.e., bonelike) or cementoid (i.e., cementum-like) material (Fig. 24-30).31,103,266 In a primate study, bridging of the root end with osteodentin was reported after vital pulpectomy and canal medication with Ca(OH)2/parachlorophenol paste. The material appeared to be distinct from but continuous with the cementum, dentin, and preden-tin at the root apex.58 The closure of the apex may be partial or complete, but minute communications with the periapical tissues are consistently seen (see Fig. 24-28, B; Fig. 24-29, C; and Fig. 24-30). For this reason, apexification stimulated by

Apexification does not occur when the apex of the tooth penetrates the cortical plate. To be successful, the apex must be completely within the confines of the medullary space.

Apexification TechniqueIn the apexification technique, the canal is cleaned and disin-fected in line with the principles defined in Chapter 6. The use of a rubber dam is mandatory, and resourcefulness may be needed to isolate partially erupted or damaged teeth in children.

The access opening may require some extension to fully unroof pulp horns, but care should be taken not to heavily instrument the already thin and relatively fragile walls of the root.

The length of the canal is established by radiographs because the absence of an apical constriction may make electronic methods unreliable.122,138 A constant drying point, determined with paper points, may provide helpful additional information on length.14 Irrigation is central to the debride-ment of immature teeth, and with proper precautions, opera-tors should not hesitate to benefit from the antimicrobial and tissue-solvent properties of NaOCl. Sonic, ultrasonic, and other vibratory devices capable of activating the irrigant within the canal may be advantageous,291 and benefit may also come from the use of small brushes of the sort that are designed for interproximal tooth brushing or the application of etchants to post channels. After thorough debridement, the canal is dried and medicated with a fluid Ca(OH)2 paste, carried into the canal with a Lentulo spiral or injected from a

FIG. 24-30 Histologic section of a dog’s tooth after calcium hydroxide apexification. A, Cementum-like mineralized tissue is closing the wide-open root end. Debris is apparent in the canal because of inadequate debridement before filling. B, Higher magnification shows cellular detail; the periodontal ligament is free of inflam-mation. Root canal filling material was lost in the histologic preparation. Note the presence of tissue communica-tion through the apical barrier (stain, H&E).

A B


reduced cost of clinical time, and the ability to securely restore the tooth at an earlier stage.49 The risk of tooth fracture due to long-term Ca(OH)2 medication is also eliminated.307

MTA Barrier Technique (see Fig. 24-28; also Figs. 24-31 and 24-32)In the apexification technique, the canal is cleaned and disin-fected as described for Ca(OH)2 apexification. Lee et al.151 have suggested that the tissue pH may affect the hydration reaction and final physical properties of MTA, and it has become stan-dard practice to medicate canals for at least 1 week with Ca(OH)2 to raise the acidic pH of the inflamed periapical tissues before permanent sealing.

When the tooth is free of signs and symptoms of infection, it is reisolated with a rubber dam and the Ca(OH)2 is washed free, often with the help of ultrasonics and small brushes. After it is dried with large, sometimes inverted, premeasured paper points, the canal is filled incrementally with MTA, which is delivered to the canal with a dedicated MTA carrier or depos-ited in small pellets from an amalgam gun. The material can then be worked up the canal with premeasured pluggers, or inverted paper-points, set some 1 to 3 mm short of the root end, often with the help of sonic or ultrasonic energy to settle the material.308 Apical matrices have not generally been con-sidered necessary to limit the flow of MTA, although impressive-looking results may be obtained by packing the apical region with calcium sulfate before MTA application.283 An apical plug 4- to 5-mm thick is usually considered optimal (see Fig. 24-31, B).289 The adequacy of the apical plug is verified radiographically.

All excess MTA is removed from the canal walls by scrub-bing with large, moistened paper points or brushes. Meticulous cleanup is important to allow optimal bonding of the subsequent composite resin restoration, which will extend deeply into the canal and offer internal reinforcement of the fragile root.

A very wet cotton pellet is placed in the canal to provide moisture for the setting reaction. The pellet should not be in contact with the MTA because fibers of the cotton can become impregnated into the material. Excess water in the access

pastes must always be followed by obturation of the canal with a permanent root canal filling, traditionally of thermoplastic gutta-percha and sealer, although MTA would be a good con-temporary alternative.

Although the apexification technique with Ca(OH)2 has enjoyed considerable tooth-preserving success, the many disadvantages of this protracted treatment have justified a search for alternatives, such as artificial barrier techniques, with their potential for more rapid treatment, and regenera-tion techniques, with their potential for continued tooth development.

Artificial Apical Barrier Techniques (see Fig. 24-28, C)Coviello and Brilliant41 reported the use of tricalcium phos-phate as an apical barrier in 1979. The material was packed into the apical 2 mm of the canal, against which gutta-percha was compacted. The treatment was completed in one appoint-ment, and radiographic assessment confirmed successful apexification comparable to that achieved with Ca(OH)2. Calcium hydroxide powder has also been used successfully as an apical barrier against which to pack gutta-percha.248

The use of MTA as an apical barrier was first reported in 1996,281 and subsequent clinical investigations in animals252 and humans217,242,260 have established this as the standard, with biologic outcomes in terms of periapical healing and root-end closure at least comparable to those treated with Ca(OH)2.

217 Simon et al.260 treated 57 teeth in patients with a mean age of 18 years (standard deviation, 12 years). Of the 43 teeth with at least 12-month follow-up, healing had occurred in 81%. More recently, a series of 17 nonvital immature incisors in children with a mean age of 11.7 years was followed up for a mean of 12.5 months. This study reported 94.1% clinical success, with radiographic healing in 76.5% and a further 17.6% uncertain.242 One study of 38 cases also suggested that the presence of a preoperative periapical lesion had no influ-ence on the outcome.195 This approach to the problem of root-end closure allows treatment to be completed on a short time scale, with advantages including improved patient compliance,

FIG. 24-31 Mineral trioxide aggregate (MTA) apical barrier apexification procedure and restoration with bonded composite. A, Maxillary right central incisor with a large periapical lesion. The patient is undergoing orthodontic treatment. B, After placement of MTA in the apical 4 mm of the canal. C, Six months later; the entire canal coronal to the MTA apical barrier is filled with bonded composite resin. Note that calcification has occurred periapically as orthodontic treatment has continued. D, Thirty months after treatment; the periapical lesion has healed.

A B C D


bond the canal according to the manufacturer’s instructions, with proper washout of etchant and avoiding gross pooling of unfilled resin. Complete resin infiltration of dentin cannot be guaranteed in the depths of a root canal, and the potential exists that host-derived metalloproteinases liberated by acid etching may degrade resin-dentin bonds with time. Flushing the preparation after etching with a synthetic protease inhibi-tor, such as 2% chlorhexidine, may help counter some of these adverse events.33

Clear light-transmitting posts (e.g., Luminex System, Dentatus USA, New York) have been developed to ensure com-plete bonding of deep increments of light-activated composite. This may be less of an issue with dual-curing materials.

In the Luminex technique, the clinician places a light-curing composite resin in the canal, building up 2-mm incre-ments with care to avoid trapping air bubbles. The Luminex post is placed to the depth of the preparation, and the com-posite is cured by transmitting light through the post. After curing, the plastic post is trimmed to the cervical line, and the incisal opening is restored.

If a core is needed for crown placement, a Luminex post without serrations is used for curing the composite. Because the composite does not bond to the smooth post, it can be gently removed and a corresponding metal Dentatus post cemented into the space with a resin cement. A composite buildup for crown retention may then be completed.

A variety of commercial quartz and glass fiber post systems are also available for use in such applications, ensuring the delivery of light deep into the canal system and offering the potential for internal reinforcement (see Fig. 24-28, C).245 The heads of fiber posts should always be covered with com-posite resin to prevent them from absorbing oral fluids and delaminating.

NEW HORIZONS FOR PULP REGENERATIONUntil recently, few treatment options were available for the nonvital, permanent immature tooth. On confirming pulp necrosis, efforts could be made to preserve the tooth by apexi-fication, or it could be extracted within a broader orthodontic treatment plan. This view has recently been challenged by a

preparation is dried with cotton pellets, and the opening is sealed with a provisional restorative material, such as Cavit. At a subsequent appointment, the tooth is reisolated and the hard set of the MTA verified with an endodontic file or probe. If for some reason the MTA has not hardened, the canal can be recleansed and the procedure repeated before final bonded restoration.

Restoration After ApexificationImmature teeth, particularly those that are pulpless and have undergone apexification, are at high risk of fracture. It has been reported that, within 3 years of long-term Ca(OH)2 medication and root filling with gutta-percha, 28% to 77% of immature teeth suffered a cervical root fracture.46 The degree of dental development appeared to be a key variable. Clinically, it is the impression of the authors that rapid MTA plug techniques, in combination with the internal placement of bonded com-posite resin, appear to have virtually eliminated cervical root fractures. Many of the studies are laboratory based, using simu-lated rather than real immature teeth, but the use of contem-porary dentinal bonding techniques has been shown to strengthen endodontically treated teeth to levels close to those of intact teeth.100,110,136 A 2004 study149 demonstrated signifi-cantly greater resistance to root fracture after placement of a 4-mm thick apical plug of MTA followed by an intracanal composite resin, compared with MTA followed by gutta-percha and sealer. Root reinforcement has also been reported to be improved by the cementation of a metal post within the channel created by removal of a light-transmitting composite curing post.34 The potential of fiber-reinforced posts would also appear great,26,251 though little clinical evidence has yet been published on the clinical treatment of immature teeth.

Alternative materials that have been suggested to bond and reinforce fragile roots include resin-modified glass ionomer cements95 and, most recently, Resilon.277 However, the evidence on Resilon remains contentious,303 and the ideal of predictable bonding and tooth reinforcement throughout the length of the root canal system has not yet been achieved.276

Bonding of dual- or light-curing composite resin directly over the MTA plug, with no interposing layer of gutta-percha, has become an established clinical method (see Fig. 24-28, C, and Fig. 24-31, C). The clinician should take care to etch and

FIG. 24-32 Apexification with mineral trioxide aggregate (MTA) barriers in a mandibular permanent molar. A, Periapical lesion reveals open apices in this pulpless molar. B, Apical plugs of MTA and the remainder of the pulp space are restored with bonded composite resin. C, Two years later; closure of the root ends with cementum.

A B C


number of ground-breaking reports in which nonvital imma-ture teeth with clear evidence of pulp breakdown and periapi-cal suppuration were encouraged to resume root formation (length and wall thickness), possibly by the regeneration of pulp tissue (see also Chapter 10).15,37,128,132,279 Success is believed to depend on the activity of a newly identified population of stem cells, the so-called stem cells from apical papilla (SCAP) cells (Fig. 24-33, A), a hidden treasure with enormous poten-tial for tissue regeneration and bioroot engineering.121

The potential of bioengineering is huge, and work contin-ues to optimize scaffolds that may encourage revascularization of the pulp space and to explore the options of seeding cell populations into the properly sterilized pulp spaces of imma-ture teeth.182 Our call for action has never been louder as we seek effective, biologically based treatments for our pediatric patients.

ACKNOWLEDGMENTThe authors of this chapter acknowledge with gratitude the legacy of former principal authors Joe H. Camp and Anna B. Fuks, whose meticulous and steadfast work has authoritatively informed clinicians and scientists over many decades, and whose wisdom lays the foundations for this edition.

FIG. 24-33 Schematic representation of pulp regeneration. A, Immature, nonvital permanent tooth, showing the location of the apical papilla with its rich collection of stem cells. B, After the canal has been medicated, classically with a triantibiotic paste, it is overinstrumented to encourage bleeding up to the cervical level. A subsequent blood clot is overlaid with MTA and a sealing restoration, forming a scaffold for invasion by stem cells from the apical papilla (i.e., SCAP cells). C, Pulp regeneration is expected to allow continued root formation in a previously pulpless tooth.

Immature toothwith necrotic pulp

Compositecoronal

seal

MTA seal

Blood clotscaffoldinvaded

by SCAP New pulptissue

Root formation:length and wallthickness

A B C

SCAP

REFERENCES1. Aeinehchi M, Eslami B, Ghanbariha M, et al: Mineral

trioxide aggregate (MTA) and calcium hydroxide as pulp-capping agents in human teeth: a preliminary report, Int Endod J 36:225, 2003.

2. Agamy HA, Bakry NS, Mounir MMF, et al: Comparison of mineral trioxide aggregate and formocresol as pulp-capping agents in pulpotomized primary teeth, Pediatr Dent 26:302, 2004.

3. Aguilar P, Linsuwanont P: Vital pulp therapy in vital permanent teeth with cariously exposed pulp: A systematic review, J Endod 37:581, 2011.

4. Al-Zayer MA, Straffon LH, Feigal RJ, et al: Indirect pulp treatment of primary posterior teeth: A retrospective study, Pediatr Dent 25:29, 2003.

5. Alacam A: Long term effects of primary teeth pulpotomies with formocresol, glutaraldehyde-calcium hydroxide and glutaraldehyde-zinc oxide eugenol on succedaneous teeth, J Pedod 13:307, 1989.

6. Andreasen FM: Transient apical breakdown and its relation to color and sensibility changes after luxation injuries to teeth, Endod Dent Traumatol 2:9, 1986.

7. Andreasen J, Andreasen F, Andersson L: Textbook and colour atlas of traumatic injuries to the teeth, ed 4, Philadelphia, 2008, Wiley-Blackwell.

8. Andreasen JO, Ravn JJ: The effect of traumatic injuries to primary teeth on their permanent successors. II. A clinical and radiographic follow-up study of 213 teeth, Scand J Dent Res 79:284, 1971.

9. Andreasen JO, Ravn JJ: Epidemiology of traumatic dental injuries to primary and permanent teeth in a Danish population sample, Int J Oral Surg 1:235, 1972.

10. Andrew P: The treatment of infected pulps in deciduous teeth, Br Dent J 98:122, 1955.

11. Aponte AJ, Hartsook JT, Crowley MC: Indirect pulp capping success verified, J Dent Child 33:164, 1966.

12. Armstrong RL, Patterson SS, Kafrawy AH, et al: Comparison of Dycal and formocresol pulpotomies in young permanent teeth in monkeys, Oral Surg Oral Med Oral Pathol 48:160, 1979.

13. Avram DC, Pulver F: Pulpotomy medicaments for vital primary teeth. Surveys to determine use and attitudes in

pediatric dental practice and in dental schools throughout the world, ASDC J Dent Child 56:426, 1989.

14. Baggett FJ, Mackie IC, Worthington HV: An investigation into the measurement of the working length of immature incisor teeth requiring endodontic treatment in children, Br Dent J 181:96, 1996.

15. Banchs F, Trope M: Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? J Endod 30:196, 2004.

16. Barcelos R, Santos MPA, Primo LG, et al: ZOE paste pulpectomies outcome in primary teeth: a systematic review, J Clin Pediatr Dent 35:241, 2011.

17. Barthel CR, Rosenkranz B, Leuenberg A, et al: Pulp capping of carious exposures: treatment outcome after 5 and 10 years—a retrospective study, J Endod 26:525, 2000.

18. Belobrov I, Parashos P: Treatment of tooth discoloration after the use of white mineral trioxide aggregate, J Endod 37:1017, 2011.

19. Bennett CG: Pulpal management of deciduous teeth, Pract Dent Monogr 64:1, 1965.

20. Berk H, Krakow AA: Endodontic treatment in primary teeth. In Goldman HM, et al, editors: Current therapy in dentistry, vol 5, St Louis, 1974, Mosby.

21. Bevelander G, Benzer D: Morphology and incidence of secondary dentin in human teeth, J Am Dent Assoc 30:1079, 1943.

22. Bjørndal L: Indirect pulp therapy and stepwise excavation, J Endod 34:S29, 2008.

23. Bjørndal L, Reit C, Bruun G, et al: Treatment of deep caries lesions in adults: randomized clinical trials comparing stepwise vs direct complete excavation, and direct pulp capping vs partial pulpotomy, Eur J Oral Sci 118:290, 2010.

24. Block RM, Lewis RD, Sheats JB, et al: Cell-mediated immune response to dog pulp tissue altered by formocresol within the root canal, J Endod 3:424, 1977.

25. Bogen G, Kim JS, Bakland LK: Direct pulp capping with mineral trioxide aggregate: an observational study, J Am Dent Assoc 139:305, 2008.

26. Bonfante G, Kaizer OB, Pegoraro LF, et al: Fracture strength of teeth with flared root canals restored with glass fibre posts, Int Dent J 57:153, 2007.

27. Borum MK, Andreasen JO: Sequelae of trauma to primary maxillary incisors. I. Complications in the primary dentition, Endod Dent Traumatol 14:31, 1998.

28. Burnett S, Walker J: Comparison of ferric sulfate, formocresol, and a combination of ferric sulfate/formocresol in primary tooth vital pulpotomies: a retrospective radiographic survey, J Dent Child 69:44, 2002.

29. Caldwell RE, Freilich MM, Sandor GK: Two radicular cysts associated with endodontically treated primary teeth: rationale for long-term follow-up, Ont Dent 76:29, 1999.

30. Calişkan MK: Pulpotomy of carious vital teeth with periapical involvement, Int Endod J 28:172, 1995.

31. Camp JH: Continued apical development of pulpless permanent teeth after endodontic therapy, master’s thesis, Bloomington, 1968, School of Dentistry, Indiana University.

32. International Agency for Research on Cancer: IARC classifies formaldehyde as carcinogenic to humans, press release no 153. Available at: www.iarc.fr/pageroot/PRELEASES/prl153a.html. Accessed August 20, 2004.

33. Carrilho MRO, Geraldeli S, Tay F, et al: In vivo preservation of the hybrid layer by chlorhexidine, J Dent Res 86:529, 2007.

34. Carvalho CAT, Valera MC, Oliveira LD, et al: Structural resistance in immature teeth using root reinforcements in vitro, Dent Traumatol 21:155, 2005.

35. Casagrande L, Bento LW, Dalpian DM, et al: Indirect pulp treatment in primary teeth: 4-year results, Am J Dent 23:34, 2010.

36. Casagrande L, Falster CA, Di Hipolito V, et al: Effect of adhesive restorations over incomplete dentin caries removal: 5-year follow-up study in primary teeth, J Dent Child 76:117, 2009.

37. Chueh LH, Huang GTJ: Immature teeth with periradicular periodontitis or abscess undergoing apexogenesis: a paradigm shift, J Endod 32:1205, 2006.

http://www.iarc.fr/pageroot/PRELEASES/prl153a.html

http://www.iarc.fr/pageroot/PRELEASES/prl153a.html


38. Cohenca N, Karni S, Rotstein I: Transient apical breakdown following tooth luxation, Dent Traumatol 19:289, 2003.

39. Coll JA: Predicting pulpectomy success and its relationship to exfoliation and succedaneous dentition, Pediatr Dent 18:57, 1996.

40. Cotes O, Boj JR, Canalda C, et al: Pulpal tissue reaction to formocresol vs ferric sulfate in pulpotomized rat teeth, J Clin Pediatr Dent 21:247, 1997.

41. Coviello J, Brilliant JD: A preliminary clinical study on the use of tricalcium phosphate as an apical barrier, J Endod 5:6, 1979.

42. Cox CF, Hafez AA, Akimoto N, et al: Biocompatibility of primer adhesive and resin composite systems on non-exposed and exposed pulps of non-human primate teeth, Am J Dent 11:s55, 1998.

43. Croll TP, Pascon EA, Langeland K: Traumatically injured primary incisors: a clinical and histological study, ASDC J Dent Child 54:401, 1987.

44. Cvek M: Treatment of non-vital permanent incisors with calcium hydroxide. I. Follow-up of periapical repair and apical closure of immature roots, Odontol Revy 23:27, 1972.

45. Cvek M: A clinical report on partial pulpotomy and capping with calcium hydroxide in permanent incisors with complicated crown fracture, J Endod 4:232, 1978.

46. Cvek M: Prognosis of luxated non-vital maxillary incisors treated with calcium hydroxide and filled with gutta-percha: a retrospective clinical study, Endod Dent Traumatol 8:45, 1992.

47. Cvek M, Cleaton-Jones PE, Austin JC, et al: Pulp reactions to exposure after experimental crown fractures or grinding in adult monkeys, J Endod 8:391, 1982.

48. Cvek M, Lundberg M: Histological appearance of pulps after exposure by a crown fracture, partial pulpotomy, and clinical diagnosis of healing, J Endod 9:8, 1983.

49. Damle SG, Bhattal H, Loomba A: Apexification of anterior teeth, J Clin Pediatr Dent 36:263, 2012.

50. Dandashi MB, Nazif MM, Zullo T, et al: An in vitro comparison of three endodontic techniques for primary incisors, Pediatr Dent 15:254, 1993.

51. Davis MJ, Myers R, Switkes MD: Glutaraldehyde: an alternative to formocresol for vital pulp therapy, ASDC J Dent Child 49:176, 1982.

52. de Amorim RG, Leal SC, Frencken JE: Survival of atraumatic restorative treatment (ART) sealants and restorations: a meta-analysis, Clin Oral Invest 16:429, 2012.

53. Dean JA, Avery DR, McDonald RE: McDonald and Avery’s dentistry for the child and adolescent, ed 10, St Louis, 2011, Mosby/Elsevier.

54. American Academy of Pediatric Dentistry: Reference manual: clinical guideline on pulp therapy for primary and young permanent teeth, Pediatr Dent 25:87, 2003.

55. Dominguez MS, Witherspoon DE, Gutmann JL, et al: Histological and scanning electron microscopy assessment of various vital pulp therapy materials, J Endod 29:324, 2003.

56. Doyle TL, Casas MJ, Kenny DJ, et al: Mineral trioxide aggregate produces superior outcomes in vital primary molar pulpotomy, Pediatr Dent 32:41, 2010.

57. Dummer PM, Hicks R, Huws D: Clinical signs and symptoms in pulp disease, Int Endod J 13:27, 1980.

58. Dylewski JJ: Apical closure of non-vital teeth, Oral Surg Oral Med Oral Pathol 32:82, 1971.

59. Easlick KA: Operative procedures in management of deciduous molars, Int J Orthod 20:585, 1934.

60. Eidelman E, Odont D, Holan G, et al: Mineral trioxide aggregate vs formocresol in pulpotomized primary molars: a preliminary report, Pediatr Dent 23:15, 2001.

61. El Meligy OAS, Avery DR: Comparison of mineral trioxide aggregate and calcium hydroxide as pulpotomy agents in young permanent teeth (apexogenesis), Pediatr Dent 28:399, 2006.

62. Elliott RD, Roberts MW, Burkes J, et al: Evaluation of the carbon dioxide laser on vital human primary pulp tissue, Pediatr Dent 21:327, 1999.

63. Emmerson C: Pulpal changes following formocresol applications on rat molars and human primary teeth, J South Calif Dent Assoc 27:309, 1959.

64. England MC Jr, Best E: Noninduced apical closure in immature roots of dogs’ teeth, J Endod 3:411, 1977.

65. Erdem AP, Guven Y, Balli B, et al: Success rates of mineral trioxide aggregate, ferric sulfate, and formocresol pulpotomies: a 24-month study, Pediatr Dent 33:165, 2011.

66. Evans D, Reid J, Strang R, et al: A comparison of laser Doppler flowmetry with other methods of assessing the vitality of traumatised anterior teeth, Dent Traumatol 15:284, 1999.

67. Falster CA, Araujo FB, Straffon LH, et al: Indirect pulp treatment: in vivo outcomes of an adhesive resin system vs calcium hydroxide for protection of the dentin-pulp complex, Pediatr Dent 24:241, 2002.

68. Farooq NS, Coll JA, Kuwabara A, et al: Success rates of formocresol pulpotomy and indirect pulp therapy in the treatment of deep dentinal caries in primary teeth, Pediatr Dent 22:278, 2000.

69. Farsi N, Alamoudi N, Balto K, et al: Clinical assessment of mineral trioxide aggregate (MTA) as direct pulp capping in young permanent teeth, J Clin Pediatr Dent 31:72, 2006.

70. Fayle SA, Welbury RR, Roberts JF: British Society of Paediatric Dentistry: a policy document on management of caries in the primary dentition, Int J Pediatr Dent 11:153, 2001.

71. Fei AL, Udin RD, Johnson R: A clinical study of ferric sulfate as a pulpotomy agent in primary teeth, Pediatr Dent 13:327, 1991.

72. Feigal RJ, Messer HH: A critical look at glutaraldehyde, Pediatr Dent 12:69, 1990.

73. Feltman EM: A comparison of the formocresol pulpotomy technique and Dycal pulpotomy technique in young permanent teeth, master’s thesis, Bloomington, 1972, School of Dentistry, Indiana University.

74. Finn SB: Morphology of primary teeth. In Finn SB, editor: Clinical pedodontics, ed 3, Philadelphia, 1967, Saunders.

75. Fischer DE: Tissue management: a new solution to an old problem, Gen Dent 35:178, 1987.

76. Fishman SA: Success of electrofulguration pulpotomies covered by zinc oxide and eugenol or calcium hydroxide: a clinical study, Pediatr Dent 18:385, 1996.

77. Frank AL: Therapy for the divergent pulpless tooth by continued apical formation, J Am Dent Assoc 72:87, 1966.

78. Fuchino T: Clinical and histopathological studies of pulpectomy in deciduous teeth, Shikwa Gakuho 80:971, 1980.

79. Fuks AB: Ferric sulfate versus dilute formocresol in pulpotomized primary molars: long-term follow up, Pediatr Dent 19:327, 1997

80. Fuks AB: Current concepts in vital pulp therapy, Eur J Paediatr Dent 3:115, 2002.

81. Fuks AB, Bimstein E: Clinical evaluation of diluted formocresol pulpotomies in primary teeth of schoolchildren, Pediatr Dent 3:321, 1981.

82. Fuks AB, Bimstein E, Bruchim A: Radiographic and histologic evaluation of the effect of two concentrations of formocresol on pulpotomized primary and young permanent teeth in monkeys, Pediatr Dent 5:9, 1983.

83. Fuks AB, Bimstein E, Guelmann M, et al: Assessment of a 2% buffered glutaraldehyde solution in pulpotomized primary teeth of school children, ASDC J Dent Child 57:371, 1990.

84. Fuks AB, Cosack A, Klein H, et al: Partial pulpotomy as a treatment alternative for exposed pulps in crown-fractured permanent incisors, Endod Dent Traumatol 3:100, 1987.

85. Fuks AB, Eidelman E, Pauker N: Root fillings with Endoflas in primary teeth: a retrospective study, J Clin Ped Dent 27:41, 2002.

86. Fulling HJ, Andreasen JO: Influence of maturation status and tooth type of permanent teeth upon electrometric and thermal pulp testing, Scand J Dent Res 84:286, 1976.

87. Fulling HJ, Andreasen JO: Influence of splints and temporary crowns upon electric and thermal pulp testing procedures, Scand J Dent Res 84:291, 1976.

88. Fulton R, Ranly DM: An autoradiographic study of formocresol pulpotomies in rat molars using 3H-formaldehyde, J Endod 5:71, 1979.

89. Fuss Z, Trowbridge H, Bender IB: Assessment of reliability of electrical and thermal pulp testing agents, J Endod 12:301, 1986.

90. Garcia-Godoy F, Novakovic DP, Carvajal IN: Pulpal response to different application times of formocresol, J Pedod 6:176, 1982.

91. Garcia-Godoy F: Evaluation of an iodoform paste in root canal therapy for infected primary teeth, ASDC J Dent Child 54:30, 1987.

92. Garcia-Godoy F, Ranly DM: Clinical evaluation of pulpotomies with ZOE as the vehicle for glutaraldehyde, Pediatr Dent 9:144, 1987.

93. Gerlach E: Root canal therapeutics in deciduous teeth, Dent Surv 8:68, 1932.

94. Glendor U: On dental trauma in children and adolescents: incidence, risk, treatment, time and costs, Swed Dent J Suppl 140:1, 2000.

95. Goldberg F, Kaplan A, Roitman M, et al: Reinforcing effect of a resin glass ionomer in the restoration of immature roots in vitro, Dent Traumatol 18:70, 2002.

96. Goldmacher VS, Thilly WG: Formaldehyde is mutagenic for cultured human cells, Mutat Res 116:417, 1983.

97. Granath LE, Hagman G: Experimental pulpotomy in human bicuspids with reference to cutting technique, Acta Odontol Scand 29:155, 1971.

98. Greenberg M: Filling root canals of deciduous teeth by an injection technique, Dent Dig 67:574, 1964.

99. Gruythuysen R, Van Strijp G, Wu MK: Long-term survival of indirect pulp treatment performed in primary and permanent teeth with clinically diagnosed deep carious lesions, J Endod 36:1490, 2010.

100. Guelmann M, Bookmyer KL, Villalta P, et al: Microleakage of restorative techniques for pulpotomized primary molars, J Dent Child 71:209, 2004.

101. Guthrie TJ, McDonald RE, Mitchell DF: Dental pulp hemogram, J Dent Res 44:678, 1965.

102. Hadeer AA, Niveen SB, Maha MFM, et al: Comparison of mineral trioxide aggregate and formocresol as pulp-capping agents in pulpotomized primary teeth, Pediatr Dent 26:302, 2004.

103. Ham JW, Patterson SS, Mitchell DF: Induced apical closure of immature pulpless teeth in monkeys, Oral Surg Oral Med Oral Pathol 33:438, 1972.

104. Hamaguchi F, Tsutsui T: Assessment of genotoxicity of dental antiseptics: ability of phenol, guaiacol, p-phenolsulfonic acid, sodium hypochlorite, p-chlorophenol, m-cresol or formaldehyde to induce unscheduled DNA synthesis in cultured Syrian hamster embryo cells, Jpn J Pharmacol 83:273, 2000.

105. Hargreaves KM: Seltzer and Bender’s the dental pulp, ed 2, Chicago, 2010, Quintessence.

106. Hayashi M, Fujitani M, Yamaki C, et al: Ways of enhancing pulp preservation by stepwise excavation: a systematic review, J Dent 39:117, 2011.

107. Heasman PM, McCracken G: Harty’s dental dictionary, ed 3, London, 2007, Churchill Livingstone.

108. Heide S: Pulp reactions to exposure for 4, 24 and 168 hours, J Dent Res 59:1910, 1980.

109. Heide S, Kerekes K: Delayed partial pulpotomy in permanent incisors of monkeys, Int Endod J 19:78, 1986.

110. Hernandez R, Bader S, Boston D, et al: Resistance to fracture of endodontically treated premolars restored with new generation dentine bonding systems, Int Endod J 27:281, 1994.

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


112. Hill SD, Berry CW, Seale NS, et al: Comparison of antimicrobial and cytotoxic effects of glutaraldehyde and formocresol, Oral Surg Oral Med Oral Pathol 71:89, 1991.

113. Hobson P: Pulp treatment of deciduous teeth. Part 2. Clinical investigation, Br Dent J 128:275, 1970.

114. Holan G: The diagnostic value of coronal dark-gray discoloration in primary teeth following traumatic injuries, Pediatr Dent 18:224, 1996.

115. Holan G: Tube-like mineralization in the dental pulp of traumatized primary incisors, Endod Dent Traumatol 14:279, 1998.

116. Holan G: Development of clinical and radiographic signs associated with dark discolored primary incisors following traumatic injuries: a prospective controlled study, Dent Traumatol 20:276, 2004.

117. Holan G, Eidelman E, Fuks AB: Long-term evaluation of pulpotomy in primary molars using mineral trioxide aggregate or formocresol, Pediatr Dent 27:129, 2005.

118. Holan G, Fuks AB: A comparison of pulpectomies using ZOE and KRI paste in primary molars: a retrospective study, Pediatr Dent 15:403, 1993.

119. Holan G, Topf J, Fuks AB: Effect of root canal infection and treatment of traumatized primary incisors on their permanent successors, Endod Dent Traumatol 8:12, 1992.

120. Huang GTJ: Apexification: the beginning of its end, Int Endod J 42:855, 2009.

121. Huang GTJ, Sonoyama W, Liu Y, et al: The hidden treasure in apical papilla: the potential role in pulp/dentin regeneration and bioroot engineering, J Endod 34:645, 2008.

122. Hulsmann M, Pieper K: Use of an electronic apex locator in the treatment of teeth with incomplete root formation, Endod Dent Traumatol 5:238, 1989.

123. Ibricevic H, Al-Jame Q: Ferric sulfate as pulpotomy agent in primary teeth: 20-month clinical follow-up, J Clin Pediatr Dent 24:269, 2000.

124. Ingle JI, Bakland LK, Baumgartner JC: Ingle’s endodontics, ed 6, New York, 2008, Decker.

125. Innes NP, Evans DJ, Stirrups DR: The Hall technique: a randomized controlled clinical trial of a novel method of managing carious primary molars in general dental practice—acceptability of the technique and outcomes at 23 months, BMC Oral Health 7:18, 2007.

126. Innes NPT, Stirrups DR, Evans DJP, et al: A novel technique using preformed metal crowns for managing carious primary molars in general practice: a retrospective analysis, Br Dent J 200:451, 2006.

127. Ireland RL: Secondary dentin formation in deciduous teeth, J Am Dent Assoc 28:1626, 1941.

128. Iwaya SI, Ikawa M, Kubota M: Revascularization of an immature permanent tooth with apical periodontitis and sinus tract, Dent Traumatol 17:185, 2001.

129. Jacobsen I: Criteria for diagnosis of pulp necrosis in traumatized permanent incisors, Scand J Dent Res 88:306, 1980.

130. Jeng HW, Feigal RJ, Messer HH: Comparison of the cytotoxicity of formocresol, formaldehyde, cresol, and glutaraldehyde using human pulp fibroblast cultures, Pediatr Dent 9:295, 1987.

131. Jordan ME: Operative dentistry for children, New York, 1925, Dental Items of Interest Publishing.

132. Jung IY, Lee SJ, Hargreaves KM: Biologically based treatment of immature permanent teeth with pulpal necrosis: a case series, J Endod 34:876, 2008.

133. Junn DJM, McMillan P, Bakland LK, Torabinejad M: Quantitative assessment of dentin bridge formation following pulp capping with mineral trioxide aggregate (MTA), J Endod 24:278, 1998.

134. Kaiser JH: Management of wide-open canals with calcium hydroxide. Cited by Steiner JC, Dow PR, Cathey GM: Inducing root end closure of non-vital permanent teeth, J Dent Child 35:47, 1968.

135. Karp WB, Korb P, Pashley D: The oxidation of glutaraldehyde by rat tissues, Pediatr Dent 9:301, 1987.

136. Katebzadeh N, Clark Dalton B, Trope M: Strengthening immature teeth during and after apexification, J Endod 24:256, 1998.

137. Kennedy DB, el-Kafrawy AH, Mitchell DF, et al: Formocresol pulpotomy in teeth of dogs with induced pulpal and periapical pathosis, ASDC J Dent Child 40:208, 1973.

138. Kim YJA, Chandler NP: Determination of working length for teeth with wide or immature apices: a review, Int Endod J 46:483, 2013.

139. Klein H: Pulp responses to an electric pulp stimulator in the developing permanent anterior dentition, ASDC J Dent Child 45:199, 1978.

140. Koenigs JF, Heller AL, Brilliant JD, et al: Induced apical closure of permanent teeth in adult primates using a resorbable form of tricalcium phosphate ceramic, J Endod 1:102, 1975.

141. Kopel HM, Bernick S, Zachrisson E, et al: The effects of glutaraldehyde on primary pulp tissue following coronal amputation: an in vivo histologic study, ASDC J Dent Child 47:425, 1980.

142. Kotsanos N, Arizos S: Evaluation of a resin modified glass ionomer serving both as indirect pulp therapy and as restorative material for primary molars, Eur Arch Paediatr Dent 12:170, 2011.

143. Kubota K, Golden BE, Penugonda B: Root canal filling materials for primary teeth: a review of the literature, ASDC J Dent Child 59:225, 1992.

144. Laboratory, Physical and Theoretical Chemistry: 2006. “New Age” Pulp Therapy: Personal Thoughts on a Hot Debate. Available at: http://physchem.ox.ac.uk/MSDS/CR/cresol.html. Accessed August 15, 2007.

145. Landau MJ, Johnsen DC: Pulpal responses to ferric sulfate in monkeys, J Dent Res 167(Special issue):215, 1988.

146. Langeland K, Dowden WE, Tronstad L, et al: Human pulp changes of iatrogenic origin, Oral Surg Oral Med Oral Pathol 32:943, 1971.

147. Laurence RP: A method of root canal therapy for primary teeth, master’s thesis, Atlanta, 1966, School of Dentistry, Emory University.

148. Laurent P, Camps J, About I: Biodentine TM induces TGF-β1 release from human pulp cells and early dental pulp mineralization, Int Endod J 45:439, 2012.

149. Lawley GR, Schindler WG, Walker WA III, et al: Evaluation of ultrasonically placed MTA and fracture resistance with intracanal composite resin in a model of apexification, J Endod 30:167, 2004.

150. Laws AJ: Pulpotomy by electro-coagulation, N Z Dent J 53:68, 1957.

151. Lee YL, Lee BS, Lin FH, et al: Effects of physiological environments on the hydration behavior of mineral trioxide aggregate, Biomats 25:787, 2004.

152. Lekka M, Hume WR, Wolinsky LE: Comparison between formaldehyde and glutaraldehyde diffusion through the root tissues of pulpotomy-treated teeth, J Pedod 8:185, 1984.

153. Lemon RR, Steele PJ, Jeansonne BG: Ferric sulfate hemostasis: effect on osseous wound healing. I. Left in situ for maximum exposure, J Endod 19:170, 1993.

154. Liu H, Zhou Q, Qin M: Mineral trioxide aggregate versus calcium hydroxide for pulpotomy in primary molars, Chin J Dent Res 14:121, 2011.

155. Liu JF, Chen LR, Chao SY: Laser pulpotomy of primary teeth, Pediatr Dent 21:128, 1999.

156. Lloyd JM, Seale NS, Wilson CF: The effects of various concentrations and lengths of application of glutaraldehyde on monkey pulp tissue, Pediatr Dent 10:115, 1988.

157. Loh A, O’Hoy P, Tran X, et al: Evidence-based assessment: evaluation of the formocresol versus ferric sulfate primary molar pulpotomy, Pediatr Dent 26:401, 2004.

158. Loos PJ, Han SS: An enzyme histochemical study of the effect of various concentrations of formocresol on connective tissues, Oral Surg Oral Med Oral Pathol 31:571, 1971.

159. Loos PJ, Straffon LH, Han SS: Biological effects of formocresol, ASDC J Dent Child 40:193, 1973.

160. Lucas Leite ACG, Rosenblatt A, Da Silva Calixto M, et al: Genotoxic effect of formocresol pulp therapy of deciduous teeth, Mutat Res 747:93, 2012.

161. Machida Y: Root canal therapy in deciduous teeth, Jpn Dent Assoc J 36:796, 1983.

162. Mack ES: Personal communication with former chapter author, Joe Camp, 1967.

163. Mack RB, Dean JA: Electrosurgical pulpotomy: a retrospective human study, ASDC J Dent Child 60:107, 1993.

164. Mack RB, Halterman CW: Labial pulpectomy access followed by esthetic composite resin restoration for nonvital maxillary deciduous incisors, J Am Dent Assoc 100:374, 1980.

165. Maltz M, Alves LS, Jardim JJ, et al: Incomplete caries removal in deep lesions: a 10-year prospective study, Am J Dent 24:211, 2011.

166. Maltz M, Garcia R, Jardim JJ, et al: Randomized trial of partial vs stepwise caries removal: 3-year follow-up, J Dent Res 91:1026, 2012.

167. Mansukhani N: Pulpal reactions to formocresol, master’s thesis, Urbana, 1959, University of Illinois.

168. Marsh PD: Dental plaque as a microbial biofilm, Caries Res 38:204, 2004.

169. Mass E, Zilberman U: Clinical and radiographic evaluation of partial pulpotomy in carious exposure of permanent molars, Pediatr Dent 15:257, 1993.

170. Mass E, Zilberman U: Long-term radiologic pulp evaluation after partial pulpotomy in young permanent molars, Quint Int 42:547, 2011.

171. Mass E, Zilberman UL: Endodontic treatment of infected primary teeth, using Maisto’s paste, ASDC J Dent Child 56:117, 1989.

172. Mass E, Zilberman U, Fuks AB: Partial pulpotomy: another treatment option for cariously exposed permanent molars, ASDC J Dent Child 62:342, 1995.

173. Massler MM, Mansukhani H: Effects of formocresol on the dental pulp, J Dent Child 26:277, 1959.

174. Matsumiya SS, Susuki A, Takuma S: Atlas of clinical pathology, vol 1, Tokyo, 1962, Tokyo University Press.

175. Mejàre I, Cvek M: Partial pulpotomy in young permanent teeth with deep carious lesions, Endod Dent Traumatol 9:238, 1993.

176. Mendoza A, Enrique Solano Reina J, Garcia-Godoy F: Evolution and prognosis of necrotic primary teeth after pulpectomy, Am J Dent 23:265, 2010.

177. Messer LB, Cline JT, Korf NW: Long term effects of primary molar pulpotomies on succedaneous bicuspids, J Dent Res 59:116, 1980.

178. Milnes AR: Persuasive evidence that formocresol use in pediatric dentistry is safe, J Can Dent Assoc 72:247, 2006.

179. Milsom KM, Tickle M, Blinkhorn AS: Dental pain and dental treatment of young children attending the general dental service, Br Dent J 192:280, 2002.

180. Morawa AP, Straffon LH, Han SS, et al: Clinical evaluation of pulpotomies using dilute formocresol, ASDC J Dent Child 42:360, 1975.

181. Mulder GR, van Amerongen WE, Vingerling PA: Consequences of endodontic treatment of primary teeth. II. A clinical investigation into the influence of formocresol pulpotomy on the permanent successor, ASDC J Dent Child 54:35, 1987.

182. Murray PE, Garcia-Godoy F, Hargreaves KM: Regenerative endodontics: a review of current status and a call for action, J Endod 33:377, 2007.

183. Murray PE, Smith AJ, Garcia-Godoy F, et al: Comparison of operative procedure variables on pulpal viability in an ex vivo model, Int Endod J 41:389, 2008.

184. Myers DR: Effects of formocresol on pulps of cariously exposed permanent molars, master’s thesis, Memphis, 1972, University of Tennessee.

http://physchem.ox.ac.uk/MSDS/CR/cresol.html

http://physchem.ox.ac.uk/MSDS/CR/cresol.html


185. Myers DR, Battenhouse MR, Barenie JT, et al: Histopathology of furcation lesions associated with pulp degeneration in primary molars, Pediatr Dent 9:279, 1987.

186. Myers DR, Durham LC, Hanes CM, et al: Histopathology of radiolucent furcation lesions associated with pulpotomy-treated primary molars, Pediatr Dent 10:291, 1988.

187. Myers DR, Pashley DH, Lake FT, et al: Systemic absorption of 14C-glutaraldehyde from glutaraldehyde-treated pulpotomy sites, Pediatr Dent 8:134, 1986.

188. Myers DR, Pashley DH, Whitford GM, et al: The acute toxicity of high doses of systemically administered formocresol in dogs, Pediatr Dent 3:37, 1981.

189. Myers DR, Pashley DH, Whitford GM, et al: Tissue changes induced by the absorption of formocresol from pulpotomy sites in dogs, Pediatr Dent 5:6, 1983.

190. Myers DR, Shoaf HK, Dirksen TR, et al: Distribution of 14C-formaldehyde after pulpotomy with formocresol, J Am Dent Assoc 96:805, 1978.

191. Myers K: The effects of mineral trioxide aggregate on the dog pulp, J Endod 22:198, 1996.

192. Nadin G, Goel BR, Yeung CA, et al: Pulp treatment for extensive decay in primary teeth, Cochrane Database Syst Rev 1:CD003220, 2003.

193. Nair PNR, Duncan HF, Pitt Ford TR, et al: Histological, ultrastructural and quantitative investigations on the response of healthy human pulps to experimental capping with mineral trioxide aggregate: a randomized controlled trial, Int Endod J 42:422, 2009.

194. Nanci A: Ten Cate’s oral histology, development, structure and function, ed 7, St Louis, 2008, Mosby.

195. Nayar S, Bishop K, Alani A: A report on the clinical and radiographic outcomes of 38 cases of apexification with mineral trioxide aggregate, Eur J Pros Rest Dent 17:150, 2009.

196. Nelson S, Ash M: Wheeler’s dental anatomy, physiology and occlusion, ed 9, St Louis, 2010, Saunders.

197. Nematollahi H, Sahebnasagh M, Parisay I: Comparison of electrosurgical pulpotomy with zinc oxide eugenol or zinc polycarboxylate cements sub-base, J Clin Pediatr Dent 36:133, 2011.

198. Nevins A, Finkelstein F, Laporta R, et al: Induction of hard tissue into pulpless open-apex teeth using collagen-calcium phosphate gel, J Endod 4:76, 1978.

199. Nishino M: Clinico-roentenographical study of iodoform-calcium hydroxide root filling material Vitapex in deciduous teeth, Shoni Shikagaku Zasshi (Japanese Journal of Pedodontics) 18:20, 1980.

200. Nocentini S, Moreno G, Coppey J: Survival, DNA synthesis and ribosomal RNA transcription in monkey kidney cells treated by formaldehyde, Mutat Res 70:231, 1980.

201. Nosrat A, Seifi A, Asgary S: Pulpotomy in caries-exposed immature permanent molars using calcium-enriched mixture cement or mineral trioxide aggregate: a randomized clinical trial, Int J Paediatr Dent 23:56, 2013.

202. Nosrat IV, Nosrat CA: Reparative hard tissue formation following calcium hydroxide application after partial pulpotomy in cariously exposed pulps of permanent teeth, Int Endod J 31:221, 1998.

203. Nurko C, Ranly DM, García-Godoy F, et al: Resorption of a calcium hydroxide/iodoform paste (Vitapex) in root canal therapy for primary teeth: a case report, Pediatr Dent 22:517, 2000.

204. Oen KT, Thompson VP, Vena D, et al: Attitudes and expectations of treating deep caries: a PEARL Network survey, Gen Dent 55:197, 2007.

205. Orban BJ: Oral histology and embryology, ed 4, St Louis, 1957, Mosby.

206. Oringer MJ: Electrosurgery in dentistry, ed 2, Philadelphia, 1975, Saunders.

207. Ørstavik D, Hongslo JK: Mutagenicity of endodontic sealers, Biomats 6:129, 1985.

208. Papagiannoulis L: Clinical studies on ferric sulfate as a pulpotomy medicament in primary teeth, Eur J Paediatr Dent 3:126, 2002.

209. Working Group on Action to Control Chemicals Committee: The carcinogenicity of formaldehyde (2005-2006). Available at: www.hse.gov.uk/aboutus/hsc/iacs/acts/watch/130105/p6.pdf. Accessed June 10, 2007.

210. Pashley EL, Myers DR, Pashley DH, et al: Systemic distribution of 14C-formaldehyde from formocresol-treated pulpotomy sites, J Dent Res 59:602, 1980.

211. Patel S, Dawood A, Pitt Ford T, et al: The potential applications of cone beam computed tomography in the management of endodontic problems, Int Endod J 40:818, 2007.

212. Payne RG, Kenny DJ, Johnston DH, et al: Two-year outcome study of zinc oxide eugenol root canal treatment for vital primary teeth, J Can Dent Assoc 59:528, 1993.

213. Peron LCB, Burkes EJ, Gregory WB: Vital pulpotomy utilizing variable concentrations of paraformaldehyde in rhesus monkeys, J Dent Res 55:B129, 1976.

214. Pinkham JR, Cassamassimo P, Fields HW, et al: Pediatric dentistry: infancy through adolescence, ed 4, St Louis, 2005, Saunders.

215. Pitt Ford TR, Torabinejad M, Abedi HR, et al: Using mineral trioxide aggregate as a pulp-capping material, J Am Dent Assoc 127:1491, 1996.

216. Polydorou O, Pelz K, Hahn P: Antibacterial effect of an ozone device and its comparison with two dentin-bonding systems, Eur J Oral Sci 114:349, 2006.

217. Pradhan DP, Chawla HS, Gauba K, et al: Comparative evaluation of endodontic management of teeth with unformed apices with mineral trioxide aggregate and calcium hydroxide, J Dent Child 73:79, 2006.

218. Primosch RE: Primary tooth pulp therapy as taught in predoctoral pediatric dental programs in the United States, Pediatr Dent 19:118, 1997.

219. Puapichartdumrong P, Ikeda H, Suda H: Influence of the pulpal components on human dentine permeability in vitro, Int Endod J 38:152, 2005.

220. Qudeimat MA, Barrieshi-Nusair KM, Owais AI: Calcium hydroxide vs mineral trioxide aggregates for partial pulpotomy of permanent molars with deep caries, Eur Arch Paediatr Dent 8:99, 2007.

221. Rabinowitch BZ: Pulp management in primary teeth, Oral Surg Oral Med Oral Pathol 6:542, 1953.

222. Ranly DM: Glutaraldehyde purity and stability: implications for preparation, storage, and use as a pulpotomy agent, Pediatr Dent 6:83, 1984.

223. Ranly DM: Pulpotomy therapy in primary teeth: new modalities for old rationales, Pediatr Dent 16:403, 1994.

224. Ranly DM, Amstutz L, Horn D: Subcellular localization of glutaraldehyde, Endod Dent Traumatol 6:251, 1990.

225. Ranly DM, Garcia-Godoy F, Horn D: Time, concentration, and pH parameters for the use of glutaraldehyde as a pulpotomy agent: an in vitro study, Pediatr Dent 9:199, 1987.

226. Ranly DM, Horn D: Distribution, metabolism, and excretion of [14C] glutaraldehyde, J Endod 16:135, 1990.

227. Ranly DM, Horn D, Zislis T: The effect of alternatives to formocresol on antigenicity of proteins, J Dent Res 64:1225, 1985.

228. Ricketts DN, Kidd EA, Innes N, et al: Complete or ultraconservative removal of decayed tissue in unfilled teeth, Cochrane Database Syst Rev 3:CD003808, 2006.

229. Riekman GA, el Badrawy HE: Effect of premature loss of primary maxillary incisors on speech, Pediatr Dent 7:119, 1985.

230. Rifkin A: The root canal treatment of abscessed primary teeth: a 3- to 4-year follow-up, ASDC J Dent Child 49:428, 1982.

231. Rimondini L, Baroni C: Morphologic criteria for root canal treatment of primary molars undergoing resorption, Endod Dent Traumatol 11:136, 1995.

232. Ritwick PC, Cuisia ZV, Dahir P, Musselman RJ: MTA pulpotomies in the primary molars of children: results after 3 years. Paper presented at the meeting of the International Association for Dental Research, New Orleans, October 2003.

233. Roberts SC Jr, Brilliant JD: Tricalcium phosphate as an adjunct to apical closure in pulpless permanent teeth, J Endod 1:263, 1975.

234. Robertson A, Lundgren T, Andreasen JO, et al: Pulp calcifications in traumatized primary incisors: a morphological and inductive analysis study, Eur J Oral Sci 105:196, 1997.

235. Rodd HD, Waterhouse PJ, Fuks AB, et al: Pulp therapy for primary molars, Int J Paediatr Dent 16(Suppl 1):15, 2006.

236. Rølling I, Poulsen S: Formocresol pulpotomy of primary teeth and occurrence of enamel defects on the permanent successors, Acta Odontol Scand 36:243, 1978.

237. Ruemping DR, Morton TH Jr, Anderson MW: Electrosurgical pulpotomy in primates: a comparison with formocresol pulpotomy, Pediatr Dent 5:14, 1983.

238. Sadrian R, Coll JA: A long-term followup on the retention rate of zinc oxide eugenol filler after primary tooth pulpectomy, Pediatr Dent 15:249, 1993.

239. Salako N, Joseph B, Ritwik P, et al: Comparison of bioactive glass, mineral trioxide aggregate, ferric sulfate, and formocresol as pulpotomy agents in rat molar, Dent Traumatol 19:314, 2003.

240. Sanchez ZMC: Effects of formocresol on pulp-capped and pulpotomized permanent teeth of rhesus monkeys, master’s thesis, Ann Arbor, 1971, University of Michigan.

241. Sarkar NKS, Saunderi B, Moiseyevai R, Berzins DW, Kawashima I: Interaction of mineral trioxide aggregate (MTA) with a synthetic tissue fluid, J Dent Res 81:A391, 2002.

242. Sarris S, Tahmassebi JF, Duggal MS, et al: A clinical evaluation of mineral trioxide aggregate for root-end closure of non-vital immature permanent incisors in children: a pilot study, Dent Traumatol 24:79, 2008.

243. Savage NW, Adkins KF, Weir AV, et al: A histological study of cystic lesions following pulp therapy in deciduous molars, J Oral Pathol 15:209, 1986.

244. Schmitt D, Lee J, Bogen G: Multifaceted use of ProRoot MTA root canal repair material, Pediatr Dent 23:326, 2001.

245. Schmoldt SJ, Kirkpatrick TC, Rutledge RE, et al: Reinforcement of simulated immature roots restored with composite resin, mineral trioxide aggregate, gutta-percha, or a fiber post after thermocycling, J Endod 37:1390, 2011.

246. Schröder U: Effect of an extra-pulpal blood clot on healing following experimental pulpotomy and capping with calcium hydroxide, Odontol Revy 24:257, 1973.

247. Schroder U, Wennberg E, Granath LE, et al: Traumatized primary incisors: follow-up program based on frequency of periapical osteitis related to tooth color, Swed Dent J 1:95, 1977.

248. Schumacher JW, Rutledge RE: An alternative to apexification, J Endod 19:529, 1993.

249. Seale NS, Glickman GN: Contemporary perspectives on vital pulp therapy: views from the endodontists and pediatric dentists, Pediatr Dent 30:261, 2008.

250. Selliseth NE: The significance of traumatised primary incisors on the development and eruption of permanent teeth, Trans Eur Othod Soc 46:443, 1970.

251. Seto B, Chung KH, Johnson J, et al: Fracture resistance of simulated immature maxillary anterior teeth restored with fiber posts and composite to varying depths, Dent Traumatol 29:394, 2013.

252. Shabahang S, Torabinejad M, Boyne PP, et al: A comparative study of root-end induction using osteogenic protein-1, calcium hydroxide, and mineral trioxide aggregate in dogs, J Endod 25:1, 1999.

253. Shaw DW, Sheller B, Barrus BD, et al: Electrosurgical pulpotomy: a 6-month study in primates, J Endod 13:500, 1987.

254. Sheller B, Morton TH Jr: Electrosurgical pulpotomy: a pilot study in humans, J Endod 13:69, 1987.

255. Shulman ER, McIver FT, Burkes EJ Jr: Comparison of electrosurgery and formocresol as pulpotomy techniques in monkey primary teeth, Pediatr Dent 9:189, 1987.

256. Sigurdsson A: Pulpal diagnosis, Endod Topics 5:12, 2003.

http://www.hse.gov.uk/aboutus/hsc/iacs/acts/watch/130105/p6.pdf

http://www.hse.gov.uk/aboutus/hsc/iacs/acts/watch/130105/p6.pdf


257. Simancas-Pallares MA, Díaz-Caballero AJ, Luna-Ricardo LM: Mineral trioxide aggregate in primary teeth pulpotomy: a systematic literature review, Med Oral Patol Oral Cir Bucal 15:e942, 2010.

258. Simon M, van Mullem PJ, Lamers AC: Formocresol: no allergic effect after root canal disinfection in non-presensitized guinea pigs, J Endod 8:269, 1982.

259. Simon S, Perard M, Zanini M, et al: Should pulp chamber pulpotomy be seen as a permanent treatment? Some preliminary thoughts, Int Endod J 46:79, 2013.

260. Simon S, Rilliard F, Berdal A, et al: The use of mineral trioxide aggregate in one-visit apexification treatment: a prospective study, Int Endod J 40:186, 2007.

261. Smith NL, Seale NS, Nunn ME: Ferric sulfate pulpotomy in primary molars: a retrospective study, Pediatr Dent 22:192, 2000.

262. Srinivasan V, Patchett CL, Waterhouse PJ: Is there life after Buckley’s formocresol? I. A narrative review of alternative interventions and materials, Int J Paediatr Dent 16:117, 2006.

263. Stanton WG: The non-vital deciduous tooth, Int J Orthod 21:181, 1935.

264. Starkey PE: Management of deep caries of pulpally involved teeth in children. In Goldman HM, et al, editors: Current therapy in dentistry, vol 3, St Louis, 1968, Mosby.

265. Starkey PE: Treatment of pulpally involved primary molars. In McDonald RE, et al, editors: Current therapy in dentistry, vol 7, St Louis, 1980, Mosby.

266. Steiner JC, Dow PR, Cathey GM: Inducing root end closure of nonvital permanent teeth, J Dent Child 35:47, 1968.

267. Steiner JC, Van Hassel HJ: Experimental root apexification in primates, Oral Surg Oral Med Oral Pathol 31:409, 1971.

268. Straffon LH, Han SS: Effects of varying concentrations of formocresol on RNA synthesis of connective tissues in sponge implants, Oral Surg Oral Med Oral Pathol 29:915, 1970.

269. Subramaniam P, Gilhotra K: Endoflas, zinc oxide eugenol and Metapex as root canal filling materials in primary molars: a comparative clinical study, J Clin Pediatr Dent 35:365, 2011.

270. Subramaniam P, Konde S, Mathew S, et al: Mineral trioxide aggregate as pulp capping agent for primary teeth pulpotomy: 2-year follow up study, J Clin Pediatr Dent 33:311, 2009.

271. Sweet CA: Procedure for the treatment of exposed and pulpless deciduous teeth, J Am Dent Assoc 17:1150, 1930.

272. Swenberg JA, Kerns WD, Mitchell RI, et al: Induction of squamous cell carcinomas of the rat nasal cavity by inhalation exposure to formaldehyde vapor, Cancer Res 40:3398, 1980.

273. Tabarsi B, Parirokh M, Eghbal MJ, et al: A comparative study of dental pulp response to several pulpotomy agents, Int Endod J 43:565, 2010.

274. Tagger E, Sarnat H: Root canal therapy of infected primary teeth, Acta Odontol Pediatr 5:63, 1984.

275. Tagger E, Tagger M, Sarnat H: Pulpal reactions to glutaraldehyde and paraformaldehyde pulpotomy dressings in monkey primary teeth, Endod Dent Traumatol 2:237, 1986.

276. Tay FR, Pashley DH: Monoblocks in root canals: a hypothetical or a tangible goal? J Endod 33:391, 2007.

277. Teixeira FB, Teixeira ECN, Thompson JY, et al: Fracture resistance of roots endodontically treated with a new resin filling material, J Am Dent Assoc 135:646, 2004.

278. Teplitsky PE: Formocresol pulpotomies on posterior permanent teeth, J Can Dent Assoc 50:623, 1984.

279. Thibodeau B, Trope M: Pulp revascularization of a necrotic infected immature permanent tooth: case report and review of the literature, Pediatr Dent 29:47, 2007.

280. Thompson VP, Craig RG, Curro FA, et al: Treatment of deep carious lesions by complete excavation of partial removal: a critical review, J Am Dent Assoc 139:705, 2008.

281. Tittle KWF, Farley J, Linkhardt M, Torabinejad M: Apical closure induction using bone growth factors and mineral trioxide aggregate, J Endod 22:198, 1996.

282. Trask PA: Formocresol pulpotomy on (young) permanent teeth, J Am Dent Assoc 85:1316, 1972.

283. Trope M: Treatment of immature teeth with non-vital pulps and apical periodontitis, Endod Topics 14:51, 2006.

284. Turner C, Courts FJ, Stanley HR: A histological comparison of direct pulp capping agents in primary canines, ASDC J Dent Child 54:423, 1987.

285. Tziafas D: The future role of a molecular approach to pulp-dentinal regeneration, Caries Res 38:314, 2004.

286. Tziafas D, Koliniotou-Koumpia E, Tziafa C, et al: Effects of a new antibacterial adhesive on the repair capacity of the pulp-dentine complex in infected teeth, Int Endod J 40:58, 2007.

287. Tziafas D, Molyvdas I: The tissue reactions after capping of dog teeth with calcium hydroxide experimentally crammed into the pulp space, Oral Surg Oral Med Oral Pathol 65:604, 1988.

288. Tziafas D, Pantelidou O, Alvanou A, et al: The dentinogenic effect of mineral trioxide aggregate (MTA) in short-term capping experiments, Int Endod J 35:245, 2002.

289. Valois CRA, Costa ED Jr: Influence of the thickness of mineral trioxide aggregate on sealing ability of root-end fillings in vitro, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 97:108, 2004.

290. van Amerongen WE, Mulder GR, Vingerling PA: Consequences of endodontic treatment in primary teeth. I. A clinical and radiographic study of the influence of formocresol pulpotomy on the life span of primary molars, ASDC J Dent Child 53:364, 1986.

291. Van Der Sluis LWM, Versluis M, Wu MK, et al: Passive ultrasonic irrigation of the root canal: a review of the literature, Int Endod J 40:415, 2007.

292. van Mullem PJ, Simon M, Lamers AC: Formocresol: a root canal disinfectant provoking allergic skin reactions in presensitized guinea pigs, J Endod 9:25, 1983.

293. van Velzen SKT, Feltkamp-Vroom TM: Immunologic consequences of formaldehyde fixation of autologous tissue implants, J Endod 3:179, 1977.

294. Venham LL: Pulpal responses to variations in the formocresol technique: a histologic study, master’s thesis, Columbus, 1967, College of Dentistry, Ohio State University.

295. Vij R, Coll JA, Shelton P, et al: Caries control and other variables associated with success of primary molar vital pulp therapy, Pediatr Dent 26:214, 2004.

296. Waterhouse PJ: “New age” pulp therapy: personal thoughts on a hot debate, Pediatr Dent 30:247, 2008.

297. Waterhouse PJ, Nunn JH, Whitworth JM: Prostaglandin E2 and treatment outcome in pulp therapy of primary molars with carious exposures, Int J Paediatr Dent 12:116, 2002.

298. Webber RT: Apexogenesis versus apexification, Dent Clin North Am 28:669, 1984.

299. Weber CM, Alves LS, Maltz M: Treatment decisions for deep carious lesions in the Public Health Service in Southern Brazil, J Public Health Dent 71:265, 2011.

300. Wemes JC, Jansen HWB, Purdell-Lewis D, et al: Histological evaluation of the effect of formocresol and glutaraldehyde on the periapical tissues after endodontic treatment, Oral Surg Oral Med Oral Pathol 54:329, 1982.

301. Wemes JC, Purdell-Lewis D, Jongeblood W, et al: Diffusion of carbon-14–labeled formocresol and glutaraldehyde in tooth structures, Oral Surg Oral Med Oral Pathol 54:341, 1982.

302. Wilkins RJ, Macleod HD: Formaldehyde induced DNA protein crosslinks in Escherichia coli, Mutat Res 36:11, 1976.

303. Wilkinson KL, Beeson TJ, Kirkpatrick TC: Fracture resistance of simulated immature teeth filled with Resilon, gutta-percha, or composite, J Endod 33:480, 2007.

304. Witherspoon DE, Small JC, Harris GZ: Mineral trioxide aggregate pulpotomies: a case series outcomes assessment, J Am Dent Assoc 137:610, 2006.

305. Yacobi R, Kenny DJ, Judd PL, et al: Evolving primary pulp therapy techniques, J Am Dent Assoc 122:83, 1991.

306. Yanpiset K, Vongsavan N, Sigurdsson A, et al: Efficacy of laser Doppler flowmetry for the diagnosis of revascularization of reimplanted immature dog teeth, Dent Traumatol 17:63, 2001.

307. Yassen GH, Platt JA: The effect of nonsetting calcium hydroxide on root fracture and mechanical properties of radicular dentine: a systematic review, Int Endod J 46:112, 2013.

308. Yeung P, Liewehr FR, Moon PC: A quantitative comparison of the fill density of MTA produced by two placement techniques, J Endod 32:456, 2006.

309. Zurcher E: The anatomy of the root canals of the teeth of the deciduous dentition and of the first permanent molars, New York, 1925, William Wood & Co.

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