Fundamentals of Dentin/Pulp Histology

The pulps of primary and permanent teeth are histologically and functionally similar.^248,249 Odontoblasts are the dentin-forming cells that line the periphery of the pulp chamber and extend their cytoplasmic processes into its tubular structure. They become increasingly crowded as they retreat centrally, and tubular density therefore increases in deep dentin (Fig. 23-1). A cell-free zone is located just below the odontoblastic layer and contains an extensive plexus of nerves (Raschkow’s plexus) and blood capillaries that may support and regulate odontoblast activity and provide sensory innervation to the pulp. Raschkow’s plexus does not fully mature until the late stages of root formation, and pulp sensitivity tests may therefore be inconclusive in immature permanent teeth. Beneath the cell-free zone is the cell-rich zone of Höhl, a band of tissue containing uncommitted cells capable of differentiation into odontoblast-like cells should primary odontoblasts be lost.¹¹⁰ The core of the dental pulp contains larger blood vessels and nerves which are surrounded by loose connective tissue.²⁰⁴ The volume of perfusion through the incomplete apices of immature teeth is considerable and underpins the enormous reparative capacity of young pulps in the face of injury.

FIG. 23-1 Odontoblasts move closer as they retreat centrally on an ever-diminishing pulp circumference. Deep dentin contains wider and more closely arranged dentinal tubules, making it more porous than superficial dentin.

Chapter 12 provides a more detailed review of tissue structure and functions within the dentin-pulp complex, and Box 23-1 provides relevant key points.

Dentinogenic Response to Injury

Without dentin, the pulp would be a highly sensitive and vulnerable organ, and in the absence of a pulp, the defensive capacity of dentin would be limited. The tissues are therefore inseparable and work together as a functional complex.

Key responses of the dentin-pulp to injury include the deposition of tertiary dentin, which increases the distance between the injury and the pulp, and a reduction in dentin permeability by the formation of sclerotic dentin.³⁰⁹ Chapter 13 further discusses pulpal responses to injury.

The nature and quality of the tertiary dentin depend on its tubular structure and influence local dentin permeability. In the case of a mild injury, the odontoblasts responsible for primary odontogenesis can frequently survive the challenge and are stimulated to secrete tertiary, reactionary dentin (Fig. 23-2) beneath the site of injury.²⁷⁵ Because the original odontoblasts are responsible for this matrix secretion, tubular continuity and communication with the primary dentin matrix will be present [see Fig. 23-2, B; Fig. 23-3, A].¹⁸⁴

FIG. 23-2 Schematic representation of tertiary reactionary dentin. A, A mild insult to dentin, such as dental caries that does not extend deeply to threaten survival of primary odontoblasts. B, Liberation of dentin matrix components such as TGF-β leads to upregulation of odontoblast activity, with deposition of a reactionary dentin matrix whose tubular pattern is continuous with underlying tissue.

FIG. 23-3 Histologic sections of tertiary reactionary and reparative dentin. A, Reactionary dentin: histologic section showing tubular continuity. B, Reparative dentin: histologic section showing lack of continuity.

(From Pinkham JR, Casamassimo PS, McTigue DJ, et al: Pediatric dentistry: infancy through adolescence, ed 4, St Louis, 2005, Saunders; Courtesy Carlos Alberto S. Costa, DMD, PhD.)

When the injury is severe, as in pulp exposure, the affected odontoblasts may die. Since odontoblasts are postmitotic cells with no capacity for renewal, their replacement must come from elsewhere. If suitable conditions exist in the pulp, a new generation of odontoblast-like cells may differentiate, probably from the cell-rich zone, and secrete a tertiary, reparative dentin matrix (Fig. 23-4). Because this dentin is formed by a new generation of cells, discontinuity in the tubular structure will occur, with a subsequent reduction in tissue permeability (Fig. 23-3, B).³¹

FIG. 23-4 Schematic representation of tertiary reparative dentin. A, A significant insult, such as deep caries, which kills primary odontoblasts in a localized area of pulp. B, New odontoblast-like cells differentiate from cell-rich zone. C, Secretion of a tertiary reparative dentin matrix commences. Tubular structure is irregular and has no continuity with underlying tissue.

A critical question that arises is “What are the factors responsible for triggering the stimulation of odontoblastic activity?” Although much still has to be learned about the molecular control of cell activity in general and odontoblastic activity in particular, one family of growth factors, the transforming growth factor superfamily (specifically TGF-βs)¹¹⁰ has been reported to have extensive effects on the mesenchymal cells of many connective tissues.¹⁸⁰

During tooth development, the odontoblasts secrete TGF-βs, and some of them remain sequestered within the dentin matrix. These TGF-βs may be released during any process leading to tissue dissolution, such as dental caries or the use of acid etching.³⁰⁹ Dentin matrix should not be considered an inert dental hard tissue but rather a potential tissue store of a cocktail of bioactive molecules (particularly growth factors) waiting to be released if appropriate tissue conditions prevail.³⁰⁹

In contrast to reactionary responses, reparative dentinogenesis represents a more complex sequence of biologic processes. Migration and differentiation of pulpal progenitor cells must take place, creating a new generation of odontoblast-like cells before matrix secretion. A series of stereotypic wound-healing reactions will occur in the pulpal connective tissue, including vascular and cellular inflammatory reactions.

In vitro and in vivo experiments on reparative odontogenesis demonstrate that the noninflamed pulp constitutes an appropriate environment where competent pulp cells (potential preodontoblasts) can differentiate into new odontoblast-like cells, forming reparative dentin.^171,203,212

Reactions to Dental Caries

When the carious process advances from enamel into dentin, sclerotic dentin is formed by the apposition of minerals into and between the dentinal tubules (intratubular and intertubular dentin), and reactionary tertiary dentin is secreted. Sclerotic dentin can be seen in radiographs as a radiopaque area as the aforementioned apposition of minerals increases the radiopacity of this dentin.

The quality and amount of tertiary dentin depend on the depth and rate of progression of the carious lesion. The faster the lesion progresses, the poorer and more irregular the reactionary dentin. In addition, if the noxious irritant is too intense, the cytoplasmic processes of the odontoblasts degenerate, and “dead tracts” are formed.

When the carious process advances more rapidly than the elaboration of reactionary dentin, blood vessels of the pulp dilate, and scattered inflammatory cells become evident, particularly subjacent to the area of the involved dentinal tubules. If the carious lesion remains untreated, a frank exposure will eventually occur. The pulp will react, resulting in an acute inflammatory infiltrate, and the previously chronic pulpitis will become acute. A small abscess may develop under the region of the exposure, and cells of the chronic inflammatory series may accumulate farther away from the central area of irritation. The remainder of the pulp may be uninflamed (chronic partial pulpitis with acute exacerbation). As the exposure progresses, the pulp may undergo partial necrosis, followed in some instances by total necrosis.

Drainage is apparently the factor determining whether partial or total necrosis occurs. If the pulp is open and drainage can occur, the apical tissue may remain uninflamed or chronically inflamed. If drainage is impeded by food packing or a restoration, the entire pulp may become necrotic.¹¹⁰

Reactions to Restorative Procedures

The principal factors affecting the dentin-pulp complex during restorative procedures (e.g., cavity and crown preparation) are the cutting of the dentin, the generation of heat, and the desiccation of the tissue. When uninvolved dentin is operated on, as in extension for prevention or in crown preparation, tubules unprotected by reactionary dentin are cut. The tissue reaction that occurs is similar to that occurring with caries: intratubular and intertubular mineralization takes place, resulting in sclerotic dentin, followed by the formation of tertiary dentin. Remaining dentin thickness (RDT) is apparently the most significant factor determining pulp survival and the secretion of tertiary reactionary dentin. Maximal reactionary dentin was observed in a study wherein the cavity RDT was between 0.5 and 0.25 mm. The reduced reactionary dentin beneath cavities with an RDT below 0.25 mm (described in the same study) appeared to be related to reduced odontoblastic survival.¹⁸⁸ In these deep cavities, little more than 50% of the odontoblasts survived, whereas in shallow cavities, odontoblastic survival was about 85% or greater, and despite the cutting of the odontoblastic process, the cells responded by secreting reactionary dentin. The same authors demonstrated that the choice of restorative material influenced the secretion of reactionary dentin to a lesser extent than the RDT. The effect of cutting dentin can be observed histologically as a calciotraumatic band, which represents an interruption of the apposition between the secondary and tertiary dentin.

Pulp reactions to restorative procedures can be mild or severe, depending on the technique used. When the technique is gentle, the reaction will be mild, and minor alterations in the odontoblastic layer can be observed as a result of fluid accumulation. In a severe reaction, the nuclei of the odontoblasts may be aspirated into the dentinal tubules, hemorrhage may be present, and inflammation is extensive, sometimes resulting in cell necrosis. A gentle technique implies using appropriate cooling and minimal pressure. Cutting a cavity without using water cooling might lead to irreversible changes in the pulp because of the heat generated at the tip of the bur. The application of pressure increases the damage. Prolonged air blasts are also deleterious to the pulp. To prevent the generation of heat and damage to the pulp, the following measures should be taken: (1) The cavity preparation should be as shallow as possible, respecting the principles of cavity preparation and embracing contemporary partial and serial caries excavation techniques (see later); (2) suitably sized, sharp burs should be used, balancing the need for conservatism with the risks of localized overcutting with small burs; (3) appropriate cooling should be employed and minimum pressure exerted; and (4) excessive drying of dentin by air syringe should be avoided.²²⁶

Reactions to Dental Materials

There is substantial evidence that adverse responses within the dentin-pulp complex to restorative materials are more closely linked with microbial agents than with irritant or toxic components of the materials themselves.²²

The routine lining of cavities has long been advocated as a means of pulp protection. Both calcium hydroxide (Ca[OH]₂) and zinc oxide eugenol (ZOE) cements have proven track records for promoting pulp health by destroying residual microorganisms in the depths of cavity preparations.^{14,69,147,153} The antimicrobial and remineralizing potential of glass ionomer cements has been recognized during the last 2 decades,¹⁶⁶ and the importance of marginal seal has been supported by evidence on favorable pulp outcomes following bonded composite restorations.^{42-44,145,277,292}

Researchers²⁰¹ have begun to use the term artificial enamel to describe their aspirations of hybrid-layer formation²⁰² and impervious, pulp-protecting barriers formed by resin-based materials. The response of the pulp to direct contact with dental materials is of special importance in the primary and young permanent teeth of children where pulp capping, pulpotomy, and apexification procedures are important modalities of treatment.

A variety of materials, medicaments, antiseptics, antiinflammatory agents, antibiotics, and enzymes have been used as pulp-capping agents, but Ca(OH)₂ has been the standard by which all others were judged.^9,58,110 Before 1930, when Hermann¹¹⁵ introduced Ca(OH)₂ as a successful pulp-capping agent, pulp therapy consisted of devitalization with arsenic and other fixative agents. Hermann demonstrated the formation of “secondary dentin” (now termed tertiary dentin) over the amputation sites of vital pulps capped with Ca(OH)_2.

In 1938, Teuscher and Zander²⁹⁶ introduced Ca(OH)₂ in the United States, confirming complete dentinal bridging with healthy radicular pulp under Ca(OH)₂ dressings. Further reports firmly established Ca(OH)₂ as the pulp-capping agent of choice. After these early works, many studies have reported on various forms of Ca(OH)₂, with success rates ranging from 30% to 98%.⁸² The dissimilar results have been attributed to variables in study design, including the model (human or animal), tooth selection, area of the pulp involved (coronal or cervical), type of Ca(OH)₂ employed, outcome criteria, and study duration.

When Ca(OH)₂ is applied directly to pulp tissue, necrosis of the adjacent pulp tissue and inflammation of the contiguous tissue occur. Dentin bridge formation occurs at the junction of the necrotic tissue and the vital inflamed tissue. Although Ca(OH)₂ works effectively, the exact mechanisms are not fully understood. Compounds of similar alkalinity (pH 11) cause liquefaction necrosis when applied to pulp tissue, but Ca(OH)₂ maintains a local state of alkalinity necessary for bone or dentin formation. Beneath the region of coagulation necrosis, cells of the underlying pulp tissue differentiate into odontoblast-like cells and elaborate dentin matrix.¹¹⁰

Occasionally, in spite of successful bridge formation, the pulp remains chronically inflamed or becomes necrotic. Internal resorption may occur after pulp exposure and capping with Ca(OH)₂. In other cases, complete mineralization of the remaining pulp tissue occludes the canals and greatly complicates any future attempts at root canal treatment.

It was postulated³³⁰ that calcium diffused from a Ca(OH)₂ dressing into the pulp to participate in reparative dentin formation. Experiments with radioactive ions, however, have shown that calcium ions from the circulation, not from the Ca(OH)₂ pulp cap are involved in bridge formation.^16,227,260 Calcium hydroxide promotes bridge formation by creating low-grade irritation in the underlying pulpal tissue, a phenomenon observed even after short-term application and removal of the material.⁵⁴

Different forms of Ca(OH)₂ have produced markedly different responses when applied as a pulp cap.^291,305 The reactions to Dycal (DENTSPLY/Caulk, Milford, DE), Prisma VLC Dycal (DENTSPLY/Caulk), Life, and Nu-Cap (GC America, Alsip, IL) have been shown to be similar.^279,280,291 The chemically altered tissue created by application of these compounds is resorbed first, and the bridge is then formed in contact with the capping material.^302,305 With Ca(OH)₂ powder and nonsetting products such as Pulpdent Paste (Pulpdent Corp, Watertown, MA) the bridge forms at the junction of the chemically altered tissue and the remaining subjacent vital pulp tissue. The altered tissue degenerates and disappears, leaving a void between the capping material and the dentin bridge. For this reason, a bridge can be visualized better on radiographs with products such as Pulpdent Paste than with the other commercial compounds. The quality of the dentin bridging was equally good with either material. Investigators have, however, highlighted the frequent occurrence of porosities and tunnel defects in Ca(OH)₂-generated dentin bridges.⁴⁸ A related study⁴⁷ further demonstrated long-term evidence that Ca(OH)₂ becomes softened and allows leakage, resulting in recurrent pulpal inflammation and necrosis after 1 to 2 years. Despite its widespread use, the body of good evidence on Ca(OH)₂ pulp capping is surprisingly limited,²¹⁴ and efforts to improve the body of evidence or develop well-documented alternatives are justified.

Mineral Trioxide Aggregate

Favorable pulp responses have been reported following the use of MTA.^{1,140,198,200,228} When compared with Ca(OH)₂, MTA produced significantly more dentinal bridging in a shorter period of time with significantly less pulpal inflammation. Dentin deposition also began earlier with MTA.

MTA is a biocompatible material with an antibacterial effect similar to that of Ca(OH)₂ and the property of providing a biologically active substrate for cell attachment. This feature makes it effective in preventing microleakage and improving the prognosis of treatment. MTA has been shown to promote pulp healing with dentin bridge formation and minimal inflammatory reaction in exposed pulps in monkeys²²⁸ and humans,²⁰⁰ and its dentinogenic effect in short-term capping experiments was demonstrated in dogs.⁷¹ The material was approved for use by the United States Food and Drug Association (FDA). Following promising preliminary studies,² it has been shown to provide impressive results for pulp capping (Fig. 23-5) and pulpotomy treatments in young permanent teeth^27,326 and for pulpotomies in the primary dentition.^3,63

FIG. 23-5 Pulpal response to mineral trioxide aggregate (MTA) capping after 3 months observation. Distal macrophotographic view of the mesial half of a maxillary left third molar (tooth 28 [FDI]) shows remnants of restorative and capping material (CP) and a distinct hard-tissue bridge (BR) across the exposed pulp (PU). The photomicrograph (B) is part of a histologic section of the specimen in (A). Note mineralized hard-tissue barrier (BR) stretching across full length of exposed pulp (B).

(Reproduced from Nair PNR, Duncan HF, Pitt Ford TR, Luder HU: Histological, ultrastructural and quantitative investigations on the response of healthy human pulps to experimental capping with mineral trioxide aggregate: a randomised controlled trial. Int Endod J 41:128, 2008.)

Root Formation

According to Orban,²¹⁵ development of the roots begins after enamel and dentin formation has reached the future cementoenamel 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 formation, the apical foramen of each root has a wide opening limited by the epithelial diaphragm. The dentinal walls diverge apically, 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. 23-7, A). When root length is established, the sheath disappears, but dentin deposition continues internally within the roots.

FIG. 23-7 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 deposition of dentin (shaded areas). Small fins and branches are present between the two canals. C, Canals are completely divided; root resorption has begun.

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 there is formation of dentin islands within 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. 23-7, B). (See Chapter 12 for a complete description of pulp and dentin formation.)

As growth proceeds, the root canal is narrowed by continued 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. 23-7, 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 of time than in the permanent tooth because of the shorter length of the primary roots.

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. 23-6).²⁰⁴

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, significantly 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. Figs. 23-8 and 23-9 show silicone models of root canals, and Fig. 23-10 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 computerized tomography²²¹ is bringing greater understanding of such anatomic features to practicing clinicians.

FIG. 23-8 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 division of the canal in model on left.

FIG. 23-9 Maxillary primary canine and silicone model of the root canal. A, Mesial surface. B, Model of the root canal.

FIG. 23-10 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 distofacial and palatal canals. B, Same tooth from the distal view. Note wide area of pulp tissue connection between distofacial and palatal canals.

(Courtesy Paul Dummer and Sue Bryant, Cardiff University, UK.)

Primary Root Canal Anatomy

To 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.²⁰⁵ To understand some of the variations in the primary root canal systems requires an understanding of root formation (see previous discussion and Box 23-2).

Primary Anterior Teeth

The morphology of root canals in primary anterior teeth resembles the form and shape of the roots of the teeth themselves (see Figs. 23-8 and 23-9). 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. 23-8, A).

Primary Molars

Often, primary molars have the same number and position of roots as the corresponding permanent molars (see Fig. 23-10). 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 permanent 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. 23-7, B and Fig. 23-10).

In primary teeth, the deposition of secondary dentin has been reported to occur after root-length completion.^24,117,134 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.¹¹⁷

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 separation of the root canal into two or more individual canals. Many fine connecting branches or lateral fibrils form a connecting network between the facial and lingual aspects of the root canals (see Fig. 23-10).

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 ramifications of the pulp are common in primary molars, occurring in 10% to 20%.^117,331

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.

History and Characteristics of Pain

The character of any presenting pain is first identified in the history. Distinction should, wherever possible, be made between provoked and spontaneous pain.

Provoked pain is usually triggered by a thermal or 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. 23-11), soreness associated with tooth exfoliation, or eruption of permanent teeth.

FIG. 23-11 Pain and bone loss caused by food impaction in interproximal 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.

By contrast, spontaneous pain is not consistently associated with an external stimulus, may arise at any time of the day, or wake the child from sleep. In both primary and young permanent teeth, spontaneous pain and provoked pain which continues long after the causative factor is withdrawn are usually associated with extensive, irreversible pulpal inflammation extending into the root canals.¹⁰⁵ Primary teeth with a history of spontaneous toothache are unreliable candidates 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. Since 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).

Clinicians faced with an apparently graphic pain history should not, however, neglect to conduct a proper clinical examination, since other conditions such as papillitis caused by interproximal food impaction may mimic pulpitic pain.

Equally, the absence of pain should not encourage clinical complacency, since varying degrees of pulp degeneration or even complete necrosis can be encountered without any report of pain. Children may thus present without any complaint, despite extensive carious lesions and draining parules. Those who have developed early childhood caries (e.g., nursing bottle caries), may equally have no experience of their teeth feeling any other way and have no special pain history to report.²²⁶

Clinical Examination

A careful extraoral and intraoral examination is of great importance in identifying teeth with pulpal involvement. Signs such as tooth discoloration, gross caries, redness and swelling of the vestibulum, or draining parules may strongly suggest pulpal pathoses. In addition, attention should be paid to teeth with extensive fractured and missing restorations or restorations with carious marginal breakdown. All may indicate involvement of the pulp through the relatively thin and porous dentin of the cavity floor.

Palpation, Percussion, and Mobility

Fluctuation, felt by palpating a swollen mucobuccal fold, may be the expression of an acute dentoalveolar abscess before exteriorization. Bone destruction following a chronic dentoalveolar abscess can also be detected by palpation.

Though 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 inflammation 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 ipsilateral 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.

Sensitivity to percussion may reveal a painful tooth in which pulpal breakdown has resulted in acute periradicular periodontitis. Exceptions include recently traumatized teeth. Care should be taken in percussing the teeth of children; one author²²⁶ has recommended the gentle use of a fingertip rather than the end of a dental mirror.

Pulp Tests

Standard electrical and thermal pulp provocation tests are of limited value in the primary dentition and in young permanent teeth with incompletely developed apices.⁹ Although these tests may indicate the presence of some vital responsive tissue, they will not give reliable data on the extent of pulpal inflammation. Many children with perfectly normal teeth do not respond to the electrical pulp tester even at the higher settings. Equally, young patients may give unreliable responses to such provocation tests because of apprehension, fear, or general management problems.

The unreliability of electronic methods in immature permanent teeth has been reported in several studies.^91,92,94,148 One author¹⁴⁸ 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 ascertaining 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.^91,92,94,148 Heat is unreliable as a diagnostic test in young children.⁹²

Laser Doppler flowmetry has been reported^68,272,328 to be reliable for diagnosing pulpal vitality in immature permanent teeth, but the equipment has not been perfected for clinical use⁶⁸ and is cost prohibitive. It is also affected by blood pigmentation in discolored crowns.

Radiographic Examination

Clinical examination should be supplemented where appropriate with high-quality radiographs. Interradicular 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, exposed on a small film by a paralleling technique. The integrity of the lamina dura of the affected tooth should be compared with that of adjacent or contralateral teeth.²²⁶

Current radiographs are essential in examining for caries, restoration integrity, previous endodontic treatments, and resorptive and periapical changes in primary and young permanent teeth. In children, interpretation of radiographs is complicated by physiologic root resorption of primary teeth and incompletely formed roots of permanent teeth. If the clinician 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 antimere 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. What may appear as an intact barrier of secondary or tertiary dentin overlying the pulp may actually be a perforated mass of irregularly calcified and carious dentin overlying a pulp with extensive inflammation.⁵⁸

The presence of calcified masses within the pulp is an important diagnostic sign (Fig. 23-12). Mild, chronic irritation to the pulp stimulates tertiary reactionary dentin formation. When the irritation is acute and of rapid 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.⁵⁸ 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 metamorphosis within the coronal pulp chamber would not in isolation warrant pulpectomy and root canal treatment.

FIG. 23-12 Calcified mass in the pulp chamber. There is internal and external root resorption. Calcified mass (arrow) is an attempt to block a massive carious lesion. Because of resorption, this tooth should be extracted. Note bone loss in the bifurcation area.

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. 23-12). Pathologic bone and root resorption indicates advanced pulpal degeneration that has 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 permanent teeth, are usually at the apices.

Internal resorption occurs frequently in the primary dentition after pulpal involvement. It is always associated with extensive inflammation,¹⁰⁵ 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 internal resorption has become advanced enough to be seen on radiographs, there is usually a perforation of the root by the resorption (Fig. 23-13). In some instances, however, the process is reversible and self-correcting, and the resorbed area becomes filled with mineralized tissue.^110,219 If a perforation of the root occurs in a primary tooth because of internal resorption, all forms of pulp therapy are contraindicated. 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).^110,219

FIG. 23-13 Pulpotomy failure. Note internal resorption that has perforated the pulp chamber floor and resulted in a furcal radiolucency.

In immature permanent teeth, it is often difficult to assess the extent of apical closure. Plain-film images are frequently misleading, since under normal conditions, they show the mesiodistal plane of the tooth but give little information in 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 the mesiodistal. 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 convergent root canal, whereas in the faciolingual plane, the root canal is divergent. Equally, canals which are apically diverging in the faciolingual view may be parallel or converging in the mesiodistal view. Again, contemporary three-dimensional imaging techniques are beginning to improve understanding, both in the research laboratory (Fig. 23-14) and in the clinic.²²¹

FIG. 23-14 Three-dimensional tomographic images of an immature maxillary canine. A, Faciolingual view. B, Mesiodistal view. Such imaging techniques are bringing new anatomic awareness to both the research laboratory and the clinic.

(Courtesy Paul Dummer and Sue Bryant, Cardiff University, UK.)

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

It 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.²²⁶

Restorative Diagnosis: Pulpal Exposures and Hemorrhage

It has been reported that the size of the exposure, the appearance 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 excessive^58,226,282 or deep purple colored²²⁶ 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),^58,282 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. This rule does not apply for young permanent teeth with incomplete root development, 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 nature of 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.²²⁶

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 MTA pulp cap may be a better candidate for a pulpotomy, apexification, or pulp regeneration (see later section on immature permanent teeth).

Investigators¹⁰⁵ attempted to use the first drop of hemorrhage from an exposed pulp site as a diagnostic aid for 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, including percussion, electrical pulp test, thermal tests, mobility, and history of pain, was obtained. 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 evidence 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 mediators (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 following vital pulpotomy in extensively carious primary molars has been reported.³¹⁹ Thirty-nine primary molars with no history of spontaneous pain had blood samples harvested from the radicular pulp stumps immediately following coronal pulp amputation. Enzyme immunoassay of the samples for PGE₂ detected the inflammatory mediator in all samples. A wide range of concentrations was detected, and it was shown that the concentration of PGE₂ detected correlated positively with radiologic signs of failure following treatment. The authors tempered their findings by describing the dependence upon a single inflammatory mediator 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 diagnostic kit to assess the extent of pulp inflammation does not yet exist. Therefore, despite research in this area, clinicians still rely upon empirical clinical findings to diagnose the inflammatory status of the pulp.

Diagnosis Following Traumatic Injuries in Children

The details of trauma management are considered in Chapter 17. Injuries to the primary dentition are common, occurring in 1 in 3 children by the age of 5 years.^11,99 Diagnosis following traumatic injuries requires consideration of other factors in addition to those previously discussed. The most frequent injury in the primary dentition is tooth displacement due to less dense bone and shorter roots. Healing varies from normal without sequela to canal calcification or pulpal necrosis. Canal calcification may vary from an amorphous material resembling osteodentin to a partial or complete closure of the canal.^121,247

Pulp Diagnosis and Treatment Planning After Trauma

Treatment guidelines are almost nonexistent concerning healing and complications following trauma in primary teeth. The literature is devoid of histologic or microbiologic studies in this area. Borum and Andreasen²⁹ in a study of 545 traumatized primary maxillary incisors found that 53% developed pulpal necrosis, and 25% developed canal obliteration. The age of the patient, degree of tooth displacement, concurrent crown fracture, and amount of root resorption were factors influencing pulpal necrosis and calcification. Teeth with a coronal fracture were less likely to suffer calcific obliteration of the root canal than those which had been luxated.

When making a decision upon treatment, the proximity of the primary tooth to the permanent successor is an important consideration. Treatment least likely to damage the permanent tooth should be chosen.^9,29 Studies present conflicting data on the merits of treating or extracting traumatized primary teeth. Some have suggested no relationship,^11,12 others have shown more extensive developmental disturbances if the primary tooth is treated and preserved.²⁶⁶

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.^29,125

Pulpal necrosis ranging from 50% to 82% is reported^{29,120,125,263} in traumatized primary incisors with dark gray discoloration, compared to 25% in those with no discoloration. One author⁴⁹ points out that color change in the absence of other clinical findings is unreliable. 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 injuries.^130,136 Yellow or brown-tinted discoloration usually indicates calcification of the pulp space; a gray color is usually associated with pulpal necrosis. A return to normal after transient coronal discoloration^8,38 and transient apical breakdown up to 4 months’ duration³⁸ have been reported.

Indirect Pulp Therapy in Primary Teeth

Indirect pulp treatment (IPT) in the primary dentition is considered a contemporary, effective approach to a deep carious lesion in the absence of signs or symptoms of irreversible pulp pathosis.²⁶⁵ 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 clinical and radiographic examination, direct evaluation of the cavity preparation, and a good knowledge of tooth anatomy and the caries process.¹⁴

The aims of IPT are²⁵⁰ to arrest the carious process, provide conditions conducive to the formation of reactionary dentin, and promote remineralization of the altered dentin that was left. This in turn is expected to promote pulpal healing and preserve/maintain the vitality of the pulp.

Direct Pulp Capping in Primary Teeth

The lifespan of the average primary tooth from initial development to exfoliation is significantly shorter than that of a 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. Further, 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.¹¹⁰

Carious pulpal exposures in primary teeth should not be direct pulp capped. 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.^7,250 Under these circumstances, it is presumed that the conditions for a favorable pulpal response are optimal.

Pulpotomy in Primary Teeth

The AAPD guidelines⁷ 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. Evidence of successful pulp therapy includes those features listed in Box 23-3.

For all pulpotomy procedures for the cariously exposed vital pulp of primary teeth, the procedure common to all is the complete amputation of coronal pulp tissue. Following this, and once hemostasis has been achieved, a decision is made on the wound dressing or technique to apply to the pulp stumps.

Some of the options available are listed below, and the success of all depends upon ensuring that the residual pulp tissue is correctly diagnosed as healthy or reversibly inflamed.

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. Yet despite these, formocresol and in particular one of its constituents, formaldehyde (FAD), has come under close 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 over the safety of these materials make it clear that additional research on the use of these and other pharmacotherapeutic agents is required.

Nonpharmacologic hemostatic techniques have been recommended, including electrosurgery^{169,253,269,270} and laser therapy.⁶⁴ Research involving human clinical trials on both these techniques is sparse; nevertheless, electrosurgical pulpotomy is currently being taught in several dental schools. Comprehensive reviews of the techniques and agents used in vital pulp therapy and discussion of possible new modalities are available in the literature.^236,278,318

Technique of Coronal Pulp Amputation

Removal of the coronal pulp tissue is a process common to whichever pulpotomy procedure is chosen for the cariously exposed vital primary tooth. Following successful coronal amputation and hemostasis (Fig. 23-15, A-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. Fig. 23-15, C-H provides a schematic overview of the options and expected outcomes.

FIG. 23-15 Illustration to show three different approaches to the radicular pulp following coronal pulp amputation during pulpotomy in an extensively carious primary molar. A, Primary molar with caries extending to the pulp. Note inflammatory response in coronal pulp. B, Tooth has undergone removal of the coronal pulp. Radicular pulp tissue is healthy and has stopped bleeding. C, A 1:5 dilute solution of formocresol may be applied to 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 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 within the root canals. G, Mineral trioxide aggregate (MTA) is placed directly over the radicular pulp stumps, and the tooth is provided with an intracoronal restoration as before. H, The radicular pulp tissue remains vital beneath the MTA; a calcific bridge may form over time beneath the MTA.

Stages in the Technique of Coronal Pulp Amputation

1. Following the initial diagnosis of probable vital pulpal involvement, the primary tooth is anesthetized and isolated with a rubber dam.

2. All caries are removed, and the observation of bleeding from exposure sites indicates vital (if inflamed) coronal pulp tissue (Fig. 23-16, A-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. 23-16, C-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. Completely dry cotton pellets should not be used; fibers of the cotton will be incorporated into the clot and when removed will cause hemorrhage. 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 filaments 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, it can be reentered with a small round bur to amputate the suspected inflamed tissue; the canal is then rinsed again, and cotton pellet pressure is applied.

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.

FIG. 23-16 Clinical stages of a vital pulpotomy using ferric sulfate solution. A, Extensive dental caries affecting a mandibular first primary molar. Note proximity of 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 bleeding coronal pulp prior to amputation. D, Roof of pulp chamber removed completely. E, A 15.5% solution of ferric sulfate is applied to radicular pulp stumps using a dento-infuser tip supplied by the manufacturer. F, Hemostasis is evident at 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 of Vidya Srinivasan, Edinburgh Dental Institute, UK.)

Once bleeding has stopped at the radicular pulp stumps, the wounds are managed according to one of the following pulpotomy techniques (see Fig. 23-15):

• Application of dilute formocresol solution for 5 minutes

• Application of 15% ferric sulfate solution for 15 seconds (Fig. 23-16, E-F)

• Permanent placement of MTA

• Electrosurgical manipulation of the wound surfaces

• Laser manipulation of the wound surfaces

Formocresol Pulpotomy

Formocresol and the Permanent Successor

The 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 teeth^187,251 to an increase in defects and positional alterations of the underlying permanent tooth.¹⁸¹ It should be pointed out that studies of this nature are follow-up studies long after treatment, without 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, with some studies finding no consistent effect^187,312 and some reporting early exfoliation.^119,185

Unlike the tissue response to Ca(OH)₂, no dentin bridge should be anticipated after applying formocresol to exposed pulp tissue (see Fig. 23-15, C-D). However, narrowing of the root canal through the continued deposition of dentin by the preserved radicular pulp may be observed in some cases (Fig. 23-17).

FIG. 23-17 Narrowing of the apical region of the root canal following formocresol pulpotomy. Histologic section of tooth showing deposition of new dentin along the walls of the apical region of the root canal.

Criteria for Success

Failure of a formocresol pulpotomy is usually detected on radiographs (see Fig. 23-13). 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 the deposition of calcified tissue. In the primary molars, radiolucency develops in the bifurcation or trifurcation area. In the anterior teeth, a radiolucency may develop at the apices or lateral to the roots. With more destruction, the tooth becomes excessively mobile; a sinus tract usually develops. It is rare for pain to occur with the failure of a formocresol pulpotomy. Consequently, unless patients receive follow-up checks after a formocresol pulpotomy, failure may be undetected. When the tooth 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.^32,259 An amorphous, eosinophilic material shown to contain phenolic groupings similar to those present in medicaments was found in the lesions. Other researchers¹⁹⁴ have observed furcal lesions in untreated, pulpally involved primary molars containing granulomatous tissue with stratified squamous epithelium, suggesting the potential for cyst formation. In a subsequent study involving failed, pulpotomized primary molars, most specimens were diagnosed as furcation cysts.¹⁹⁵ These findings emphasize the importance of periodic follow-up to endodontic treatment on primary teeth. Fig. 23-18 shows a favorable long-term outcome following a formocresol pulpotomy in a mandibular primary molar.

FIG. 23-18 Five-year follow-up of a primary tooth with a formocresol pulpotomy. A, Pretreatment radiograph showing deep caries on lower right first and second primary molars. B, One-year posttreatment radiograph. C, Five-year follow-up radiograph. Note eruption of lower right first permanent molar and first bicuspid.

Glutaraldehyde Pulpotomy

Glutaraldehyde has been a suggested alternative to formocresol 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.^290,322 Fixed pulp tissue may be replaced with dense collagenous tissue over time.¹⁵⁰ Studies have also demonstrated less systemic distribution than was thought to occur with formocresol.^{57,159,196,220,321}

Glutaraldehyde has been shown to be rapidly metabolized with little toxic effect.^{118,137,143,196,240} It has also been demonstrated that although glutaraldehyde has antigenic action similar to formocresol, it is of a lower potential.^237,239 However, there are perceived problems with the use of glutaraldehyde as a pulpotomy agent:

Despite the perceived enhanced safety of glutaraldehyde with respect to formocresol, it did not gain favor over formocresol for pulpotomy in the primary dentition.^17,76

Ferric Sulfate Pulpotomy

Mineral Trioxide Aggregate Pulpotomy

Electrosurgical Pulpotomy

Laser Pulpotomy

Several reports have appeared in the literature on the use of the carbon dioxide laser for performing vital pulpotomies on primary teeth.^64,161 Investigators⁶⁴ 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 identified in one of the formocresol-treated teeth and two of the laser-treated teeth. They 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 should be conducted 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.

Other researchers¹⁶¹ 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 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 calcification 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 formocresol. 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 formocresol. Until such an agent, instrument, or technique is found, ferric sulfate, MTA, or formocresol (one-fifth dilution) can be used with equal confidence in primary tooth pulpotomies.^84,250,278

Pulpectomy in Primary Teeth

The 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 impact upon clinical technique, pulpectomy and root canal obturation of primary teeth with irreversibly inflamed or necrotic pulp can be a clinically successful option.

In brief, these features are:

Effect of Resorption on Canal Anatomy and Apical Foramina

In 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 23-7).

BOX 23-7 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 interradicular septum.

As resorption progresses, the apical foramen may not correspond to the anatomic apex of the root but be coronal to it. Subsequently, radiographic establishment of the root canal length may be challenging (Fig. 23-19). 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.²⁴⁴ Because of these factors, use of an apex locator is not reliable to establish canal length.

FIG. 23-19 Primary maxillary canine. A, Facial view, where apical foramen appears to be at the apex of the root. B, Physiologic root resorption has occurred at the palatal aspect of the root; apical foramen is positioned more coronally and will not be coincident with the perceived radiographic apex of the tooth.