In summary, orthograde root canal treatment has a high degree of predictability both in normal and complex cases. Some limitations exist, but the potential for a favorable outcome is significant. As indicated previously, the shaping and cleaning performed as part of root canal treatment are directed against microbial challenges to the root canal system.188 Microbes can breach dental hard-tissue barriers through several avenues, the most common being dental caries (Fig. 9-7).
Pulpal reactions may be observed as soon as the diffusion barrier (the remaining dentin thickness) is sufficiently permeable for bacteria or their toxins to affect the pulp35 (Fig. 9-7). Under experimental conditions, pulpal inflammation can be detected only a few hours after topical application of bacterial components to exposed dentin.28 In an established lesion, a bacterial ecosystem evolves, with synergisms and antagonisms among the microorganisms (see Chapter 15). These interactions play an important role in the course of the disease, when intraradicular biofilms develop and bacteria invade dentinal tubules.159 Two key factors initiate and modify inflammatory reactions, such as the development of microabscesses in subodontoblastic regions: the penetration of bacterial components and the release and diffusion of inflammatory mediators.
The stereotypic pulpal defense reaction is hard-tissue deposition (Figs. 9-7 and 9-8) by primary and secondary odontoblasts.35 Hard tissue is laid down as a response to a stimulus (reactionary or reparative dentinogenesis) and thus takes place within a defined spatial relationship to that stimulus, occurring slightly apical to the lesion.
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Figure 9-5 Possibilities and limitations of orthograde endodontic therapy. In this case, a large lesion in the right maxilla was enucleated and histologically diagnosed as a radicular cyst. A, Preoperative occlusal plane radiograph shows a large periradicular lesion in the right maxilla, as well as two separated instruments in tooth #7 (arrow).B, Postoperative periapical radiograph of tooth #7 and necrotic tooth #8, which were obturated after calcium hydroxide dressings had been placed for two weeks. Obturation was done with laterally compacted gutta-percha and Roth's 801 sealer. C, Two lentulo spiral fragments removed from tooth #7 (ruler gradation is 0.5 mm). D, Histologic slide shows both respiratory epithelium (arrow) and squamous epithelial lining and inflammatory cells, supporting the diagnosis. (Ccourtesy Dr. I. Hegyi.)
Hard-tissue deposition is a natural event with aging310 (secondary dentinogenesis), which creates a higher degree of treatment difficulty in older patients. Clinicians note a radiographically detectable decrease in the size of the pulp space that occurs most often in the coronal regions but also can be seen in the more apical areas. This condition is not a contraindication to orthograde endodontic therapy; however, it requires additional attention to clinical procedures such as preenlargement and prebending of hand files (discussed later in the chapter).
The process of calcific metamorphosis is a response to traumatic injury.14 It is characterized by a reduction in the size of both the radicular and coronal pulp spaces. Conversely, teeth with signs of hard-tissue deposition caused by bacterial attack show an initial reduction of pulp space size coronally, which may involve the pulp chamber and canal orifices (Fig. 9-7). This situation calls for meticulous preparation of an access cavity and preenlargement of canal orifices in a nondestructive manner. Depending on the timing of inoculation and the number of microbes, hard-tissue deposition also may occur more apically.145
Reparative dentin may form a diffusion barrier sufficient for the pulp to recover, depending on the severity of the bacterial challenge and the capability of the defense mechanisms.163 Unfortunately, no consensus exists on the best therapy to allow this recovery to occur.29
Further into the disease progress, and if the carious lesion persists, bacteria may be present in sufficient concentrations to induce pulpal inflammation. This is triggered by molecular signals (e.g., cytokines), which are released from cells such as macrophages and neutrophils well before microbes are actually present intrapulpally (see Chapter 13). At this stage, with a diagnosis of reversible pulpitis, endodontic treatment may be avoidable, provided the source of the irritants is removed.
To deliver adequate endodontic therapy, the clinician must understand that apical periodontitis is the endpoint of a disease flow that in most cases originates coronally, either with carious lesions or a traumatized pulp (Fig. 9-7). As stated previously, opportunistic bacteria may invade dental hard tissue, and their byproducts eventually may reach the pulp space (see Chapter 15). Host response factors, such as the recruitment of neutrophil granulocytes and local development of neurogenic inflammation, act against microbial invasion, but this line of defense may succumb to the challenge if the carious defect is not repaired. Then, after microabscesses form, circulation changes occur; coronal and subsequently radicular pulp may become nonperfused and thus necrotic.
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Figure 9-6 Root canal therapy as part of a comprehensive treatment plan. The patient, who was recovering from intravenous drug addiction, requested restorative dental treatment. Because of extensive decay several teeth had to be extracted, and nine teeth were treated endodontically. Root canal treatment was aided by nickel-titanium rotary instruments, and obturation was done with lateral compaction of gutta-percha and AH26 as the sealer. Microsurgical retrograde therapy was performed on tooth #8, and the distobuccal root of #14 had to be resected. Metal-free adhesively luted restorations were placed, and missing mandibular teeth were replaced by implants. A, Preoperative intraoral status, showing oral neglect. B, Postoperative intraoral status at 4-year followup, showing fully functional, metal-free, tooth-colored reconstructions. C, Panoramic radiograph at 4-year recall shows sound periradicular tissues in relation to endodontically treated teeth. (Restorations done by Dr. Till N. Göhring.)
At various points in this process, bacterial factors such as lipopolysaccharides and peptidoglycans134 can reach periapical tissues through apical and accessory foramina. Zones of bone resorption (appearing as radiolucencies) may develop, depending on the balance between microbial virulence factors and host defenses.272 The development of apical periodontitis is associated with a significantly less encouraging prognosis after orthograde endodontic treatment.62,261,263
One school of thought emphasizes the importance to successful endodontic therapy of cleaning and filling lateral and accessory canals.227,314 Clinical radiographs of artfully done cases support this position; the contribution of accessory canals to lesion development in certain cases seems highly likely (Fig. 9-2). However, this pathogenesis depends on the volume of accessory canals and the amount of bacteria harbored in them. Another subject of controversy is the clinical importance and mechanisms of dentinal tubule infection158,159,197 with bacteria and fungi (Fig. 9-9).
In most cases lesions are associated with the main root canal systems (Figs. 9-1 and 9-3 to 9-5) and form periapically around the main foramina. The main canal unquestionably has the highest bacterial load, and important studies link reduction of the viable intracanal bacterial load to favorable outcomes for endodontic therapy.138,196,261 Therefore a primary aim of all endodontic procedures, and most notably of cleaning and shaping, is to remove canal contents, specifically infective microorganisms.2
A wide spectrum of possible strategies exists for attaining the goal of removing the canal contents and eliminating infection. Lussi et al165 introduced a minimally invasive approach to removing canal contents and accomplishing disinfection that did not involve the use of a file (the noninstrumentation technique [NIT]). This system consisted of a pump, a hose, and a special valve that was cemented into the access cavity (Fig. 9-10, A) to provide oscillation of irrigation solutions (1% to 3% sodium hypochlorite [NaOCl]) at a reduced pressure. Although several in vitro studies164,166,167 demonstrated that canals can be cleaned and subsequently filled using this system (Fig. 9-10, B and C), preliminary clinical results have not been as convincing (Fig. 9-10, D).15
At the opposite end of the spectrum is a treatment technique that essentially removes all intraradicular infection through extraction of the tooth in question (Fig. 9-10, C). Almost invariably, periradicular lesions heal after extraction of the involved tooth.
Clinical endodontic therapy takes place somewhere along this spectrum of treatment strategies. This is reflected in some of the controversies that surround the cleaning and shaping process, such as how large the apical preparation should be and what are the correct diameter, length, and taper.135
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Figure 9-7 Progression of pulpal disease and the development of periradicular pathosis. A carious lesion leads to contact of toxins and microbes with the coronal pulp, resulting in inflammation and infection. The stereotypic defense reaction of dental pulp then occurs: hard-tissue deposition. This reaction may lead to repair or to additional hard-tissue deposition (e.g., as calcific metamorphosis). The next step may be formation of microabscesses, changes in circulation during inflammation, and ultimately progression of infection into the radicular pulp space. Finally, periradicular osseous lesions may develop if the bacterial challenge persists. (Courtesy Dr. H.-U. Luder and T. Häusler.)
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Figure 9-8 Evidence of coronal hard-tissue deposition. A, Periapical radiograph of tooth #19 shows evidence of reduced coronal and radicular pulp space. B, Intraoral photograph, taken through an operating microscope (×25), of access cavity of the tooth shown in A; note the calcific metamorphosis.
The foundation of the endodontic treatment plan is an adequate diagnostic process (see Chapter 1), which includes obtaining diagnostic radiographs from various angles. Also, the restorability and periodontal status of teeth to be treated endodontically must be determined; in some cases buildups or crown lengthening is required for preendodontic restoration to allow proper isolation, to create pulp chambers that retain irrigants, and to facilitate interappointment temporary restorations. In many cases the existing restoration may have to be removed so that an adequate diagnosis can be made and the immediate cause of endodontic treatment can be assessed.1
Once the decision has been made to initiate endodontic treatment, the clinician must integrate his or her knowledge of dental anatomy, immunology, and bioengineering science with clinical information. The intent of this chapter is to assist clinicians with that task and to provide a much-condensed background in radicular anatomy, pulpal pathophysiology, and nickel-titanium metallurgy.
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Figure 9-9 Presence of microorganisms inside the main root canal and dentinal tubules. A, Scanning electron micrograph of a root canal surface shows a confluent layer of rod-shaped microbes. (×3000.) B, Scanning electron micrograph of a fractured root with a thick smear layer and fungi in the main root canal and dentinal tubules. (Acourtesy Professor C. Koçkapan;Bcourtesy Dr. T. Waltimo.)
Endodontic therapy has been compared to a chain, and it has rightfully been pointed out that the chain is only as strong as each individual link. For the purposes of this chapter, shaping and cleaning of the root canal system is considered a decisive link, because shaping determines the efficacy of subsequent procedures. It includes mechanical debridement, the creation of space for the delivery of medicaments, and optimized canal geometries for adequate obturation.198 These tasks are attempted within a complex anatomic framework, as recognized in the early twentieth century by Walter Hess124 (Fig. 9-11) (see Chapter 7).
Unfortunately, canal preparation results are adversely affected by the highly variable root canal anatomy.9,10,126,180,205 This fact is especially true for conventional hand instruments and to a lesser degree for most nickel-titanium rotary instruments.31,198 Therefore the radicular anatomy is briefly reviewed as it pertains to cleaning and shaping.
Root canal curvature can be assessed clinically from radiographs, preferably taken from various angles. However, it is well documented that curves in the mesiodistal plane often are greater than those in the more readily accessible buccooral plane.66,208 In vitro a full account of three-dimensional canal anatomy can be seen with interactive micro-computed tomographic (μCT) reconstructions (Figs. 9-12 and 9-13).
The clinician must understand the five commonly encountered canal paths (i.e., canals that merge, curve, recurve, dilacerate, or divide).227 All five situations are risk factors for file breakage and should be carefully evaluated, as is done for more basic considerations such as the estimated canal length, position of the primary curve, canal diameter, and apical topography.
Early anatomic studies108,109,148 evaluated the position and topography of the apical foramina and the position of the apical constriction. These studies found that the physiologic foramen, or canal terminus, was located up to 1 mm coronal to the anatomic apex, or root tip. This observation has been confirmed by later studies.81,176
Clinically, the landmark detected from radiographs (the radiographic apex) does not necessarily coincide with the anatomic apex because of projection artifacts. Taken together, these observations suggest that shaping to the radiographic apex is likely to produce overinstrumentation past the apical foramen, with possible clinical sequelae of postoperative pain and inoculation of microorganisms into periapical spaces.27,29,84,111
Foramen diameter was also an issue in both early109,148 and more recent studies.41,81,176,273 The smallest canal diameter, called the apical constriction, was located 0.5 to 0.7 mm coronal to the canal terminus.109,148 A wide range of diameters has been reported in that region, from 0.2 to about 1 mm41,141-143,148,176; the concept of a single apical constriction has also been challenged.81 Moreover, studies have shown that clinicians usually underestimate apical dimensions.315 Clearly, the apical anatomy presents the clinician with major challenges (Fig. 9-14), such as apically dividing canals, nonround cross sections, and deltalike configurations. In addition, canal cross sections that are wide buccolingually314 are difficult to instrument with rotary techniques.