Lars Bjorndal
9.1 Diagnostic Challenges of Deep Caries and Traumatic Pulp Exposure
Prevention of apical periodontitis begins with the evaluation of whether the pulp can be preserved or not. The task of assessing the actual stage of pulpal infection and inflammation has been and still is today a major challenge [61]. Stringent means of pulpal diagnosis are largely lacking. It is particularly important to: 1) establish an exact threshold for unwanted inflammation that inevitably leads to necrosis; 2) estimate whether an exposed dentine pulp complex pulp should be avoided; and 3) in case of exposure, decide if a pulp capping or pulpotomy procedure is possible or if a pulpectomy is necessary.
This essential diagnostic problem of estimating degrees of pulp inflammation and infection has led to different treatment concepts for deep carious lesions. These concepts range from a strictly conservative approach, leaving affected dentine and the pulp underneath the restoration, to radical pulp removal and root filling. Questionnaire surveys based on radiographic illustration of deep carious lesion have shown that there is a huge variation among dentists in their choice among the treatment modalities for a given situation [64, 76, 85, 86]. In clinical practice, the decision whether to save the pulp or not varies even when supplementary subjective and objective diagnostic data are added [85]. The majority of dentists lean toward an invasive approach suggesting that a pulpectomy should be carried out [64, 86]. The variation in choice of treatment may also be a consequence of an unclear definition of what constitutes a deep carious lesion, as well as of a lack of unambiguous clinical signs and symptoms for defining the status of the pulp. Clinical research should strive to improve the evidence base both for the diagnostic procedures and for the choice of therapy associated with the different clinical situations. In practice, this means that we need clearer definitions of deep lesions based on solid clinical evidence, and we need sophis- ticated technologies for measurements of inflammation. While there is active clinical research in this field, many questions are still unanswered.
9.1.1 Deep Caries as an Endodontic Problem
Endodontics as a discipline holds the key for providing optimal “pulpal care" Endodontology has a natural focus on aseptic strategies that is fundamental and mandatory for a successful preservation of pulp vitality. This includes the preparation of an aseptic working field using rubber dam isolation and application of a disinfection agent. Lack of asepsis and use of contaminated instruments in deep caries treatment, as well as the potential introduction of carious dentine fragments into an exposed pulp, is likely to be the main reason why conservative approaches to treatment so often fail. In general dental practice, focus on an aseptic working field using rubber dam in these situations is variable at best. A great majority of practitioners treat deep caries and associated pulpal exposures without regard to asepsis [15, 44, 70, 82], which makes pulpcapping procedures a vulnerable modality from the outset. Clear guidelines are needed, and efforts should be made to ensure that protocols for treatment of deep caries and pulp capping are recognized as strictly aseptic procedures with predictable outcomes, rather than simple and easy methods just hoping to avoid a pulpectomy [49].
This chapter deals with the dilemma of correctly diagnosing the pulpal status in deep caries. Also addressed is the biological platform for understanding why the dentine pulp complex is able to produce a hard tissue barrier. Moreover, the various modalities for managing the disease of the inflamed pulp are reviewed, including approaches to avoid pulp exposure.
9.2 Discerning Pulpal Diagnosis
Most often the cause of a pulp exposure and subsequent endodontic intervention is caries [14]. Therefore, the diagnostic dilemma is best illustrated by the scenario of a deep carious lesion. From a classical endodontic viewpoint, the consideration of the actual status of pulp inflammation immediately emerges. It is generally recognized that signs and symptoms as presented by the patient or during an objective examination do not per- mit an accurate diagnosis of the histologic status of the pulp; consequently, it is difficult to assess whether a pulpal inflammation is reversible or not [26, 78, 79] (see also Chapter 10). From a histopathological/bacteriological viewpoint, the point of no return for unwanted and irreversible inflammation in the pulp can be defined as the stage where the invading microorganisms have entered the pulp space either through tertiary dentine or directly into the pulp [66, 69]. However, this critical threshold of infection is difficult to detect clinically. Particularly, deep lesions with risk of pulp exposure during caries removal should be better defined by added information on progression stage and penetration depth, lesion activity and estimated length of progression time (patient age). These elements of defining the carious lesion are further detailed below.
9.2.1 The Penetration Depths of Carious Lesions
Clinically, defining the depth of a deep carious lesion is usually based on dental practitioners' expectations of reaching pulp exposure fol- lowing excavation [18]. Radiographically, a deep carious lesion is in this context defined as a lesion penetrating into the pulpal quarter of the dentine, but still with a well-defined zone of radiopaque dentine separating the lesion from the pulp [7]. With further devel- opment of the carious process, demineralized dentine may be seen to affect the entire thickness of the dentine; caries may then be defined as extremely deep [17]. Examples of deep and extremely deep lesions are shown in Figure 9.1.
Based on knowledge from caries histo- pathology, the infected carious dentine is initially restricted to the so-called outer zone of the demineralized dentine. This outer zone is non-remineralizable and decomposed with degraded collagen [31], whereas the inner zone being the most advanced part of the carious process includes a radiopaque/ hypermineralized zone, which is actually keeping the microorganisms from directly entering the pulp. When this hypermineralized zone is broken down, the carious lesion has microorganisms penetrating into the critical area of tertiary dentine and the pulp [66]. At this stage clinical symptoms may occur that are useful in defining a diagnosis of irre- versible pulpitis, corresponding well with the presence of bacteria within the pulp [69].
Figure 9.1 (a) A deep carious lesion defined with a lesion penetration into the pulpal quarter of the dentine. A well-defined zone of radiopaque dentine is separating the carious lesion from the pulp (arrow). (b) An extremely deep carious lesion extending through the entire thickness of the dentine, no evidence of a radiopaque zone of dentine, but there may be thin radiopaque lines within the pulp chamber (arrows).
Therefore, the careful examination of lesion depths on bitewing radiographs becomes a substitute for evaluation of the risk of bacterial invasion into the pulp. The exact degree of carious lesion progression has seldom been described in literature dealing with pulp capping [10]. This means that there is probably a wide variation among cases with regard to the extent of dentine and pulp infection, which could be one explanation of the difficulties in comparing studies and in predicting the outcome following direct pulp capping. It is definitively important whether the capping procedure is performed within a deep or extremely deep carious scenario versus an iatrogenic exposure. In the latter case, the capping procedure is done after preparation for a filling or a crown that has exposed the pulp, e.g., a pulp horn, and the local pulp has not been affected by caries. Such information is seldom specified in clinical reports [10, 28], but it probably represents a major difference in outcome. A pulp exposed during carious tissue removal would have a much higher risk of becoming infected during treatment, whereas an iatrogenic exposure stands a fair chance of remaining free from infecting bacteria (see also later).
9.2.2 Pulp Inflammation - a Two-edged Sword
Caries is the common reason for performing root canal treatments, particularly in vital cases [14], and is a main cause of pulp inflammation. An update on pulp inflammation and caries pathology is briefly presented. The view of seeing pulp inflammation under caries as an irreversible process that cannot be stopped is no longer tenable. It was based on the belief that if carious dentine was left behind intentionally, it would represent a strong, permanent challenge to the subjacent pulp, and sustained inflammation was to be expected. Even if carious tissue removal and pulp capping was performed on such an inflamed pulp, the inflammation was expected to run its own course and eventually lead to necrosis and clinical failure [63]. Pulp inflammation does not necessarily lead to the pulp becoming necrotic and infected. Rather, a low-grade inflammation provides a platform for repair and regeneration [23]. When the source of injury is removed, the pulp may still have the capacity and potential to provide an upregulation of hard-tissue-forming cells including odontoblasts [81]. In addition, pulp reactions to caries are dynamic in nature and differ in response to slowly versus rapidly progressing carious lesions. The dentine-pulp complex lays down reactionary, tertiary dentine formed by primary odontoblast cells in response to a low-grade/slowly progressing lesion environment (typically adult/older patient, lesion penetration half into the dentine) [8]. In contrast, subjacent to a rapidly progressing lesion (young patient, lesion in inner quarter of dentine), the tertiary dentine, if present at all, is characterized by a decreasing presence of dentinal tubules, eventually being completely atubular, by a process called fibrodentinogenesis [6]. Here the primary odontoblasts have decayed and died, and the reaction should be seen as repair and not regeneration [68].
9.2.3 Untreated Caries a Model to Understand Reparative Dentine
Figure 9.2, using different teeth for the different stages, illustrates the progression of untreated occlusal lesion in molar teeth. The carious dentine shrinks due to the extensive loss of mineral, and a gap or slit is created laterally along the enamel-dentine junction, which provides the pathway for a massive infection. This gap, that is undermining sound enamel, comprises a biofilm [12]. Clinically the lateral spread of infection [9] appears as a milky change of dentine translucency surrounding the cavity (Figure 9.2b arrows). During mastication, the undermined enamel breaks off and a large dentine surface is exposed to the environment (Figure 9.2c). This in turn creates a change in the growth conditions for the cariogenic biofilm. Even though the lesion is deep, the large, exposed surface causes it to change into a more slowly progressing lesion, and a massive formation of reparative dentine formation is often noted subjacent to these open deep lesions. Histologically, a new layer of tubular dentine is laid down on top of the atubular dentine [8]. Unfortunately, while the pulp may be only reversibly inflamed, when deep lesions progress to the extent where the enamel has been broken severely down, these teeth may no longer be salvageable.
The key message of this “natural history” of caries progression is that when the outer lesion environment changes, reducing the cariogenic load, the pulp may react with reparative dentine formation. In principle, this knowledge may enable us to convert lesion activity by conservative treatment approaches to deep carious lesions: if we can change the environment over an active lesion, we may be able to support the production of effective reparative dentine. Another message is that the formation of reparative dentine per se is not a permanent sign of bio- logical, or treatment, success. New bacterial infection will always challenge any type of new tertiary dentine barrier that has been laid down. Thus, while the formation of a dentine barrier is a step in the right direction of maintaining pulpal vitality, permanent elimination and control of dentine infection is essential for a lasting preservation of the pulp.
Figure 9.2 (a, b, c) The "natural history" of untreated caries. Three progressing stages of a deep lesion, where (a) undermined enamel eventually (b) breaks off due to mastication (arrows), converting the lesion environment from a "closed" to (c) an "open" environment converting the central part of the lesion into a slowly progressing environment. Changing the outer environment during the course of the carious process turns the active, rapid lesion into a slower or even arrested phase. Courtesy of Dr Lars Bjorndal.
Table 9.1 Clinical and radiographic characteristics of reversible and irreversible pulpitis.
|
Diagnostic factors |
Pulp condition |
|
|
Reversible pulpitis |
Irreversible pulpitis |
|
|
Spontaneous toothache |
No |
Yes |
|
Pulp response to cold and electricity |
Yes |
Yes |
|
Lingering pain to cold |
No |
Possible |
|
Lingering pain to heat |
No |
Yes |
|
Pain relief from cold |
No |
Possible |
|
Swelling |
No |
No |
|
Increased mobility |
No |
Possible |
|
Tenderness to biting/percussion |
Possible |
Yes |
|
Radiographic signs of apical bone destruction |
Possible |
Possible |
Table 9.1 lists some variables describing features of clinical caries. Combined with subjective, objective and para-clinical information, a pragmatic approach is presented for dividing the status of pulp into normal or reversible pulpitis versus irreversible pulpitis.
9.3 The Pulp Biology Associated with Pulp Capping
9.3.1 Hard Tissue Formation
Numerous experimental, animal studies have provided evidence that the dentine pulp complex has the biological capacity of laying down tertiary dentine formation following sealing of a pulp exposure, with the prerequi- site that the pulp per se is without infection. The classical Kakehashi study [45] is well known for documenting the fundamental role of root canal infection for the development of apical periodontitis; but it also showed that the exposed pulps of germ-free rats, i.e., in the absence of bacteria, healed with the formation of tertiary dentine. It is beyond the scope of this chapter to further detail the basic biological interactions causing this to happen, but the following items will be briefly discussed: the origin of dentinal repair cells, hemostasis, biological and sealing properties of the capping material.
9.3.2 Stimuli Causing Tertiary Dentine and Origin of Dentinal Repair Cells
Tertiary dentine is defined as new dentine produced in relation to an external injury [6]. The subdivision of tertiary dentine into reactionary dentine (dentine laid down by primary odontoblast cells) and reparative dentine (hard tissue laid down by other cells than the primary odontoblasts) simply reflects the type of the external stimuli that has caused it to happen and was illustrated above in relation to caries [8, 68]. A completely atubular pattern is typical for a very rapidly progressing carious lesion, but it can also be seen in the pulp underneath an acute, iatrogenic trauma, caused by, for example, an insufficiently water-cooled rotating bur during cavity preparation. The atubular dentine or fibrodentine may also occur as a physiological phenomenon in teeth without signs of external injuries [6], e.g., at the tip of a pulp horn or on the floor of the pulp chamber [19], and reflect a mineralization potential of pulpal stem cells, not only the odontoblast.
Indeed, tertiary dentine can be produced by non-primary odontoblast cells, as seen following pulp exposure, where the re-establishment of a dentinal bridge formation can be expected following a successful pulp-capping procedure (Figure 9.3). Dentine bridge formation following a pulp-capping procedure reveals many non-mineralized parts or so-called “tunnel defects” that could easily be invaded by microorganisms [24]. Therefore, the placement of a bacteria-tight, coronal seal securing long-term control of contamination is mandatory after a capping procedure.
9.3.3 Hemostasis
For any pulp capping (or pulpotomy) proce- dure to be successful, it is commonly held that hemostasis is obtained and blood clot formation between the capping material and the pulp tissue is avoided. This is important for the proper placement of the capping material on a dry cavity base; moreover, the presence of a blot clot has been linked to higher risk of infection [71, 72]. The means of obtaining hemostasis seems of little importance, particularly for capping of a sound pulp. A clinical trial investigated different hemostatic protocols using either saline, sodium hypochlorite, or chlorhex- idine digluconate prior to pulp capping with calcium hydroxide, and found no difference among the liquids in the expression of specific gluco-proteins related to pulpal repair [4]. Moreover, a randomized clinical trial has shown improved outcome if a disinfection agent is applied in the hemostatic protocol prior to the application of a capping material [88]. On the other hand, it may also be seen as a contradiction that the blood clot should in fact be removed. It contains numerous potentially bioactive molecules, which could contribute to and benefit a repair process. In fact, revascularization protocols actively induce bleeding [32, 33]. Current pulp- capping protocols are most probably far from making a full biological benefit of the healing potential of the pulp.
Figure 9.3 Histological evidence of reparative dentine in human following direct pulp capping.
9.3.4 The Pulp-capping Materials
The majority of evidence is from calcium hydroxide in various preparations, both in animal as well as in human studies. However, many of the studies in human suffer from a low level of evidence. For one thing, a control group is missing in many of these studies [28]. Furthermore, numerous pulp-capping studies have tested the materials in an uncontaminated environment, i.e., using teeth with non-inflamed pulps and no caries. This is relevant for various trauma and/or iatrogenic scenarios where a relatively sound pulp is exposed. However, capping the cariously exposed pulp may represent the most common clinical situation, and capping procedures should be tested under these more realistic conditions. In particular, whereas bioengineered anti-inflammatory pulp-capping materials have been around for quite some time [49], the lack of realistic clinical testing is an impediment to clinical acceptance. Marketing for new pulp-capping materials often runs ahead of robust clinical evidence. However, recent reviews provides some evidence for a superior outcome with the hydraulic calcium silicate cements, in particular various forms of the mineral trioxide aggregate material (MTA) [52, 91]. However, as high-quality randomized clinical trials comparing and testing capping materials are still lacking, the relative performance of different materials for capping is largely unknown (see also below).
9.4 Criteria for Assessing Success of Vital Pulp Therapies
A number of signs and symptoms converge to form a definition of successful treatment. As patients are well aware, absence of clinical symptoms, such as pain or discomfort,
spontaneous or induced, is essential. Recording of symptoms is therefore one important part of success/failure assessment. A necrotic pulp may be a sequel to treatment/infection, but does not necessarily lead to symptoms; therefore, assessment of pulpal sensibility by thermal or electrical testing is necessary. Finally, the pulp may become infected with development of apical periodontitis, which is reflected in periapical control radiographs. It should be noted that in some trauma cases, inflamed pulps may induce periapical radiographic changes known as transient apical breakdown [3], and the pulp is salvageable. Radiographs may at times also be suitable for monitoring dentine bridge and tertiary dentine formation. The use of cone beam CT may represent a refinement for detecting changes also in the tissue responses to pulp- capping procedures. It appears that cariously affected, vital pulps may have radiographically visible changes at the apex more easily detectable by CBCT, and that monitoring treatment by CBCT may be a more sensitive technique for observing differences among pulp-capping methods [37].
9.5 Indirect Pulp Capping and Stepwise Excavation
Traditionally, complete caries removal was seen as appropriate for any and all carious lesions. However, clinical and experimental evidence has gradually been building up a far more nuanced concept for dealing with deep and extremely deep lesions [39, 47, 67, 74]. Complete carious tissue removal to sound dentine (non-selective carious tissue removal) is clearly contraindicated in several instances [41, 75]. Randomized clinical follow-up studies have shown that a stepwise excavation approach to deep carious lesions as defined in this chapter (Figure 9.1) is preferable to com- plete carious tissue removal procedure in one visit: the incidence of pulpal exposure was reduced, and the patients had more vital teeth with less pain and without apical periodontitis after 5 years. A partial carious tissue removal procedure with a permanent filling placed at the same appointment may perform successfully [21, 29]; for deciduous teeth, this concept has been taken to its extreme by the so-called Hall technique, where a stainless steel crown is cemented directly over carious teeth, which shows similar, high success rates [40, 42]. However, from a clinical, endodontic viewpoint, a clear definition of lesion depth is difficult, and the evidence gained on welldefined deep carious lesions as well as on an adult population is limited. Therefore, the classical, indirect pulp-capping procedure [47], permanently leaving carious dentine behind based on one-stage carious removal, cannot currently be recommended for deep carious lesions in adults. It is unknown to what extent retained carious dentine will shrink, which may impair the coronal restoration and increase the risk for pulpal complications. With the less invasive carious removal strate- gies, an insufficient temporary or permanent coronal seal may also lead to failure including pulpal and apical pathosis [18, 56].
As discussed above, conversion of the outer lesion environment to one less conducive to caries progression can explain why a less aggressive, stepwise carious tissue removal concept is possible. The aim of the first stage of stepwise excavation is therefore to change the cariogenic environment (Figure 9.4a-b).
Active carious dentine is clinically recognized as a soft, discolored, and wet tissue (Figure 9.4c), becoming darker, harder, and drier when arrested (Figure 9.4d). After the first carious tissue removal procedure the active carious dentine is left under a calcium hydroxide base material followed by a glass-ionomer temporary restoration (Figure 9.4c). On reentry after 8 to 12 weeks, remaining caries is removed non-selectively until dentine with hardness comparable to unaffected dentine is encountered. While it is difficult to judge, in radiographs, the quality and extent of the ter- tiary dentine being laid down between visits (arrows, Figure 9.4d) [54], it appears that this is not clinically relevant for the procedure.
Figure 9.4 The principal changes during stepwise excavation. (a) The deep lesion has undermined enamel and an undisturbed cariogenic biomass. The active carious dentine is light brown/light yellow in color, and it is relatively wet and soft. (b) After first stage carious tissue removal leaving light and soft dentine close to the pulp (insert is a clinical example) (c) A calcium hydroxide base material and a temporary seal is made. (d) After the treatment interval (2-9 months later), the carious dentine appears darker, drier and harder (insert is a clinical example). (e) Non-selective carious tissue removal during the second stage leaves hard, tertiary dentine in the cavity floor (insert is a clinical example). (f) The permanent restoration can now be placed and on tissue that do not shrink further.
The stepwise excavation procedure reduces the risk of pulpal exposure significantly com- pared with immediate, complete caries excavation [16]. The clinical result of leaving behind carious dentine in between two stages is that carious dentine changes into signs of more chronic or arrested caries [13, 55]. Arrest of carious dentine after a treatment interval is associated with a reduction in the degree of infection [13, 65]. The arrest also induces underlying changes stimulating hard tissue formation, which may add to the fact that the incidence of pulp exposures is lower for teeth treated by stepwise excavation com- pared with complete excavation at the first sitting. Moreover, if exposure should occur during the second excavation stage, there is evidence that the outcome following a pulp capping is improved compared to capping of exposures occurring during the first visit [51]; this may be related to the different level of infection in the first and second stage of a stepwise excavation approach. During the process of carious dentine arrestment the retained dentine shrinks; this creates a gap subjacent to the temporary restoration. The second stage is therefore also aimed at opti- mizing the final cavity for the permanent restoration.
9.6 Pulp Capping of the Uninflamed Pulp (Class I)
This is the conventional pulp-capping proce- dure done after a complicated trauma leading to superficial exposure of the pulp or after an accidental perforation. The pulp is judged to be clinically sound and without inflammation prior the treatment. The perforation is small (preferably <1 mm in diameter) and is located in the coronal third of the crown pulp chamber, e.g., a pulp horn. It is essential that the cavity be effectively sealed with a coronal permanent restoration. Given the presumption of a clinically sound pulp, the tooth has been asymptomatic before the perforation. Perforations occurring after excavation of deep caries cannot be treated by this modality. Randomized studies have documented dismal results for capping of pulp exposure after excavation of deep caries, with only around 5% pulp survival after some five years [11], confirming earlier retrospective data [5].
9.7 Pulp Capping of the Cariously Involved Pulp (Class II)
This modality applies to carious lesions where the preservation of a vital pulp is especially important, such as in teeth with incom- plete root formation. The carious lesion has caused demineralization into the pulpal one fourth of the dentine or more. For pulp cap- ping to be indicated, the pulp must be vital with no reported pain indicative of irreversible pulpitis. This is a more refined treatment protocol, because a severe microbial challenge is expected. There are promising results with this method, but it is currently based on observational data only [20, 53, 57], and randomized studies are yet lacking. Furthermore, the data on outcome with this procedure has been gathered primarily in children, and even though the carious lesion has been extremely deep, the clinical diagnosis has always been “reversible pulpitis” with no spontaneous, lingering pain.
9.8 Partial Pulpotomy
Partial pulpotomy, widely known as the “Cvek” pulpotomy, was first applied to traumatic pulp exposures in young teeth. The superficial part of a contaminated and possibly infected exposed coronal pulp is removed aseptically and a calcium hydroxide dressing or capping material is placed over the exposure [25, 30]. Partial pulpotomy has also been applied to deep carious lesions [58-60, 92], but with a limited number of reported cases with long-term follow-up data [1]. The retention of the capping material may be improved following this modality, e.g. with complicated crown fractures in single-rooted teeth [25], but the important rationale for the procedure is that the superficial and expected necrotic and infected pulp tissue at exposure site is removed. In the young patient with incomplete root formation, the advantages are two-fold: (a) root formation may run to com- pletion; and (b) secondary and some tertiary dentine is formed, whereby the cervical part of the tooth is strengthened and the risk of cervical fractures may be decreased. The added opening of the exposure site for the removal of potential inflamed tissue should be as small as possible, because a higher risk of failure may be expected in children with larger exposure sites [22]. However, clinical trials comparing direct pulp capping with partial pulpotomy in adults with carious exposures could not show a difference between the two treatment modalities in this clinical situation [11].
Figure 9.5 The difference between (a) direct pulp capping and (b) partial pulpotomy. Partial pulpotomy entails active removal of inflamed/infected superficial pulp tissue, and provides improved retention of the capping agent.
9.9 Pulpotomy
The rationale for this procedure is to remove completely the coronal pulp tissue, thereby increasing the chance of eliminating any infected pulpal tissue. It is a standard method for vital pulp treatment in deciduous teeth, where pulp chamber dimension makes pulp-capping procedures more difficult to perform. The case selection criteria for full pulpotomy in non-carious teeth are com- plicated crown fractures and teeth with incomplete root formation. See Figure 9.5.
As for other vital pulp therapies, signs and symptoms of irreversible pulpitis, e.g., lingering or persistent pain following ther- mal provocation (this may be difficult to estimate in children) are absolute contrain- dications. Radiographically, care must be taken to differentiate the radiolucency of a follicle associated with a root-open tooth from a chronic apical periodontitis [89].
A serial case report found that pulpotomy could be a permanent treatment option in adults in cases of reversible pulpitis [80]. There is also evidence to suggest that irreversible pulpitis can be treated successfully with pulpotomy [27, 90]. Pulpotomy can certainly be considered as an intermediate treatment option in managing carious vital pulp exposures of permanent teeth with closed root apices serving as a substitute for extraction when root canal treatment for some reason cannot be performed [2]. Clinical testing comparing pulpotomy with conventional pulpectomy is needed for a complete assessment of the indications for this procedure.
9.10 Treatment Details for Pulp-preserving Techniques
General: Isolation by rubber dam, peripheral caries removal, and chemical surface disinfection is mandatory in all clinical situations with deep caries and/or when an exposure has already occurred. After surface disinfection, sterile instruments are used for removal of carious tissue and cavity preparation. Hemostasis must be obtained without a thick coagulum. This is usually achieved within 5 min. by rinsing with sterile saline or sodium hypochlorite. If hemostasis is not obtained, pulpectomy should be performed. Calciumhydroxideor calcium-silicate-based cements are used for capping as well as pulpotomy procedures, with a minimum thickness of 1.5 mm. A temporary or permanent filling placed under aseptic conditions completes the procedure. Clinical and radiographic follow-up is mandatory.
Stepwise excavation: After rubber dam isolation and surface disinfection, the super- ficial discolored and wet tissue (Figure 9.4c) is selectively removed to the extent that a temporary restoration can be made. Light and softened dentine is left under a calcium hydroxide base material followed by a glass- ionomer restoration (Figure 9.4c). After 8 to 12 weeks, the cavity is re-entered and the darker, harder, and drier dentine closer to the pulp is removed non-selectively with sterile excavators, leaving only dentine that is firm with a hardness comparable to sound dentine (Figure 9.4d). This process also eliminates the potential problem associated with shrinkage following arrestment of carious dentine, as the base of the cavity following second stage should not be able to shrink further, optimizing the interface between the permanent restoration and cavity.
Accidental or traumatic perforations (Class I): After rubber dam isolation and surface disinfection, the cavity and the perforation are gently rinsed with sterile saline to remove debris and to establish a clean and non- bleeding wound. Spraying of the exposure site as well as application of pressure by a cotton pellet may provoke hemorrhage. If hemostasis is not achieved after 5 minutes, the pulp-capping option is discarded and pulpectomy initiated. After placement of the capping material, the permanent restoration is placed, preferably immediately after capping but at any rate within days, as this improves the outcome significantly [5].
Capping of the cariously involved pulp (Class II): After rubber dam isolation and surface disinfection, carious tissue is removed with the guidance of a detector dye, and the use of loupes or an operating microscope as well as enhanced illumination is mandatory. Excavation continues until no dye is visible at the dentine margins of the exposure. No enlargement of the exposure site is attempted. After application of the capping material, it is covered by a glass-ionomer cement, followed by a bonded coronal restoration. A two-step procedure is recommended if necessary for clinical control of setting of the capping material. A case following the principles for a Class II pulp cap is shown in Figure 9.6.
Partial pulpotomy: After rubber dam isolation and surface disinfection, an end-cutting diamond operating at high speed with copious irrigation is used to remove approximately 2 mm of the underlying coronal pulp tissue. When the superficial pulp cutting is accom- plished and hemostasis is obtained, the proce- dure is identical to that used for pulp capping of a carious pulp exposure. See Figure 9.5.
Pulpotomy: After rubber dam isolation and surface disinfection, a sterile diamond bur in a high-speed hand piece under water spray is used to remove the entire coronal pulp tissue, with the amputation wound located at the orifice 1-2 mm into the root canal. For singlerooted teeth, the amputation wound should be placed in the cervical region 2-3 mm below the collar of the tooth. A paper point (blunt end toward the capping material) is a simple tool for compacting the capping material for proper placement and sealing of the material. A thickness up to 4-5 mm of the cement is desirable, if possible. A two- step procedure is recommended if clinical control of setting of the amputation material is needed, but may not be necessary [48]. A clinical case is demonstrated in Figure 9.7.
Figure 9.6 Clinical example of a Class II direct pulp capping. (a) Preoperative radiograph reveals a deep lesion and no apical pathosis. (b) After non-selective carious removal using the operating microscope, no carious dentine is retained, and hemorrhage is stopped. (c) The capping agent (MTA) is placed in increments. (d) Postoperative radiograph with permanent restoration in place (e) 1-year follow-up and (f) 2-year follow-up. Case courtesy of Dr Phu Le.
9.11 The Available Evidence for Relative Merit of Treatment Procedures for Vital Pulps
9.11.1 Scenarios for Multiple Outcomes and Follow-up Treatment
Based on published data, it is possible to make simulated scenarios for establishing a cost-effectiveness analysis of various vital pulp therapies [77]. Such an analysis does not improve on existing data but can expand our interpretation of them. In an example on the outcome of vital pulp treatment [77] a scenario was created by the following assumptions: (i) a deeply carious molar with a sensible, non-symptomatic (painless) pulp exposed during caries excavation, subjected to (ii) either direct pulp capping using calcium hydroxide or MTA followed by direct restoration, or root canal treatment (vital pulpectomy) with a cast coronal restoration. The carious lesion could be approximal as well as occlusal. Various potential scenarios were followed using a state transition diagram simulating the lifetime of such a tooth (Figure 9.8). Based on data collected before 2014, the model suggests that an optimal scenario for successful direct pulp capping is younger patients (< 40 yrs) with exposures occlusal in posterior teeth, whereas older patients (>40 yrs) with approximal exposures in anterior teeth represent the other extreme, where many cases more quickly needed endodontic treatment after complications.
Figure 9.7 (a) A 10-year-old girl presenting for endodontic treatment 4 days after emergency treatment of the lacerated lip with sutures, but no dental treatment. (b) Clinical and (c) radiographic examination showed a complicated crown fracture with (d) exposure of pulp horns (white arrow). The patient had an exaggerated non-lingering response to cold test and a positive response to electric pulp testing reflecting a diagnosis of reversible pulpitis. (e) After adequate dental dam isolation, approximately 3 mm of coronal pulp was removed with copious water spray with a diamond-coated bur. (f) A calcium silicate-based cement was placed immediately over the pulp tissue, followed by a layer of glass ionomer and a composite restoration. (g) After 1-year follow-up, the patient remained asymptomatic and the tooth responded to electric pulp test without any signs or symptoms of discoloration or (h) radiographic signs of apical pathosis. (i, j) Small-volume cone beam computer tomography (CBCT) revealed a dense mineralized zone. Case courtesy of Dr Anibal Diogenes.
Figure 9.8 State transition diagram illustrating the lifetime of a tooth with an exposed, sensible, non-symptomatic pulp given various event options.
Figure 9.9 illustrates a failed direct pulp capping (Class II) where capping of an approximal exposure, while technically well performed, resulted in pulpal necro- sis, infection and apical periodontitis. Given the poorer prognosis of treatment of established apical periodontitis compared to pulpectomy, the choice of capping the inflamed pulp in this case increased the cost and probably shortened the life span of the tooth.
9.11.2 Strategies for Obtaining Optimal Clinical Evidence
Treatment options for pulps affected by well-defined deep caries are stepwise caries removal or direct pulp capping, partial or full pulpotomy, or pulpectomy. For extremely deep carious only pulp invasive tretaments are recommended. Current evidence point to a more conservative approach in the sense that the pulp may survive the less invasive techniques better than previ- ously thought. Further evidence for selection of the appropriate technique must rely on data from carefully performed clinical studies, preferably with a randomized design. Important aspects in designing such trials include well-defined inclusion criteria; e.g. a better definition of lesion size and lesion activity may lead to more accurate data analysis (Table 9.2, Figure 9.10); power calculations for sample size estimation; central randomization; and unbiased, i.e. blinded recording of outcome.
Figure 9.9 Clinical example of a Class II direct pulp-capping procedure (male, 48 years). (a) Preoperative radiograph reveals a deep lesion and no apical pathosis. (b) Carious tissue removal shows that the lesion is located deep down at the approximal site. (c) An small build-up filling is placed at the margin to facilitate asepsis. (d) A bleeding exposure is noted. (e) Hemostasis is about to be reached. (f) Application of calcium silicate cement. (g) After 3 months, the patient presents with a sinus tract and apical periodontitis. (h) An immediate postoperative radiograph of completed root canal treatment. Case courtesy of Dr Pim Buurman.
9.11.3 Lack of Standardization in Clinical Trials
Table 9.3 is a list of recent, randomized clinical trials covering the topics presented in this chapter. Although these studies were not meant to be compared, they all have the same inclusion criteria: a deep carious lesion and signs of reversible pulpitis. However, the treatments vary from pulpotomy to indirect pulp capping and stepwise excavation, reflecting that no global consensus or tradition as yet dominate the choice of treatments of vital pulp therapy. Moreover, details vary widely even when the treatment is supposedly the same, indicating the need for more standardization for the performance of clinical trials.
Table 9.2 Carious dentine status and prognosis following a pulp-preserving treatment.
|
Clinical signs of dentine surrounding a pulp exposure |
Prognosis following a direct pulp capping Class II in relation to carious activity status of suggested event |
|
Soft, wet, and yellowish discolored dentine |
+ ( Performed in relation to a deep or extremely deep carious lesion) |
|
Firm, dry, and dark discolored dentine |
++ (Performed after second stage during stepwise excavation) |
|
Hard, dry, and gray dentine |
+++ (Performed in medium-sized lesion or as an iatrogenic exposure (pulp horn)) |
Figure 9.10 Clinical criteria for inclusion in trials. More precise data of the lesion environment that is going to be capped will lead to a better platform for inclusion criteria into trials, hence a better interpretation of data (a) Carious tissue removal in a lesion with signs of arrested lesion activity, reflecting a darker and more firm appearance of dentine. (b) When pulp exposure takes place the prognosis has been reported to be better than for exposures under an active lesion environment with a much lower level of infection than an active lesion environment [51]. Case courtesy of Dr Miguel Marqeus.
9.11.4 Choice of Capping Materials
Even though some studies suggest a histologically better response beneath MTA compared with calcium hydroxide, (i.e. a more homog- enous dentine bridge and less or no inflammation) [87] and clinical cohort studies also favor MTA [62], calcium hydroxide is still considered suitable for successful pulp preserving treatments. Several studies have failed to show a significant difference between the two types of capping agents. It appears that the size of the exposure is more important than the choice of capping material [22]. A randomized, multicenter practice-based study designed to reflect better the real clinical situation also did not find a significant difference in treatment outcome with the two materials, although, again, the tendency was for MTA to give better results [38].
Adherence to protocol and the establishment of a bacteria-free cavity and pulp wound is probably a key issue [20, 24], and the translation of this basic knowledge to clinical practice is probably the greatest challenge.
9.11.5 Status of Current Clinical Evidence
Data may be collected from all levels of the evidence pyramid, from simple case series to cohort and comparative studies of varying quality. However, of the many randomized, controlled clinical trials in humans (Table 9.3) comparing different capping materials, several may be underpowered, which makes inferences to clinical practice questionable [43, 46, 84]. In addition, an adequate randomization procedure is not always done, but is critical for adequate interpretation of the intervention effect [34]. Even well-designed randomization procedures run the risk of ending with case characteristics (in casu, lesion depths) having an uneven distribution between the groups tested. [50]. Thus high- level, scientific recommendations can hardly be made for proper choice of capping materials based on current studies [73].
Table 9.4 is a suggested cross-tabulation relating each intervention procedure to its current level of evidence.
Table 9.3 Examples of randomized clinical trials of capping agents and pulp-preserving interventions.
|
Jang et al. 2015 [43] |
Kang et al. 2015 [46] |
Hashem et al. 2015 [37] |
Bjorndal et al. 2017 [11] |
|
|
Study material |
||||
|
Teeth |
Permanent |
Deciduous |
Permanent |
Permanent |
|
Caries |
y & n |
y |
y |
y |
|
Pulp status |
Reversible pulpitis |
? |
Reversible pulpitis |
Reversible pulpitis |
|
Age |
>19 yrs |
3-10 yrs |
Median 28 yrs |
Median 29 yrs |
|
Trial |
||||
|
Intervention |
15% |
? |
20% |
20% |
|
Power |
80% |
? |
80% |
90% |
|
Group size |
23 |
47 to 48 |
36 |
156-158 |
|
Material |
ProRoot MTA vs Endocem |
ProRoot MTA vs OrthoMTA vs RetroMTA |
Glass ionomer vs Biodentine |
Dycal/Ketac cem |
|
Variable |
Age; occlusal vs axial surface |
— |
Cavity size; CBCT |
Procedure |
Table 9.3 (Continued)
|
Jang et al. 2015 [43] |
Kang et al. 2015 [46] |
Hashem et al. 2015 [37] |
Bjorndal et al. 2017 [11] |
|
|
Protocol |
||||
|
Indirect pulp capping |
x |
|||
|
Stepwise excavation |
x |
|||
|
Immediate capping |
x |
x |
||
|
Pulpotomy |
x |
|||
|
Outcome assessment |
||||
|
Observation time |
1 yr |
1 yr |
1 yr |
5 yrs |
|
Pulp test |
x |
x |
x |
x |
|
Radiography |
a |
a |
x |
x |
|
Clinical pulpal diagn |
a |
a |
x |
a |
|
Outcome variable |
||||
|
Material |
nsd |
nsd |
nsd |
|
|
Method |
CBCT more sensitive |
|||
|
Treatment procedure |
Stepwise better than immediate |
|||
|
Other |
axial cavity worse |
|||
a: moderate precision of registration nsd: no significant difference
Table 9.4 Cross-tabulation of treatments and diagnostic factors with estimation of evidence when applicable (++ treatment comparison RCT-based), (treatments observation-based +).
|
Diagnostics factors |
|||||||
|
Treatments |
Sound dentine (trauma) |
Age young |
Age old |
Radiograph deep carious lesion (pulpa 1/4) |
Radiograph Extremely deep carious lesion (pulpa 4/4) |
Reversible pulpitis |
Irreversible pulpitis |
|
Direct pulp capping Class I |
yes(+) |
yes |
yes |
no (++) |
no |
yes |
no |
|
Direct pulp capping Class II |
no |
yes |
yes |
yes (+) |
yes (+) |
yes |
no |
|
Partial pulpotomy |
yes (+) |
yes |
no |
no (++) |
no |
yes |
no |
|
Pulpotomy |
yes |
yes |
yes |
? (+) |
? |
yes |
yes |
|
Stepwise excavation |
— |
yes |
yes |
yes (++) |
no |
yes |
no |
|
Indirect pulp capping (ad modem Kerkhove et al.) |
— |
yes |
yes |
yes (+) |
no |
yes |
no |
|
Partial excavation/ selective carious tissue removal. |
— |
yes |
? |
? |
? |
yes |
no |
9.12 Future Perspectives of More Advanced Biological Approaches
The cells involved in dentinal repair of repar- ative type are often described as secondary odontoblast-like cells, and they originate from differentiated stem cell/progenitor cells. These cells can be expressed in various places (niches) around the pulp and are typically associated with blood vessels [36]. Thus, repair processes are not restricted to the area close to the original dentine, and the ubiquitous presence of these cells explains why both a superficial pulp capping as well as a deeper pulpotomy can be carried out with a successful dentine bridge formation. How ever, it is still unclear exactly which cells of the stem cell/progenitor cell populations actually participate in dentinal repair [35]. These cells express numerous mesenchymal and embryonic cell markers, reflecting a variation in the stem cells/progenitors in the pulp [83]. In short, more research is needed before clinical practice can truly benefit on a larger scale.
Improved information on the origin of cells involved in dentinal and pulpal repair will obviously guide the content of future treatment protocols on revitalization and regenerative endodontic procedures, including techniques and materials for pulp capping and pulpotomies (see Chapter 10).
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