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Vital Pulp Treatment Modalities: The Management of Deep Caries Using Selective and Non‐Selective Removal of Carious Tissue, Stepwise Excavation and Indirect Pulp Capping
Helena Fransson1 and Lars Bjørndal2
1 Department of Endodontics, Faculty of Odontology, Malmö University, Malmö, Sweden
2 Cariology and Endodontics, Section of Clinical Oral Microbiology, Department of Odontology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Introduction
When you first become a dentist and perhaps later pursue a career within a specialty, you are or should be in your comfort zone. You are supposed to make qualified judgements and decisions and carry out the treatments that are expected and evidence‐based. You are an expert in the field. However, acquired expertise is not permanent as the considered best choice of treatment for a given health state may change over time, perhaps due to the impact of new research or a change in the demographics of the population. Within endodontics, the tradition has been to address two main domains: the exposed vital pulp or the infected, necrotic root canal system associated with apical periodontitis. In short, the prevention or treatment of apical periodontitis has been the focus of endodontics. The question arises as to how far back in the disease development we would like to go to prevent apical periodontitis. Does it include excavation of carious tissue in order to prevent pulp exposure?
Often, pulp inflammation has been described without the associated cause (1). In this chapter, we will focus on caries being the cause of inflammation, as it is one of the main indications for endodontic treatment (2, 3). An insight into the dynamics of the pulp inflammation due to progressing stages of caries is presented. Instead of simply presenting a case with a deep carious lesion being the cause of further treatment, it seems relevant to describe the carious lesion in more detail. Is it possible to introduce a threshold for deciding on the need for an invasive pulp treatment, or would the prognosis of the tooth be improved if pulp exposure was avoided?
It is perhaps the norm that dentists limiting their practice to endodontics only receive referrals on root canal treatments that often have already been initiated; perhaps an emergency treatment has been performed or attempts to negotiate the root canals have been made. It is tempting to suggest that these dentists rarely perform primary carious‐tissue removal close to the pulp, even though such a dentist should have extensive theoretical knowledge about the pulp and its healing capacity. However, there is a trend within the endodontic field that dentists and endodontists should also have knowledge on the treatment when pulp exposure should be avoided. This is important not only for pre‐ and postgraduate students but also for the trained endodontist in educating and training general dentists.
The development and updating of clinical guidelines are examples of ways to help dentists to keep up with any changes regarding established treatments and to inform about potential new treatment concepts. In this chapter, recently updated publications on evidence and guidelines on the treatment of deep carious lesions will be included. From the perspective of a general dental practitioner, this should form part of being an engaged and motivated dentist. It is, however, a difficult task to implement new knowledge and change the behaviours or traditions related to treatment. At the beginning of this chapter, we will present the treatment modalities as well as the indications based on a pragmatic subdivision of an extensive carious lesion into three classes.
Vital Pulp Treatment Modalities Aiming Not to Expose the Pulp
Based on understanding the biological concepts behind treatment recommendations, the goal is to provide the reader with tools to adopt a minimally invasive approach, such as the vital pulp treatments in teeth with well‐defined deep carious lesions, as outlined in Table 4.1.
Table 4.1 Definitions of the vital pulp treatment modalities presented in this chapter were modified after a position paper from the European Society of Endodontology (4).
Source: Adapted from the European Society of Endodontology.
Treatment | Definition |
---|---|
Non‐selective caries removal | Complete removal of soft and firm carious dentine from the periphery and central aspects of the cavity until hard dentine is reached |
Selective caries removal | A collective name for several treatments: selective caries removal in one‐stage and stepwise excavation |
Selective caries removal in one‐stage | Application of a biomaterial onto a dentine barrier in an indirect one‐stage selective carious‐tissue removal technique. Removal of soft or firm dentine. Immediate placement of a permanent restoration |
Stepwise excavation | Application of a biomaterial in an indirect two‐stage selective carious‐tissue removal technique. Temporary restoration placement between visits and re‐entry after 6–12 mo. The first stage involves selective carious removal to soft dentine to the extent that it facilitates proper placement of a temporary restoration, and the second stage involves removal to firm dentine – the final placement of a permanent restoration |
Indirect pulp capping | Application of a biomaterial onto a thin dentine barrier in a one‐stage carious‐tissue removal technique generally to hard dentine. Leaves neither soft nor firm carious dentine behind. Considered more aggressive than selective carious‐tissue removal in one‐stage and stepwise excavation. However, if the excavation is successful, pulp exposure is avoided. The problem is that the frequency of unintended exposures will be more frequent than for selective caries removal in one‐stage or stepwise excavation |
Indications – A Pragmatic Subdivision of Extensive Carious Lesions
For the management of extensive carious lesions, the clinical dilemma is obvious, as the presence of infected dentine is not an objective clinical measure. Concomitantly, it is not possible to monitor the degree of pulpal inflammation at the chairside based on the patient’s symptoms or other clinical findings (5). So what is meant by a ‘deep carious lesion’. The traditional wording of ‘complete’ and ‘partial’ removal of carious tissue is not precise and has unclear elements, and you may speculate on what is actually meant when the words are used. Is it the partial removal of microorganisms or demineralized dentine?
The International Caries Consensus Collaboration have carried out a comprehensive qualitative analysis of the nomenclature for excavation and treatment options, attempting to simplify the topic and making it more suitable for dental practice (6, 7). This practice‐based terminology on carious‐tissue removal is based on the features of the carious tissue and presented in Figure 4.1 (8).
The common subdivision of caries diagnoses in thirds, denoting caries superficialis, media and profunda is a widely accepted terminology (9). However, for extensive carious lesions, the diagnosis caries profunda can further be subdivided into three classes, which could be related to evidence‐based treatments (10).
Caries Profunda 1
Radiographic features: This stage is defined as a lesion penetrating 2/3–3/4 of the dentine, with a radiopaque zone separating the advancing front of the lesion and the pulp.
Histologic features: Microorganisms are located in the carious dentine. Evidence of chronic pulp inflammation, but not associated with invasion of microorganisms into the pulp cavity (Figure 4.2).
Recommended treatment: Selective carious removal in one step to either soft or firm dentine (Figure 4.3e–h). This particular lesion class is most often treated with a selective caries removal strategy (11–13).
Caries Profunda 2
Radiographic features: This stage, described as deep caries, is defined as a lesion penetrating 3/4 or more of the dentine, but still with a radiopaque zone separating the advancing front of the lesion and the pulp.
Histologic features: Microorganisms are located in the carious dentine. Evidence of chronic pulp inflammation with a low probability of the presence of invading microorganisms in the pulp cavity (Figure 4.2).
Recommended treatment: Stepwise excavation (Figure 4.3a–d). Evidence for selective carious removal in one step to either soft or firm dentine is available but mainly based on children and adolescent patients. See also Table 4.1 (13).
Caries Profunda 3
Radiographic features: This stage, described as extremely deep caries, is defined as a lesion penetrating the entire thickness of the dentine without a radiopaque zone separating the advancing front of the lesion and the pulp.
Histologic features: Microorganisms are located in the carious dentine, tertiary dentine and within the pulp cavity. The pulpal status includes severe inflammation associated with partial or full necrosis in the pulp cavity (Figure 4.2).
Recommended treatment: Pulpectomy or root canal treatment. Pulpotomy including partial pulpotomy may also be considered, but comparative studies with longer follow‐up are lacking (14–16).
Understanding Caries Pathology – A Reason to ‘Dare’ Leaving Carious Dentine Behind
The Non‐cavitated Enamel‐Dentine Lesion
Dental tissues represent a unique entity that, over a lifetime, sustains its physiological properties despite a multitude of various external stimuli and/or injuries affecting the tooth surface. The enamel layer is not considered a tissue but a secretory product from past ameloblast cells that have laid down a matrix that is systematically packed with rod and inter‐rod enamel. Ultrastructurally, these enamel crystals are oriented in different directions. The enamel layer is not a solid barrier but allows for a transportation route along the direction of the enamel crystals, making it possible to transfer external stimuli from the periphery of the enamel into the dentine in an exceptionally organized manner. On this basis, the early topographic signs of carious enamel demineralization (the ‘white spot lesion’) is considered a time‐dependent development (17, 18). The reason for the 3D configuration with the cone‐shaped approximal enamel lesion is due to a time difference between the central versus the peripheral parts of the enamel. That is, the central and deepest lesion penetration reflects the oldest part of the lesion, where the cariogenic biofilm has been located for the longest time. This is seen subjacent to the approximal contact area, whereas the peripheral part can be interpreted as the youngest lesion front, hence the site of the youngest biofilm accumulation (19).
As the lesion progresses towards the enamel–dentine junction, there is a notable early response from the dentine–pulp complex. In fact, even before the demineralization has reached the enamel–dentine junction, it has been suggested that cells in the odontoblast‐predentine region, including the subodontoblastic cells, respond to noxious stimuli (20, 21). This demonstrates that the enamel should not be seen as an absolute physical barrier.
As the non‐cavitated enamel lesion develops closer to the dentine, the next reaction is initiated with the mineral content increasing within the dentinal tubules. Many of the thousands of dentinal tubules with their finger‐like projections will respond to an early cariogenic stimulus, but when the odontoblast cell responds, it may resemble an accelerated ageing process. This process is restricted to a local area subjacent to the enamel lesion. Notably, at this non‐cavitated stage of lesion penetration, no pH drop has created dentine mineral loss yet, making it plausible that the early dentine mineral increase seen within the dentinal tubules could be related to a cellular reaction and not purely a chemo‐physical reprecipitation of dissolved mineral.
When the demineralized enamel reaches the enamel–dentine junction, the first clinical visible signs of dentine mineral loss appear as a yellow‐brownish discolouration of the dentinal matrix. Evidence indicates that as long as there is an intact rod‐/inter‐rod structure separating the surface biofilm aligning the enamel from the dentine, the number of microorganisms reaching the dentine does not have as significant influence on the severity of caries progression. Although studies show early invaders of microorganisms into subjacent dentine even in non‐cavitated enamel (22, 23), such patterns do not represent the typical microbial spread into carious dentine, being more likely associated with a gradual breakdown of the enamel layer (24, 25). From this, it is understood that the odontoblast cells respond to a very shallow carious lesion by trying to defend the pulp from penetrating bacterial products.
As the growth of the enamel lesion extends laterally, the peripheral and less advanced aspects eventually reach the enamel–dentine junction, repeating the sequence of events, developing a hypermineralized/translucent zone and demineralizing dentine (19).
Overall, the progression of the enamel–dentine lesion takes place from the enamel surface and is guided along the enamel rods.
As the extent of dentine demineralization increases, it is suggested that bioactive dentine matrix components fossilized in the primary dentine matrix during development are released and participate in the tertiary dentinogenesis process (26).
Notably, even before many microorganisms have invaded the dentine, a rather complex series of pulp‐dentinal responses have occurred without any severe pulp inflammation.
The Approximal and Occlusal Cavitated Carious Lesion
The microbiological ecosystem within the carious lesions penetrates deeper and deeper as the demineralized enamel breaks down. A cavity is eventually formed, mainly due to the forces from mastication. The characteristics of the cavitated enamel lesion where the dentine is clinically exposed comprise several ecologically important elements:
- The dentine is invaded by a significant number of microorganisms.
- The possibility of cleaning and removing the cariogenic biofilm is compromised, leading to an undisturbed progression, a so‐called ‘closed’ ecosystem (27).
- The focus of a microbial spread is no longer from the enamel surface along the microstructures of the enamel layer but spreads into the dentinal tubules as well as the gap created at the enamel–dentine junction due to shrinkage of the demineralized dentine, also described as retrograde demineralization (Figure 4.2).
- In untreated extensive occlusal lesions, the undermined enamel breaks down; the growth condition for the biofilm may then change considerably, creating a so‐called ‘open’ lesion environment showing temporary signs of caries arrest (Figure 4.4).
Additional consequences of the above changes are that when microorganisms invade the dentine, it is always with a zone of non‐infected demineralized dentine ahead, both at the lateral front as well as in the advancing central front. Unfortunately, it has long been a clinical dilemma to define the border where the infected dentine ends and the demineralized but non‐infected dentine begins. More than 50 years ago, Fusayama and co‐workers (28, 29) carried out a series of studies trying to characterize the infected versus the affected zones of carious dentine, providing more evidence to the concept of leaving affected dentine behind. The innermost affected dentine, although having altered consistency, did not need to be removed, as it had the potential to remineralize (30). In addition, the concept of separating the excavation procedure into two stages in teeth with deep carious lesions raised the understanding about the possibility of leaving infected dentine in the most pulpal part of the cavity and sealing the cavity with a restoration. Bacterial samples from the carious dentine indicated a clear reduction in the infection status just by a superficial removal of infected dentine (31). In other words, changing the cariogenic environment without completely removing all infected carious dentine and restoring the tooth with a well‐placed ‘tight’ seal has proven to be an accepted treatment concept for initiating arrestment of the carious lesion. During this process, the carious dentine darkens markedly through the Maillard reaction (32).
The extent of bacterial invasion into the pulp cavity has been illustrated by the classical study by Reeves and Stanley (33), showing that when the microorganisms enter the innermost tertiary dentine, there were histological signs of severe pulp inflammation, considered irreversible. However, in a clinical context, it has been unclear when exactly this could occur during excavation. In other words, this classical study did not study a correlation between the radiographic depth of the carious lesion and the degree of bacterial penetration. Recently, a combined analysis of the microbial profile in two well‐defined extensive stages of carious lesion formations provided some insights concerning the threshold when microorganisms can be present in the pulp cavity and, thus, the need for a more invasive approach than any selective removal (34).
Cavitated Deep and Extremely Deep Carious Lesions
As the carious lesion progresses, the infected advancing front also progresses, but typically with an innermost zone of demineralized dentine without microorganisms. Based on a sample of freshly extracted teeth, the bacterial penetration is confined to primary dentine in well‐defined deep lesions without reaching the pulp, as shown in Figure 4.5.
In summary, a deep carious lesion in the pulpal quarter with a radiopaque zone separating the lesion from the pulp tends to have no bacteria. It is without signs of necrosis or severe inflammatory infiltrate. In contrast, severe inflammatory infiltrates and partial necrosis are typically seen in teeth with deep carious lesions with no radiopaque zone separating the lesion from the pulp. Moreover, the pulp inflammation is often located in the coronal part of the pulp, indicating that even in severely infected pulp cavities, the radicular pulp can appear without histological signs of inflammation.
Untreated carious lesions change their ecosystem over time, and it is recognized that the growth condition for the cariogenic biofilm may change dramatically. As described above, a temporary clinical arrest of lesion activity can take place due to a sudden breakdown of undermined enamel and the creation of a much more open environment (Figure 4.4a–e); the open exposed dentine becomes darker and also harder (35). The darkening of exposed carious dentine is also a very familiar sign in root carious lesions (36, 37). Histologically, the inflammatory infiltrates may still be present but accompanied by the formation of tertiary reactionary dentine formation.