Managing the Exposed Pulp
2.3.3.1 Direct Pulp Capping
2.3.3.2 Partial Pulpotomy
2.3.3.3 Full Pulpotomy
2.3.3.4 Pulpectomy
2.3.4 Immature Roots
2.4 Materials Used in Vital Pulp Treatment 2.4.1 The Role of the Material 2.4.2 Calcium Hydroxide 2.4.3 Resin‐Based Adhesives 2.4.4 Hydraulic Calcium Silicate Cements 2.4.5 Resin‐Based Hydraulic Calcium Silicate Cements 2.4.6 Glass Ionomer Cements 2.4.7 Experimental Agents Used in Vital Pulp Treatment 2.4.8 Tooth Restoration After VPT
2.5 Clinical Outcome and Practicalities 2.5.1 Vital Pulp Treatment Outcome 2.5.2 Discolouration 2.5.3 Setting Time and Handling
2.1 Introduction
Preserving the health of the dental pulp, or at least part of it, is important when treating a vital tooth with a deep unexposed cavity or exposed pulp, particularly if the root formation is incomplete. There is a long tradition of treating deep cavities and exposed dental pulp by performing procedures such as pulp capping and partial and complete pulpotomy. An improved understanding of the regenerative capacity of the dentine–pulp complex and the introduction of new hydraulic calcium silicate cements (HCSCs) has stimulated a new wave of research and treatment strategies in this area. The aim of this chapter is to evaluate the pulpal healing response, the range of vital pulp treatment (VPT) procedures, and the nature of the materials employed in the management of deep caries and exposed pulp.
2.2 Maintaining Pulp Vitality
2.2.1 Why Maintain the Pulp?
Maintaining healthy pulp tissue is preferable to root canal treatment (RCT), which can be complex, destructive, time‐consuming, and expensive for both patients and clinicians. Preserving all or at least part of the dental pulp is important after pulp exposure, especially when the tooth is immature and root formation is not yet complete [1]. The need for a more conservative approach to management of the inflamed pulp is a more biologically based and minimally invasive treatment strategy compared with pulpectomy and has recently been encouraged in editorials and position statements [1, 2]. Besides reducing intervention, this biological concept also maintains pulp developmental, defensive, and proprioceptive functions [3, 4]; VPT is generally considered technically easier to execute than RCT [5]. From a longitudinal perspective, advocating less aggressive dentistry reduces overtreatment and limits the ‘restorative cycle’ concept [6], whilst also improving the cost‐effectiveness of treatment [7]. Finally, with the surge in research and interest in regenerative endodontics [8], biomaterial developments [9], and the need to therapeutically utilize dental pulp stem cell (DPSC) populations [10], VPT has reemerged as an area of significant interest to both patients and dentists [11].
2.2.2 Pulpal Irritants
Although the pulp can be challenged by microbial, mechanical, and chemical stimuli, necrosis will not result without the presence of microorganisms [12]. Caries has traditionally been considered the principal cause of pulpal damage, and although falling in prevalence, it is now manifesting more commonly in disadvantaged and elderly populations [13–15]. Whilst inflammation of the pulp is evident even in shallow carious lesions [16, 17], it is not until the carious process is deep and comes within 0.5 mm of the pulp that the pulpitic response significantly intensifies [18]. As a result, before it reaches this stage, the damage is likely to be reversible. This forms the basis of predictable operative dentistry, in that the pulp should recover after removal of carious dentine and insertion of a suitable dental restorative material [19]. Microbial challenge, however, is not limited to caries, as bacterial microleakage is also a common cause of pulpitis and subsequent necrosis due to oral microorganisms colonizing the ‘gap’ between the restoration and the tooth [20]. Prevention of microleakage using lining material is no longer considered good practice [21], but dentine bonding agents and incremental placement of resin‐based composites will reduce the risk of bacterial colonization [22], particularly if there is sufficient residual dentine thickness (RDT).
Views on the irritant effect of dental materials on the pulp have changed over the last 50 years. The idea that their toxicity to pulp tissue leads to pulpal necrosis has been questioned by several operators [20, 23, 24], who point to microbial contamination and leakage as the decisive factor in sustained pulpal inflammation. That said, there is also good evidence to suggest that some materials are more biocompatible and ‘pulp‐friendly’ than others, with the adverse toxic effects of dental resins on pulp cells being repeatedly highlighted [25, 26]. Alternatively, the positive biological responses of HCSC [9] have led to recent suggestions that deep carious lesions should be lined with HCSC after deep caries removal [27]. Other nonmicrobial irritants such as bleaching procedures, particularly chairside ‘power’ techniques, can lead to rises in pulpal temperature and pulpitis [28]; however, whilst these are increasingly common as treatment strategies, the pulpal changes seen are generally reversible and are not catastrophic in nature [29, 30].
2.2.3 Pulpal Healing After Exposure
The odontoblast cell is responsible for forming primary dentine during tooth development, the more slowly deposited secondary dentine throughout the life of the tooth, and, when ‘irritated’, tertiary dentine in the pulp tissue adjacent to the source of challenge [31]. Dependent on the stimulant severity, tertiary dentine deposition can be either reactionary or reparative (Figure 2.1) [32]. Reactionary dentine is formed by an upregulation of existing odontoblast activity when the dentine–pulp complex is exposed to a relatively mild stimulus (e.g. shallow or slowly progressing carious disease process), whilst reparative dentine is formed generally after a stronger stimulus has led to odontoblast cell death (e.g. deep caries or traumatic exposure) [32, 33]. At a cellular level, reparative dentine is believed to be produced following cytodifferentiation of pulpal progenitor cells (DSPCs or other progenitor cells) and the formation of a new generation of odontoblast‐like cells [1, 32, 33]. Although this description of reparative dentinogenesis represents the currently accepted theory, others have highlighted the influence of other cells such as fibroblasts or fibrocytes as secretory cells [34, 35]. The cellular differentiation is guided by the influence of growth factors and other bioactive molecules released from both the dentine matrix and the
