5
Vital Pulp Treatment Modalities: Direct Pulp Capping
Till Dammaschke
Department of Periodontology and Operative Dentistry, University of Münster, Münster, Germany
Is Exposing the Pulp a Problem? An Introduction
As early as 1756, Philipp Pfaff (1713–1766; Royal Prussian Court Dentist to Frederick the Great) recognized that the vitality of the dental pulp could be preserved after exposure by providing it with a small cap made of thin gold foil (1). In the absence of suitable expertise for root canal preparation and obturation, interest in such treatment measures was high, and they were widely used, as the only alternative to maintaining pulp vitality was usually extraction of the tooth to relieve pain. In the following centuries, attempts were made to preserve pulp vitality under all circumstances, and as a result, a plethora of different materials and methods for direct pulp capping were propagated. Unfortunately, these methods were often not suitable for successfully maintaining pulp vitality and were usually doomed to failure (2). Therefore, in 1922, Hans‐Hermann Rebel (1889–1967) formulated his doctrine: ‘An exposed pulp is a lost organ’ (3). Some years later, around 1930, Bernhard W. Hermann (1884–1954) introduced calcium hydroxide as an agent for maintaining pulp vitality and was able to prove histologically that vital pulp treatment (VPT) can be successfully performed using this material if the indication is correct (4, 5). Nevertheless, the doctrine formulated by Rebel a hundred years ago has persisted even today so that some dentists are of the opinion that exposure of the pulp tissue must be avoided at all costs, and it is, therefore, preferable to leave carious dentine in the cavity beneath the filling. Furthermore, many possess the opinion that – if pulp exposure does occur – vital extirpation and root canal treatment are unavoidable.
Both doctrines have been proven not to be true. It is now known that the principle of wound healing at the pulp is no different from that of other tissues of the body. Wound healing is always the programmed response of the host to an injury. The goal is to regenerate or repair the tissue (6). Thus, there has been an encouraging renaissance of interest in VPT. The purpose of direct pulp capping is to protect the pulp tissue and stimulate new hard tissue formation through an appropriate wound dressing. This should preserve the vitality of the tooth (7, 8).
It is well known that teeth can be preserved in the long term by adequately performing root canal treatment. For example, several years ago, the so‐called ‘Toronto study’ showed that in teeth with apical lesions, the success rate four to six years after root canal treatment was 79% and without initial apical lesions (e.g. after vital extirpation) 93% (9). However, one problem with root canal‐treated teeth is that a non‐vital tooth can be loaded with more than twice the masticatory force compared with a vital tooth before the proprioceptors respond (10, 11). This means that root canal‐treated teeth do not register foreign bodies in food, for example, until they bite down harder, which in the long term can lead to mechanical overload and fracture of the tooth. Other problems that can occur after root canal treatment include increased susceptibility to caries due to increased plaque accumulation and altered microflora (12) and tooth discolouration (13). Root canal treatment may also prove to be more complex than initially anticipated, which may affect the success of the treatment. If the initial root canal treatment is unsuccessful, a more complex procedure (re‐treatment or apicectomy) may be required to save the tooth (14, 15).
In contrast, direct pulp capping is a non‐invasive, comparatively simple technique that can be performed with a significantly lower expenditure of time than root canal treatment, does not entail costly restorations and is, therefore, cost‐effective (16). In addition, the vital pulp offers the best protection against the invasion of microorganisms into the root canal system. When correctly indicated and performed, direct pulp capping is associated with high success rates comparable with root canal treatment (14, 15).
Management of Traumatic and Iatrogenic Pulp Exposures
The pulp can either be exposed during caries excavation or as a consequence of trauma. In the case of dental trauma, the enamel and dentine can be fractured by the application of force, so that the pulp tissue is exposed (Figure 5.1). These so‐called ‘complicated’ crown fractures predominantly affect caries‐ and restoration‐free teeth of juvenile patients. Therefore, the dentine around the exposure area is free of microbial colonization (17–19). The same applies when the pulp is exposed by the removal of sound dentine during operative procedures, the so‐called iatrogenic exposure of the dental pulp (20). In both cases, the prognosis of direct pulp capping can be considered good, since the existence of a ‘healthy’ pulp that has not been damaged by caries and is therefore capable of regeneration can be assumed (18, 19). In the case of trauma with additional dislocation injuries, however, the situation may be aggravated by the fact that the blood supply and thus the defence capability of the pulp tissue of the fractured tooth is compromised (21).
Figure 5.1 Tooth 21 with a complicated crown fracture after trauma, resulting in exposure of the pulp. The prognosis of direct pulp capping can be considered good, since the tooth is caries‐free and there were no microorganisms in the dentine and near the pulp before the trauma.
Preparation of cavities or crowns could also lead to an exposure of dentinal tubules, so direct access for bacterial toxins to the pulp is created without exposing the pulp tissue itself (20). In adolescents, an additional complication is that the dentine‐pulp complex is even more susceptible to microbial contamination due to the presence of very wide dentinal tubules (17).
If saliva and, thus, microorganisms from the oral cavity penetrate the portion of the crown pulp exposed by trauma or iatrogenically, the pulp tissue must be considered microbially contaminated. The depth of this contamination correlates with the duration of exposure of the pulp tissue to the oral cavity. The longer the exposed area remains unattended, the deeper the microorganisms penetrate into the pulp tissue. Therefore, in both cases, i.e. after traumatic as well as iatrogenic exposure of the pulp, VPT must be performed as quickly as possible (17).
It is known from animal experiments that traumatic or iatrogenic pulp exposure leads to superficial alterations in the pulp tissue (22), but the microbial contamination after an exposure time of 2 hours to a maximum of 24 hours can be classified as low, so direct pulp capping is still possible (23, 24). In the case of a longer pulp exposure time of up to seven days, an infection or inflammation to a depth of approximately 2 mm can be assumed (18, 19). In this case, direct pulp capping is no longer indicated. Instead, a partial or complete pulpotomy must be performed (see Chapter 8. Vital Pulp Treatment for Traumatic Dental Injuries). In general, however, partial pulpotomy after trauma has a higher certainty of success than direct pulp capping and is, therefore, to be favoured in these cases.
With regard to tooth survival, higher success rates are generally reported in the literature for direct pulp capping in these teeth compared with carious teeth, since there has presumably been no or only minimal contamination of the pulp tissue with microorganisms prior to capping (17, 25). Thus, iatrogenic exposure of the pulp in caries‐free dentine or after tooth trauma provides ideal conditions for VPT in most cases and should not be reserved only for children and adolescents (18, 19).
In contrast, caries invasion of the pulp leads to microbial infection of the pulp, resulting in pulp inflammation (26). As a result, the pulp has a reduced capacity to respond and heal compared with mechanical exposure, where there is no pre‐existing inflammation (25).
Indications for Direct Pulp Capping
The basic prerequisite for successful VPT is vital pulp tissue that is capable of regeneration. The problem is that the exact condition of the pulp is difficult to determine clinically (27). In most cases, a textbook distinction is made between reversible and irreversible pulpitis. This clinical diagnosis is based on objective but also subjective findings. According to the definition, in reversible pulpitis, the inflammation is assumed to subside and the pulp should return to normal. In irreversible pulpitis, the vital pulp has a high level of inflammation that is not compatible with healing (28).
Clinically, reversible pulpitis is characterized by pain that is tied to a stimulus. The painful tooth can be localized by the patient, and the sensibility test is positive (29). Histologically, there are moderate signs of inflammation, migrated lymphocytes and plasma cells, hyperaemia, a decrease in cell count, odontoblasts appear flatter and most importantly, no or hardly any bacteria in the pulp chamber. In contrast, in irreversible pulpitis, irritation stimulated, sustained pain or even spontaneous pain, pain on heat, with the offending tooth not clearly locatable by the patient. The sensibility test is positive, which makes diagnosis difficult for the dentist. Histologically, there are signs of inflammation with polymorphonuclear neutrophilic granulocytes, micro‐abscesses and even partial necrosis caused by bacteria that have already invaded the pulp chamber (30).
The presence of microorganisms in the pulp tissue is decisive for whether pulpitis can heal (reversible) or not (irreversible). However, this cannot be readily determined clinically, as irreversible pulpitis can be clinically asymptomatic in 14–60% of cases (29, 31). Thus, in pulpitis, the histologic findings frequently deviate from the clinical picture. Thus, in 15.6% of cases, the clinical and histological diagnosis do not coincide (30). In other histological examinations, a discrepancy between clinical and histological findings could even be shown in 60–80% of cases, i.e. pulpal changes were clinically underestimated (‘hypodiagnosis’) (32, 33).
The clinical classification of the symptoms into reversible and irreversible pulpitis, therefore, says little about the actual regenerative capacity of the tissue and is therefore increasingly questioned (27). It merely facilitates the treatment decision for the practitioner, as a schematic approach can be taken (7).
Spontaneous pain or even pain in response to a stimulus (e.g. in the sensibility test) does not provide a reliable indication of the condition of the pulp. Even with irreversible pulpitis, a patient does not necessarily respond to a cold or heat test with pain. Pain does not correlate with the extent of inflammation, is always subjective and cannot be detected histologically (34).
If the pulp tissue is exposed during treatment, the bleeding of the tissue can be used for diagnostic purposes. The extent of the pulp haemorrhage can be considered a more reliable diagnostic method than the sensibility test and pain symptoms. If the pulp tissue is free of inflammation or if only superficial inflammation has occurred as a result of the caries, the pulp bleeding is weak. If, on the other hand, microorganisms or bacterial toxins have already penetrated the pulp and the inflammatory reaction extends deeper into the tissue, the pulp bleeding is more severe. The extent of bleeding may, therefore, reflect the degree of pulp inflammation. Prolonged or severe bleeding is indicative of irreversible pulpitis. Therefore, pulp tissue with severe or persistent haemorrhage has been reported to have a significantly worse chance of healing (35–38). But, not all studies have shown this, e.g. Careddu and Duncan could proof that prolonged bleeding time (as well as preoperative tenderness to percussion) was not an indicator of higher failure rates (39).
In clinical studies, haemostasis was achieved within six minutes after partial or total pulpotomy in 84% of cases in teeth with symptoms of irreversible pulpitis, and the pulp was vital after capping (40, 41). Clinically, it should, therefore, be possible to control pulp haemorrhage within approximately five minutes (7), although it must be emphasized that scientific evidence as to the prolonged bleeding time above which the pulp must be considered unsuitable for vital preservation is still lacking (27). Several studies reported successful VPT even after bleeding times of up to 25 minutes (42, 43).
The exact correlation between haemorrhage and pulp inflammation is still unclear. However, it can be concluded that in a healthy, uninfected pulp, pulp haemorrhage stops on its own or can be easily controlled, whereas in an inflamed pulp, profuse haemorrhage should be expected (35–38) (Figure 5.2a,b).
Factors Affecting the Outcomes of Direct Pulp Capping
Patient Age
Patient age per se is not a contraindication for direct pulp capping. In patients of advancing age, the regenerative power of the pulp tissue seems to decrease (8, 17) as pulp volume, vascularity, immune defence and functional repair mechanisms decrease (44, 45). However, in principle, direct pulp capping can be successfully performed in older patients (Figure 5.3a,b). However, the chronological age of the patient does not necessarily correlate with the healing capacity of the pulp. Rather, the biological age of the tissue is relevant, i.e. the history of a tooth during its functional period. Teeth with a history of trauma, extensive restorations, or intrapulpal mineralization tend to have a worse prognosis than teeth with a primary carious defect (8, 17) (Figure 5.4).
Figure 5.2 (a) Pronounced bleeding from the pulp tissue exposed over a small area is an indication that microorganisms have invaded the pulp. Instead of direct capping, partial pulpotomy may be indicated in this case. (b) Correct haemostasis after exposure of the pulp tissue with NaOCl 3%. This is a proxy measure that no microorganisms have penetrated the tissue and that there is, therefore, a high probability of being able to preserve the pulp vitality by direct capping.
Figure 5.3 (a) Preoperative radiograph of a 77‐year‐old patient shows caries distal to Tooth 35. Exposure of the pulp occurred during caries excavation. The patient’s age does not contraindicate an attempt at vital preservation. (b) Radiograph of the Tooth 35 five years after direct capping with a hydraulic calcium silicate cement (Biodentine). No pathological changes could be detected apically on Tooth 35. The patient, now 82 years old, was symptom‐free and the tooth was unremarkable in the sensitivity and percussion tests. Tooth 34 had to undergo root canal treatment in the meantime.
Figure 5.4 The intrapulpal hard tissue formations on the molar teeth may indicate pre‐damage of the pulp, as the tissue reacts to inflammation with mineralization. This is caused by the extensive restorations with presumably preceding caries. The regenerative capacity of the pulp may then be limited – regardless of the age of the patient.
Exposure Size
It is known from many studies that the exposure size has no influence on the success of direct pulp capping. The requirement that the exposure area of the pulp chamber should be a maximum 1 mm2 in size cannot be sustained today. When treating the pulp after trauma or partial pulpotomy, the pulp tissue is exposed over a large area. Nevertheless, direct pulp capping can be successful as long as infection of the tissue with microorganisms can be avoided (8, 17) (Figure 5.5). However, it should be kept in mind that if the pulp is exposed over a large area during caries excavation, large‐scale penetration of bacteria into the dentine has probably also occurred. This extensive contamination of the tissue may reduce the chances of success of direct pulp capping. If necessary, a partial pulpotomy can be performed in this case (see Chapter 6. Vital Pulp Treatment Modalities: Pulpotomy – Partial and Complete).
Figure 5.5 If the pulp tissue is not inflamed, the size of the pulp exposure has no influence on the success of direct pulp capping.
Location of the Pulp Exposure
The position of the pulp exposure has been discussed as a factor influencing the prognosis of direct pulp capping. However, presumably, the location of the cavity (occlusal or incisal versus cervical or lateral) does not influence the success of direct pulp capping. Nor do there appear to be significant differences in prognosis for specific tooth groups (anterior, premolars, molars) or jaws (maxillary or mandibular) (8, 17).
Microorganisms
Only a non‐inflamed, bacteria‐free pulp can maintain vitality in the long term, i.e. in the absence of microbial infections, human dental pulp shows a proven regenerative capacity when directly capped with calcium hydroxide suspension or hydraulic calcium silicate cement (HCSC) (7, 8). Microorganisms and their metabolites play a crucial role in the development of pathogenic pulpal changes and periapical diseases. Kakehashi et al. demonstrated in a histological study of germ‐free rats that in the absence of microorganisms, the pulp has the regenerative power to close an exposure site by hard tissue regeneration, even in the absence of capping material or final restoration. The presence or absence of microorganisms is the determining factor in the healing of exposed pulp tissue (46).
Due to the protected location of bacteria in the dentinal tubules during the carious process, phagocytosis (killing of microorganisms) by defence cells from the bloodstream does not occur until the pulp tissue is in direct contact with the caries (47–49). This is a major problem with direct pulp capping because pulp tissue infected with microorganisms loses its regenerative capacity (50)
It does not even have to be the microorganisms directly that cause inflammation of the pulp tissue. It is sufficient that metabolic products produced by the bacteria, so‐called endotoxins, such as lipopolysaccharides and lipoteichoic acid, diffuse into the pulp via dentinal tubules to cause an inflammatory reaction (51–54). Therefore, to exclude pulp infection during or after direct pulp capping, treatment should always be performed with sterile instruments under dental dam application. The caries should be completely excavated and the cavity disinfected and definitively restored with a bacteria‐proof restoration (7, 8).
Caries Excavation
With regard to the preservation of the vitality of the pulp, the therapy of deep, caries‐altered dentine has been the subject of controversial discussion for decades. The recommended therapeutic spectrum ranges from leaving the carious dentine largely intact to complete excavation into the caries‐free dentine. The following different and partly contradictory concepts can be distinguished: Ultraconservative caries excavation, selective caries excavation, two‐stage incomplete caries excavation, two‐stage complete caries excavation and complete caries excavation (55, 56).
With the exception of two‐stage and complete caries excavation, all other excavation concepts deliberately leave dentinal caries in place close to the pulp. Thus (in the spirit of Rebel (3)), avoiding pulp exposure is the prime objective. The idea behind this is to apply a tight adhesive seal over the remaining carious dentine and thus cut off the caries bacteria from access to fermentable carbohydrates (substrate). The bacteria are said to ‘starve’ under the filling without a substrate supply. Recently, therefore, the so‐called ‘selective caries excavation’ has been recommended as an alternative to complete caries excavation (55, 56). The pros and cons of different concepts of caries excavation are not the focus of this chapter on direct pulp capping. However, the following considerations should be kept in mind: In addition to cariogenic bacteria, which metabolize carbohydrates from food, certain anaerobic asaccharolytic bacteria, which use nitrogenous substrates for energy, also occur in infected dentine. Proteins and glycoproteins from demineralized collagen and tissue fluid from the dentinal tubules serve as food. These anaerobic asaccharolytic bacteria, therefore, do not require a substrate supply from ‘outside’ and can remain active even under dense, dentine‐adhesive fillings. The degradation products of these microorganisms can then lead to chronic inflammation of the pulp tissue (57–60).
Bacteria left in the dentine always pose a risk of caries recurrence and, even after the microorganisms have died, form a reservoir of endotoxins. They can maintain inflammatory processes in the pulp (61). Endotoxins readily diffuse through 0.5 mm thick dentine (51). Endotoxins that have penetrated the pulp release inflammatory mediators from odontoblasts and macrophages, leading to chronic inflammation of the pulp tissue (54). Therefore, even inactive caries histologically lead to changes in the pulp tissue (62). Consequently, histologically, chronic pulp inflammation may occur after ‘selective caries excavation’. Due to the bacterial infection, ideal healing is not to be expected. However, the teeth are clinically asymptomatic and react inconspicuously to a sensibility test. Patients’ clinical responses to the sensibility test may not correlate with histologic findings (63–65). Therefore, merely considering the absence of clinical symptoms after ‘selective caries excavation’ as a treatment success is too short‐sighted. Only histological analysis can assess the actual condition of the dental pulp tissue after ‘selective caries excavation’ (26, 27). Such histological studies prove that the pulp remains free of inflammation in the long term after ‘selective caries excavation’ has been lacking. Therefore, these clinical results of ‘selective caries excavation’ should be interpreted with caution. A direct comparison of ‘selective caries excavation’ with complete excavation and subsequent capping of the pulp showed that ‘selective caries excavation’ histologically leads to chronic inflammation of the pulp in 68–100% of cases and thus to a failure of the treatment. In contrast, complete caries excavation followed by indirect or direct pulp capping with calcium hydroxide resulted in histological failure in only 7–33%. In all cases, patients were clinically symptom‐free throughout the follow‐up period of three months to five years (63, 64). Accordingly, a higher probability of success of ‘selective caries excavation’ compared with VPT after pulp exposure cannot be established (7). Hence, the current statement of the American Association of Endodontists (AAE) on VPT calls for complete caries removal and the elimination of all infected tissues (66). Thus, to prevent bacterial contamination of the pulp, the goal of caries excavation should be to completely remove the infected dentine – even at the risk of exposing the pulp tissue – and to directly cap the pulp with biocompatible and potentially bioactive materials (e.g. HCSC).
Haemostasis and Cavity Disinfection
As already mentioned, adequate haemostasis must be ensured if pulp tissue is exposed. Pulp haemorrhage should be easily controlled. Increased bleeding may indicate a higher degree of inflammation in the pulp, leading to a reduced ability to repair (26). In addition to pulp diagnostics, it is also important that the capping material be applied directly onto the exposed pulp tissue. No blood residue should remain between the wound dressing and the pulp tissue. A blood coagulum restricts the formation of hard tissue and thus pulp healing, since a blood coagulum is a breeding ground for possibly remaining pathogenic microorganisms. In addition, chemotactic inflammatory mediators are released into the pulp tissue, which leads to a chronic inflammatory state of the pulp and not to healing (67, 68).
A third reason for effective haemostasis is that the moisture and contamination of the dentine near the exposed site due to bleeding may make it more difficult to get a pulp‐capping material to adhere to dentine. If the capping material does not adhere properly to the dentine, leaks occur and microorganisms can migrate into the pulp (26).
Haemostasis can ideally be performed together with cavity disinfection. Traditionally, hydrogen peroxide (H2O2) was often used to clean the cavity after caries excavation. It acts as a peroxidase on tissue catalases, releasing nascent oxygen. H2O2 has a little corrosive or toxic effect on pulp tissue, shows good haemostasis in exposed pulp and mechanical cleaning effects due to foaming in contact with blood. However, the disinfecting effect of H2O2 is mostly overestimated and may not be sufficient for cavity disinfection in the context of caries excavation (8). Histologically, it has been found that after haemostasis with H2O2, emphysema formation may occur in the pulp, which has a negative effect on healing (69).
Sodium hypochlorite (NaOCl) at a concentration of about 3% seems to be much more suitable in this case. NaOCl is effective in haemostasis, has a disinfecting effect on dentine surfaces, and removes blood, fibrin and biofilm residues from dentine surfaces, as well as dentine chips and damaged pulp cells from the superficial pulp tissue. NaOCl has a non‐toxic effect on pulp tissue and does not appear to interfere with the healing of the exposed pulp. It is even possible that the high pH of NaOCl is beneficial to pulp healing. NaOCl at concentrations below 2.5% is probably not sufficiently effective in terms of disinfection and haemostasis. Concentrations above 5%, on the other hand, may be too aggressive and thus damaging to the tissue (8).
Nevertheless, a histological study showed that after rinsing for 15 minutes with 5 ml NaOCl 5.25%, dissolution effects occurred on the vital pulp tissue, but these were limited to the superficial three to five cell layers. There were no changes in deeper pulp areas and no changes in the dentine. Presumably, the perfused pulp tissue buffers the effect of NaOCl (70). Due to this superficial tissue‐dissolving effect, a kind of ‘chemical amputation’ of the pulp probably occurs, whereby irreversibly damaged pulp cells are removed (71). Therefore, a randomized clinical trial clearly demonstrated that the use of NaOCl for cavity disinfection significantly improves success rates in direct pulp capping. In 84 patients, the pulp was exposed during complete caries excavation. After irrigation of the pulp wound with either isotonic saline (0.9% NaCl) or NaOCl (2.5%) and direct pulp capping with MTA, survival rates after one year were only 55% in the saline group but 89% in the NaOCl group (71).
Conversely, it could be disadvantageous that NaOCl negatively influences the adhesion of dentine adhesives and composite resins to dentine. However, the reported data is inconsistent in this respect. For some dentine adhesives, dentine pretreatment with NaOCl has no significant effect on the adhesion of the resin‐based composite restoration (72). To be on the safe side, the cavity should be rinsed again with water before definitive adhesive restoration (7, 8).
Chlorhexidine digluconate (CHX) at a concentration of 2% is a possible alternative to NaOCl (73). Histologically, there was no significant difference in pulp healing and pulp tissue morphology after haemostasis with NaOCl (0.5–5.25%) and CHX (2%) in direct pulp capping. Both solutions showed no negative effects on the pulp tissue (74, 75). However, in general, the disinfecting effect of CHX 2% on carious dentine is lower than that of NaOCl (76). Therefore, CHX mouth rinsing solutions in a concentration of 0.1–0.2% should not be used here, as they are neither sufficiently antimicrobial nor sufficiently haemostatic.
In paediatric dentistry, ferric sulphate has been recommended for arresting pulp haemorrhage on deciduous teeth. In permanent teeth, these haemostatic agents such as ferric sulphate, aluminium chloride and other materials are not indicated because they would ‘mask’ the true inflammatory state of the pulp due to their high effectiveness in stopping bleeding (77). One might thus be tempted to directly cap a pulp that is irreversibly inflamed. Moreover, these substances are tissue‐damaging and may interfere with wound healing (78). Thus, after haemostasis with ferric sulphate, postoperative discomfort was significantly more common after direct pulp capping (26).
Selection of the Pulp Capping Material
Calcium hydroxide suspensions have been considered the universal standard material for maintaining pulp vitality since the first publications by B. W. Hermann around 1930 (4, 5). The desirable properties of calcium hydroxide include an initial high alkaline pH, which is responsible for stimulating cells and enzymes of the pulp. It neutralizes both the low pH acids produced by cariogenic bacteria and bacterial toxins, inhibits macrophages and, thus, inflammation, exhibits antibacterial properties and promotes defence mechanisms and pulp tissue repair. The disadvantages of calcium hydroxide include poor sealing to dentine, mechanical instability and resorption over time (79). The slow decay of calcium hydroxide after hard tissue formation may lead to microleakage and allow slow penetration of microorganisms through defects (80). Tunnel defects have been demonstrated in the hard tissue formed after direct pulp capping with calcium hydroxide, through which bacteria and their toxins may then secondarily enter the pulp (81).
In order to compensate for the disadvantages of aqueous calcium hydroxide suspensions, in the 1960s, other delivery forms of calcium hydroxide such as hard setting cement (calcium salicylate ester cement; e.g. Dycal, Dentsply Sirona or Kerr Life, Kerr Dental) were developed. In contrast to aqueous calcium hydroxide suspension, hard‐setting calcium hydroxide cements offer a better seal of the dentine‐pulp complex. But, these preparations show a lower release of hydroxyl ions, resulting in a lower pH value and a significantly weaker antimicrobial effect (79, 82). In addition, hard‐setting calcium salicylate ester cement dissolves under the overlaying restoration in the long term (79, 83) and, therefore, does not provide the necessary permanent support for the main filling (84). Hard tissue formation under calcium salicylate ester cement develops more slowly and is less uniform. Hard tissue regeneration is, therefore, weaker compared to aqueous calcium hydroxide suspensions. In addition, inflammation occurs more frequently (68, 85, 86). Some additives necessary for the setting of calcium hydroxide cements may possibly have a toxic effect on the pulp (86). Hence, salicylate ester‐based hard‐setting calcium hydroxide cement cannot be recommended as a first‐choice agent for direct pulp capping (7, 8, 17).
HCSCs consist of a cement powder mixed with water. The main components of the powder are tri‐ and/or dicalcium silicate, which are also found in Portland cement. During hydration, i.e. when the cement sets, calcium hydroxide is formed, i.e. calcium and hydroxyl ions are released (87). Identical to calcium hydroxide preparations, calcium ions have a positive effect on pulp cell regeneration. HCSC, therefore, stimulates the mitotic index of pulp cells (88). Hydroxyl ions contribute to a sustained alkaline pH (89, 90) and stimulate the release of growth factors and cytokines from the surrounding dentine, which also amounts to the formation of reparative hard tissue (91). In addition to calcium hydroxide, silicon is released during the HCSC setting (92). The exact function of silicon in hard tissue formation is unclear, but it probably plays a role in the early stages of mineralization (93) and contributes to the induction of hard tissue formation (94). Furthermore, silicon can remineralize demineralized dentine in vitro (95). Another key advantage of HCSCs in pulp capping is that they interfere with the modulation of inflammatory and pain mediators at the molecular level. Application of HCSC to the exposed pulp tissue results in decreased vascularization and vasodilation, as well as decreased recruitment of inflammatory cells. As a result, tissue pressure within the pulp decreases, and so does the pain response. Therefore, after pulp capping, both inflammatory responses and pain are suppressed. This has a positive effect on the healing process and the patient´s well‐being after treatment (96).
The setting properties of HCSCs are not affected by the presence of tissue fluids or blood. They are, therefore, also referred to as ‘hydraulic’ cement, as they set in contact with both air and water (87). HCSC forms a tight bond to the dentine. The small particle size of HCSC allows penetration of these cement particles into the dentinal tubules (97), which produces adhesion to dentine comparable to that of glass ionomer cement (98). In combination with the alkaline pH, this also helps to trap residual cariogenic bacteria at the transition from dentine to HCSC, thus preventing bacterial advancement, caries progression and persistent pulp damage (99).
Upon contact with calcium‐ and phosphate‐containing (body) fluids, these cements exhibit hydroxyapatite‐like crystal formation on their surfaces (100, 101). Osteoblasts, cementoblasts, periodontal ligament cells and (in the case of capping) pulp cells, therefore, deposit directly on the HCSC surface, as the material is recognized as ‘non‐foreign’, which explains the biocompatibility of these cement (102).
Overall, all data available to date indicate that HCSC is a biocompatible, non‐cytotoxic material that promotes an antibacterial environment and surface morphology favourable for the reparative formation of hard tissue. HCSC stimulates the release of dentine matrix components necessary for hard tissue repair and regeneration in mechanically exposed healthy and partially inflamed pulps (7, 103). However, odontoblast‐like cells and the formation of dentine or dentine‐like tissue could not be detected after direct pulp capping with an HCSC (RetroMTA; BioMTA, Daejeon, Korea). Therefore, the newly formed hard tissue was not ‘regular dentine’ and does not appear to be the product of the differentiation of pulp cells into odontoblasts (104). This observation is identical to the results after direct pulp capping with calcium hydroxide (105). Therefore, hard tissue formation after direct pulp capping appears to be dystrophic intrapulpal mineralization in response to therapy (104, 105).
The advantages of these HCSCs compared to the typically used calcium hydroxide products are the higher mechanical strength, the lower solubility and the better sealing of the dentine. Disadvantages of calcium hydroxide are avoided when using HCSC: dissolution of the capping material as well as mechanical instability and, thus, long‐term protection against bacterial microleakage. HCSCs appear very promising in pulp vitality preservation. Recent studies seem to support their potential and extended use in maintaining pulp vitality (8, 103).
ProRoot MTA (Tulsa/Dentsply, Tulsa, OK, USA) was the first HCSC to be introduced into dentistry in the mid‐1990s. One disadvantage of ProRoot MTA is that it can cause discolouration of the tooth. This can be particularly problematic in the pulp capping of anterior teeth after trauma (106). The discolouration is due to heavy metals contained in the MTA, such as bismuth oxide (used as a radiographic contrast agent) (107, 108) or iron (109). The discolouration is mainly caused by the oxidation of these metals after contact with NaOCl or the uptake of blood components (109, 110). Other HCSCs contain less or small amounts of heavy metals and their potential to discolour teeth is minimal. HCSCs with zirconia, zirconia, or tantalum oxide as the radiographic contrast agent are particularly stable in colour (106).
Since the introduction of ProRoot MTA, a variety of new HCSCs have been developed, such as Biodentine (Septodont, St. Maur‐des Fossés, France) (111). Thus, more than 40 different HCSCs are currently commercially available internationally. Studies have demonstrated physicochemical and bioinductive properties comparable to MTA, indicating a promising application in vital maintenance (111, 112). In general, HCSCs are superior to all calcium hydroxide products in maintaining pulp vitality, with no significant differences between the various HCSCs in terms of mode of action (113).
In contrast to HCSC and calcium hydroxide, all light‐, dual‐ or auto‐curing materials containing monomers such as dentine adhesives or composite resins are not suitable for pulp capping. This also applies to composite resins where calcium hydroxide, Portland cement or calcium silicate has been added as a filler (7, 8, 17). (For further details, see Chapter 7. Vital Pulp Treatment: Material Selection.)
Definitive Restoration
In order to reliably prevent (re)contamination of the dentine‐pulp complex, the cavity must be restored with a bacteria‐proof, definitive filling in the same treatment appointment after direct pulp capping. Ideally, this should be done with a dentine‐adhesive and resin‐based composite restoration. If the cavity is only restored with a temporary material (such as glass ionomer cement) after direct pulp capping, the success rate of VPT decreases significantly (14, 114). If a bacteria‐proof, definitive filling is not possible in the same treatment session, this argues against the attempt to preserve pulp vitality (7, 8) (Box 5.1).
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