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REVIEW
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Henry F Duncan, PN Ramachandran Nair, Thomas R Pitt Ford
Vital pulp treatment: a review
Henry F Duncan
Key words
calcium hydroxide, mineral trioxide aggregate, pulp capping, pulpotomy
Preserving the health of the dental pulp, or part of it, is important when treating a vital tooth with an exposed pulp; particularly, if the tooth is immature and root formation is incomplete. There is a long tradition of treating the exposed dental pulp by pulp capping. An improved understanding of pulp biology, the development of mineral trioxide aggregate and the advent of regenerative therapies have heralded a new wave of research and treatment methods in this area. The intention of this review is to evaluate the past, present and future of vital pulp treatment in endodontics.
Division of Restorative Dentistry & Periodontology, Dublin Dental School & Hospital, Trinity College Dublin, Dublin 2, Eire Tel: +353 1 6127356 Fax: +353 1 6711255 Email: hal.duncan@dental.tcd.ie
PN Ramachandran Nair Institute of Oral Biology, Centre of Dental and Oral Medicine, University of Zurich, Zurich, Switzerland
Thomas R Pitt Ford Department of Conservative Dentistry, Guy’s Campus, King’s College London Dental Institute, London, UK
Introduction
Rationale for pulp capping
Exposure of the dental pulp may be the result of caries, trauma, or may occur iatrogenically during routine cavity preparation; this is a clinical reality that requires optimal treatment. When managing the exposed pulp the options include direct pulp capping, pulpotomy and pulpectomy. Direct pulp capping is defined as a procedure in which the pulp is covered with a protective dressing or base placed directly over the pulp at the site of the exposure1. The only difference between pulpotomy and pulp capping is that with the former, additional tissue is removed from the exposure site2,3. Pulpectomy is defined as a procedure in which the pulp is totally removed, followed by root canal treatment1.
If possible, maintaining an intact, healthy pulp is preferable to endodontic treatment, which may be complex, time-consuming and expensive4. Preserving the dental pulp, or part of it, is important when treating a vital tooth with an exposed pulp; particularly, if the tooth is immature and root formation is not yet complete. In these cases the maintenance of a healthy pulp allows continued root formation. The need for a more conservative approach in endodontics was highlighted in 1989, when it was suggested that it seemed ironic in the days of biological know-how that so much time is dedicated to removing rather than conserving pulp tissue5. Preserving the pulp should be encouraged within the discipline of modern endodontics; it is
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What are the criteria for successful pulp capping? The treatment outcome for pulp capping has, traditionally, been evaluated clinically and radiographically15,16. Healing has been described when a continuous hard tissue barrier was found and the residual pulp was free of inflammation17. For a successful outcome, the formation of hard tissue such as a dentine bridge (hard tissue factors) and the maintenance of healthy pulpal tissue (soft tissue factors) are considered essential.
Hard tissue factors Most studies examining hard tissue formation have used animal models. Studies that used human teeth
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The concept of pulp capping is not new, with the earliest reports dating back to the 18th century, when a piece of gold was placed over the exposed vital pulp in an attempt to promote healing6. Since then, and in keeping with many other medical practices, pulp capping has enjoyed swings in popularity with numerous investigations citing the advantages and disadvantages of the technique. In 1922, it was stated that ‘the exposed pulp is a doomed organ’7. Unfortunately, this often-quoted phrase has endured and indeed remained despite the volumes of new research on the subject. Perhaps much of the reluctance to accept pulp capping can be explained by the often unpredictable and poor results when compared with more conventional forms of treatment such as root canal treatment. Studies in the 1950s reported a successful outcome of between 60 to 70% for direct pulp capping compared with over 80% for conventional root canal treatment8-10. Later studies demonstrated a successful outcome of 80 to 90%11-14 for pulp capping, which approached or even exceeded that of conventional root canal treatment.
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more conservative, more biologically acceptable and less technically demanding than pulpectomy.
pyrig No Co t fo rP ub lica were examined in a recent systematic review18. It wastion te e concluded that none of the studies were a chigh ssofe n
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evidence-based level. It was further concluded that high-quality studies are still required. In previous studies, it was postulated that the presence of a hard tissue barrier was so important after pulp capping that it should be detectable by direct clinical examination prior to placement of the definitive restoration16. However, others felt that radiographic verification of secondary dentine deposition at the site of exposure was all that was necessary to consider the procedure a success15. The need for dentine bridge formation is based on the premise that pulp capping is a procedure designed to heal the pulpal exposure and return the hard tissue to its normal structure and function. Successful hard tissue bridge formation was considered a prerequisite for longterm control of post-operative infection in vital pulp therapy19 and, therefore, without it, a pulp-capping procedure cannot be considered a success. However, this concept is not universally accepted. Another view is that a successful outcome with pulp capping requires only survival of the asymptomatic vital pulp and the presence or absence of a dentine bridge is not important12. The need for the development of a dentine bridge has remained controversial in pulp capping. Many researchers have suggested that any bridge that is formed is often poorly mineralised and porous20,21 and therefore is of secondary importance in protecting the pulp from bacteria and subsequent infection. The limitations of radiographs in assessing dentine bridge formation have been demonstrated and it has been pointed out that although the bridge may look acceptable on a radiograph, it may be perforated20. It was also suggested that to confirm an unbroken dentine bridge, it is necessary to examine serial histological sections (Figs 1a and 1b). Therefore, the notion of an impervious dentine bridge is a ‘myth’. Other histological research corroborates this, showing that 90% of dentinal bridges contained ‘tunnel’ defects and 41% were associated with inflammation or necrosis21. However, it should be noted that in this study, no attempts were made to reduce marginal leakage and only amalgam was used to seal over the pulp-capping material. Others have disputed the value of the above research22,23 by pointing out that dentine itself is porous and contains dead tracts, and the apparent porosity of the dentine barrier is not unlike that found in freshly cut dentine and is of little clinical significance24.
pyrig No Co 249 t fo rP ub lica tio Experimental findings suggest that extensive accun te mulation of PMNs, which is usually an indication of inss e n c e
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fection, put the pulp at risk of tissue necrosis. However, in the absence of bacteria, even inflamed pulps have good healing potential26. Unfortunately, it is not possible to accurately determine the histopathological status of the pulp just from clinical signs and symptoms27,28. Therefore, pain history, sensitivity testing and radiography are currently the only methods of assessment available to aid the clinician when determining treatment outcome. This presents a preoperative problem when deciding which teeth are likely to be suitable for the capping procedure. Apart from the role of inflammation in treatment failure, it is also important to consider the soft tissue response during healing, following placement of a pulp-capping material. The cellular processes have been investigated, mainly with the use of calcium hydroxide (Ca(OH)2)29,30. Ca(OH)2 is strongly alkaline and it appears that this high pH causes a local necrosis in the surface of the pulp. In addition, the alkalinity prevents bacterial infection, thereby reducing inflammation and providing a more stable environment for repair31. Pulpal cells proliferate and migrate
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Fig 1a Hard tissue formation on the pulpal aspect of hardsetting calcium hydroxide (Dycal) capping material (arrow) and a thick, calcified hard tissue barrier (C) at a distance from the capping material with gaps at the periphery.
Fig 1b Higher magnification of Fig 1a gap or ‘tunnel’ defects (D) are evident peripherally, associated with engorged blood vessels (arrow) and surrounding acute and chronic inflammatory cells (original magnification ǂ100). Adapted from Nair et al103.
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It has been suggested that in addition to hard tissue formation, the residual pulp should be free from the infiltration of inflammatory cells17. The aim of vital pulp therapy should be to minimise pulpal injury and to harness the natural regenerative capacity of the dentine–pulp complex. Inflammation is a response to injury and the presence of polymorphonuclear leucocytes (PMNs) and chronic inflammatory cells is indicative of failure of the procedure. It should be remembered that when pulpal exposure occurs, the buffering effect of the dentine is lost and the pulp tissue is rendered more sensitive to potential adverse interactions25.
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In the absence of a dentine bridge, wounded pulp tissue is much closer to the surface and more susceptible to exposure to oral fluids and attack by bacteria23. In a clinical situation, if the coronal restoration ‘leaks’, the presence and the quality of a dentine bridge is likely to be of greater importance compared with a restoration that ‘seals’.
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Fig 2 Carious maxillary second molar.
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It has been demonstrated that the key factor in healing after pulpal exposure was the absence of microorganisms and infection33. Several other investigators have since confirmed that microbial irritants and microleakage of restorations are the dominant causes of pulpal inflammation34-37. Caries in the dentine or leaking restorations will allow bacteria and their byproducts to invoke varying degrees of pulpal inflammation. Even if the carious process has not reached the pulp and is only at the outer dentine, pulpal inflammation may still be evident38. When the carious lesion approaches the pulp, the severity of the inflammatory response increases, and when it is within the last 0.5mm, the pulp becomes acutely inflamed39. As a result, this accounts for poor predictability when pulp capping teeth with carious exposures8,40 compared with vital, non-caries-related exposures. It also highlights the need to reduce the effects of further contamination from microleakage. The reason that teeth with
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to the injury site after 2 weeks29 and appear to undergo an odontoblast-like differentiation; thereafter they begin to form collagen and the mineralised dentine bridge29,30,32. This bridge walls off the pulp and offers further protection to the soft tissue. The signalling process responsible for this differentiation remains to be elucidated31 but may be due to the Ca(OH)2 solubilising bioactive molecules in the dentine19. However, there may be aberrations in this signalling process, as the initial dentine bridge is usually osteodentine type, rather than tubular orthodentine. It, therefore, seems that pulp-capping materials act as relatively nonspecific inducers of reparative dentinogenesis31.
pyrig No Co t fo rP ub lica carious exposures (Figs 2 and 3) have limited and un-tion t certain potential for healing is because ofethe sssustained e nc e
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period of bacterial infection, which leads to inflammation and reduced pulpal defence capabilities41. Carious exposure of the pulp has a detrimental effect on outcome, yet the majority of experimental studies in humans involved healthy teeth, limiting the confounding factors and aiding comparisons18,42-45. Unfortunately, studies undertaken in ideal, caries-free conditions may have limited clinical relevance18. In experimental studies on healthy teeth, the influence of wound infection and the associated inflammatory processes is not at play46. Attempts have been made to mimic the effects of wound infection in animal studies47-49. In one such study, the effects of bacterial microleakage were investigated using a variety of capping materials, all surface-sealed with zinc oxide eugenol (ZOE) cement49. It was found that a range of materials when surface-sealed with ZOE cement were well tolerated by the dental pulp tissue and did not impair or negatively affect pulpal wound healing. On the other hand, if bacteria were present at the tooth/ restoration interface, severe inflammatory breakdown was seen. It was concluded that healing of pulp exposures was not significantly affected by any particular type of capping agent, but rather on the material’s ability to prevent microleakage. This was corroborated by other work, which showed that surface sealing of the cavity prevented microleakeage, and thereby reduced pulpal inflammation37.
Pulp-capping techniques Traditionally, pulp-capping techniques involve materials placed onto the pulp as a dressing, to stimulate the
Fig 3 Caries removed, haemorrhage controlled and pulpal exposure visible.
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What materials are used as pulp-capping agents? A plethora of materials have been used as potential pulp-capping materials15. As mentioned earlier, the healing of a pulpal exposure is not dependent on the effect of a particular type of material, but on the reaction to the capping agent and the surface sealing to prevent bacterial leakage37,48-50. However, although pulpal repair is possible with a range of capping agents, an important proviso is that the environment should not only be free from infection, but the capping agent should, subsequently, become relatively innocuous46. Therefore, the predictability and potential success of pulp capping is influenced by the capping agent chosen. For this reason, over the last 50 years, Ca(OH)2 has been the ‘gold standard’ in pulp-capping therapy. Recently, resin composite and mineral trioxide aggregate (MTA) have shown promise as alternatives.
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Apart from encouraging hard tissue formation, the ideal properties of a pulp-capping material45 are that it should: • maintain vitality and function of the dental pulp (biocompatible) • aid formation of a dentine bridge (encourage good thickness and quality hard tissue formation) • have appropriate mechanical properties (including being insoluble in water) • adhere to dentine (seals to prevent microleakage) • be simple to handle clinically.
The introduction of Ca(OH)2 to endodontics in 1930 stimulated renewed interest in pulp capping51. The effect of Ca(OH)2 on the exposed pulp has been investigated extensively over the last 70 years6,17,24,29,42,52-54. During this time, Ca(OH)2 has established itself as the capping agent of choice. The beneficial effect of Ca(OH)2 is thought to be due to the hydroxyl ions; they exert a caustic effect that leads to superficial necrosis at the wound6. Coagulation necrosis results, demarcating the vital tissues, and the pulp is stimulated to defend and repair29. Studies using auto-radiation demonstrated that the calcium forming the bridge came from the underlying tissues and not from the Ca(OH)255,56. Originally, it was thought that calcium ions from the material itself contributed to the dentine bridge. Therefore, how does Ca(OH)2 stimulate a reparative dentinogenic response? As discussed earlier, it appears that the alkalinity may dampen the inflammatory response and provide a relatively sterile environment for repair to occur31. Pulp cells were seen to migrate to the area within 2 weeks of Ca(OH)2 placement29. Thus, it would appear that Ca(OH)2 has a relatively non-specific effect as an inducer of dentinogenesis; perhaps it exploits endogenous biologically active molecules19. Nevertheless, the actual mechanism of action remains unclear57. Traditional non-setting Ca(OH)2 powder and water irritates the exposed pulpal surface and a necrotic layer is formed in contact with the material. Subsequent dentine bridge formation occurs on the vital aspect of the necrotic zone, resulting in persistence of the zone between the Ca(OH)2 and the bridge29. The advent of hard-setting Ca(OH)2 cements, such as Dycal (Dentsply, Addlestone, Weybridge, Surrey, UK) altered the histological picture; against this pulp-capping agent there is less caustic damage to the underlying pulp during hard tissue barrier formation. It appeared the necrotic layer still formed, but it is then removed by phagocytes and replaced with granulation tissue52. In addition, Dycal did not appear to delay dentine bridge formation compared with other Ca(OH)2 pulp-capping agents (although radiographic detection of the dentine bridge was more difficult). Over the last 30 years, hard-setting Ca(OH)2 products have become the material of choice for pulp capping. Experimental pulpotomies in human teeth using Ca(OH)2 have shown a successful outcome of ENDO (Lond Engl) 2008;2(4):247–258
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deposition of reparative dentine and repair the wound. This principle is still considered the gold standard for pulp capping and most of the research is directed at finding new materials that will behave more predictably and provide a better seal than those currently in use46. Recently, biological approaches to pulp capping have evolved using bioactive molecules. In addition, lasers have been evaluated as potential adjuncts to the traditional pulp-capping technique.
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During the late 1990s, in an attempt to replace Ca(OH)2 as the pulp-capping agent of choice, much attention was directed towards the use of dentine-bonding agents and resin cements. The trend stemmed largely from developments in adhesive dentistry and has the advantage of resin cements bonding to dentine and enamel. Previous studies55,61,62 have demonstrated that calcium salts were not essential for the formation of reparative dentine and that dentine bridging occurred even under non-calcium materials such as wax, acrylic resin and amalgam, placed on the amputated pulps of rat molars. With the aforementioned agents, the reparative dentine was quantitatively less, but it was similar in structure to that under Ca(OH)2 pulp caps.
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89% after 6 months42 and predictable formation of dentine bridges44. However, clinically, the outcome of pulp capping with Ca(OH)2 remains unpredictable due to the need for intimate contact, without an intervening blood clot, between the pulp and the capping agent42. If clot formation was allowed to occur, only 22% of the teeth showed healing17. It was suggested that the reasons for the failure could be due to the clot or its components neutralising the effects of the Ca(OH)2 or interfering with healing. Nevertheless, it could simply be that the clot produced an inadequate seal, which leads to the pulp becoming infected. Another drawback of Ca(OH)2 is that although it has the short-term advantage of stimulating dentine bridge formation quickly, in the long term it does not maintain a long and enduring seal against bacterial microleakage58. It has been demonstrated that the Dycal under amalgam restorations were soft in over 70% of cases59. In addition, there was substantial washout of Ca(OH)2 bases/linings under amalgam restorations60; this may be due to the surface seal not offering long-term protection against bacterial microleakage. This underlines the need for a carefully placed base over the pulp-capping material9,48. Ideally, it would be advantageous if the pulp-capping agent has good sealing characteristics as this would reduce the chances of bacterial leakage into the pulp. For this reason, other materials have been investigated as potential pulpcapping agents. The hope is that the alternatives will be easier to use, lead to an improved seal and aid formation of better quality dentine barriers.
pyrig No Co t fo rP ub lica More recently, there is some scientific data to sup-tion t e port the practice of acid-etching the e exposed ss e n cpulp
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followed by bonding techniques. Adhesive systems were compared with Dycal in exposed monkey pulps and it was found that although the Dycal samples showed a significantly higher incidence of bridging at 30 days, at 60 days there was no significant difference between the groups63. These results have been verified by others64,65. However, the need to control haemorrhage is paramount with resin-based systems and, therefore, they are considered technique sensitive. Using an animal model, 147 pulps were etched with phosphoric acid and three different resin bonding systems were placed over the exposure23. The experimental groups were compared with the control group using Ca(OH)2. It was found that etching tended to encourage renewed bleeding from the pulp, which was difficult to control. In addition, 45% of the cases subsequently became non-vital and a dentine bridge was only formed in 35% of the cases. In contrast, in the Ca(OH)2 group, only 7% of the teeth became non-vital and 82% formed dentine bridges. It was concluded that until a modification or another technique has been scientifically proven to be superior to Ca(OH)2, the use of the ‘total etch’ technique in pulp capping is contraindicated. It is unclear as to why there are such wide variations in results in these studies. It has been suggested that perhaps resins are not the ideal material for pulp capping25 as polymerisation shrinkage and contraction stresses increase the risk of bacterial microleakage. In addition, leachable resin monomers may have adverse effects on the pulp66. A recent study on 46 healthy human teeth, using immunohistochemical analysis, compared Ca(OH)2 with a dentine-bonding system; it was concluded that Ca(OH)2 remains the material of choice for the treatment of accidental pulp exposure67.
Mineral trioxide aggregate MTA was developed in the mid 1990s as a root-end filling material68,69. It has since been recommended as a pulp-capping agent70. The use of MTA in endodontics has been reviewed in the literature71. The constituents of MTA have been examined using x-ray energy dispersive analysis in a scanning electron microscope and x-ray diffraction72. It was found that the constituents of MTA were similar to
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One of the drawbacks of using Ca(OH)2 as a pulpcapping agent is that being neither adhesive to dentine nor sealing particularly well, it fails to provide good long-term protection58. Scientific evidence exists, at least in studies conducted in vitro, that verifies the good sealing ability of MTA68,73-78. The results have generally demonstrated MTA to seal significantly better than the other materials tested.
Fig 4 White MTA (ProRoot MTA, Dentsply) advertised as a one-visit pulp-capping agent.
specimens showed less pulpal inflammation and more complete dentine bridge formation than the Ca(OH)2 specimens. It was concluded that MTA has potential as a pulp-capping agent. Other studies have found that pulpal inflammation was reduced and the thickness and tubular structure of the dentine bridges were better with the MTA compared with the Ca(OH)2 controls81,84.
Human studies Solubility Ideally a pulp-capping agent should be insoluble as it will come into contact with pulpal tissue and dentinal tubule fluid in situ. The physical properties of MTA have been compared with other dental materials including amalgam, intermediate restorative material (IRM) and ethoxybenzoic acid cement (EBA)69. It was concluded from the study that amalgam, EBA and MTA showed no signs of solubility in water.
Animal studies MTA has been investigated as a pulp-capping agent in several animal studies70,79-87. Most of the studies have compared MTA with Ca(OH)270,79-81 although some have only analysed MTA83,85,86 or Portland cement82,88. Other studies have compared MTA with Ca(OH)2 and a dentine-bonding agent84 or MTA with bioactive glass, ferric sulphate and formocresol87. The pulps of 12 teeth from four monkeys were exposed and then capped with either MTA or Ca(OH)270. After 5 months the teeth were processed and examined histologically. It was found that the MTA
The clinical and radiographic results of direct pulp capping in human primary89-96 and permanent13,14,97-99 teeth using MTA have been reported; all these studies involved carious teeth. In contrast, there are only six publications involving caries-free teeth in which the response of human pulp to MTA has been studied histologically43,100-103. In one study, 11 pairs of maxillary third molar teeth were pulp capped with either MTA or Ca(OH)2; they were examined histologically after various postoperative intervals of up to 6 months. The results favoured the use of MTA, although more studies with larger sample sizes were needed43. Unfortunately, in this study, there was an unusually high drop-out rate. Of the 22 pulp capped teeth, only 14 were available for histological examination. Another prospective randomised study involving 33 third molar teeth compared hard-setting Ca(OH)2 with MTA103. Following pulp capping, the teeth were extracted at predetermined time intervals of 1 week, 1 month and 3 months. The specimens were processed for qualitative and quantitative evaluation by correlative light and transmission electron microscopy. The pulp wounds capped with MTA were mostly free from inflammation
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Portland cement, but the two commercially available versions, grey and white MTA (ProRoot MTA, Dentsply, Addlestone, Weybridge, Surrey, UK), differed in some of their constituents. Aluminium and iron were present in the grey, but not white, MTA (Fig 4). Many studies have examined the behaviour and properties of MTA and it is prudent, for the sake of this review, to compare and contrast these properties with the ideal properties of a pulp-capping agent45.
Sealing ability
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Fig 5 A selected serial section of MTA pulp cap at 1 week demonstrating capsule formation (arrow) and the absence of inflammatory cells (original magnification ǂ16). Adapted from Nair et al103.
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Fig 6a Macrophotographic view of the mesial half of a human maxillary third molar showing remnants of the restorative material (C) and MTA capping material (D) at 3 months. Note the distinct hard tissue bridge (arrow) (original magnification ǂ6). Adapted from Nair et al103.
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Fig 6b Photomicrograph of part of the histological section as shown in Fig 6a of a MTA cap at 3 months. Note that the thick mineralized barrier (arrow) stretched across the entire length of the exposed pulp (original magnification ǂ8). Adapted from Nair et al103.
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Fig 7 Correlative transmission electron micrograph of the same hard tissue bridge (B) and subjacent pulp (C) as Fig 6b. The bridge is lined on the pulpal side by cuboidal cells (D) and there is a cytoplasmic projection extending into the bridge, reminiscent of a developing dentinal tubule (arrow) (original magnification ǂ21,000). Adapted from Nair et al103.
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5 to 7). Furthermore, the dentine bridge–pulp interface was lined by cells with cytoplasmic processes projecting into invaginations of the bridge; this is indicative of odontoblast-like cells formation and the initiation of tubular dentine formation. In contrast, in the Ca(OH)2 group, pulpal inflammation was a common feature at all time intervals; hard tissue barrier formation was less consistent and the bridges formed had numerous tunnel defects (Fig 1b). It was concluded that MTA was clinically easier to use and should be the material of choice for direct pulp capping instead of hard-setting Ca(OH)2 cements. Other histological studies on pulp capping comparing Ca(OH)2 with MTA have either corroborated these findings100,104 or found both materials to be equally effective101,102. There are four longitudinal case series studies looking at MTA in vital pulp treatment13,14,97,98 involving carious permanent teeth. These clinical and radiographic studies have reported a successful outcome of over 90% at 18 to 24 months13,98 and up to 9 years14. Although these results are promising, they should only be considered as preliminary in nature as there were no controls and the number of treated cases was generally small. In addition, care must be exercised in extrapolating the results as most of the teeth treated were in young patients (only one of the studies included teeth in patients over 16 years old14). The limitation of observational research was addressed in a recent prospective study comparing Ca(OH)2 with MTA using 51 permanent carious teeth99. The average age of the patients was 10 years old and the follow-up period ranged from 25.4 to 45.6 months. No significant differences in outcome were found between the two materials; both materials were reported to be successful, in excess of 90%.
Other approaches to pulp capping
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There are new strategies in vital pulp therapy including lasers105 and regenerative techniques106. These newer areas of research will not only increase our understanding of the tertiary dentinogenesis process, but hopefully in the future, adjuncts or replacements will emerge to replace conventional treatment approaches.
pyrig No Co 255 t fo rP ub lica tio at the pulp–dentine border regulating tissue-specific n t processes of tertiary dentinogenesis19. It has long been e ss e n c e n
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To sterilise the wound surface and achieve a bloodless field, lasers have been suggested as a possible aid to pulp capping. Lasers have the ability to vaporise and coagulate, and in doing so, seal small blood vessels107. A plethora of lasers exists for use in dentistry and many different types have been investigated for their efficacy in pulp capping. The majority of the studies involved either the CO2 or Nd:YAG lasers107. The application of laser treatment directly on to pulpal tissue was first reported in an animal model using a CO2 laser108. The pulps of 34 teeth were exposed and subjected to eight blasts of the laser before being sealed with Dycal. After 1 month, the teeth were extracted and then examined histologically. It was concluded that, compared with the control samples, teeth exposed to the laser exhibited a faster and more constant reactionary dentinogenesis. However, the study was only preliminary in nature and the control groups were poorly defined. A concern with laser use on the dental pulp is the risk of pulpal damage, due to heat generation. Irreversible damage has been reported when lasers were used directly on the pulp109. However, other studies have reported the thermal effects of sterilisation and coagulation to be beneficial and it was suggested that lasers may be an invaluable tool in pulp capping110-112. Overall, laser pulp capping studies are limited and due to the large number of different techniques used, comparisons are difficult. Although the results so far form a basis for further research it must be remembered that lasers are expensive and may not be available to every practising clinician. In addition, clear safety parameters must be established to prevent damage to pulpal tissue prior to recommendation for routine clinical use105.
Regenerative therapy Recent biological advancements in developing a regenerative approach to pulp capping have centred on dentine-pulp stem cell therapy. Not only is the possibility of new and future treatment techniques being explored, possible mechanisms for defensive dentinogenesis during pulpal irritation are also being revealed. The ultimate goal of regenerative pulp therapy is to reconstitute a normal tissue continuum
known that dental pulp cells have the potential to develop into odontoblasts and this ability allows pulp tissue considerable ability to regenerate and repair. However, the exact molecular mechanisms involved are unclear29,113,114. It was recently hypothesised that dentine repair may be similar to bone repair, with the osteoinductive properties of dentine being due to a group of signalling proteins with multiple biological actions115,116. There has been much research in this area, exploring the molecular processes underlying tertiary dentinogenesis. It was demonstrated that the application of EDTA-soluble dentine components to unexposed cavities of animal teeth resulted in stimulation of odontoblasts117, and in a follow-up study118 the application of these products resulted in the formation of a zone of tertiary dentine. In addition, it has been suggested that caries-induced demineralisation of dentine releases bioactive molecules that initiate dentinogenesis57. It was concluded that dentine extracellular matrix is not an inert material, but contains bioactive molecules, which are available for release during pulp healing and repair. The activity of these bioactive molecules has also been investigated in controlled experiments, and it was concluded that the molecules acted as bioactive pulp-capping agents119,120. The possible benefits of bioactive pulp-capping agents are that they may be an improvement on conventional pulp-capping agents such as Ca(OH)2 or other artificial materials that can only produce a small amount of reparative dentine120. It is thought that these bioactive agents could produce larger amounts of dentine over exposed pulps, which would, therefore, offer better protection against microleakage and pulp infection119. However, an overproduction of dentine could lead to future management problems including canal obliteration and large areas of mineralisation in the coronal pulp31. It is also tempting to overlook the importance of infection control in preventing failure, when developing these new technologies. It is difficult to extrapolate the results to clinical application as the research, mostly in vitro or in animals, is still preliminary in nature. Therefore, critical questions, such as the type of carrier, the dose–response effects and the possible side-effects remain unanswered. Although the results so far reported are promising, there is still the need for further research. In a review by Tziafas19, it was con-
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Preserving the health of the dental pulp is an important aspect of modern endodontics. If successful, pulp preservation is more conservative and less technically demanding than pulpectomy. Therefore, pulp capping should form part of a clinician’s treatment armamentarium. The advent of MTA has provided renewed impetus in vital pulp treatment and this material is likely to supersede Ca(OH)2 as the agent of choice for pulp capping. Although the exact mechanisms are unknown, MTA and Ca(OH)2 appear to harness endogenous, biologically active molecules, thereby inducing dentinogenesis. This can result in successful pulpal healing if the pulp is not irreversibly inflamed and attention is given to preventing microleakage. The future of vital pulp treatment may involve development of regenerative techniques and further understanding the role of bioactive molecules. It is important that longitudinal prospective studies using modern materials are conducted to improve our knowledge and provide the necessary evidence base to support clinical practice.
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cluded that bioactive molecules should be subject to careful evaluation in well-designed preclinical investigations as well as clinical trials before they are introduced into general use. It was also concluded that, at least in the short term, modern materials capable of exploiting active molecules should be used.
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