|Vital Pulp Therapy|
|Date: 09/08/2011 16:26|
Vital Pulp Therapy
Vital Pulp Therapy - GEORGE BOGEN, NICHOLAS P. CHANDLER
Image resized (Original file: 300x432
Healing is a matter of time, but it is sometimes also a matter of opportunity.
Vital pulp therapy is broadly defined as treatment initiated to preserve and maintain pulp tissue in a healthy state, tissue that has been compromised by caries, trauma, or restorative procedures. The objective is to stimulate the formation of reparative dentin to retain the tooth as a functional unit. This is particularly important in the young adult tooth, where apical root development may be incomplete. This chapter describes advances in direct pulp capping and pulpotomy, where the treatment has been redefined by newly developed materials and protocols that are rapidly replacing long accepted strategies. The focus is directed toward the preservation of the pulpally involved permanent tooth, based on the premise that pulp tissue has an innate capacity for repair in the absence of microbial contamination.1
During the last decade, exceptional progress was made in the field of vital pulp therapy. Materials used in the past were both biologic and nonbiologic.2 Since the concept of indirect pulp capping was first documented in the eighteenth century by Pierre Fauchard, clinicians have recognized the innate capacity of the pulp tissue to initiate repair after injury from trauma, caries, or mechanical exposure.3 The first documented instance of vital pulp therapy is attributed to Phillip Pfaff, who placed gold foil against an exposed pulp with the intention to promote pulpal healing.4 Since the beginning of modern dentistry, researchers have endeavored to better understand and expand their knowledge of pulp physiology, microbiology, and caries progression. This has coincided with the quest to identify bioactive materials and physiologic mediators that consistently stimulate reparative dentin formation and protect the pulp against microbial ingress.
There is a long-held perception that pulp exposures in a carious field have an unfavorable prognosis and that more aggressive treatment, such as pulpotomy or pulpectomy, should be considered.5,6 These strategies are based on traditional treatment protocols and materials that did not provide a consistently suitable environment for pulpal repair and reparative bridge formation. Moreover, the diagnosis of the pulpal histologic condition is difficult to ascertain owing to the lack of a fundamental understanding of pulpal physiology, patient subjectivity, and the presence of inflammatory mediators that cannot be assessed clinically.7 Proper case selection, based on a new understanding of inflammatory mechanisms responsible for producing irreversible changes in pulpal tissue, can help identify teeth with a greater likelihood for favorable outcomes.
The challenge is to identify a reliable pulp capping or pulpotomy agent and a suitable delivery technique. The introduction of mineral trioxide aggregate (MTA) has opened a new frontier in vital pulp therapy and changed the perception that pulp capping in carious exposed teeth is unpredictable and therefore contraindicated. The outcome of vital pulp therapy will depend on the age of the patient, the size of the pulp, bacterial contamination, the pulp capping material, and the quality of the final restoration. The importance of establishing a differential diagnosis and proper case selection cannot be overemphasized. The pulp status must be determined carefully, establishing a differential diagnosis using multiple tests. According to the American Academy of Pediatric Dentistry, "Teeth exhibiting provoked pain of short duration, that is relieved, upon the removal of the stimulus, with analgesics, or by brushing, without signs and symptoms of irreversible pulpitis, have a clinical diagnosis of reversible pulpitis and are candidates for vital pulp therapy."8 The assessment of a definitive pulpal status prior to treatment is often difficult to establish; however, a diagnosis of reversible pulpitis increases the probability of a favorable outcome.7 A negative patient report, that is subjective and variable, does not always indicate that the pulp capping or pulpotomy procedure cannot be successful. Moreover, pain associated with cold testing prior to treatment or a pulp exposure during caries excavation does not necessarily mandate a poor prognosis for the involved tooth.
The Vital Dental Pulp
The pulp is a highly vascular tissue that has the unique distinction of being encased within a rigid chamber composed of dentin, cementum, and enamel.9 These hard tissues provide mechanical support and protection from the microorganisms associated with the oral cavity.10 The tissue performs several important functions, including dentinogenesis, immune cell defense, and nutrition and proprioreceptor cognizance. The retention and maintenance of the dental pulp are crucial to the long-term function of the tooth since during the life of the tooth, the healthy pulp produces reparative, secondary, and peritubular dentin in response to various biologic and pathologic stimuli.11
Since the vital pulp is capable of demonstrating competent immune defense mechanisms, it is desirable to preserve the vitality of an exposed pulp since its retention is crucial to the tooth's long-term survival. If the hard casing of the tooth is compromised and the pulp is subjected to microbial ingression, inflammatory changes can lead to pulp necrosis and further pathologic changes, including infection and its consequences.12,13 Circulating immunocompetent cells limit microbial challenges, and functioning proprioceptors and pressoreceptors guard against excessive occlusal loading. By contrast, structurally compromised teeth that have been endodontically treated and restored with various post and core systems are more susceptible to fracture and failure owing to the loss of protective mechanisms. Although studies show that the loss of moisture from dentin after endodontic therapy is minimal,14,15 cumulative loss of tooth structure is implicated in the failure of root-treated teeth.16
The dental pulp is composed of four distinct zones: a cell-rich zone, a core composed of major vessels and nerves, a cell-free zone, and the odontoblastic layer at the periphery. The major cell populations found in the pulp include fibroblasts, undifferentiated mesenchymal cells, odontoblasts, macrophages, and other immunocompetent cells. The odontoblasts have the distinction of forming a single layer lining the periphery of the pulp and feature odontoblastic processes extending into the dentin, sometimes to the dentoenamel junction.17-19 When the dental pulp is injured by trauma or carious exposure, the mechanism of healing is similar to that observed in normal connective tissue (see Chapter 5, "Embryology, Histology, and Physiology of the Dentin-Pulp Complex"
Wound healing is a continuous process, and a sequence of four phases of healing overlap, including hemostasis, inflammation, proliferation, and remodeling.20 After an injury, the tissue adjacent to the exposure is characterized by inflammatory cells, extravasated erythrocytes, and potentially necrotic tissue. An acute response is mounted, dominated by neutrophils in the presence of exudated fibrinogen and blood coagulation. Vascular permeability is altered when proinflammatory cytokines are released by immunocompetent cells in response to both trauma and bacterial by-products. Chemotactic signals prompt adhesion molecule interactions between leukocytes and endothelium, enabling transmigration of inflammatory cells. These cell interactions form an adhesion cascade mediated by chemoattractant/activator molecules interacting with sets of cell adhesion molecules.21
Reparative Dentin Formation
The reformation of a protective dentinal bridge by tertiary dentinogenesis is a primary goal of vital pulp therapy. The repair of pulpodentinal defects is orchestrated by the migration of granulation tissue to the site from the cell-rich and deep pulp subodontoblastic layers that differentiate into new odontoblast-like cells. Although these progenitor cells are most likely derived from undifferentiated mesenchymal cells, other cell populations migrating via the bloodstream, such as bone marrow stem cells and perivascular cells, have been proposed as possible precursors.22
The migration and proliferation of these cells were studied in nonhuman primates after direct pulp capping with calcium hydroxide (Ca(OH)2).23 At the calcium hydroxide-pulp interface, a continuous influx of newly differentiating odontoblast-type cells with initial matrix formation was observed as early as day 8. Labeled odontoblast-like cells showed differences in cell types and grain counts between zones, indicating that at least two deoxyribonucleic acid (DNA) replications had occurred between initial treatment and differentiation. Studies have suggested that the mineralization of dentin bridges is more dependent on the extracellular matrix than the pulp capping or pulpotomy material.24-26
In a transmission electron microscopic study by Hayashi, initial calcification during pulp healing, characterized by an abundance of extracellular matrix vesicles, was located between the amputated pulp surface and the forming cells that contained needle-like crystals and osmiophilic material.27 After the disappearance of the vesicular membrane, a calcified front formed as crystals and aggregate accumulated. The presence of calcium and phosphate ions within the crystals suggested that they were produced during the calcification process, similar to the calcification in other biologically normal or diseased tissues. Dentin bridge formation can be seen after 1 month at the site of the surgical wound, although pulp healing defects can be associated with different pulp capping agents and include tunnel defects, operative debris, pulpal inflammatory cell activity, and bacterial micro-leakage.28
Techniques for Generating Reparative Dentin
DIRECT PULP CAPPING
The most widely used vital pulp therapy techniques for permanent teeth include direct and indirect pulp capping and partial or complete pulpotomy. Direct pulp capping is defined as the "treatment of an exposed vital pulp by sealing the pulpal wound with a dental material placed directly on a mechanical or traumatic exposure to facilitate the formation of reparative dentin and maintenance of the vital pulp."29 The indications for direct pulp capping include exposures as a result of caries removal, tooth preparation, or trauma. Pulp tissue, jeopardized by a long-standing exposure to oral microorganisms and acute inflammation, may be unsuitable for direct pulp capping.30 Direct pulp capping for carious exposures is discussed in detail later in this chapter.
INDIRECT PULP CAPPING
Indirect pulp capping is defined as "a procedure in which a material is placed on a thin partition of remaining carious dentin that, if removed, might expose the pulp in immature permanent teeth.29 This technique shows some success in teeth with an absence of symptomatology and with no radiographic evidence of pathosis.30 It has been controversial for decades.31 The strategy involved various techniques in which caries removal was completed to a point near the pulp tissue without direct exposure. The potential for pulpal repair has been demonstrated in selected teeth with deep carious lesions where caries excavation was conservative and direct pulp exposures were avoided.32,33 Indirect pulp caps are completed using either Ca(OH)2 or zinc oxide-eugenol (ZOE) in a one- or two-stage procedure. The major difficulty with the procedure (one or two stage) is to determine at what point excavation is halted. Moreover, voids under the restorative material result during the remineralization process, in which the carious dentin dries out and loses volume. Another complication is restoration failure and rapid reactivation of a dormant lesion.34 Indirect pulp capping is not recommended as a predictable treatment for permanent teeth.
Pulpotomy is a more extensive procedure defined as "the surgical removal of the coronal portion of a vital pulp as a means of preserving the vitality of the remaining radicular portion."29 After the complete removal of the coronal pulp, a material is placed over the canal orifices. A variety of dressing materials, with varying toxicity, have been used for this purpose. They include phenol, creosote, ferric sulfate, polycarboxylate cement, glutaraldehyde, ZOE, Ca(OH)2, and formaldehyde, which mummifies the remaining tissue.35 Although studies indicate that short-term success rates are favorable, this procedure is generally advocated for deciduous teeth. Pulpotomies in young adult teeth have been completed with formocresol, although the material has distinct disadvantages.36 Aside from the issue of systemic sensitivity to the agent, experiments with primates have shown a high incidence of internal resorption.37 Also, orthograde endodontic treatment can be difficult to complete owing to changes in the canal system apical to the formocresol.38 In addition to pulpotomies performed on permanent teeth, recent studies have shown MTA to be a suitable replacement for formocresol in pulpotomy of primary molars.39,40
Partial pulpotomy (Cvek pulpotomy) is defined as "the surgical removal of a small portion of the coronal portion of a vital pulp as a means of preserving the remaining coronal and radicular pulp."29 In this instance, inflamed tissue is removed to expose deeper, healthy coronal pulp tissue.41 Direct pulp capping and partial pulpotomy are considered similar procedures and differ only in the amount of undestroyed tissue remaining after treatment.
Indications for Vital Pulp Therapy
Vital pulp therapy is indicated whenever the remaining pulp exhibits reversible pulpitis and can be selectively induced to produce a reparative barrier that protects the tissue from microbial challenges. In particular, direct pulp capping can be performed for teeth with deep caries, mechanical exposures, and traumatic injuries to maximize pulpal preservation. The outcome of treatment for direct pulp capping or pulpotomy will be determined by the initial diagnosis, which includes radiographic evaluation, pulp testing, clinical evaluation, and patient history. The intention is to postpone more aggressive therapies that could eventually lower the long-term prognosis for tooth retention and function. Teeth undergoing orthograde root canal therapy and placement of posts and cores, followed by full coverage or cuspal coverage restorations, show lower long-term survival rates than teeth with vital pulps.42-48
Vital Pulp Therapy Materials
The search for the ideal vital pulp therapy material has led researchers to investigate many different materials. These include Ca(OH)2 compounds,49-52 zinc oxide, calcium phosphate, zinc phosphate and polycarboxylate cements, calcium-tetracycline chelate, antibiotic and growth factor combinations, calcium phosphate ceramics, Emdogain, Bioglass, cyanoacrylate, hydrophilic resins, hydroxyapatite, resin-modified glass ionomers, and, recently, MTA.53-63 Other studies have included Ledermix, glycerrhetinic acid-antibiotic mix, potassium nitrate, and dimethyl isosorbide.64 Innovative methods have also been used to eliminate caries progression and stimulate the repair of affected pulpal tissue and include ozone technology, lasers, and bioactive agents that activate pulpal defenses.65-68 Favorable outcomes in direct pulp capping have varied depending on the techniques and materials, with human retrospective studies showing 30 to 85% success rates at 5 to 10 years.49-52 Researchers have strived for decades to identify and produce a pulp capping material that, ideally, would exhibit the following characteristics:69
• Stimulate reparative dentin formation
• Maintain pulpal vitality
• Release fluoride to prevent secondary caries
• Bactericidal or bacteriostatic
• Adhere to dentin
• Adhere to restorative material
• Resist forces during restoration placement
• Must resist forces under restoration during lifetime of restoration
• Provide bacterial seal
This material, long considered the "benchmark" for vital pulp therapy materials (Figure 1), has been shown to have some desirable properties, but long-term study outcomes have been variable.51,52 Beneficial characteristics include a bactericidal component owing to its high alkaline pH and the irritation of pulp tissue that stimulates pulpal defense and repair.70 Conversely, Ca(OH)2 has been shown to be cytotoxic in cell cultures, does not exclusively stimulate reparative dentin formation, shows poor marginal adaptation to dentin, and induces pulp cell apoptosis.71-73 The material can be associated with primary tooth resorption, it can degrade and dissolve beneath restorations, and it can also suffer interfacial failure upon amalgam condensation.74-76 It produces a gap between the dentin interface when used with bonding resins.77 Dentin bridges beneath Ca(OH)2 are associated with tunnel defects, and the material fails to provide a long-term seal against microleakage when used as a pulp capping agent.71,76 The disintegration of Ca(OH)2 under restorations associated with defects in the dentinal bridge can provide microorganisms with a pathway for penetration into pulpal tissue and the subsequent stimulation of circulating immune cells, inducing pulpal irritation and potential pulpal calcification and canal obliteration.
Figure 1. Pulpotomy with calcium hydroxide and amalgam. A, A 10-year-old boy with a deep carious lesion of the maxillary molar; clinical symptoms and examination indicated reversible pulpitis. B, Complete pulpotomy of the coronal pulp was done, followed by placement of a calcium hydroxide hard-setting paste and amalgam restoration. C, One-year follow-up shows additional placement of a stainless steel crown. The tooth was asymptomatic, and there were no radiographic changes. Courtesy, Dr. Leif K. Bakland.0
ADHESIVE RESINS AND RESIN-MODIFIED GLASS IONOMERS
The use of adhesive systems for direct pulp capping was first introduced by Japanese researchers in the early 1980s.78-80 Preliminary research with nonhuman primate models using ISO standards was encouraging.81-85 Exposed pulps directly capped with various resins and
[Figure 1. Pulpotomy with calcium hydroxide and amalgam. A, A 10-year-old boy with a deep carious lesion of the maxillary molar; clinical symptoms and examination indicated reversible pulpitis. B, Complete pulpotomy of the coronal pulp was done, followed by placement of a calcium hydroxide hard-setting paste and amalgam restoration. C, One-year follow-up shows additional placement of a stainless steel crown. The tooth was asymptomatic, and there were no radiographic changes.]
evaluated histologically for pulpal reaction, microbial presence, and the formation of reparative dentin formation showed favorable biocompatibility. Although these favorable results were observed in nonhuman primates, the transition was not paralleled in human subjects.86-90 Research by several investigators in humans showed unfavorable histologic reactions to the resins when placed directly against pulp tissue. Many histologic sections from these investigations were characterized by mononuclear inflammatory infiltrates, macrophages, polymorphonuclear leukocytes, multinuclear giant cells, and an absence of calcific bridge formation.86,87,90
Two clinical studies on human subjects compared direct pulp capping with either resin-modified glass ionomer cement or with a hydrophilic resin.91,92 Histologic results showed that both Vitrebond (3M Espe Dental Products, St. Paul, MN) and Clearfil Liner Bond 2 (Kuraray Co., LTD, Osaka, Japan) resulted initially in a moderate to intense inflammatory response and did not stimulate reparative dentin formation at 300 days. Further investigations in nonhuman subjects have revealed the unpredictable nature of reparative dentin formation and the contamination of reparative dentin bridges by bacteria. In a study by Murray et al., in which the hierarchy of repair was measured against microbial contamination, 18.6% of resin-based composite, 22.2% of resin-modified glass ionomer, and 47.0% of Ca(OH)2 specimens showed bacterial contamination of the reparative dentin bridge.93 This is an indication that these pulp capping materials do not allow for predictable pulpal healing, nor do they provide a favorable environment for reparative dentin formation and the exclusion of microorganisms.94,95 Repair should proceed successfully beneath the material when bacterial microleakage is precluded.
MINERAL TRIOXIDE AGGREGATE
MTA was introduced to endodontics by Lee et al. in the early 1990s.96 This bioactive silicate cement was originally composed of tricalcium silicate, tricalcium aluminate, tricalcium oxide, silicate oxide, and other mineral oxides.97 The product is currently marketed under several names around the world and in one form (ProRoot MTA, Tulsa/Dentsply, Tulsa, OK) has changed in composition since its introduction with the substitution of dicalcium silicate for tricalcium silicate and the addition of tertracalcium aluminoferrite, calcium sulfate dehydrate, and bismuth oxide; the latter was added to impart radiopacity.98 Originally a gray powder, white MTA was produced for esthetic reasons with the reduction of ferrite (Fe3O3) with no detectable change in clinical performance.98-101
[Figure 2. Comparison of dentin bridge formation using mineral trioxide aggregate (MTA) or calcium hydroxide in dog pulps. A, After 1 week, a noticeable bridge has formed subjacent to MTA. B, A comparable bridge under calcium hydroxide after 2 weeks. C, A 4-week specimen with MTA shows excellent bridge formation. D, Consistently, the bridge formation under calcium hydroxide lagged behind MTA; an example of bridge formation under calcium hydroxide after 8 weeks. CH = calcium hydroxide; DB = dentin bridge; MTA = mineral trioxide aggregate.]
The cement exhibits many favorable characteristics, which make it a superior material when used as a direct pulp capping material in adult teeth or as an agent in partial or complete pulpotomy in primary teeth.102,103 MTA is structurally similar to Portland cement, which physiochemically allows the material to set in the presence of blood and moisture.104 It exhibits a superior marginal adaptation and is nonabsorbabale, and when it cures in the presence of calcium ions and tissue fluids, it forms a reactionary layer at the dentin interface resembling hydroxyapatite in structure.104-106 Other biocompatible characteristics include a sustained alkaline pH after curing, small particle size, and a slow release of calcium ions.107 Studies have also demonstrated that MTA stimulates cytokine release, induces pulpal cell proliferation, and promotes hard tissue formation.108,109 The high alkalinity of MTA and its calcium release and sustained pH at 12.5 is most likely responsible for preventing any further microbial growth of residual microorganisms left after caries excavation. The high pH also extracts growth factors from adjacent dentin thought to be responsible for promoting dentinal bridging.108,110
Direct pulp capping with MTA has proven to be effective in stimulating tertiary dentin formation in canine models (Figure 2) and primates.60,111,112 Recent investigations have shown favorable short-term outcomes in humans when pulpotomies (partial or complete) (Figure 3) or direct pulp capping using MTA was examined.113-117 According to Tomson et al., the bioactive properties of MTA that stimulate reparative bridge formation can be attributable to the material providing a biocompatible noncytotoxic antibacterial environment.118 MTA also provides a favorable surface morphology for cell attachment and has the ability to form hydroxyapatite on its surface in the presence of tissue fluid. They hypothesized that soluble components of MTA during and after setting on the dentin interface may cause the release of growth factors
[Figure 3. Pulpotomy on young immature permanent teeth using mineral trioxide aggregate (MTA). A, Recurrent decay under a previous restoration (amalgam and stainless steel crown); clinical symptoms and examination indicated reversible pulpitis. Complete pulpotomy of coronal pulp using MTA and amalgam was done. B, Follow-up evaluation 18 months later shows continued root formation, and the tooth is asymptomatic. C, Radiograph of a maxillary molar in a 10-year-old girl shows extensive caries involvement; based on clinical symptoms and examination, the pulp was determined to be reversibly involved. After caries excavation, the coronal pulp tissue was removed and MTA was placed followed by amalgam. D, The 18-month follow-up shows normal periapical tissues, and the tooth was asymptomatic.]
and other bioactive molecules, such as transforming growth factor beta (TGF-β1) and adrenomedullin. The increased presence of these dentine extracellular proteins as the result of MTA culminates in dentin bridge formation after stimulating reparative dentinogenic mechanisms.
A current observational study examined MTA as a direct pulp capping agent using a two-visit protocol in permanent teeth in which cold testing determined a pulpal diagnosis no more severe than irreversible pulpitis.119 Teeth were selected for treatment that exhibited no detectable pathosis based on radiographic evidence and no clinical signs of swelling, furcation defects, or sinus tracts. Teeth received caries removal under magnification using a caries detector dye. Hemostasis was provided by direct contact with 5.25 to 6.0% sodium hypochlorite (NaOCl) for periods of 5 to 10 minutes. MTA was placed over the exposure, and all surrounding dentin of the pulpal roof or axial wall and teeth received interim restorations with a moist cotton pellet and unbonded Photocore (Kuraray Co., LTD).
On a second visit, after 5 to 10 days, the teeth were permanently restored with a bonded composite (Clearfil LinerBond 2 and Clearfil AP-X composite, Kuraray Co.), but only after confirmation that the MTA had set and normal responses to vitality testing were elicited. Radiographic recalls were evaluated for reparative dentin formation, pulpal calcification, continued normal root development, and the absence of pathosis. Fortynine teeth were observed for a 1- to 9-year period, with an average observation time of 3.94 years. Favorable outcomes, based on subjective symptomatology and cold testing, was 97.96%. Pulpal calcifications were seen in 10.6% (5 of 49) of cases, and all teeth (15 of 15) in younger patients showed complete root formation (apexogenesis) when open apices were present initially.119
The remarkable outcomes for direct pulp capping with MTA are attributable to distinctive properties inherent to the material. The sustained alkaline pH of the set cement is bactericidal and most likely contributes with NaOCl to the elimination of many residual microorganisms left at the dentin-pulpal interface after exposure. MTA is hygroscopic and sets in the presence of moisture, so direct contact with tissue fluids or blood does not affect the curing properties. The close adaptation of the silicate cement produces a virtually gap-free interface owing to the small particle size and precludes microleakage and bacterial ingression. MTA may also act to entomb residual microorganisms at the dentin interface. The slow release of calcium ions also allows the material to stimulate growth factors from the dental pulp and promote signaling molecules (TGF-β, interleukin [IL]-1α, IL-β, macrophage colony-stimulating factor (MCSF), that encourage hard tissue formation.108 The compressive strength and surface texture of the set cement allow strong bonding with adhesive restorations and minimal compression under heavy loading when a final restoration is placed.
Figure 2. Comparison of dentin bridge formation using mineral trioxide aggregate (MTA) or calcium hydroxide in dog pulps. A, After 1 week, a noticeable bridge has formed subjacent to MTA. B, A comparable bridge under calcium hydroxide after 2 weeks. C, A 4-week specimen with MTA shows excellent bridge formation. D, Consistently, the bridge formation under calcium hydroxide lagged behind MTA; an example of bridge formation under calcium hydroxide after 8 weeks. CH = calcium hydroxide; DB = dentin bridge; MTA = mineral trioxide aggregate. Reproduced with permission from Junn DJ.1110
Figure 3. Pulpotomy on young immature permanent teeth using mineral trioxide aggregate (MTA). A, Recurrent decay under a previous restoration (amalgam and stainless steel crown); clinical symptoms and examination indicated reversible pulpitis. Complete pulpotomy of coronal pulp using MTA and amalgam was done. B, Follow-up evaluation 18 months later shows continued root formation, and the tooth is asymptomatic. C, Radiograph of a maxillary molar in a 10-year-old girl shows extensive caries involvement; based on clinical symptoms and examination, the pulp was determined to be reversibly involved. After caries excavation, the coronal pulp tissue was removed and MTA was placed followed by amalgam. D, The 18-month follow-up shows normal periapical tissues, and the tooth was asymptomatic. Reproduced with permission from Lauer HH. Vital pulp therapy with MTA: an outcomes study [thesis]. Loma Linda (CA): Loma Linda University; CA, 2005.0
Diagnostic Criteria for Successful Outcome
Direct pulp capping and partial and complete pulpotomy are important treatment options for the immature permanent tooth. Whether the coronal pulp tissue is preserved in toto, partially removed, or removed to the base of the pulpal floor, the preservation of the radicular pulp tissue allows continuing development and apical maturation (apexogenesis) of teeth with open apices. Moreover, in cases of trauma, in which tooth development may be interrupted, induction of apexogenesis should be the clinician's primary goal, with the pulp protected and encouraged to remain vital.120-122
Before treatment can be initiated, the clinician must make a careful assessment of all available information. Important aspects of vital pulp therapy include a differential diagnosis based on medical history, radiographic evidence, patient report, percussion testing, and vitality testing. Clinical evaluation must also include assessment of mobility, periodontal probing, localized swelling, and the presence of sinus tracts. Radiographs (both periapical views and bitewings) must be assessed for the absence of periapical pathosis, furcation radiolucencies, internal or external resorption defects, and pulp calcification owing to previous restorations or trauma.
After the radiographic and clinical assessments indicate an absence of disease, subjective symptomatology must be considered. Although most patients with deep carious lesions can often experience sensitivity to heat, cold, and certain acidic or sweet foods, the subjective response to cold testing can be variable, and a short, lingering response (1-2 seconds) may not be an indication that the pulp is irreversibly involved. Studies have shown that cold testing responses in primary teeth are unpredictable, and testing may also be confounded in some individuals in immature permanent teeth.123,124 Pain to percussion is most often associated with irreversible pulpitis. In teeth with open apices with irreversible pulpitis, pulpectomy is recommended using MTA as a root-end plug to promote root-end closure (apexogenesis).122,125
All teeth that have previous restorations, or a history of trauma, have a lower prognosis for repair and tertiary dentin formation than teeth with initial caries alone.126,127 In mature permanent teeth receiving full coverage, only teeth with no previous history of restorative treatment should be considered for direct pulp capping. From a technical standpoint, pulp exposure on the occlusal surface of a full crown preparation may have the best prognosis. Pulp exposures on axial walls of full-coverage preparations are extremely difficult to treat clinically owing to the handling properties of MTA and the technical challenge of placing the material against an open vertical wall. In these cases, orthograde root canal therapy should be considered a more predictable and suitable treatment option.
The remaining tooth structure should also be considered when selecting an appropriate vital pulp treatment. In teeth exhibiting advanced caries and severe coronal breakdown, requiring full coverage, pulpotomy rather than direct pulp capping is recommended. In patients with rampant caries, pulpotomies are recommended rather than direct pulp capping since the majority of these patients will exhibit recurrent caries at a higher rate.128-130 Young patients who exhibit initial caries on all first molars can still be considered excellent candidates for direct pulp capping if the differential diagnosis indicates reversible pulpitis in all teeth evaluated. It is also evident that a favorable prognosis for vital pulp therapy diminishes with the increasing age of the patient.52,130
The diagnosis can be further confirmed at the time of pulp exposure when the pulp is visualized and hemorrhage control is assessed. In cases without bleeding, then the tissue is most likely necrotic and should be removed to a point where bleeding is encountered. A partial pulpotomy is completed with a high-speed diamond round bur with direct placement of MTA against the entire wound after achieving hemostasis. In teeth with pulp exposures, where bleeding cannot be controlled with 3 to 6% NaOCl within a 10-minute contact period, the diagnosis must be changed to irreversible pulpitis, and pulpotomy or pulpectomy is recommended. The type of vital pulp therapy delivered is based on the option that will best benefit the patient and secure the optimum prognosis for the long-term retention of the tooth.
Pulp sizes are underestimated on radiographs, possibly leading to a greater risk of an unexpected and sizeable pulpal exposure.131 The observation of Matsuo et al. that the size of an exposure has no influence on the outcome is important.132 Erroneously, clinicians probably assume that larger exposures have a poorer prognosis and may include size in their decision making. In a recent study involving the examination of simulated exposures (0.5-0.9 mm), dentists without a ruler or previous calibration overestimated exposure size by a mean of 26%.133 There may also be differences in some pulp dimensions between the genders and among racial groups.
|Date: 09/08/2011 16:30|
Re: Vital Pulp Therapy
Dental dam isolation, aided by a caries detector dye and optical magnification during caries removal may be critical implements in achieving favorable results for direct pulp capping. Fusayama et al. made considerable progress in caries research by redefining the carious process and presenting a technique for objectively removing infected tissue, thus contributing to pulpal protection and survival.135,136 They indicated that gram-positive bacteria, whose main by-product is lactic acid, first break down hydroxyapatite and collagen in the outer carious layer but spare banded collagen in the second layer, where the intermolecular cross-links are still intact.137,138 They also discovered that pulpal repair and preservation were possible in teeth sealed with bonded composites if the upper layer of two distinctive carious layers could be selectively stained and carefully removed.
Preservation of the second (caries affected) layer allowed for the exclusion of the majority of necrotic dentin and invading bacteria at the deepest point of microbial penetration, responsible for the production of proinflammatory mediators at the pulp-dentin interface. Moreover, since restoration placement was no longer dependent on retentive cavity preparations, more tooth structure could be spared, with less resultant trauma to the dental pulp.
The development of caries staining using a propylene glycol solution of Acid Red 52 dye (a common food and cosmetic coloring dye) provides visible differentiation of the two carious layers and is a selective method to remove the necrotic and infected dentin.138 The retained caries-affected layer of dentin, which contains banded, intact collagen, allows for the remineralization of the altered tissue by calcium phosphate secreted from the pulp via the dentinal tubules. In the dentinal tubules, calcium and phosphate ions induce the formation of whitlockite crystals, which block the tubules. This remineralization of caries-affected dentin has been confirmed in canine and primate models.139,140 Fusayama argued that conservative objective caries removal promotes pulpal preservation without injuring residual caries-affected dentin that is reparable and remineralizable when a bonded composite restoration is placed to prevent microbial leakage.138 Although several studies have questioned the efficacy of caries removal using a caries detector dye, the material does allow the operator to visually inspect under magnification infected dentin that may have been overlooked and potentially compromise the outcome for direct pulp capping (Figure 4).141-144
[Figure 4. Caries removal procedure. A, Clinical appearance of a mandibular molar with extensive caries after dental dam placement. B, Occlusal view after caries removal, including the use of a caries detector dye, and hemostasis using 6.0% NaOCl for a 5-minute period. Note four pulp horn exposures ranging in size from 0.5 to 2.0 mm; hemorrhaging has stopped.]
Figure 4. Caries removal procedure. A, Clinical appearance of a mandibular molar with extensive caries after dental dam placement. B, Occlusal view after caries removal, including the use of a caries detector dye, and hemostasis using 6.0% NaOCl for a 5-minute period. Note four pulp horn exposures ranging in size from 0.5 to 2.0 mm; hemorrhaging has stopped. Courtesy, Dr. George Bogan.0
Many different hemostatic agents and antimicrobial materials have been introduced into the field of vital pulp therapy. These include ferric sulfate, disinfectants such as Concepsis (Ultradent Products Inc., South Jordan, UT) and Tubulicid (Global Dental Products, North Bellmore, NY) epinephrine, and varying concentrations of hydrogen peroxide (H2O2) and NaOCl. The most commonly accepted technique has been direct pressure at the exposure site with cotton pellets moistened in sterile water or saline. Other techniques using electrosurgery and lasers have shown limited value in hemorrhage control.145 NaOCl, widely regarded as the most effective antimicrobial irrigant in endodontic therapy during chemomechanical cleaning of the root canal system, has been advocated as an agent in direct pulp capping and pulpotomy since the early 1950s.146,147 The main advantages of NaOCl not only include excellent hemostasis at the pulpal wound site, but the solution also allows for the clearance of most dentin chips, biofilm removal, chemical amputation of the blood clot and fibrin, disinfection of the cavity interface, and the removal of damaged cells from the mechanical or traumatic exposure.145,148,149 The dissolving capacity of 5.25% to 6.0% NaOCl appears to affect only the peripheral pulp cells without impairing underlying pulp tissue.150 Although concentrations of NaOCl greater than 0.025% have been shown to be adverse to wound healing as a fluid dressing in burn victims, the reaction to pulp tissue appears to be relatively benign.151
The importance of hemostasis in vital pulp therapy was demonstrated in an eloquent study by Matsuo et al., in which treatment outcomes revealed a 2-year success rate of 81.8%.132 Teeth were directly pulp-capped with a fast-setting Ca(OH)2 material after pulp exposures occurred during caries removal. Caries removal was completed under the guide of a caries detector dye, and hemorrhage control was completed with 10% NaOCl. Statistical analysis showed that the age of the patients, type of teeth, responses to thermal stimuli and percussion, and diameter of the pulpal exposure had no bearing on the success rate. The one significant measurable variable that predicted a favorable outcome was the degree to which bleeding could be arrested at the exposure site. This observation underscores the importance of proper hemostasis in the success of direct pulp capping and pulpotomy procedures.
It has been shown that higher levels of inflammatory mediators, including immunoglobulin (Ig)M, IgG, IgA, prostaglandin E2, and elastase, are present in clinically inflamed pulps.152 This suggests that greater levels of these mediators may affect the degree of intrapulpal pressure and the likelihood of securing pulpal hemostasis. In cases in which pulpal hemostasis cannot be achieved within 5 to 10 minutes, the diagnosis should be considered irreversible pulpitis, and pulpotomy or pulpectomy should be considered.
The use of undiluted NaOCl (5.25%) was investigated histologically in beagle dogs on vital pulp tissue exposed on freshly cut dentin prepared to a depth of 2 mm. After the cavities were sealed with Cavit, pulps examined at 1- and 4-week time periods were free of inflammatory cells. The use of NaOCl did not appear to cause any additional pulpal damage after the trauma of exposing dentin and vital dentinal tubules.153 Similarly, NaOCl at varying concentrations did not affect positive outcomes in primates when pulps were capped directly with adhesive resins.148,149
In a clinical evaluation by Demir and Cehreli, 1.25% NaOCl was used for 60 seconds to ensure hemorrhage control in human primary teeth that were pulp-capped with either Ca(OH)2 or various adhesive bonding agents.154 The teeth were evaluated clinically and radiographically over a period of 24 months, and the outcome revealed a 93% survival rate when exfoliations were excluded. Sodium hypochlorite hemostasis did not seem to impair the biologic repair and subsequent tertiary dentinogenesis. This was reaffirmed in a study by Vargas et al. in which pulpotomies were compared using either NaOCl or ferric sulfate (FeSO4) on primary teeth that were then restored with Intermediate restorative material (IRM) base/stainless steel crowns.155 Short-term evaluation at 1 year showed a 100% retention rate of all teeth in the NaOCl group and 79% radiographic success, higher than the FeSO4 group. Although FeSO4 is effective as a hemostatic agent and recommended as a replacement for formocresol in pulpotomies on deciduous teeth, its use is not recommended if bonded restorations are used since it interferes with the bond strength of adhesive resins.156
In a study completed on human third molars, direct pulp caps were examined histologically at 30 and 90 days after pulp capping with either Ca(OH)2 or a self-etching adhesive system after using 2.5% NaOCl for hemostasis.157 Although Ca(OH)2 appeared to perform better biologically, pulpal repair was not compromised by the use of NaOCl. When comparing hemostatic agents in healthy human pulp tissue, the exposure to 0.9% saline, 5.25% NaOCl, or 2% chlorhexidine digluconate did not incapacitate healing after direct pulp capping with Ca(OH)2 at 90 days.158 Clearly, the use of NaOCl in concentrations of 1.25 to 6.0% for direct pulpal exposures can be recommended as a relatively safe and practical method to predictably achieve hemostasis in vital pulp therapy.154,155,157,158
Another emerging potential hemostatic agent is MTAD (Biopure, Tulsa/Dentsply), an irrigant and an antimicrobial agent introduced for removal of the smear layer during nonsurgical initial endodontic treatment and retreatment.159 The solution is a mixture of tetracycline isomer (doxycycline), an acid (citric acid), and a detergent (Tween 80). The irrigant shows many desirable properties and may be a suitable replacement for ethylenediaminetetraacetic acid in conjunction with NaOCl. The solution shows an antimicrobial effect against some strains of Enterococcus faecalis, cleans the dentin-pulp tissue interface, and does not affect the flexural strength and modulus of elasticity of dentin.160-162 Initial trials with MTAD indicate favorable results when used in direct pulp capping and partial pulpotomy (Dr. Mahmoud Torabinejad, personal communication, 2007).
Direct Pulp Capping
Recommended steps for direct pulp capping with MTA using a two-visit format (Figure 5):
1. Following diagnosis, the tooth has been identified as having either reversible pulpitis or a normal healthy pulp. After profound local anesthesia, the tooth is isolated with a dental dam, further sealed with an agent such as Oraseal (Ultradent Products Inc., South Jordan, UT) or a comparable product if required, and disinfected with either chlorhexidine or NaOCl. Working under magnification is highly recommended. The undermined enamel is removed with a diamond or carbide bur, and soft debris is removed with a spoon excavator.
2. After the carious dentin is air-dried, a caries detector dye is applied for 10 seconds, and the tooth is washed and dried. Caries removal is completed with slow-speed number 4-2 carbide round burs and spoon excavators until minimal (light pink) or no profound stained dentin is evident. The caries detector is again reapplied on air-dried dentin for 10 seconds, and the process is repeated carefully (possibly five to seven applications) until no or only light pink staining is evident.
3. If a pulpal exposure occurs during the caries removal, the bleeding can be controlled by the placement of a cotton pellet moistened with 3 to 6% NaOCl for 20 to 60 seconds, and the staining and removal process is continued carefully around the exposure site until little or no staining is visible.
4. After caries removal, the exposure(s) should be hemorrhaging to some degree. A cotton pellet moistened with 3% to 6% NaOCl is placed directly against the exposure(s) for a contact time of 1 to 10 minutes. If hemostasis is not achieved within 10 minutes, the diagnosis is changed to irreversible pulpitis and more aggressive treatment is indicated. Conversely, if bleeding is not evident after pulpal exposure, the tissue is most likely necrotic, and partial or complete pulpotomy or pulpectomy must be initiated using a high-speed diamond round bur. If, during the course of caries removal, the entire pulpal roof or axial wall is removed, a pulpotomy must be considered.
5. The MTA is mixed according to the manufacturer's instructions (3:1, MTA:H2O) and will have the consistency of wet sand. The cement is brought to the site in bulk with either a hand instrument (Glick or spoon excavator) or an MTA carrier gun. The MTA should be placed directly over the exposed pulp tissue and all surrounding dentin. The material is gently patted down with a small moist cotton pellet or a dry pellet if the mixture is too wet, and when in place, it should be at least 1.5 mm thick. If MTA is pushed inadvertently into the pulp chamber, it will not impact the outcome negatively. A circumferential region of dentin and enamel measuring approximately 1.5 mm should be cleared around the MTA with a small (2 mm) moist cotton pellet placed at the end of an explorer. This will allow an adequate area for the future bonded restoration to provide an effective seal.
6. A custom-fabricated, flat (1-2 mm), moist cotton pellet is then placed over the entire area of the MTA. If the area involves a Class II preparation exposure including the axial wall, then the moist pellet may require placement in two sections. If the patient is willing to return within 4 hours, a large moist cotton pellet can be placed and the patient instructed not to eat or chew during the interim since this may disrupt the MTA placement.
7. After the cotton pellet placement, a strong interim restoration is provided, preferably an unbonded composite material that will facilitate removal during the second visit (e.g., Photocore, Kuraray). Unless amalgam is the designated restorative material, interim restorations such as
[Figure 5. Radiographic and clinical sequence showing direct pulp capping of a mandibular left molar in a 7-year-old female patient. A, Pretreatment radiograph showing caries and the presence of immature apices. B, Clinical presentation following dental dam placement. C, Caries detector stain applied after removal of undermined enamel. D, Two-millimeter pulp exposure after caries removal and 5.25% NaOCl hemostasis. E, MTA of 2.5 mm thickness placed over the entire pulpal roof. F, Radiograph of MTA with a moist cotton pellet and unbonded Photocore as the interim restoration. G, Bonded composite restoration placed over cured MTA 10 days after direct pulp capping. H, Eight-year 4-month recall radiograph showing completed root formation. The tooth has a normal response to CO2 ice testing. A, F, and G, reproduced with permission from Schmitt D et al.102]
IRM or ZOE (that are eugenol based) will interfere with adhesion and bond strengths of adhesive resins and should be avoided.163
8. The second appointment can be scheduled 5 to 10 days after MTA placement. Before attaining profound anesthesia, the patient is questioned about sensitivity, mastication comfort, or the presence of pain. The tooth is then cold-tested (CO2 ice or Endo-Ice, Hygienic Corp., Akron, OH) to confirm continued normal vitality. After injection of a local anesthetic, the tooth is isolated as before. The interim material is removed with a high-speed diamond or carbide bur under water spray. The cotton pellet is removed and the imbedded cotton fibers removed with a spoon excavator or similar hand instrument. Working with magnification is strongly recommended. The MTA is checked to ensure proper curing, and a bonded composite restoration is placed following the manufacturer's recommendations.
9. After the permanent restoration is placed, the occlusion is checked and adjusted as required. The patient is then recalled at 6 weeks, and subjective symptomatology and cold testing are evaluated. If it appears that the procedure was successful, radiographic follow-up, cold testing, and subjective symptomatology can be evaluated at 6 and 12 months. The patient can then be evaluated on a yearly basis thereafter.
Figure 5. Radiographic and clinical sequence showing direct pulp capping of a mandibular left molar in a 7-year-old female patient. A, Pretreatment radiograph showing caries and the presence of immature apices. B, Clinical presentation following dental dam placement. C, Caries detector stain applied after removal of undermined enamel. D, Two-millimeter pulp exposure after caries removal and 5.25% NaOCl hemostasis. E, MTA of 2.5 mm thickness placed over the entire pulpal roof. F, Radiograph of MTA with a moist cotton pellet and unbonded Photocore as the interim restoration. G, Bonded composite restoration placed over cured MTA 10 days after direct pulp capping. H, Eight-year 4-month recall radiograph showing completed root formation. The tooth has a normal response to CO2 ice testing. A, F, and G, reproduced with permission from Schmitt D et al.1020
ONE-STEP PULP CAPPING
According to the one manufacturer of MTA (ProRoot MTA), pulp capping can be completed in one visit. In some situations, treatment of the immature permanent tooth can be difficult, especially in young patients with challenging medical or behavioral problems that may require treatment under sedation. When one step is indicated, the manufacturer of MTA recommends the following protocol:98
1. Under a dental dam, a cavity preparation outline using high-speed burs under constant water cooling is completed.
2. If caries is present, excavate using a round bur in a handpiece at low speed or use hand instruments.
3. Rinse the cavity and exposure site(s) with 2.6% to 5% NaOCl. Heavy bleeding may be controlled with a cotton pellet moistened with sterile saline.
4. Prepare ProRoot MTA according to the listed instructions.
5. Using a small ball applicator or similar device, apply a small amount of the material over the exposure.
6. Remove excess moisture at the site with a moist cotton pellet.
7. Apply a small amount of Dyract Flow flowable compomer (Dentsply International, York, PA) (or an equivalent light-cured resin, glass ionomer liner) to cover the MTA and light-cure according to its instructions.
8. Etch the remaining cavity walls with 34% to 37% phosphoric acid gel for 15 seconds. Rinse thoroughly.
9. Dry the cavity gently, leaving the dentin moist but not wet. Apply Prime and Bond NT material or an equivalent bonding material. Cure according to its instructions.
10. Place TPH Spectrum (Dentsply/Caulk, Milford, DE) composite material or an equivalent composite resin to complete the restoration.
11. At the next appointment, assess the pulp vitality. Pulp vitality and status should be assessed clinically and radiographically every 3 to 6 months or as needed.
We recommend that caries removal be completed under magnification with the aid of a caries detector dye (step 2). Also, during MTA placement against the exposure site (step 5), a larger bulk of MTA should be placed that includes the majority of surrounding dentin at a thickness greater than 1.5 mm.
The quality of the final restoration can be critical to the long-term maintenance of pulp vitality and sustained normal function of the pulp-capped or pulpotomized tooth. Pulp inflammation is directly associated with bacterial microleakage around restorations, and the frequency varies according to the material used.164 In the absence of microleakage, the pulp will have the highest probability for wound repair and survival.165-167 It has been suggested that leaking restorations may be more harmful to pulp tissue than cavity preparations that are unfilled and left open.168 The clinician must determine an appropriate restorative material for each case that provides the best likelihood of a predictable seal against microleakage and deliver it with a high level of skill. Adhesive restorative materials are technique sensitive, and clinicians must execute treatment protocols following the manufacturer's guidelines. Specific composite materials should be matched with their respective and recommended bonding resins.169
Restorative procedures for immature permanent teeth include full-coverage restorations, composite resins, and bonded or unbonded amalgam restorations. The more conservative the restorative treatment, preserving the remaining healthy tooth structure, the higher the probability of pulp survival.138 The age of the patient, the size and depth of the cavity preparation, and the choice of restorative material are all factors affecting repair mechanisms within pulp tissue.170 Amalgam has proven to be a reliable material, inexpensive and relatively simple to place. It has disadvantages, which include esthetic concerns and potential health risks for dental providers. Restorations can be associated with coronal infractions or cuspal fracture, particularly if cusps are not protected.171-173 Amalgam may exhibit less microleakage if placed in conjunction with a bonding resin or resin-modified glass ionomer liners.164,174,175 Although retention rates of composite restorations are improving as technology advances,176,177 amalgam restorations remain a reliable, safe, and predictable long-term treatment option.178-182
Clinical recall and radiographic evaluation are the most accurate predictors for measuring survival rates in vital pulp therapy. Recall compliance is generally more challenging with successful asymptomatic cases than teeth that become irreversibly inflamed or progress to acute apical periodontitis after treatment. The importance of follow-ups after vital pulp therapy cannot be overstated since the occurrence of recurrent caries, restoration failure, poor oral hygiene, or other conditions may be present, requiring attention. Compliance rates for follow-up with child patients can be mediocre as some parents lack basic oral health knowledge and do not practice preventive care.183,184 The time sequence necessary for proper follow-up assessment is based on the common practice of the 6-month recall, usually related to the oral examination and oral prophylaxis and has recently come into question.185 Optimal recall rates should be established individually, based on the patient's need, caries index, periodontal status, symptomatology, and the need for observation of craniofacial development in younger patients.186
In an investigation in which direct pulp capping was completed with Ca(OH)2, it was determined that 3 months was an adequate time period for a tentative diagnosis of survivability.132 The same study also showed that an observation period of 21 to 24 months was sufficient to establish a prognosis for long-term pulp survival. When MTA is used in the two-visit protocol (described earlier in this chapter), the clinician has the opportunity to examine the treated tooth at 5 to 10 days. If the treatment appears successful at that appointment, the provider can confidently schedule the next follow-up at 6 weeks if possible and then at 6 and 12 months.119
In direct pulp capping and pulpotomy, with immature permanent teeth, the most reliable prognostic indicator for success is the radiographic confirmation of root-end closure (apexogenesis). Apexogenesis of the immature adult tooth is one of the key objectives in vital pulp therapy. The process encourages physiologic development and formation of the root end and should advance successfully in healthy patients at the same rate after the application of MTA, whether direct pulp capping or pulpotomy was performed.114,115,187,188
In vital teeth, this natural succession of tooth development should follow a predictable pattern viewed chronologically and compared radiographically with contralateral teeth.189 Following contralateral tooth development is an excellent way to observe the success of vital pulp therapy. In teeth that have suffered trauma, with necrotic pulps and periapical pathosis, teeth are treated to stimulate apical barrier formation (apexification). The time required to barrier formation can be variable, with times from 5 to 20 months.190 Similarly, MTA, which has been shown to be a suitable replacement for Ca(OH)2 in pulpotomy and direct pulp capping treatments, can be expected to provide apical maturation at comparable time periods.191 The human pulp and surrounding tissue have extraordinary regenerative capacity when a microbe-free environment is provided.169,192 MTA is the first of many new bioactive substances that will potentiate the ability of the dental pulp to heal, thereby retaining and maintaining its natural evolutionary function and purpose.
We wish to thank Dr. Rajneesh Roy for his contributions to this chapter.
1. Kakehashi S, Stanley HR, Fitzgerald RT. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1965;20:340-9.
2. Rutherford B, Fitzgerald M. A new biological approach to vital pulp therapy. Crit Rev Oral Biol Med 1995;6:218-29.
3. Dummet CO, Kopel MK. Pediatric endodontics. In: Ingle JI, Bakland LK, editors. Endodontics. 5th ed. Hamilton (ON): BC Decker; 2002. pp. 861-902.
4. Glass RL, Zander HA. Pulp healing. J Dent Res 1949;28:97-107.
5. Tronstad L, Mjor IA. Capping of the inflamed pulp. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1972;34:477-85.
6. Langeland K. Management of the inflamed pulp associated with deep carious lesion. J Endod 1981;7:169-81.
7. Horsted P, Sondergaard B, Thylstrup A, et al. A retrospective study of direct pulp capping with calcium hydroxide compounds. Endod Dent Traumatol 1985;1:29-34.
8. Guideline on pulp therapy for primary and young permanent teeth. American Academy of Pediatric Dentistry Clinical Affairs Committee-Pulp Therapy Subcommitte: American Academy of Pediatric Dentistry Council on Clinical Affairs. Pediatr Dent 2005;27:130-4.
9. Yu C, Abbott PV. An overview of the dental pulp: its functions and responses to injury. Aust Dent J Suppl 2007;52:S4-16.
10. Leeson TS, Leeson CR, Paparo AA. The digestive system. In: Atlas of histology. Philadelphia (PA): WB Saunders; 1988. pp. 401-8.
11. Stockton LW. Vital pulp capping: a worthwhile procedure. J Can Dent Assoc 1999;65:328-31.
12. Brannstrom M, Lind PO. Pulpal response to early dental caries. J Dent Res 1965;44:1045-50.
13. Bjorndal L, Darvann T, Thylstrupt A. A quantitative light microscopic study of the odontoblast and subodontoblastic reactions to active and arrested enamel caries without cavitation. Caries Res 1998;32:59-69.
14. Helfer AR, Melnick S, Schilder H. Determination of the moisture content of vital and pulpless teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1972;34:661-70.
15. Jameson MW, Hood JAA, Tidmarsh BG. The effects of dehydration and rehydration on some mechanical properties of human dentine. J Biomech 1993;26:1055-65.
16. Linn J, Messer HH. Effect of restorative procedures on the strength of endodontically treated molars. J Endod 1994;20:479-85.
17. Ten Cate AR. Dentin-pulp complex. In: Oral histology. 4th ed. RW Reinhardt, editor, St. Louis (MO): Mosby; 1994. p. 184.
18. Yamada T, Nakamura K, Iwaku M, Fusayama T. The extent of the odontoblast process in normal and carious human dentin. J Dent Res 1983;62:798-802.
19. Grotz KA, Duschner H, Reichert TE, et al. Histotomography of the ododontoblast processes at the dentine-enamel junction of permanent healthy human teeth in the confocal laser scanning microscope. Clin Oral Invest 1998;2:21-5.
20. Gottrup F, Andreasen JO. Wound healing subsequent to injury. In: Andreason JO, Andreason FM, editors. Textbook and color atlas of traumatic injuries to teeth. Copenhagen (Denmark): Munksgaard; 1994. pp. 13-76.
21. Albelda SM, Smith CW, Ward PA. Adhesion molecules and inflammatory injury. FASEB J 1994;8:504-12.
22. Tziafas D. Basic mechanisms of cytodifferentiation and dentinogenesis during dental pulp repair. Int J Dev Biol 1995;39:281-90.
23. Fitzgerald M, Chiego DJJ, Heys DR. Autoradiographic analysis of odontoblast replacement following pulp exposure in primate teeth. Arch Oral Biol 1990;35:707-15.
24. Oguntebi BR, Heaven T, Clark AE, Pink FE. Quantitative assessment of dentin bridge formation following pulp-capping in miniature swine. J Endod 1995;21:79-82.
25. Inoue H, Muneyuki H, Izumi T, et al. Electron microscopic study on nerve terminals during dentin bridge formation after pulpotomy in dog teeth. J Endod 1997;23:569-71.
26. Kitasako Y, Shibata S, Arakawa M, et al. A light and transmission microscopic study of mechanically exposed monkey pulps: dynamics of fiber elements during early dentin bridge formation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:224-30.
27. Hayashi Y. Ultrastructure of initial calcification in wound healing following pulpotomy. J Oral Pathol 1982;11:174-80.
28. Kitasako Y, Murray PE, Tagami J, Smith AJ. Histomorphometric analysis of dentinal bridge formation and pulpal inflammation. Quintessence Int 2002;33:600-8.
29. Glossary of endodontic terms. 7th ed. American Association of Endodontists; Chicago, (IL): 2003.
30. Marchi JJ, de Araujo FB, Froner AM, et al. Indirect pulp capping in the primary dentition: a 4 year follow-up study. J Clin Pediatr Dent 2006;31:68-71.
31. Mass E, Zilberman U, Fuks AB. Partial pulpotomy: another treatment option for cariously exposed permanent molars. J Dent Child 1995;62:342-5.
32. Hawes RR, Dimaggio JJ, Sayegh F. Evaluation of direct and indirect pulp capping [abstract]. J Dent Res 1964;43:808.
33. Jordan RE, Suzuki M. Conservative treatment of deep carious lesions. J Can Dent Assoc 1971;37:337-42.
34. Bjorndal L, Larsen T, Thylstrup A. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Caries Res 1997;31:411-17.
35. Orstavik D, Pitt Ford TR. Essential endodontology: prevention and treatment of apical periodontitis. Oxford (UK): Blackwell Science; 1998.
36. Rothman MS. Formocresol pulpotomy: a practical procedure for permanent teeth. Gen Dent 1977;25:39-41.
37. Fuks AB, Bimstein E, Bruchim A. Radiographic and histologic evaluation of the effect of two concentrations of formocresol on pulpotomized primary and young permanent teeth in monkeys. Pediatr Dent 1983;5:9-13.
38. Rolling I, Hasselgren G, Tronstad L. Morphologic and enzyme histochemical observations on the pulp of human primary molars 3 to 5 years after formocresol treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1976;42:518-28.
39. Holan G, Eidelman E, Fuks AB. Long-term evaluation of pulpotomy in primary molars using mineral trioxide aggregate or formocresol. Pediatr Dent 2005;27:129-36.
40. Caicedo R, Abbott PV, Alongi DJ, Alarcon MY. Clinical, radiographic and histological analysis of the effects of mineral trioxide aggregate used in direct pulp capping and pulpotomies of primary teeth. Aust Dent J 2006; 51:297-305.
41. Cvek M. A clinical report on partial pulpotomy and capping with calcium hydroxide in permanent incisors with complicated root fractures. J Endod 1978;4:232-7.
42. Randow K, Glantz PO. On cantilever loading of vital and non-vital teeth. An experimental clinical study. Acta Odontol Scand 1986;44:271-7.
43. Mentink AG, Meeuwissen R, Kayser AF, Mulder J. Survival rate and failure characteristics of the all metal post and core restoration. J Oral Rehabil 1993;20:455-61.
44. Torbjorner A, Karlsson S, Odman PA. Survival rate and failure characteristics for two post designs. J Prosthet Dent 1995;73:439-44.
45. Caplan DJ, Kolker J, Rivera EM, Walton RE. Relationship between number of proximal contacts and survival of root treated teeth. Int Endod J 2002;35:193-9.
46. Caplan DJ, Cai J, Yin G, White BA. Root canal filled versus non-root canal filled teeth: a retrospective comparison of survival times. J Public Health Dent 2005;65:90-6.
47. Wegner PK, Freitag S, Kern M. Survival rate of endodontically treated teeth with posts after prosthetic restoration. J Endod 2006;32:928-31.
48. De Backer H, van Maele G, Decock V, van den Berghe L. Long-term survival of complete crowns, fixed dental prostheses, and cantilever prostheses with post and cores on root-canal treated teeth. Int J Prosthodont 2007;20:229-34.
49. Haskell EW, Stanley HR, Chellemi J, Stringfellow H. Direct pulp capping treatment: a long-term follow-up. J Am Dent Assoc 1978;97:607-12.
50. Baume LJ, Holz J. Long term clinical assessment of direct pulp capping. Int Dent J 1981;31:251-60.
51. Barthel CR, Rosenkranz B, Leuenberg A, Roulet JF. Pulp capping of carious exposures treatment outcome after 5 and 10 years: a retrospective study. J Endod 2000;26:525-8.
52. Auschill TM, Arweiler NB, Hellwig E, et al. Success rate of direct pulp capping with calcium hydroxide. Schweiz Monatsschr Zahnmed 2003;113:946-52.
53. Beagrie GS, Main JH, Smith DC, Walshaw PR. Polycarboxylate cement as a pulp capping agent. Dent J 1974;40:378-83.
54. Sveen OB. Pulp capping of primary teeth with zinc oxide eugenol. Odontol Tidskr 1969;77:427-36.
55. Bhaskar SN, Beasley JD, Ward JP, Cutright DE. Human pulp capping with isobutyl cyanoacrylate. J Dent Res 1972;51:58-61.
56. Heller AL, Koenigs JF, Brilliant JD, et al. Direct pulp capping of permanent teeth in primates using a resorbable form of tricalcium phosphate ceramic. J Endod 1975;1:95-101.
57. Kashiwada T, Takagi M. New restoration and direct pulp capping systems using adhesive composite resin. Bull Tokyo Med Dent Univ 1991;38:45-52.
58. Higashi T, Okamoto H. Influence of particle size of hydroxyapatite as a capping agent on cell proliferation of cultured fibroblasts. J Endod 1996;22:236-9.
59. Yoshimine Y, Maeda K. Histologic evaluation of tetracalcium phosphate-based cement as a direct pulp-capping agent. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:351-8.
60. Pitt Ford TR, Torabinejad M, Abedi HR, et al. Using mineral trioxide aggregate as a pulp-capping material. J Am Dent Assoc 1996;127:1491-4.
61. Stanley HR, Clark AE, Pameijer CH, Louw NP. Pulp capping with a modified bioglass formula (#A68-modified). Am J Dent 2001;14:227-32.
62. Olsson H, Davies JR, Holst KE, et al. Dental pulp capping: effect of Emdogain Gel on experimentally exposed human pulps. Int Endod J 2005;38:186-94.
63. Zhang W, Walboomers XF, Jansen JA. The formation of tertiary dentin after pulp capping with a calcium phosphate cement, loaded with PLGA microparticles containing TGF-beta1. J Biomed Mater Res A 2007 [In press].
64. Miyashita H, Worthington HV, Qualtrough A, Plasschaert A. Pulp management for caries in adults: maintaining pulp vitality. Cochrane Database Syst Rev 2007;18:CD004484.
65. Moritz A, Schoop U, Goharkhay K, Sperr W. The CO2 laser as an aid in direct pulp capping. J Endod 1998;24:248-51.
66. Goldberg M, Six N, Decup F, et al. Bioactive molecules and the future of pulp therapy. Am J Dent 2003;16:66-76.
67. Dahnhardt JE, Jaeqqi T, Lussi A. Treating open carious lesions in anxious children with ozone. A prospective controlled clinical study. Am J Dent 2006;19:267-70.
68. Olivi G, Genovese MD, Maturo P, Docimo R. Pulp capping: advantages of using laser technology. Eur J Paediatr Dent 2007;8:89-95.
69. Cohen BD, Combe EC. Development of new adhesive pulp capping materials. Dent Update 1994;21:57-62.
70. Cox CF, Subay RK, Ostro E, Suzuki S, Suzuki SH. Tunnel defects in dentin bridges: Their formation following direct pulp capping. Oper Dent 1996;21:4-11.
71. Schroder U. Effect of calcium hydroxide-containing pulp capping agents on pulp cell migration, proliferation, and differentiation. J Dent Res 1985;66:1166-74.
72. Andelin WE, Shabahang S, Wright K, Torabinejad M. Identification of hard tissue after experimental pulp capping using dentin sialoprotein (DSP) as a marker. J Endod 2003;29:646-50.
73. Goldberg M, Lasfargues JJ, Legrand JM. Clinical testing of dental materials—histological considerations. J Dent 1994;22:S25-8.
74. Via W. Evaluation of deciduous molars by treated pulpotomy and calcium hydroxide. J Am Dent Assoc 1955;50:34-43.
75. Barnes IM, Kidd EA. Disappearing Dycal. Br Dent J 1979;147:111.
76. Cox CF, Suzuki S. Re-evaluating pulp protection: calcium hydroxide liners vs. cohesive hybridization. J Am Dent Assoc 1994;125:823-31.
77. Goracci G, Mori G. Scaning electron microscopic evaluation of resin-dentin and calcium hydroxide dentin-interface with resin composite restorations. Quintessence Int 1996;27:129-35.
78. Inokoshi S, Iwaku M, Fusayama T. Pulpal response to a new adhesive resin material. J Dent Res 1982;61:1014-19.
79. Yamani T, Yamashita A, Takeshita N, Nagai N. Histopathological evaluation of the effects of a new dental adhesive resin on dog dental pulps. J Jpn Prosth Soc 1986;30:671-8.
80. Matsuura T, Katsumata T, Matsuura T, et al. Histopathological study of pulpal irritation of dental adhesive resin. Part 1. Panavia EX. Nihon Hotetsu Shika Gakkai Zasshi 1987;31:104-15.
81. Tarmin B, Hafez AA, Cox CF. Pulpal response to a resin-modified glass-ionomer material on nonexposed and exposed monkey pulps. Quintessence Int 1998;29:535-42.
82. Cox CF, Hafez AA, Akimoto N, et al. Biocompatibility of primer, adhesive and resin composite systems on nonexposed and exposed pulps of non-human primate teeth. Am J Dent 1998;11:S55-63.
83. Akimoto N, Momoi Y, Kohno A, et al. Biocompatibility of Clearfil Liner Bond 2 and Clearfil AP-X system on nonexposed and exposed primate teeth. Quintessence Int 1998;29:177-88.
84. Tarim B, Hafez AA, Suzuki SH, et al. Biocompatibility of Optibond and XR-Bond adhesive systems in nonhuman primate teeth. Int J Periodontics Restorative Dent 1998;18:86-99.
85. Tarim B, Hafez AA, Suzuki SH, et al. Biocompatability of compomer restorative systems on nonexposed dental pulps of primate teeth. Oper Dent 1997;22:149-58.
86. Gwinnett J, Tay FR. Early and intermediate time response of the dental pulp to an acid etch technique in vivo. Am J Dent 1997;10:S35-44.
87. Hebling J, Giro EMA, deSouza Costa CA. Biocompatibility of an adhesive system applied to exposed human dental pulp. J Endod 1999;25:676-82.
88. Mjor IA. Pulp-dentin biology in restorative dentistry. Part 7: the exposed pulp. Quintessence Int 2002;33:113-35.
89. Horsted-Bindslev P, Vilkinis V, Sidlauskas A. Direct capping of human pulps with a dentin bonding system or with calcium hydroxide cement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;96:591-600.
90. Accorinte Mde L, Loguercio AD, Reis A, et al. Adverse effects of human pulps after direct pulp capping with different components from a total-etch, three-step adhesive system. Dent Mater 2005;21:599-607.
91. do Nascimento ABL, Fontana UF, Teixeira HM, de Souza Costa CA. Biocompatibility of a resin-modified glass-ionomer cement applied as pulp capping in human teeth. Am J Dent 2000;13:28-34.
92. de Souza Costa CA, Lopes do Nascimento AB, Teixeira HM, Fontana UF. Response of human pulps capped with a self-etching adhesive system. Dent Mater 2001;17:230-40.
93. Murray PE, Hafez AA, Smith AJ, Cox CF. Hierarchy of pulp capping and repair activities responsible for dentin bridge formation. Am J Dent 2002;15:236-43.
94. Murray PE, Garcia-Godoy F. The incidence of pulp healing defects with direct capping materials. Am J Dent 2006;19:171-7.
95. Olsson H, Petersson K, Rohlin M. Formation of a hard tissue barrier after pulp capping in humans. A systematic review. Int Endod J 2006;39:429-42.
96. Lee SJ, Monsef M, Torabinejad M. The sealing ability of a mineral trioxide aggregate for repair of lateral root perforations. J Endod 1993;19:541-4.
97. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. J Endod 1995;21:349-53.
98. Dentsply Tulsa Dental. ProRoot MTA [product literature].
99. Holland R, de Souza V, Nery MJ, et al. Reaction of rat connective tissue to implanted dentin tubes filled with a white mineral trioxide aggregate. Braz Dent J 2002;13:23-6.
100. Ferris DM, Baumgartner JC. Perforation repair comparing two types of mineral trioxide aggregate. J Endod 2004;30:422-4.
101. Menezes R, Bramante CM, Letra A, et al. Histologic evaluation of pulpotomies in dog using two types of mineral trioxide aggregate and regular and white Portland cements as wound dressings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:376-9.
102. Schmitt D, Lee J, Bogen G. Multifaceted use of ProRoot MTA root canal repair material. Pediatr Dent 2001;23:326-30.
103. Torabinejad M, Chivian N. Clinical applications of mineral trioxide aggregate. J Endod 1999;25:197-205.
104. Torabinejad M, Higa RK, McKendry DJ, Pitt Ford TR. Dye leakage of four root-end filling materials: effects of blood contamination. J Endod 1994;20:159-63.
105. Torabinejad M, Smith PW, Kettering JD, Pitt Ford TR. Comparative investigation of marginal adaptation of mineral trioxide aggregate and other commonly used root-end filling materials. J Endod 1995;21:295-9.
106. Sarkar NK, Caicedo R, Ritwik P, et al. Physiochemical basis of the biologic properties of mineral trioxide aggregate. J Endod 2005;31:97-100.
107. Moghaddame-Jafari S, Mantellini MG, Botero M, et al. Effect of ProRoot MTA on pulp cell apoptosis and proliferation in vitro. J Endod 2005;31:387-91.
108. Koh ET, Pitt Ford TR, Torabinejad M, McDonald F. Mineral trioxide aggregate stimulates cytokine production in human osteoblasts. J Bone Miner Res 1995;10S:S406.
109. Andelin WE, Shabahang S, Wright K, Torabinejad M. Identification of hard tissue after experimental pulp capping using dentin sialoprotein (DSP) as a marker. J Endod 2003;29:646-50.
110. Tziafas D, Pantelidou O, Alvanou A, et al. The dentinogenic effect of mineral trioxide aggregate (MTA) in short-term capping experiments. Int Endod J 2002;35:245-54.
111. Junn DJ. Quantitative assessment of dentin bridge formation following pulp-capping with mineral trioxide aggregate [master's thesis]. Loma Linda (CA): Loma Linda University; 2000.
112. Faraco IM Jr, Holland R. Response of the pulp of dogs to capping with mineral trioxide aggregate or a calcium hydroxide cement. Dent Traumatol 2001;17:163-6.
113. Aeinehchi M, Eslami B, Ghanabriha M, Saffar AS. Mineral trioxide aggregate (MTA) and calcium hydroxide as pulp capping agents in human teeth: a preliminary report. Int Endod J 2003;36:225-31.
114. Witherspoon DE, Small JC, Harris GZ. Mineral trioxide aggregate pulpotomies: a case series outcome assessment. J Am Dent Assoc 2006;137:610-18.
115. Barrieshi-Nusair KM, Qudeimat MA. A prospective clinical study of mineral trioxide aggregate for partial pulpotomy in cariously exposed permanent teeth. J Endod 2006;32:731-5.
116. Iwamoto CE, Adachi E, Pameijer CH, et al. Clinical and histological evaluation of white ProRoot MTA in direct pulp capping. Am J Dent 2006;19:85-90.
117. Farsi N, Alamoudi N, Balto K, Mushayt A. Clinical assessment of mineral trioxide aggregate (MTA) as direct pulp capping in young permanent teeth. J Clin Pediatr Dent 2006;31:72-6.
118. Tomson PL, Grover LM, Lumley PJ, et al. Dissolution of bio-active dentine matrix components by mineral trioxide aggregate. J Dent 2007;35:636-42.
119. Bogen G, Kim JS, Bakland LK. Direct pulp capping with mineral trioxide aggregate: an observational study. [In press]
120. Gutmann JL, Heaton JF. Management of the open (immature) apex. 1. Vital teeth. Int Endod J 1981;14:166-72.
121. Fuks AB. Pulp therapy for the primary and young permanent dentitions. Dent Clin North Am 2000;44:571-96.
122. Shabahang S, Torabinejad M. Treatment of teeth with open apices using mineral trioxide aggregate. Pract Periodontics Aesthet Dent 2000;12:31.
123. Fulling HJ, Andreasen JO. Influence of maturation status and tooth type of permanent teeth upon electrometric and thermal pulp testing. Scand J Dent Res 1976;84:286-90.
124. Karibe H, Ohide Y, Kohno H, et al. Study on thermal pulp testing of immature permanent teeth. Shigaku 1989;77:1006-13.
125. Bortoluzzi EA, Souza EM, Reis JM, et al. Fracture strength of bovine incisors after intra-radicular treatment with MTA in an experimental immature tooth model. Int Endod J 2007;40:684-91.
126. Abou-Rass M. The stressed pulp condition: an endodontic restorative diagnostic concept. J Prosthet Dent 1982;48:264-7.
127. Mjor IA. Pulp-dentin biology in restorative dentistry. Part 5: clinical management and tissue changes associated with wear and trauma. Quintessence Int 2001;32:771-88.
128. Brambilla E, Garcia-Godoy F, Strohmenger L. Principles of diagnosis and treatment of high-caries-risk subjects. Dent Clin North Am 2000;44:507-40.
129. Tinanoff N, Douglass JM. Clinical decision making for caries management in children. Pediatr Dent 2002;24:386-92.
130. Camp J. Pediatric endodontic treatment. In: Cohen S, Burns RC, editors. Pathways of the pulp. 7th ed. St. Louis (MO): Mosby;1998. pp. 718-58.
131. Chandler NP, Pitt Ford TR, Monteith BD. Pulp size in molars: underestimation on radiographs. J Oral Rehabil 2004;31:764-9.
132. Matsuo T, Nakanishi T, Shimizu H, Ebisu S. A clinical study of direct pulp capping applied to carious-exposed pulps. J Endod 1996;22:551-6.
133. Gracia TB. Accuracy of size estimations by dentists of simulated pulp exposures and cavity preparations. MDS (endodontics) research report. Otago (New Zealand): University of Otago; 2006.
134. Chandler NP, Pitt Ford TR, Monteith BD. Coronal pulp size in molars: a study of bitewing radiographs. Int Endod J 2003;36:757-63.
135. Fusayama T, Okuse K, Hosoda H. Relationship between hardness, discoloration, and microbial invasion in carious dentin. J Dent Res 1966;45:1033-46.
136. Fusayama T, Kurosaki N. Structure and removal of carious dentin. Int Dent J 1972;22:401-11.
137. Sato Y, Fusayama T. Removal of dentin guided by Fuchsin staining. J Dent Res 1976;55:678-83.
138. Fusayama T. A simple pain-free adhesive restorative system by minimal reduction and total etching. St. Louis (MO): Ishiyaku EuroAmerica Publishing; 1993.
139. Kato S, Fusayama T. Recalcification of artificially decalcified dentin in vivo. J Dent Res 1970;49:1060-7.
140. Tatsumi T. Physiological remineralization of artificially decalcified monkey dentin under adhesive composite resin. J Stom Soc Jpn 1989;56:47-74.
141. Kidd EA, Joyston-Bechal S, Beighton D. The use of a caries detector dye during cavity preparation: a microbiological assessment. Br Dent J 1993;174:245-8.
142. Lennon AM, Attin T, Buchalla W. Quantity of remaining bacteria and cavity size after excavation with FACE, caries detector dye and conventional excavation in vitro. Oper Dent 2007;32:236-41.
143. Zacharia MA, Munshi AK. Microbiological assessment of dentin stained with a caries detector dye. J Clin Pediatr Dent 1995;19:111-15.
144. Yazici AR, Baseren M, Gokalp S. The in vitro performance of laser fluorescence and caries-detector dye for detecting residual carious dentin during tooth preparation. Quintessence Int 2005;36:417-22.
145. Garcia-Godoy F, Murray PE. Systemic evaluation of various haemostatic agents following local application prior to direct pulp capping. Braz J Oral Sci 2005;4:791-7.
146. Hirota K. A study on the partial pulp removal (pulpotomy) using four different tissue solvents. J Jpn Stomatol Soc 1959;26:1588-603.
147. Sudo C. A study on partial pulp removal (pulpotomy) using NaOCl (sodium hypochlorite). J Jpn Stomatol Soc 1959;26:1012-24.
148. Cox CF, Hafez AA, Akimoto N, et al. Biocompatibility of primer, adhesive and resin composite systems on nonexposed and exposed pulps of non-human primate teeth. Am J Dent 1998;11:S55-63.
149. Hafez AA, Cox CF, Tarim B, et al. An in vivo evaluation of hemorrhage control using sodium hypochlorite and direct capping with a one-or two-component adhesive system in exposed nonhuman primate pulps. Quintessence Int 2002;33:261-72.
150. Rosenfeld EF, James GA, Burch BS. Vital pulp tissue response to sodium hypochlorite. J Endod 1978;4:140-6.
151. Heggers JP, Sazy JA, Stenberg BD, et al. Bactericidal and wound-healing properties of sodium hypochlorite solutions: the 1991 Lindberg Award. J Burn Care Rehabil 1991;12:420-4.
152. Nakanishi T, Matsuo T, Ebishu S. Quantitative analysis of immunoglobulins and inflammatory factors in human pulpal blood from exposed pulps. J Endod 1995;21:131-6.
153. Tang HM, Nordbo H, Bakland LK. Pulpal response to prolonged dentinal exposure to sodium hypochlorite. Int Endod J 2000;33:505-8.
154. Demir T, Cehreli ZC. Clinical and radiographic evaluation of adhesive pulp capping in primary molars following hemostasis with 1.25% sodium hypochlorite: 2-year results. Am J Dent 2007;20:182-8.
155. Vargas KG, Packham B, Lowman D. Preliminary evaluation of sodium hypochlorite for pulpotomies in primary molars. Pediatr Dent 2006;28:511-17.
156. Salama FS. Influence of zinc-oxide eugenol, formocresol, and ferric sulfate on bond strength of dentin adhesives to primary teeth. J Contemp Dent Pract 2005;6:14-21.
157. Elias RV, Demarco FF, Tarquinio SB, Piva E. Pulp responses to the application of a self-etching adhesive in human pulps after controlling bleeding with sodium hypochlorite. Quintessence Int 2007;38:67-77.
158. Silva AF, Tarquinio SBC, Demarco FF, et al. The influence of haemostatic agents on healing of healthy human dental pulp tissue capped with calcium hydroxide. Int Endod J 2006;39:309-16.
159. Torabinejad M, Cho Y, Khademi AA, et al. The effect of various concentrations of sodium hypochlorite on the ability of MTAD to remove the smear layer. J Endod 2003;29:233-9.
160. Machnick TK, Torabinejad M, Munoz CA, Shabahang S. Effect of MTAD on flexural strength and modulus of elasticity of dentin. J Endod 2003;29:747-50.
161. Torabinejad M, Shabahang S, Aprecio RM, Kettering JD. The antimicrobial effect of MTAD: an in vitro investigation. J Endod 2003;29:400-3.
162. Shabahang S, Torabinejad M. Effect of MTAD on Enterococcus faecalis-contaminated root canals of extracted human teeth. J Endod 2003;29:576-9.
163. al-Wazzan KA, al-Harbi AA, Hammad IA. The effect of eugenol-containing temporary cement on the bond strength of two resin composite core materials to dentin. J Prosthodont 1997;6:37-42.
164. Murray PE, Hafez AA, Smith AJ, Cox CF. Bacterial microleakage and pulp inflammation associated with various restorative materials. Dent Mater 2002;18:470-8.
165. Bergenholtz G, Cox CF, Loesche WJ, Syed SA. Bacterial leakage around dental restorations: its effect on the dental pulp. J Oral Pathol 1982;11:439-50.
166. Cox CF, Keall CL, Keall HJ, et al. Biocompatibility of surface-sealed dental materials against exposed dental pulps. J Prosthet Dent 1987;57:1-8.
167. Pashley DH, Pashley EL, Carvalho RM, Tay FR. The effects of dentin permeability on restorative dentistry. Dent Clin North Am 2002;46:211-45.
168. Sasafuchi Y, Otsuki M, Inokoshi S, Tagami J. The effects on pulp tissue of microleakage in resin composite restorations. J Med Dent Sci 1999;46:155-64.
169. Murray PE, Smith AJ. Saving pulps—a biological basis. An overview. Prim Dent Care 2002;9:21-6.
170. Murray PE, About I, Lumley PJ, et al. Postoperative pulpal and repair responses. J Am Dent Assoc 2000;131:321-9.
171. Van Nieuwenhuysen JP, D'Hoore W, Carvalho J, Qvist V. Long-term evaluation of extensive restorations in permanent teeth. J Dent 2003;31:395-405.
172. Wahl MJ, Schmitt MM, Overton DA, Gordon MK. Prevalence of cusp fractures in teeth restored with amalgam and with resin-based composite. J Am Dent Assoc 2004;135:1127-32.
173. Halbach S, Vogt S, Kohler W, et al. Blood and urine mercury levels in adult amalgam patients of a randomized controlled trial: interaction of Hg species in erythrocytes. Environ Res 2007 [In press].
174. Marchiori S, Baratieri LN, de Andrada MA, et al. The use of liners under amalgam restorations: an in vitro study on marginal leakage. Quintessence Int 1998;29:637-42.
175. Luz MA deC, Ciaramicoli-Rodrigues MT, Garone Netto N, De Lima ACP. Long-term clinical evaluation of fracture and pulp injury following glass-ionomer cement or composite resin applied as a base filling in teeth restored with amalgam. J Oral Rehabil 2001;28:634-9.
176. Gaengler P, Hoyer I, Montag R. Clinical evaluation of posterior composite restorations: the 10-year report. J Adhes Dent 2001;3:185-94.
177. Gordan VV, Mondragon E, Watson RE, et al. A clinical evaluation of a self-etching primer and a giomer restorative material: results at eight years. J Am Dent Assoc 2007;138:621-7.
178. Collins CJ, Bryant RW, Hodge KLV. A clinical evaluation of posterior composite resin restorations: 8-year findings. J Dent 1998;26:311-17.
179. DeRouen TA, Martin MD, Leroux BG, et al. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. J Am Dent Assoc 2006;295:1784-92.
180. Martin MD, Woods JS. The safety of dental amalgam in children. Exp Opin Drug Saf 2006;5:773-81.
181. Bernardo M, Luis H, Martin MD, et al. Survival and reasons for failure of amalgam versus composite posterior restorations placed in a randomized clinical trial. J Am Dent Assoc 2007;138:775-83.
182. Soncini JA, Maserejian NN, Trachtenberg F, et al. The longevity of amalgam versus compomer/composite restorations in posterior primary and permanent teeth: findings from the New England Children's Amalgam Trial. J Am Dent Assoc 2007;138:763-72.
183. Jamieson WJ, Vargas K. Recall rates and caries experience of patients undergoing general anesthesia for dental treatment. Pediatr Dent 2007;29:253-7.
184. Primosch RE, Balsewich CM, Thomas CW. Outcomes assessment an intervention strategy to improve parental compliance to follow-up evaluations after treatment of early childhood caries using general anesthesia in a Medicaid population. ASDC J Dent Child 2001;68:102-8.
185. Mettes D. Insufficient evidence to support or refute the need for 6-monthly dental check-ups. What is the optimal recall frequency between dental checks? Evid Based Dent 2005;6:62-3.
186. Nikiforuk G. Optimal recall intervals in child dental care. J Can Dent Assoc 1997;63:618-24.
187. Weisleder R, Benitez CR. Maturogenesis: is it a new concept? J Endod 2003;29:776-8.
188. Patel R, Cohenca N. Maturogenesis of a cariously exposed immature permanent tooth using MTA for direct pulp capping: a case report. Dent Traumatol 2006;22:328-33.
189. Ballesio I, Marchetti E, Mummolo S, Marzo G. Radiographic appearance of apical closure in apexification: follow-up after 7-13 years. Eur J Paediatr Dent 2006;7:9-34.
190. Sheehy EC, Roberts GJ. Use of calcium hydroxide for apical barrier formation and healing in non-vital immature permanent teeth: a review. Br Dent J 1997;183:241-6.
191. El-Meligy OAS, Avery DR. Comparison of mineral trioxide aggregate and calcium hydroxide as pulpotomy agents in young permanent teeth (apexogenesis). Pediatr Dent 2006;28:399-404.
192. Chueh LH, Huang GT. Immature teeth with periradicular periodontitis or abscess undergoing apexogenesis: a paradigm shift. J Endod 2006;32:1205-13.
|Date: 04/05/2013 11:14|
Re: Vital Pulp Therapy
Really Great to know about this Vital Pulp Therapy. This is really great treatment for teeth. It is really beneficial for lot of patients.