Vital pulp therapy is designed to preserve and maintain pulpal health in teeth that have been exposed to trauma, caries, restorative procedures, and anatomic anomalies. The treatment can be completed for permanent teeth that show reversible pulpal injuries, and the outcomes depend on a variety of factors. The prime objective in vital pulp therapy is to initiate the formation of tertiary reparative dentin or calcific bridge formation. This procedure is essential for the preservation of involved immature permanent teeth where root development may be incomplete and preservation of arch integrity is critical during maxillofacial development.
Recent advances in pulp biology and dental materials have provided alternative treatment strategies for healthy and partially inflamed pulps. Vital pulps can be successfully treated if the clinician has an improved understanding of diagnosis and case selection, hemostasis, caries removal, magnification systems, bioactive capping materials, bonded composites, and other restorative materials. The treatment is particularly valuable in young permanent teeth that have not attained their complete adult length and exhibit thin-walled roots and wide-open apices.
Immature teeth may require up to 5 years or more to gain apical closure after emergence into the oral cavity. They are characterized by large dentinal tubules that allow increased permeability for microbial penetration. The vulnerability and perceived poor prognosis of vital pulp treatment for immature permanent teeth have prompted aggressive treatment recommendations that include extraction. Alternately, with an accurate diagnosis and early intervention, new strategies for pulp preservation promote a domain for continued hard tissue formation that encourages apexogenesis. Maintaining pulp vitality in these teeth reduces the probability of fracture, through continued growth and natural strengthening of the tooth structures.
The introduction of mineral trioxide aggregate (MTA) and other bioceramic or calcium silicate-based cements (CSCs), along with advanced treatment strategies, has markedly changed the long-held concept that pulp capping after carious pulp exposure should be avoided. According to Seltzer and Bender, “Pulp capping is a questionable procedure even under ideal circumstances.” They further stated that “pulp capping should be discouraged for carious pulp exposures, since microorganisms and inflammation are invariably associated.” The perception that outcomes for direct pulp capping in a carious field are inconsistent and problematic is based on traditional protocols and materials that did not generate a favorable milieu for hard tissue formation. This perspective has encouraged clinicians to deliver alternative treatments, such as pulpotomy or pulpectomy, particularly in immature permanent teeth. This rigid approach is further complicated by the difficulty in establishing the appropriate diagnosis because clinical signs, symptoms, and radiographic evidence may not accurately reflect the histologic condition of the involved pulp tissue ( Fig. 23-1 ). However, based on a better understanding of pulp physiology, caries microbiology, and the inflammatory mechanisms responsible for irreversible changes in pulp tissue, teeth with the potential for repair and continued vitality can now be more readily identified and predictably treated.
Advances in our knowledge of pulpal physiology and immunology, together with recently introduced dental materials, have markedly changed the treatment approaches for teeth with involved pulps. Bioactive CSCs, such as MTA, have changed the perception that treating direct carious pulp exposures is unpredictable and therefore contraindicated. From the introduction of indirect pulp capping by Pierre Fauchard in the eighteenth century, dentistry has recognized the innate reparability of the dental pulp when exposed to injury. Subsequent advances have been complemented by newly developed dental materials that provide superior sealing properties and protect the pulp from microorganisms and their toxic by-products.
A goal in vital pulp therapy has been to identify bioactive pulp capping and pulpotomy agents and implement a consistent treatment regimen that favors pulp preservation. It is recognized that outcomes for vital pulp therapy can vary, depending on the age of the patient, extent of bacterial contamination, and degree of pulp inflammation. Perhaps of greater importance may be the choice of pulp capping material and the quality of the permanent restoration. Appropriate case selection, through a detailed differential diagnosis using multiple tests paired with a careful radiographic interpretation, is paramount for establishing the best treatment for the problem tooth. In its guidelines, the American Academy of Pediatric Dentistry (AAPD) states, “Teeth exhibiting provoked pain of short duration relieved with over-the-counter analgesics, by brushing, or upon the removal of the stimulus without signs and symptoms of irreversible pulpitis, have a clinical diagnosis of reversible pulpitis and are candidates for vital pulp therapy.”
In young patients, assessment of pulpal status before treatment is often difficult, but the probability of favorable outcomes increases with a diagnosis of reversible pulpitis or normal pulp (AAPD). Furthermore, subjective and sometimes negative patient reports or pain associated with cold testing does not absolutely signify that the pulp capping or pulpotomy procedure will be unsuccessful. Because pulpal disease is microbial in nature, this chapter describes the microbiology of caries and the associated physiologic reactivity of pulp tissue. Based on the understanding that pulp tissue has an innate potential for repair in the absence of bacterial contamination, the chapter reviews new treatment concepts in vital pulp therapy intended for the ultimate preservation of the pulpally involved permanent tooth.
The Living Pulp
As reviewed in Chapter 12 , the dental pulp is a highly vascular and innervated loose connective tissue that has the unusual distinction of being enclosed within a rigid envelope composed of enamel, dentin, and cementum. These hard tissues impart mechanical support and offer protection from the oral microbiota. When these tissues are examined together embryologically and histologically, they may be referred to as the dentin-pulp complex. The pulp tissue accomplishes several important functions, including immune cell defense and surveillance, nutrition, dentinogenesis, and proprioreceptor recognition. Healthy pulp tissue can generate reparative hard tissue, secondary, and peritubular dentin in response to assorted biologic and pathologic stimuli. The maintenance of dental pulp vitality, therefore, is essential to the long-term retention and normal functioning of the tooth.
The dental pulp encompasses four distinct structural zones: a cell-rich zone, and core, composed of major vessels and nerves; a cell-free zone; and the odontoblastic layer that lines the entire pulp periphery. The cell-rich zone demonstrates a greater density of undifferentiated mesenchymal cells and fibroblasts than is present in the pulp proper. The central pulp core consists of nerve fibers, blood vessels, fibroblasts, undifferentiated mesenchymal stem cells, immunocompetent cells, ground substance, and collagen fibers. The cell-free zone of Weil is subjacent to the odontoblast layer and is linked by capillaries, fibroblastic processes, and an extensive network of unmyelinated nerve fibers. The odontoblastic zone lines the pulp circumference as an epithelioid layer and includes the large, columnar-shaped odontoblasts, nerve fibers, capillaries, and dendritic cells.
Vital pulp tissue comprises various cell populations that include fibroblasts or pulpoblasts, undifferentiated mesenchymal cells, odontoblasts, macrophages, dendritic cells, and other immunocompetent cells. The cells of the subodontoblastic layer and odontoblasts form a thin border between the inside margin of the dentin and the periphery of the pulp; this border is known as the Höehl cell layer. The odontoblasts are tall, columnar-shaped cells separated from the mineralized dentin by predentin and characterized by processes that extend into the dentin and possibly to the dentinoenamel junction. Odontoblasts are credited with formation of the mineralized predentin-dentin matrix, which is composed of an assortment of molecules, including phosphoproteins, glycoproteins, proteoglycans, and sialoproteins. Repair mechanisms in the dental pulp are similar to those observed in normal connective tissue injured by trauma. When the enamel and dentin are challenged and the pulp exposed to advancing microorganisms, inflammatory changes can induce pulp necrosis, which precedes progressive pathologic changes that can include infection and its complications.
Pressoreceptors and proprioreceptors protect the dentin-pulp complex against excessive occlusal loading while circulating immune competent cells confront bacterial challenges. Pulpless teeth with minimal remaining tooth structure that undergo root-filling procedures and are restored with post and core systems combined with cuspal coverage restorations are more vulnerable to irreparable fracture because of the loss of any protective proprioceptive mechanisms. Investigations have shown that moisture depletion from dentin and the relative reduction of tooth stiffness are minimal after root canal treatment. Although root canal treatment can prolong tooth survival, the cumulative loss of tooth structure from it and restorative care may precipitate tooth loss. Root-filled teeth also demonstrate an increased susceptibility to recurrent caries, either because of poor marginal integrity of the permanent restoration or as a result of the modification of the biologic environment in these teeth.
The pulp undergoes physiologic, pathologic, and defensive changes during its life. These age-related transitions include continued dentin apposition, causing gradual narrowing of pulp volume and circumference. The atrophy results in fibrosis, dystrophic calcification, degeneration of odontoblasts, and increased cellular apoptosis. The aging of human dental pulp cells is primarily characterized by the formation of reactive oxygen species and senescence-related beta-galactosidase activity. In addition, sensitivity to dental pain is reduced due to a decrease in fast-conducting A-delta fibers and diminished pulp repair, partly attributed to decreases in the levels of substances such as alkaline phosphatase. An array of extracellular matrix macromolecules regulated by pulp cell activity contributes to tissue differentiation and growth, defense mechanisms, reactions to inflammatory stimuli, and the formation of calcified tissues.
A comparison analysis of gene expression levels that reflect the activity of biologic cell function, proliferation, differentiation, and development found them markedly higher in young pulps compared to older dental pulps. Analyses of young dental pulps indicated a greater expression level in cell and tissue differentiation, proliferation, and development of the lymphatic, hematologic, and immune systems compared to older dental pulps where the apoptosis pathway is highly expressed. Although A-beta fiber function remains constant with aging, a decrease in A-delta fibers with age may reduce the perception of dental pain transmitted by these faster-conducting fibers. Pulp volume and root canal lumen dimensions also diminish with advancing age as a result of continual deposition of dentin. These age-related changes in tissue differentiation and organization, growth regulation, defense mechanisms, responses to inflammatory stimuli, and the deposition of calcified tissue are regulated by pulp cell activity and an assortment of extracellular matrix molecules.
Pulpal Response to Caries *
* Adapted from Hahn and Liewehr.
The advance of invading microorganisms in carious lesions is the essential cause of pulpal inflammation and potential tissue necrosis. Acidogenic gram-positive bacteria, predominantly oral streptococci and lactobacilli, produce metabolic by-products during active caries that demineralize enamel and dentin. Immune responses and pulpal inflammation occur when the caries front advances to within 1.5 mm of the pulp and bacterial antigens and metabolites diffuse through the dentinal tubules. The main by-product in active carious lesions is lactic acid, which contributes to the demineralization of tooth structure. If the bacterial challenge continues, immune cell responses lead to increased inflammation and edema, initially characterized clinically by pulpal pain. Inflammation is a complex protective biologic response designed to remove injurious stimuli produced by pathogens and reestablish pulpal equilibrium. Prolonged inflammation in the low-compliance environment of the pulp space eventually leads to pulp disintegration and apical pathosis.
The caries invasion is initially blocked by protective innate immune responses; it progresses to an adaptive immune response when bacteria directly approach the pulp. The pioneer microbes during caries progression first encounter a positive outward flow of dentinal fluid, characterized by the deposition of immunoglobulins and serum proteins that slow the diffusion of bacterial antigens. Potent microbial metabolites, such as lipoteichoic acid and lipopolysaccharide, also activate the innate immune system. The bacterial by-products stimulate signaling by Toll-like receptors in odontoblasts when the odontoblasts first encounter the carious front. They also stimulate proinflammatory cytokines, including interleukin-1, interleukin-8, interleukin-12, tumor necrosis factor alpha, vascular endothelial growth factor, and transforming growth factor beta (TGF- β ). Vascular endothelial growth factor promotes vascular permeability and angiogenesis. Dentin mineralization and matrix metalloproteinase secretion are also induced by the increased expression of TGF- β. Caries bacteria also activate complement pathways and induce the proinflammatory cytokine interferon gamma, which is responsible for killing phagocytosed bacteria by activated macrophages. Odontoblasts also participate in the adaptive response to microbial invasion of dentin by the synthesis of a modified mineralized matrix known as reactionary dentin, a structurally altered hard tissue characterized by diminished tubularity. As microorganisms advance toward the pulp, the modified helical structure in reparative dentin effectively constricts tubular lumen diameter and forms an active barrier against advancing pathogens ( Fig. 23-2 ).
As pulpitis progresses, vasoactive neuropeptides contribute to increased vascular permeability and intrapulpal blood flow. Increases in neuropeptide concentration and nerve sprouting characterize neurogenic inflammation, which can cause a transient increase in interstitial tissue pressure and contribute to painful pulpitis. Immune cells attempt to control neurogenic inflammation with the secretion of peptides such as somatostatin and β- endorphin . The primary effector cells in innate responses include natural killer cells, neutrophils, monocytes, and macrophages. Immature dendritic cells and T cells contribute to immunosurveillance during the progression of caries. Macrophages participate in the innate and adaptive immune responses by eliminating both pathogens and senescent cells while contributing to tissue homeostasis by repairing and remodeling tissue after inflammation.
Cytokines are small, cell-signaling proteins secreted by innate immune cells that induce phagocyte extravasation during inflammation. Chemokines secreted by odontoblasts, fibroblasts, immature dendritic cells, and macrophages stimulate leukocyte recruitment by directing monocyte and neutrophil migration extravascularly to sites of infection. Persistent infection engages the adaptive immune system, which can lead to edema and increased intrapulpal pressure, causing tissue destruction, acute phase protein production, and cell death, leading to tissue necrosis. As the caries front progresses to the pulp, prompt clinical intervention, through removal of decay and bacterial antigens before irreversible pulpitis commences, can resolve pulpal inflammation and promote recovery.
Reparative Bridge Formation
The foremost objective in vital pulp therapy is to encourage protective hard tissue barrier formation after injury. The process is initiated when regenerated odontoblast-like cells recruited from the cell-rich zone and subodontoblastic layer advance the repair of pulpodental defects after migration of highly vascularized tissue to the site. The repair process after pulp capping is characterized by four steps: (1) moderate inflammation, (2) recruitment and advance of dedicated adult reserve stem (progenitor) cells, (3) proliferation of the progenitor cells, and (4) terminal differentiation. Strong evidence supports the role of inflammation as a prerequisite for tissue repair to proceed.
The osteoblast/odontoblast-like progenitors responsible for reparative calcific bridge formation are either fibroblasts, inflammatory cells that undergo phenotypic conversion, or potentially resident stem cells activated by cytokines released during the inflammatory process. Progenitor cell differentiation may also be modulated during inflammation by activation of antigen-presenting dendritic cells or triggered by specific odontoblast and fibroblast membrane receptors. Currently, the origin of the differentiated odontoblast-like cells remains controversial. Fibroblasts, perivascular cells, bone marrow stem cells, and undifferentiated mesenchymal stem cells have all been proposed as potential progenitors. A recent histologic study, however, suggests that the amorphous, atubular calcified repair tissue formed subjacent to the calcium hydroxide (CH) placed on the pulp wound in the absence of odontoblasts is produced by pulpal fibroblasts. Therefore, such mineralized hard tissue is not genuine dentin, but repair tissue that has been called “reparative dentin,” for lack of a better term.
Odontoblast replacement in nonhuman primates directly after pulp exposures capped with CH has been examined during the cell migration and replication stages. Newly differentiating odontoblast-type cells showing initial matrix formation were demonstrated as early as day 8 at the CH-pulp interface. The continual influx of labeled differentiating cells indicated that the original derivation was from the deeper, central pulp tissue that required two DNA replications before terminal differentiation. Investigations have also indicated that reparative bridge mineralization may be more dependent on the extracellular matrix than on the capping material selected.
During healing, initial calcification immediately after pulp amputation is characterized by a proliferation of extracellular matrix vesicles situated between the forming cells and the injured pulp surface. The formation of needle-like crystals and osmophilic material within vesicles proceeds with an accumulation of crystals and aggregate at the calcified fronts, along with the disappearance of the vesicular membrane. The crystals produced during the calcification process are associated with phosphate and calcium ions, similar to fundamental calcification processes shown by other normal and pathologic calcified tissues. Defects in pulpal healing and dentinal bridge formation are associated with different pulp capping materials and include pulpal inflammation, bacterial microleakage, operative debris, and tunnel defects.
Procedures for Generating Hard Tissue Barriers
Direct Pulp Capping
The treatment options for permanent teeth that encourage pulp preservation include direct and indirect pulp capping and partial or complete pulpotomy. Direct pulp capping is defined as “placing a dental material directly on a mechanical or traumatic vital pulp exposure” and “sealing the pulpal wound to facilitate the formation of reparative dentin and maintenance of the vital pulp.” The procedure is indicated for pulp exposures incurred as a result of caries removal, trauma, or tooth preparation. When mechanical exposures occur during tooth preparation, the exposed tissue is generally not inflamed. However, in cases of trauma or carious exposure, the degree of inflammation is the key predetermining prognostic factor. According to the American Association of Endodontists, “In a carious pulp exposure, underlying pulp is inflamed to a varying or unknown extent.” The major challenge in direct pulp capping is the proper identification and removal of the acutely inflamed or necrotic tissue compromised by longstanding exposure to oral microorganisms.
Pulpotomy
Pulpotomy, or pulp amputation, is a more intrusive procedure defined as “the removal of the coronal portion of the vital pulp as a means of preserving the vitality of the remaining radicular portion: may be performed as emergency procedure for temporary relief of symptoms or therapeutic measure, as in the instance of a Cvek pulpotomy.” After complete amputation of the coronal pulp, a capping material is placed over the pulp floor and the remaining exposed tissue in the canal orifices. Dressing materials of varying toxicity have been used for this purpose, including ferric sulfate, creosote, phenol, zinc oxide eugenol, polycarboxylate cement, glutaraldehyde, CH, and formaldehyde; some of these dressing materials embalm any remaining tissue.
The procedure is recommended for primary teeth for which short-term outcomes are generally favorable. Formocresol has been the accepted “standard” universal pulpotomy agent in primary teeth and is recommended for young adult teeth; however, it has considerable drawbacks that put into question its continued use in humans. It has been identified as carcinogenic and genotoxic, and experiments have shown a high incidence of internal resorption in nonhuman primate models. Changes in the root canal system apical to formocresol placement can also create challenges when orthograde root canal treatment is attempted. Comparative studies have demonstrated MTA to be an appropriate replacement for formocresol for primary molar pulpotomy. Recent investigations also support the use of MTA and other CSCs for application in pulpotomy procedures in permanent teeth.
Partial Pulpotomy
Partial pulpotomy (shallow pulpotomy, or Cvek pulpotomy) is defined as the removal of a small portion of the vital coronal pulp as a means of preserving the remaining coronal and radicular pulp tissues. After the pulp has been exposed and is visualized after hemostasis, inflamed or necrotic tissue is removed to uncover deeper, healthy pulp tissue in the pulp chamber. Partial pulpotomy and direct pulp capping can be viewed as similar procedures, but they differ in the amount of vital pulp tissue remaining after treatment. Partial pulpotomy is the preferred option in elective treatment procedures for teeth diagnosed with anatomic anomalies, such as dens invaginatus.
Indirect Pulp Capping
Indirect pulp capping is defined by the AAPD as “a procedure performed in a tooth with a deep carious lesion approximating the pulp but without signs or symptoms of pulp degeneration. Indirect pulp treatment is indicated in a permanent tooth diagnosed with a normal pulp with no signs or symptoms of pulpitis or with a diagnosis of reversible pulpitis.” The treatment can be completed as a one-step or two-step procedure (stepwise technique) with the objective of arresting the active carious lesion. Indirect pulp capping has been shown to be an effective technique for caries and patient management in the primary dentition, but it remains controversial in permanent teeth. The technique is similar for both primary and permanent teeth, except that permanent teeth require reentry for the removal of residual carious tissue; reentry also is considered necessary to confirm reactionary dentin formation. However, data from a recent investigation have questioned the need to reopen cavities to remove residual infected dentin in a subsequent visit.
The treatment requires prudent case selection, including identification of asymptomatic patients with no suspicion of irreversible pulpitis. Pulp exposures are avoided during caries excavation by removal of the superficial demineralized necrotic dentin and then the removal of the peripheral dentin. After excavation, the remaining carious dentin is lined with CH and sealed with a provisional material, such as intermediate restorative material (IRM) or a resin-modified glass ionomer (RMGI). The patient returns in 8 to 12 weeks for placement of a permanent coronal restoration. Advocates of indirect pulp capping argue that pulp healing can be compromised if the carious dentin barrier is removed during excavation and that the prognosis of vital pulp therapy (direct exposure) is unfavorable. A challenging aspect of indirect pulp capping is determining the exact boundary point where caries excavation is terminated. Therefore, the technique is based primarily on subjective criteria and the operator’s skill. Further complicating the process is the presence of potential voids under the provisional restoration; during the mineralization process, these can permit dentin to lose volume during desiccation. Another drawback is the rapid reactivation of dormant lesions after restoration failure. However, in younger patients with management issues, indirect pulp capping has shown promising results for immature permanent teeth in which the apical foramina are large, the canal walls are thin, and pulp vascularization is pronounced.
Indications for Vital Pulp Therapy
Vital pulp therapy is recommended for all teeth diagnosed with reversible pulpitis or partially inflamed pulps in which the remaining healthy tissue can be conserved to generate a hard tissue barrier that seals and protects the pulp from future microbial insult. The introduction of new bioactive materials, along with modified protocols, make more teeth with deep caries, traumatic injuries, and mechanical exposures viable candidates for innovative pulp therapies designed to potentiate and maintain pulpal survival. Treatment outcomes for direct pulp capping and pulpotomy procedures depend on multiple factors, beginning with a differential diagnosis that takes into account pulp testing, radiographic evaluation, clinical evaluation, and the patient history to determine a rational prognosis. Outcomes also depend on case selection, hemostatic agents, choice of pulp capping material, and the integrity of the sealed permanent restoration. The underlying purpose in vital pulp therapy is to avoid or delay root canal therapy and advanced restorative care because these, together, may reduce long-term tooth survival compared to teeth with vital pulps. *
* References .
Materials for Vital Pulp Therapy
A variety of pulp dressing materials have been investigated and used over the past century to encourage bridge formation and pulp preservation. A short list of compounds includes CH products, calcium phosphate, zinc oxide, calcium-tetracycline chelate, zinc phosphate and polycarboxylate cements, Bioglass, Emdogain, antibiotic and growth factor combinations, Ledermix, calcium phosphate ceramics, cyanoacrylate, hydrophilic resins, RMGI cements, hydroxyapatite compounds and, recently, MTA and other CSCs. † Other strategies designed to arrest invasive caries and promote repair of underlying tissues include the use of lasers, ozone technology, silver diamine fluoride, and bioactive agents that stimulate pulpal defense mechanisms. ‡ Retrospective investigations have shown varying success rates of 30% to 85% for direct pulp capping in humans, depending on the method, hemostatic agent, and dressing material used. § The search to identify and produce the ideal pulp capping material continues, and remarkable progress has been made in pulp preservation research in the past decade.
† References .
‡ References .
§ References .
Calcium Hydroxide
Calcium hydroxide has long been considered the universal standard for vital pulp therapy materials. The introduction of CH into dentistry is credited to Hermann in the 1920s. Although the material demonstrates many advantageous properties, long-term study outcomes in vital pulp therapy have been inconsistent. Desirable characteristics of CH include an initial high alkaline pH, which is responsible for stimulating fibroblasts and enzyme systems. It neutralizes the low pH of acids, shows antibacterial properties, and promotes pulp tissue defense mechanisms and repair. The drawbacks of CH include weak marginal adaptation to dentin, degradation and dissolution over time, and primary tooth resorption. Reparative bridge formation subjacent to CH can also be characterized by tunnel defects. * Histologically, CH demonstrates cytotoxicity in cell cultures and has been shown to induce pulp cell apoptosis.
* References .
Tunnel defects have been demonstrated in reparative hard tissue bridges associated with both CH and CSCs. However, the primary difference between the two pulp therapy agents is that CH products are absorbable over time and dimensionally unstable. The slow disintegration of the CH after hard tissue barrier formation can allow microleakage, thus permitting a slow ingress of microorganisms through calcific bridge defects. This can induce subsequent pulpal degeneration, further leading to potential dystrophic calcification and pulpal necrosis. Over extended periods, this problematic outcome of CH pulp capping can complicate nonsurgical root canal treatment if required.
Clinical retrospective investigations have shown variable success rates over 2- to 10-year recall periods for direct CH pulp capping in humans. Two current studies have examined the efficacy of CH as a direct pulp capping agent. One study examined the survival rate of 248 pulp-capped teeth that were diagnosed either as having normal pulps or as exhibiting spontaneous pain; the researchers found an overall survival rate of 76.3% with an average recall period of 6.1 years. Treatment outcomes were less favorable for teeth showing spontaneous pain, in older compared to younger patients, and in teeth restored with glass ionomer cements. The probability of pulps becoming nonvital after CH pulp capping was greater within the first 5 years of treatment.
The second study observed 1,075 teeth directly pulp capped with a CH-based agent; these teeth had either healthy pulps or showed signs of reversible pulpitis. Inclusion criteria limited pulp chamber roof exposures to no larger than 2 mm in diameter. Successful outcomes were 80.1% after 1 year and 68% after 5 years; this diminished to 58.7% after a 9-year observation period.
The results of the two studies indicate increasing failure rates over time, attributable to absorption of the material under permanent restorations proximal to mineralized bridges with tunnel defects. Another investigation has confirmed decreasing success rates with CH pulp capping with extended recall periods. Calcium hydroxide clearly has many favorable characteristics as a vital pulp therapy agent. However, the material also demonstrates inherent physical weaknesses and can no longer be considered the preferred universal agent in vital pulp therapy ( Fig. 23-3 ).
Resin-Modified Glass Ionomer Cements and Hydrophilic Resins
Adhesive systems were introduced in the early 1980s as potential agents for direct pulp capping of cariously and mechanically exposed pulps. These materials include RMGI cements, composite resins, and hydrophilic resins. Hydrophilic resins and RMGI cements initially showed favorable outcomes in preliminary pulp capping investigations with nonhuman primates based on standards set by the International Organization for Standardization (ISO). However, the transitional use of these materials in human subjects did not demonstrate the corresponding biocompatibility or consistent reparative bridge formation. Investigations that have examined responses of resin-based materials in human teeth have demonstrated unfavorable histologic reactions when the material is placed directly or in close proximity to pulp tissue. Histologic sections from these studies typically demonstrate the presence of inflammatory cell infiltrates consistent with pulp cell cytotoxicity, subclinical adhesive failures at the pulp interface, and a profound absence of biocompatibility. *
* References .
Research data have shown that increasing concentrations of triethylene glycol dimethacrylate (TEGDMA), a common dentin bonding compound, differentially increase the levels of apoptotic and necrotic cell populations after direct exposure. Moreover, even low levels of TEGDMA diminish alkaline phosphatase activity and calcium deposition, thus inhibiting pulp cell mineralization and potential reparative bridge formation. Alternatively, adhesive resins have shown some promise when combined with additives or growth factors, such as hydroxyapatite powder, dental matrix protein-derived synthetic peptides, calcium chloride (CaCl 2 ), calcium phosphate, and antibacterial agents, including 12-methacryloyloxydodecylpyridinium bromide (MDPB). It is evident that bonding agents used for direct pulp capping do not predictably generate a favorable environment for pulp healing and hard tissue formation. However, hydrophilic resins and RMGI cements provide excellent seals when they are combined with light-cured composites in permanent restorations and then placed directly over pulp capping materials such as MTA.
Mineral Trioxide Aggregate (MTA)
Mineral trioxide aggregate was introduced as a pulp capping material by Torabinejad and associates in the mid-1990s. Most preliminary experimental and current clinical data in vital pulp therapy are based on the proprietary material ProRoot MTA (Tulsa/Dentsply, Tulsa, Oklahoma). The cement consists of hydraulic calcium silicate powder containing various oxide compounds, including calcium oxide, ferric oxide, silicon oxide, sodium and potassium oxides, magnesium oxide, and aluminum oxide. The material exhibits favorable physiochemical characteristics that stimulate reparative dentinogenesis by recruitment and activation of hard tissue–forming cells, contributing to matrix formation and mineralization. Soluble cytokines and growth factors that mediate wound repair of the dentin-pulp complex are nested in the extracellular matrix, and MTA stimulates reparative hard tissue formation by sequestering these growth factors and cytokines embedded in the surrounding dentin matrix. Calcium hydroxide and calcium silicate hydrate, the principal by-products formed during hydration of mixed MTA, contribute to a sustained alkaline pH. The setting properties of the hydroscopic silicate cements are not affected by the presence of tissue fluids or blood.
During the setting process, the gradual release of calcium ions encourages reparative barrier formation by promoting signaling molecules, such as vascular endothelial growth factor (VEGF), macrophage colony-stimulating factor (MCSF), TGF- β , and interleukins IL-1 β and IL-1 α . MTA demonstrates superior marginal adaptation to dentin compared to CH-based agents; MTA forms an adherent interfacial layer during mineral nucleation at the dentin surface that appears similar in composition to hydroxyapatite when examined with X-ray diffraction, energy-dispersive X-ray analysis, and scanning electron microscopy (SEM).
If the pulp is injured, wound healing and the repair process can advance only after the initiation of the inflammatory reaction. Similar to CH, MTA induces an inflammatory cascade that results from calcium ion release and the creation of an alkaline environment, producing tissue necrosis. Both MTA and CH have been shown to stimulate and increase the Höehl cell mitosis index in rodent models. MTA activates the migration of progenitor cells from the central pulp to the injury site and promotes their proliferation and differentiation into odontoblast-like cells without inducing pulp cell apoptosis. MTA also stimulates in vitro the production of messenger ribonucleic acid (mRNA) and increases protein expression of the mineralized matrix genes and cellular markers crucial for mineralization after matrix formation.
Gray MTA has been shown to enhance cell proliferation and survival of cultured human dental pulp stromal cells. The biocompatibility of set MTA up-regulates the expression of transcription factors, angiogenic factors, and gene products, such as dentin sialoprotein, osteocalcin, and alkaline phosphatase. Odontoblast signaling proteins are essential in the differentiation of progenitor cells into the odontoblast-like cells responsible for repair and hard tissue deposition. After MTA pulp capping, both sialoprotein and osteopontin have been observed in the fibrodentin matrix at the exposure site during the process of reparative hard tissue formation.
Dental pulp cells differentiate into the odontoblastic cell line in the presence of the signaling molecules, such as TGF- β , heme oxygenase-1 enzyme, and bone morphogenetic proteins BMP-2, BMP-4, and BMP-7. MTA most likely up-regulates fibroblast secretion of BMP-2 and TGF- β 1 and therefore stimulates and promotes mineralization and hard tissue regeneration. * MTA induces a time-dependent environment that is proinflammatory and promotes wound regeneration through up-regulation of cytokines. Immunohistochemical analyses show that cytokines, including myeloperoxidase, inducible nitric oxide synthase, VEGF, nuclear factor-kappa B (NF- κ B), activating protein-1, and cyclooxygenase-2, show increased expression in the presence of MTA. Cytokine up-regulation is responsible for inducing biomineralization by producing apatite-like clusters on collagen fibrils at the MTA-dentin interface. MTA does not affect the generation of reactive oxygen species, thereby positively influencing cell survival. MTA also has been shown to improve the secretion of IL-1 β , Il-6, and IL-8. However, an inhibitory effect on dental pulp cells has been demonstrated in the presence of MTA, which may be attributed to the release of aluminum ions. The data indicate that MTA promotes a biocompatible, noncytotoxic, antibacterial environment and surface morphology that are favorable for reparative calcific bridge formation. MTA stimulates the release of the dentin matrix components necessary for hard tissue repair and regeneration in mechanically exposed healthy and partially inflamed pulps ( Figs. 23-4 to 23-6 ). †
* References .
† References .
Calcium Silicate–Based Cements (CSCs)
A variety of new bioactive CSCs or bioceramic materials have been developed since the introduction of MTA. Preliminary investigations with CSCs have demonstrated physiochemical and bioinductive properties comparable to those of MTA, indicating the potential future application of these materials in vital pulp therapy. Some of these tricalcium-based materials include BioAggregate (Innovative Bioceramix, Vancouver, British Columbia), Biodentine (Septodont, Cambridge, Ontario, Canada), MTA-Angelus, MTA Bio, and MTA Branco (MTA-Angelus, Londrina PR, Brazil). Other formulations include EndocemMTA (Maruchi, Wonju-si, Gangwon-do, South Korea) and Endosequence root repair material (Brasseler USA, Savannah, Georgia). Additional compounds are currently undergoing clinical investigations to establish their safety and efficacy.
The main components of MTA and the new CSCs are tricalcium silicate and dicalcium silicate, major components of Portland cement. Hydraulic tricalcium silicates promote reparative barrier formation by up-regulation of transcription factors after gaining immediate strength on hydration. However, research data are limited on direct pulp capping and pulpotomy treatments in humans using these new bioceramic products.
BioAggregate is a bioinductive tricalcium cement that can induce mineralization in osteoblast cells by increasing levels of osteocalcin, collagen type 1, and osteopontin gene expression. Hydration of the cement results in the formation of calcium silicate hydrate and CH, showing high concentrations of silica and calcium phosphate. This characteristic is consistent with materials used in vital pulp therapy to promote hard tissue formation. Investigations using X-ray diffraction show the material to have a composition similar to that of MTA, but BioAggregate contains tantalum rather than bismuth oxide to provide radiopacity. BioAggregate demonstrates remarkable biocompatibility compared to MTA, inducing cell differentiation in both human periodontal ligament and gingival fibroblasts. Both fresh and set mixtures of MTA and BioAggregate have shown antimicrobial properties effective against Enterococcus faecalis in vitro when combined with equal amounts of human dentin powder. The material also shows a greater resistance to dislodgement in an acidic environment compared to MTA, in addition to higher fracture resistance when used as a filling material.
Biodentine is a tricalcium silicate–based cement that also demonstrates exceptional bioactive properties with potential for both direct and indirect pulp capping procedures. The cement has a short setting time of 10 minutes and does not induce genotoxic or cytotoxic effects when measured with the Ames mutagenicity test. It is considered a biocompatible dentin replacement material for use under various restorative materials as a base or liner, and it does not alter human pulp fibroblast cytodifferentiation. SEM analysis demonstrates the sealing ability of Biodentine to be similar to that of MTA; Biodentine forms needle-like crystals resembling apatite at the dentin interface. The material induces odontoblast-like cell differentiation, stimulates biomineralization, and promotes hard tissue formation when used as a pulp capping material.
Another promising material for vital pulp therapy is MTA-Angelus, which has a basic formulation of 25% bismuth oxide and 75% Portland cement. The composition eliminates calcium sulfate, providing a short setting time of 10 minutes, which is preferable for one-visit pulp capping or pulpotomy procedures ( Fig. 23-7 ). Variations in bismuth oxide and the presence of iron characterize the chemical composition of MTA-Angelus, and the crystalline structures formed on hydration are similar to gray and white ProRoot MTA. MTA-Angelus and ProRoot MTA have been compared experimentally as pulp capping agents in intact, caries-free human teeth. Histomorphologic examination of extracted teeth revealed that the two materials produced similar responses with regard to inflammation and hard tissue formation. MTA-Angelus also demonstrates antifungal properties and a lower compressive strength than ProRoot MTA.
Endosequence root repair material shows low cytotoxicity, antibacterial activity against E. faecalis, and strong potential as a pulp capping material. Another material, calcium-enriched mixture (CEM) cement, has also demonstrated excellent physical and biologic properties in vital pulp therapy investigations.
This new generation of CSCs appears promising when used as vital pulp therapeutic agents and current investigations appear to support these materials’ future potential.
MTA Applications in Vital Pulp Therapy
Direct Pulp Capping with MTA
Controlled prospective investigations on direct pulp capping in humans using MTA against cariously exposed pulps are limited. Collectively, most studies are inconsistent with regard to case selection, treatment strategies, and clinical protocols. The subsequent spectrum of outcomes is reflected by the absence of standardized guidelines for caries removal, hemostatic agents, single- versus two-visit delivery sequences, and the choice and placement of a capping material.
Unsatisfactory outcomes for direct capping due to variations in treatment delivery and protocols were clearly demonstrated in a cohort investigation completed by predoctoral dental students. Fifty-one direct MTA pulp caps completed in a carious field were radiographically and clinically evaluated for a 12- to 27-month period. The overall success rates using Kaplan-Meier analysis were 67.7% at 1 year and 56.2% at 2 years. The poor outcome can be attributed to an absence of strict control protocols with regard to caries removal, selection of hemostatic agents, and appropriate magnification, illumination, and thickness combined with area coverage of MTA. As a result, the investigation concluded that the amount of hemorrhaging after pulp exposure was not a determining factor in the clinical outcome, contrary to other findings.
More impressive results for pulp maintenance and continued vitality after direct pulp capping procedures have been demonstrated in several other contemporary studies. An investigation examined 30 immature permanent teeth exhibiting wide-open apices directly pulp capped with MTA and restored temporarily with IRM. Definitive permanent composite restorations were placed 2 weeks later, after confirmation of pulp vitality. In these cariously exposed immature permanent teeth, the success rate at a 2-year review was 93%.
Another observational investigation examined direct pulp capping after carious exposures of mature and immature permanent teeth completed using MTA in a two-visit sequence. Forty-nine teeth were examined in patients aged 7 to 45 years over a 1- to 9-year period, with an average 3.94-year observation time. The study incorporated a strict protocol that included detector dye–aided caries excavation using the dental operating microscope, 5.25% to 6% sodium hypochlorite (NaOCl) hemostasis, thick MTA placement on pulp exposures and surrounding dentin, coupled with adhesion-based permanent restorations placed at a subsequent visit to compensate for the delayed setting properties of ProRoot MTA. Based on subjective symptomatology, cold testing, and radiographic evaluation, 97.96% of teeth showed a favorable outcome. All 15 patients with immature apices showed continued root formation, with apical closure over a 6- to 10-year period; five patients with large or multiple exposures exhibited pulpal calcification ( Fig. 23-8 ).
The improved survival outcomes seen in this MTA pulp capping study can be credited to changes in established treatment protocols and the incorporation of improved pulp capping materials. Progress in the caries removal process, magnification systems, NaOCl hemostasis, MTA selection, and adhesion technology take advantage of advances in vital pulp therapy to surpass the outcomes seen with accepted traditional methods ( Figs. 23-9 and 23-10 ).
The unique physiochemical properties of MTA also promote a superior environment for pulpal repair and bridge formation, compared to CH products. MTA is a hygroscopic cement that sets in the presence of blood and serum, produces a gap-free interface with dentin, and generates a sustained alkaline pH; in addition, the surface morphology of the hardened cement allows for predictable bonding with current adhesion systems. Growth factors necessary for hard tissue formation are activated by MTA through the gradual release of calcium ions during cement curing. The small particle size and alkaline pH contribute to the entombment of remaining cariogenic bacteria at the dentin-MTA interface, impeding bacterial ingression and caries progression and discouraging continued pulpal injury.
Pulpotomy with MTA
The decision to remove a small or large portion of the coronal pulp is based on visual inspection of the pulp tissue and the ability to achieve hemostasis after pulp exposure during either caries excavation or exposure as a result of trauma (partial or shallow pulpotomy). The coronal pulp tissue can also be removed completely to the pulp floor or cervical area (pulpotomy) in the case of molars and some premolars. The AAPD guidelines state, “A pulpotomy is performed in a tooth with extensive caries but without evidence of radicular pathology when caries removal results in a carious or mechanical pulp exposure.” If bleeding cannot be controlled after 10 minutes of direct exposure to NaOCl after removal of unhealthy tissue, complete removal of the coronal pulp to the pulp floor is the preferred option.
Sodium hypochlorite serves as an excellent diagnostic tool to differentiate irreversible from reversible pulpitis and to help determine whether to proceed with partial pulpotomy, complete pulpotomy, or pulpectomy. This decision can be of paramount importance in young permanent teeth with open apices, in which removal of tissue contaminated by microorganisms can reverse symptoms and stabilize inflamed tissue. Investigations have shown that the proliferative response of pulp tissue after exposure progresses several millimeters into the pulp from the injury site. The removal of 1 to 3 mm of peripheral tissue to access the deeper, healthy tissue, in cases of trauma or when carious exposures reveal inflamed tissue, ensures pulp survival ( Fig. 23-11 ).
Partial pulpotomy for treating direct pulp exposures in immature permanent teeth using CH products has been shown to be a reliable treatment option with proper case selection. * However, improved success rates ranging from 93% to 100% have been demonstrated using MTA for pulpotomies in permanent teeth. Moreover, pulpotomies completed with MTA in primary molar teeth do not show pathologic complications such as internal resorption, which typically are seen with CH, formocresol, and ferric sulfate.
* References .
It has been recommended that pulpectomy be avoided in immature permanent teeth with vital canal tissue so as to protect the remaining radicular pulp tissue and thus encourage continued root development and apexogenesis. However, with the introduction of MTA, predictable root-end closure and maturogenesis can be achieved with new approaches using regenerative, revascularization, and apexogenesis procedures ( Fig. 23-12 ). † Although controversy remains regarding the type and quality of tissue produced in regenerative procedures for nonvital teeth, current treatment options for immature teeth strengthen roots by increasing wall thickness and root length.
† References .
Complete pulpotomy for mature irreversibly inflamed permanent molars represents a novel approach in treating symptomatic teeth while preserving pulp canal tissue. A current randomized clinical trial compared full pulpotomies completed with MTA and CEM; the study examined postoperative pain, along with radiographic and clinical outcomes in patients diagnosed with irreversible pulpitis. At a 1-year follow-up for 413 pulpotomized teeth, the clinical success rates were 98% for MTA and 97% for CEM. Similarly, the radiographic success rates were 95% for MTA and 92% for CEM. Most patients experienced a significant reduction in pain intensity postoperatively over a 7-day period. This conservative strategy for irreversibly inflamed teeth may be beneficial for patients in underserved areas globally.
Vital Pulp Therapy Techniques
Diagnosis
A differential diagnosis based on symptoms and clinical findings is the goal in the assessment of pulp vitality. However, an accurate determination of the pulpal condition before treatment initiation can be more challenging in younger patients. Establishing a diagnosis of reversible versus irreversible pulpitis in immature teeth can be complicated by subjective symptoms and testing responses that may not accurately reflect the histopathologic condition of the involved pulp. However, efforts should be directed toward the ultimate goal of pulpal preservation and continued apexogenesis in immature permanent teeth. A diagnosis of irreversible pulpitis, based on signs and symptoms, along with clinical testing procedures, does not preclude vital pulp therapy options. Regardless of the treatment choice of pulp capping or partial or complete pulpotomy, preservation of the radicular pulp and apical papilla allows for root maturation in cases of trauma or deep caries.
Acceptable diagnostic quality intraoral radiographs of the involved tooth must be taken to evaluate accurately the extent of root formation and periradicular or furcation changes associated with the periodontal ligament and supporting bone. In young permanent teeth, the stage of root development directly influences the diagnosis and treatment options. Because the faciolingual dimension of most immature roots is greater than the mesiodistal dimension, apical closure may be difficult to determine radiographically. Teeth that demonstrate radiographic evidence of deep caries should not be planned for aggressive procedures, such as pulpectomy, without the benefit of thermal (cold) testing (see Fig. 23-1 ).
Before arriving at treatment decisions, the clinician should carefully assess all available information; the medical history, patient report, radiographic evidence, clinical evaluation, and vitality (cold) testing are recommended. Periodontal probing, mobility assessment, and the presence of any localized swelling or sinus tracts should be recorded during the evaluation. Radiographs, including bite wings and periapical views, should be evaluated for periapical and furcation pathosis, resorptive defects, and pulpal calcification resulting from trauma or previous restorations.
Subjective symptomatology can be reviewed after clinical and radiographic assessments preclude the presence of unconditional irreversible pulpal disease. Patients with deep carious lesions often experience sensitivity to cold, heat, or sweet or acidic foods, and cold tests may evoke a short lingering response of 1 to 2 seconds. This may not be a definitive indicator that the pulp is irreversibly damaged. Determination of the pulpal condition with the aid of contemporary testing methods can be challenging, even for veteran clinicians, because of possible excessive responses to pulp percussion and palpation testing in children. Clinical evidence indicates that cold testing with carbon dioxide ice is a more reliable prognosticator of pulp status in immature permanent teeth than electronic testing devices. However, a diagnosis of irreversible pulpitis or pulp necrosis should be considered for teeth that generate pain on percussion.
Recent clinical investigations have demonstrated that a diagnosis of symptomatic irreversible pulpitis and acute apical periodontitis may not proscribe pulp capping and pulpotomy procedures when MTA or other CSCs that have been shown to reverse the inflammatory process are used. Clinically, the difference between reversible and irreversible pulpitis is often determined on the basis of the duration and intensity of pain. Unprovoked spontaneous pain of long duration or unrelenting symptoms forcing sleep deprivation are consistent with irreversible pulp inflammation or an acute periapical abscess.
Another important consideration in the differential diagnosis is a patient with displacement trauma, which can display a transient apical breakdown radiographically that mimics periapical radiolucencies. Teeth that experience luxation-type injuries can discolor and may not respond to cold testing for up to 4 months before they recover normal color and vitality. Also, biologically or pharmacokinetically immunosuppressed patients may not respond to conventional treatments because of abnormal function of related repair mechanisms. Most clinical investigations clearly indicate that successful outcomes for vital pulp therapy decrease as the patient’s age increases. Although aging of the pulp diminishes pulpal volume, vascularity, and host immune responses, functional repair mechanisms can still provide favorable treatment outcomes in older patients ( Fig. 23-13 ).
The initial pulpal diagnosis can be confirmed after visualization of the exposed pulp and during hemostasis assessment. If no hemorrhaging is seen, this area of the tissue is most likely necrotic, and the tissue must be removed with a high-speed round diamond bur until bleeding is evident ( Fig. 23-14 ). After hemostasis with NaOCl, a large bulk of MTA can be placed directly against the remaining tissue. Alternatively, if hemorrhage control cannot be achieved after 10 minutes of direct contact with 3% to 6% NaOCl, the pulp is likely to be irreversibly involved, and a full pulpotomy or pulpectomy is recommended.
Although the size of the pulp exposure has no significant bearing on the final outcome, some clinicians falsely assume that larger exposures have an unfavorable prognosis. Pulp sizes are underestimated on radiographs. The size of the pulp exposures may also be overestimated, which could affect the decision-making process, leading clinicians to abandon more conservative vital pulp options. Pulp dimensions may also vary with various racial groups and between genders.
Teeth that have a history of trauma or previous restorations or that display pulpal calcification have a poorer prognosis than teeth showing only initial caries. In the selection of a specific vital pulp treatment, it is important to consider the remaining tooth structure and future restorative plan. In patients with uncontrolled caries or extensive loss of coronal structure, in which full coverage is indicated, pulpotomy rather than pulp capping is recommended.
Caries Removal
The main objective in caries removal is the identification and complete removal of the infected tissue while preserving sound tooth structure; this contributes to pulpal protection and continued vitality. Caries removal is enhanced with the aid of a caries detector dye and optical magnification; however, some studies have indicated that dyes can cause excessive and unnecessary removal of healthy tooth structure.
Caries removal has traditionally been completed somewhat subjectively using hand instruments and slow-speed burs. The procedure is performed using an explorer and tactile sense to differentiate soft from hard dentin to determine infected from noninfected dental tissue. However, this method can have shortcomings because clinicians may leave decay at the dentinoenamel junction and unnecessarily remove dentin that still has the potential to remineralize under a sealed restoration. Furthermore, it has been found that the ability to remove caries varies among operators and during different time periods for the same operator.
Investigators in the early 1970s used SEM to identify two different layers of carious dentin. Teeth show two distinct layers of carious dentin as the result of gram-positive bacteria releasing lactic acid as their main by-product. The outside carious layer subjacent to the dentinoenamel junction exhibited demineralized hydroxyapatite crystals that were dissolved by acidic bacterial byproducts; this layer also featured unbound and altered collagen denatured by microbial proteolytic enzymes. A fuchsin dye suspended in propylene glycol was used to reveal that this necrotic and infected layer could be selectively stained, identified, and removed objectively, thus preserving the inner carious layer that remained capable of remineralization. A highly significant difference in the total colony-forming units in stained and unstained dentin has been demonstrated.
The second demineralized carious layer proximal to the pulp featured degraded hydroxyapatite crystals but contained collagen with intact intermolecular cross-links unaffected by cariogenic acids and not stainable with caries detector dyes. If the second inner layer can be identified and preserved during caries excavation, the remaining pulp tissue and odontoblasts subjacent to the carious zone will be subjected to less trauma, which contributes to pulpal protection and survival. The second layer proximal to the pulp has a stronger capacity to remineralize when paired with bonded composite restorations to prevent bacterial microleakage.
The two carious layers have been further classified into four zones (pink, light pink, transparent, and apparently normal) when analyzed by atomic force microscopy and transverse digital microradiography. Consistent with previous investigations, the four zones reinforce the concept that increasing levels of demineralization decrease the peritubular dentin rating and mechanical properties of dentin.
Caries detector dyes can be considered a valuable tool in caries excavation when attempts are made to preserve remineralizable dentin and to minimize trauma to the pulp. Investigations in human, dog, and nonhuman primate models have demonstrated this regenerative characteristic in caries-affected dentin. Several studies have questioned the efficacy of caries removal using a caries detector dye. Not all stainable dentin can be classified as infected, and the absence of staining does not eliminate the potential for residual cariogenic bacteria. However, dyes allow the operator to visually inspect, under magnification, infected dentin that may have been overlooked, particularly at the dentinoenamel junction, a situation that may compromise the outcome for vital pulp therapy. Although a compromise, it may be preferable clinically to inadvertently remove a small excess amount of dentin than to leave infected tissue with active caries.
Hemostatic Agents
A wide range of hemostatic solutions and methods have been recommended to control a bleeding pulp exposure. These include various concentrations of NaOCl; 2% chlorhexidine; MTAD (DENTSPLY Tulsa Dental Specialties, Tulsa, Oklahoma); 30% hydrogen peroxide (Superoxol); ferric sulfate; disinfectants, such as Tubulicid (Global Dental Products, North Bellmore, New York); epinephrine; direct pressure with cotton pellets soaked in sterile water or saline; and the use of lasers. Sodium hypochlorite in concentrations of 1.5% to 6% is currently regarded as the most effective, safe, and inexpensive hemostatic solution for pulp capping and partial and complete pulpotomy procedures. First used as a wound antiseptic during World War I and referred to as Dakin’s solution, NaOCl became a valuable hemostatic agent in dentistry for direct pulp exposures in the late 1950s. The antimicrobial solution provides hemostasis and disinfection of the dentin-pulp interface, chemical amputation of the blood clot and fibrin, biofilm removal, clearance of dentinal chips, and removal of damaged cells at the mechanical exposure site. Concentrations of 1.5% to 6% in direct contact with pulp tissue do not appear to adversely alter pulp cell recruitment, cytodifferentiation, and hard tissue deposition. Sodium hypochlorite also shows excellent efficacy as a hemostatic agent at lower dilutions (0.5%).
When direct pulp exposures occur in a carious field, the ability to attain hemostasis remains the most crucial factor in the success of vital pulp therapy. This was demonstrated in an innovative study that examined outcomes of teeth directly pulp capped with a hard-setting CH after pulp exposures were generated during caries excavation. Caries removal during the investigation was aided by a caries detector dye, and 10% NaOCl was used for hemostasis. The 2-year success rate was 81.8%. A statistical analysis of key factors revealed that preoperative thermal responses, percussion sensitivity, the diameter of the exposure, the age of the patient, and the tooth type and location had no significant influence on the outcome. The degree of bleeding and its control at the time of exposure constituted the most critical predictor for outcome assessment. When hemostasis can be attained, pulpal repair and reparative dentin formation can proceed normally, in the absence of microbial challenges, when MTA is used as the pulp dressing.
Sodium hypochlorite is not only an effective hemostatic agent, it can also be considered an invaluable diagnostic tool for assessing the difference between irreversibly and reversibly inflamed pulps ( Fig. 23-15 ). During the inflammatory process, as cariogenic bacteria approach the pulp, higher levels of immunoglobulins (e.g., IgA, IgG, IgM) and inflammatory markers have been detected, including elastase and prostaglandin E 2 . The presence of these mediators can contribute to increased intrapulpal pressure and may play a critical role in the pathogenesis of the irreversibly inflamed pulp.
