Vital Pulp Therapy

Vital pulp therapy is performed to preserve the health status of the tooth and its ultimate position in the arch. These procedures are performed routinely in primary and permanent teeth. This review is divided into 2 parts: the first aims to illustrate the basic biology of the pulp and the effects on the pulp due to various procedures; the second focuses on the clinical aspects of treatment and the use of various dental materials during different vital pulp therapy procedures performed in the primary and permanent teeth.

Key Points

  • Vital pulp therapy for children is simple.

  • Vital pulp therapy is effective as long as proper assessment of the situation is made.

  • Treatment is performed in the appropriate fashion with strict adherence to the proper technique.

Introduction

Vital pulp therapy is performed to preserve the health status of the tooth and its ultimate position in the arch for the expected life of the tooth. In cases of a primary tooth, the length of time for expected life is measured against the expected life of the tooth in the mouth without pulp disease or pulp therapy. Cases of permanent tooth mean long-term preservation of the tooth in a healthy state in the mouth. This article reviews the rudiments of pulp therapy for children. It is recommended that practitioners gather additional information in each of the referenced areas before engaging in pulp therapy for children. Although not specifically discussed, effective local anesthesia and rubber dam usage are always required.

The first part of this article provides insight into the basic biology of the dental pulp, the mechanisms involved in inflammation, and the reactions of the pulp to various dental materials at the cellular and molecular level whereas the second part deals with the clinical aspects of treatment of the primary and permanent dentition.

Introduction

Vital pulp therapy is performed to preserve the health status of the tooth and its ultimate position in the arch for the expected life of the tooth. In cases of a primary tooth, the length of time for expected life is measured against the expected life of the tooth in the mouth without pulp disease or pulp therapy. Cases of permanent tooth mean long-term preservation of the tooth in a healthy state in the mouth. This article reviews the rudiments of pulp therapy for children. It is recommended that practitioners gather additional information in each of the referenced areas before engaging in pulp therapy for children. Although not specifically discussed, effective local anesthesia and rubber dam usage are always required.

The first part of this article provides insight into the basic biology of the dental pulp, the mechanisms involved in inflammation, and the reactions of the pulp to various dental materials at the cellular and molecular level whereas the second part deals with the clinical aspects of treatment of the primary and permanent dentition.

The dental pulp

The tooth pulp is a unique organ and is encased in a protective layer of dentin, which is encased by a layer of the enamel. Embryologically, histologically, and functionally, the dentin and the pulp are the same and are considered together, which is why they are also referred to as the pulp-dentin complex.

Zones of the Pulp

The structure of the dental pulp is similar to the other connective tissues in the body.

The mature pulp demonstrates 4 morphologic zones, including

  • 1.

    Odontoblastic layer: the outermost stratum of cells in a healthy pulp. It is subadjacent to the predentin and is composed of cell bodies of the odontoblasts, capillaries, nerve fibers, and dendritic cells. It is a highly specialized layer for the synthesis and secretion of the organic components of the dentin and has an epithelial layer that serves as a liner for the dental pulp.

  • 2.

    Cell poor zone: also called the cell free zone of Weil because it is relatively free of cells. It is subadjacent to the odontoblastic layer and is traversed by capillaries, unmyelinated nerve fibers, and cytoplasmic processes of fibroblasts.

  • 3.

    Cell-rich zone: lies subadjacent to the cell-poor zone. It has a higher number of fibroblasts with more in the central region of the pulp. The cellular components of this layer include mainly macrophages and lymphocytes. Irreversibly injured odontoblasts are replaced by cells that migrate from this layer.

  • 4.

    Pulp proper: the central mass of the pulp, which consists of larger blood vessels and nerves. The connective tissue in this zone contains collagen fibers and ground substance.

Cells of the Pulp

The pulp contains numerous cells types, which include odontoblasts, fibroblasts, macrophages, dendritic cells, lymphocytes, mast cells, and undifferentiated mesenchymal stem cells. The odontoblasts are particularly important because they are responsible for dentinogenesis both during tooth development and in the mature tooth. Odontoblasts synthesize mainly type 1 collagen, type V collagen, proteoglycans, dentin sialoprotein, and alkaline phosphatase. The odontoblasts have odontoblastic processes that extend into the dentinal tubules and occupy most of the space of the dentinal tubules. Some studies have shown that the processes are limited to the inner third of the dentin and other studies have demonstrate the processes extending to the dentinoenamel junction.

Differences in the Pulp Related to Age

Aged dental pulps have various characteristics, which include the following:

  • 1.

    Reduction of pulp chamber size

  • 2.

    Fibrosis

  • 3.

    Atrophy

  • 4.

    Loss of cellularity

  • 5.

    Dystrophic calcifications

  • 6.

    Decreased number of stem cells

  • 7.

    Degeneration of odontoblasts

At the molecular level, one study has shown a decreased expression of connexin 43 and osteocalcin in the aged human pulp, which in turn relates to the decreased viability of the odontoblasts and the pulp cells. Another study, by Matsuzaka and colleagues, demonstrated that expression of core binding factor alpha-1 subunit and dentin sialoprotein was higher in the younger pulp whereas the adult pulp demonstrated higher levels of vascular endothelial growth factor and heat shock protein 27. The investigators concluded that the defense system in younger pulps was accomplished by calcification and in adult pulp is performed by self-defense proteins and regeneration of vessels. In terms of bacterial penetration, Kakoli and colleagues showed that bacterial infection of the dentinal tubules occurs to a lesser extent in older patients than in younger patients.

Pulpal reactions to caries

The main functions of the pulp include (1) formation of dentin and (2) nutrition to the dentin, which is avascular, protective, and reparative.

The pulp is encased within the dentin. This provides the pulp a low-compliance environment and receives its blood supply from the blood vessels that traverse through the apical foramen. Some studies have reported that the pulp has some physiologic feedback mechanisms to counteract inflammation and increased tissue pressure, which in turn explains why inflammation of the pulp could be long standing and could heal if appropriate measures are taken in a timely manner.

One of the main causes of inflammation of the pulp is dental caries. Dental caries is a progressive infection of the dentin, which may lead to inflammation and ultimately necrosis of the pulp. Caries first comes into contact with the odontoblasts. These cells are important in the defense mechanism of the pulp and have been studied extensively over the past decade. There is evidence to show that odontoblasts play an active role in innate immunity. Odontoblasts are considered highly specialized cells that have been shown to express Toll-like receptors (TLRs). TLR-2 and TLR-4 have been immune-localized in human odontoblasts. Inflammation is a tightly regulated process and its main function is to eliminate pathogens and remove damaged tissue with the aim of restoring tissue homeostasis. If the caries does progress to the pulp, it leads to inflammation, which is caused by several proinflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor α, and chemokines, which cause cell death, increased vascular permeability, and an increase in inflammatory cells into the area along with production of acute phase proteins. Removal of caries may cause cessation of the inflammation but there is a continuous production of these proinflammatory cytokines, which could lead to irreversible pulpal damage followed by necrosis.

Pulpal reactions to dental materials

Once a tooth is affected by caries, some form of intervention is necessary to prevent further inflammation and ultimately necrosis. Caries excavation followed by placement of a restoration is necessary. Hence, this discussion has 2 parts: first, the materials that are placed in direct contact with the pulp, and second, restorative materials placed in the tooth after excavation of caries.

Reactions of the Pulp to Materials Used During Pulp Capping or Pulpotomy Procedures

Pulpotomy and pulp capping are indicated for teeth that have had a pulp exposure after trauma or injury, which may include the process of caries excavation in developing or mature teeth. These procedures offer good alternatives to root canal therapy for teeth with immature or mature apices when pulp is exposed with reversible injury and without signs of inflammation, offering a more conservative approach. Ultimately, the goal of treating the exposed pulp with an appropriate pulp capping material is to promote the dentinogenic potential of the pulpal cells. Historically many different materials have been used for these procedures, including resin-modified glass ionomer cements, tricalcium phosphates, hydrophilic resins, and calcium hydroxide. The success of different pulp capping materials has been measured by thickness of the dentinal bridge, morphology of the dentinal bridge, intensity of pulpal inflammation, presence of odontoblasts cells, and biocompatibility.

Historically, the material used during pulp capping procedures has been calcium hydroxide. Calcium hydroxide has been considered the gold standard for pulp capping; however, previous research has shown that it is not ideally suited for this procedure. The opponents of calcium hydroxide for direct pulp capping procedures cite 3 major causes of failure:

  • 1.

    The porosity of the dentinal bridge that is produced

  • 2.

    Calcium hydroxide adhering poorly to dentin

  • 3.

    Inability to provide a long-term seal against microleakage

The porosity of this dentinal bridge potentially allows recolonization of bacteria, thereby leading to failure of pulp capping procedures. Other studies have reported that calcium hydroxide caused a layer of necrosis of the pulp tissue when used in pulp capping procedures.

Another pulp capping material recently developed is mineral trioxide aggregate (MTA). This material has drawn much interest due to its many applications. MTA has demonstrated significantly greater frequency of dentin bridge formation, thicker and less porous dentin, and less pulp inflammation compared with calcium hydroxide. Recent research has shown that MTA, when placed in direct contact with the human dental pulp cells, differentiated them into odontoblast-like cells.

No layer of necrosis was seen in the pulp when MTA was used for pulp capping. At the cellular level, MTA has also been shown to induce the recruitment and proliferation of undifferentiated cells to form a dentinal bridge, while reducing inflammation compared with calcium hydroxide. Another study showed that MTA causes neutrophils to be recruited to the site of injury, which is important in the process of inflammation. Nair and colleagues also demonstrated decreased inflammation when MTA was used compared with calcium hydroxide. On the molecular level, MTA has been shown to induce the secretion of angiogenic factors, such as vascular endothelial growth factor, which plays an important role in healing. Other studies have shown that MTA induced cells to secrete IL-8 and IL-1β. IL-1β has been shown to induce the synthesis of collagen, resulting in a more organized response of the pulp and assisting in the healing process. Other studies in animal models have shown that MTA down-regulated inflammatory cytokines, such as interferon-gamma, CCL5 (also referred to as regulated on activation, normal T-cell expressed, and secreted [RANTES]), and IL-1α, and suppressed the proliferation of some microorganisms and inhibited the production of certain T h 1 and T h 2 cytokines.

Recently a new material has been introduced, BioAggregate (BA) (Innovative BioCeramix, Vancouver, British Columbia, Canada). BA is white nanoparticle ceramic cement with many different applications, like MTA. Studies have reported this material to have similar cytotoxicity levels as MTA De-Deus and colleagues found that BA was as biocompatible as MTA and another study reported that BA up-regulated the gene expression of collagen 1, osteocalcin, and osteopontin in osteoblasts and differentiation of human periodontal ligament fibroblasts compared with MTA. BA has also been shown have antifungal and antibacterial activity. Similar to MTA, this material induced secretion of IL-1β, IL-6, and IL-8. Further research with the new material, however, is ongoing.

Pulpal Reactions to Composite-Based Restorative Materials

Some of the more common restorative materials currently used are resin based. Although the use of these materials is aesthetically appealing in patients, they carry the risk of local and systemic adverse effects. The potential risks are direct damage to the cells (cytotoxicity) and induction of immune-based hypersensitivity reactions. Resin monomers, such as 2-hydroxyethyl methacrylate (HEMA) and triethyleneglycol dimethacrylate (TEGDMA), are shown to influence the differentiation of human pulp cells into odontoblasts. Studies have previously shown that HEMA induces apoptosis in different cell types and also in dental pulp stem cells and in odontoblast-like cells. HEMA-induced apoptosis has been linked to the decrease in intracellular glutathione levels and the production of reactive oxygen species in the cells. At the molecular level, HEMA and TEGDMA have shown to cause cell death/apoptosis in the pulp cells by a decrease in important transcription factors, such as nuclear factor κB (NF-κB) and increase in c-Jun N-terminal kinases (JNK). NF-κB is the major transcription factor that is involved in the regulation of a variety of genes responsible for survival of the cells. The activity of NF-κB is tightly regulated by cytokines and other external regulators. JNK belongs to the family of mitogen-activated protein kinases that comprise of a group of serine/threonine kinases, which are responsible for phosphorylation and mediation of signal transduction from extracellular stimuli. It is believed that activation of JNK inhibits cell growth and induces cell death. Other studies have demonstrated that HEMA causes increased phophorylation of extracellular-signal-regulated kinases (ERK 1 and 2) and decreased phosphorylation of phosphokinase B (p-AKT). The full spectrum of signals responsible for the induction apoptosis in the cells by HEMA and TEGDMA is not established yet, but it involves several different pathways. A better insight into mechanisms of toxicity of dental materials is important for understanding the potential of these materials to cause adverse health effects in a clinical setting.

Knowing the background about the dental pulp, the various cell types, and their interactions with each other and with various dental materials is important because this could ultimately lead to a better treatment modalities. Hence, the second part of this review deals with the clinical aspects of treatment of the primary and permanent dentition.

Primary dentition

Anterior

When decay or tooth preparation extends into the pulp chamber of the primary incisor or canine, first, an assessment of the vitality of the pulp must be made. This should be done before the procedure via radiographic assessment or by direct examination of pulp and its color, texture, and bleeding during the procedure. If the pulp does not bleed at all or bleeds at a hemorrhagic level, it may be infected beyond the coronal pulp, and a pulpectomy may be in order. In this instance, the coronal and radicular pulps should be removed all the way to the apex of the tooth. The radicular pulp chamber may be filled with a resorbable paste of either zinc oxide–eugenol or, preferably, calcium hydroxide with iodoform within the paste. The paste is condensed into the radicular pulp chamber after careful pulp extirpation, cleaning of the canal, and irrigation with saline. Generally, sodium hypochlorite has not been used to clean the pulp canals of primary teeth. The coronal chamber should be filled with glass ionomer or resin-modified glass ionomer. The crown is then restored with a stainless steel crown, a composite strip crown, or a preveneered, commercially available composite-faced stainless steel crown. If there are signs of early external root resorption, radiolucency beyond the confines of the pulp chamber related to the tooth or other signs of disease, or inadequate tooth structure to support a restoration, the tooth may need to be extracted.

Molars

When decay or tooth preparation extends into the coronal pulp, and the pulp is deemed vital (as described previously), a pulpotomy may be performed. The entire coronal pulp is removed circumferentially with a large round bur, pulling coronally to adequately deroof the pulp chamber and to avoid leaving any ledges or pulp tissue therein. The radicular orifices are assessed to determine that bleeding can be controlled only by direct pressure with a damp cotton piece for a minute or 2. There is some debate as to whether the remaining radicular pulp orifices should be further treated with a medicament, such as formocresol or ferric sulfate. The literature and standard of care is to use one of these agents (not discussed in this article because of the length limitations); however, there seems to be a directional change toward sealing the orifices completely as the primary objective. It is likely that recommendations going forward will require sealing the orifices as the main objective. The best sealing agents seem to be MTA or glass ionomer. Therefore, after achieving hemostasis on the radicular pulp orifices, and after using a medicament (if desired), the orifices must be sealed with one of these agents. A material that further seals, such as glass ionomer or resin-modified glass ionomer, should then be used to fill the coronal pulp chamber. A stainless steel crown is the restoration of choice after performing a primary molar pulpotomy. If the pulp tissue is nonvital or the bleeding cannot be controlled at the level of the orifice, a pulpectomy should be performed. Canals should be cleaned carefully but not significantly instrumented (primary roots are narrow and curved and there is a risk of perforation or extension beyond the apex). Canals and the pulp chamber should be filled (as described previously) for primary anterior teeth. A stainless steel crown is then used to restore the tooth. As with a primary anterior tooth, when there is disease beyond the confines of the tooth related to the tooth, consideration for extraction must be given. The tooth itself, however, is the best space maintainer, and space loss in the primary molar area is a significant long-term issue for patients. If there is the ability to retain the tooth in the mouth via pulpectomy and careful monitoring of the tooth to reduce or eliminate local infection, while waiting for a permanent molar to erupt (in the case of second primary molar infection), this treatment option may be performed with careful monitoring as a transitional treatment. In addition to maintaining the tooth, this option will ease and make a band and loop from permanent molar to primary first molar well tolerated (compared with the distal shoe appliance).

Permanent dentition

Endodontics is defined as the branch of dentistry concerned with the morphology, physiology, and pathology of the human dental pulp and periradicular tissues. The ultimate endodontics goal could be defined, however, as the prevention and/or elimination of apical periodontitis. The cause of apical periodontitis is toxic metabolites and byproducts released from microorganisms within the canal and diffused into periapical tissues, eliciting inflammatory responses and bone resorption. Thus, in clinical terms, a necrotic infected pulp is required for apical periodontitis to be present. Conversely, if the pulp is vital, there should be few or no bacteria present in the root pulp space and thus the disease (apical periodontitis) should not be present. Therefore, preservation and treatment of the vital pulp are critical for the prevention of apical periodontitis.

Vital pulp therapy in permanent teeth

Vital pulp therapy has a high success rate if the following conditions are met: (1) the pulp is not inflamed, (2) hemorrhage is properly controlled, (3) a nontoxic capping material is applied, and (4) the capping material and restoration seal out bacteria.

Indirect Pulp Therapy

Indirect pulp capping has been defined as a procedure in which a small amount of carious dentin is retained in deep areas of cavity preparation to avoid an exposure of the pulp. A medicament is then placed over the carious dentin to stimulate and encourage pulp recovery.

Indications

  • 1.

    Vital pulp

  • 2.

    Normal radiographic findings

  • 3.

    No history of spontaneous, lingering, or severe pain

  • 4.

    No extensive restoration or full crown requirements

Contraindications

  • 1.

    History of spontaneous pain or signs of irreversible pulpitis

  • 2.

    Clinical or radiographic evidence of pulpal or periradicular pathosis

  • 3.

    Carious exposure

  • 4.

    Tooth requires extensive restoration or full crown

Technique

  • 1.

    Remove soft leathery caries affected tooth structure until dentin consistency changes or pulp exposure is imminent.

  • 2.

    Disinfect the cavity using 2.5% sodium hypochlorite for at least 1 minute.

  • 3.

    Place calcium hydroxide or glass ionomer directly over the carious region.

  • 4.

    Place a permanent restoration.

In a retrospective study, Gruythuysen and colleagues examined clinically and radiographically the 3-year survival of teeth treated with indirect pulp therapy performed between 2000 and 2004. After placement of a layer of resin-modified glass ionomer as liner over carious dentin, the teeth were restored. Failure was defined as the presence of either a clinical symptom (pain, swelling, or fistula) or radiologic abnormality at recall. The survival rate was 96% for primary molars (mean survival time, 146 weeks) and 93% for permanent teeth (mean survival time, 178 weeks). This study shows that indirect pulp therapy performed in primary and permanent teeth of young patients may result in a high 3-year survival rate. Other studies had given a lower prognosis to indirect pulp therapy, however, especially in permanent teeth. With the development of more biocompatible materials with high sealing properties, these teeth might have a better outcome with direct pulp therapy.

Direct Pulp Therapy

Direct pulp capping is defined as the placement of a medicament on a pulp that has been exposed in the course of excavating the last portions of deep dental caries. The rationale behind this treatment is the encouragement of young healthy pulps to initiate a dentin bridge and wall off the exposure site. A good rule of thumb limits the diameter of the exposure site to less than 1.5 mm.

Indications

  • 1.

    Mechanically or traumatically exposed primary and young permanent teeth

  • 2.

    No history of spontaneous or irreversible inflamed pulp

  • 3.

    Vital pulp

  • 4.

    Normal radiographic findings

  • 5.

    Controlled hemorrhage

  • 6.

    Limited restorative treatment

Contraindications

  • 1.

    Spontaneous pain

  • 2.

    Large carious exposures

  • 3.

    Radiographic evidence of pulpal or periradicular pathosis

  • 4.

    Calcifications in the pulp chamber

  • 5.

    Excessive hemorrhage encountered

  • 6.

    Exposures with purulent or serous exudates

Technique

  • 1.

    Remove all peripheral caries before removing the deepest caries.

  • 2.

    Control the hemorrhage with a sterile cotton pellet moistened with sterile saline.

  • 3.

    Disinfect the cavity using 2.5% sodium hypochlorite for at least 1 minute.

  • 4.

    Place calcium hydroxide, MTAs, or BA directly over the exposure site; do not force it into the pulp.

  • 5.

    Cover the capping material with glass ionomer and restore permanently.

As discussed previously, there are various materials that have been tried and tested for pulp capping procedures. When considering the capping material, current evidence in the literature has consistently demonstrated a better outcome when using MTA. Aeinehchi and colleagues compared the use of MTA and calcium hydroxide in direct pulp capping cases using 11 pairs of third molars (patients 20–25 years old) with pulps mechanically exposed and capped with either MTA or calcium hydroxide, covered with zinc oxide–eugenol, and restored with amalgam. Teeth were extracted and then histologically evaluated at 1 week and 2, 3, 4, and 6 months. Odontoblastic layers appeared earlier; less hyperemia, inflammation, and necrosis were noted; and dentinal bridges were more pronounced in the MTA-treated teeth. In a different randomized clinical study, Nair and colleagues investigated the pulpal response to direct pulp capping in healthy human teeth with MTA versus calcium hydroxide cement (Dycal) as control. MTA was clinically easier to use as a direct pulp capping agent and resulted in less pulpal inflammation and more predictable hard tissue barrier formation than Dycal. Therefore, MTA or equivalent products should be the material of choice for direct pulp capping procedures instead of hard-setting calcium hydroxide cements.

From a clinical perspective, the control of the hemorrhage is critical to determine the level of pulp inflammation. In cases of persistent bleeding, partial pulpotomy might be indicated.

Partial Pulpotomy

According to the American Association of Endodontists glossary, partial 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 to encourage continued physiologic development and formation of the root end. In children and young adults, teeth with traumatic pulp exposure can be treated successfully (96%) with partial pulpotomy and calcium hydroxide. The procedure is also known as Cvek pulpotomy. Cvek and colleagues investigated the depth of inflammatory reactions of adult monkey pulps exposed by fracture or cavity prep at different time intervals and found that inflammation extended 1.5 mm to 2 mm into the pulp at the 48-hour mark and only 0.8 mm to 2.2 mm after 1 week. Thus, to be effective, calcium hydroxide needs to be in contact with noninflamed tissue located approximately 2 mm of pulp beneath exposure site. In 1987, Fuks and colleagues performed partial pulpotomy on 63 teeth with different types and severity of traumatic injuries and demonstrated a 94% success rate. No correlations were found between healing and size of pulp exposure, type of trauma, time frame, and root development.

Indications

  • 1.

    Carious or traumatically exposed primary and permanent teeth

  • 2.

    Vital pulp, which responds to sensitivity tests

  • 3.

    Normal radiographic findings

  • 4.

    Controlled hemorrhage

  • 5.

    Limited to moderate restorative treatment

Contraindications

  • 1.

    Spontaneous pain

  • 2.

    Radiographic evidence of pulpal or periradicular pathosis

  • 3.

    Calcifications in the pulp chamber

  • 4.

    Excessive hemorrhage encountered

  • 5.

    Exposures with purulent or serous exudates

Technique

  • 1.

    Access the tooth using a high-speed bur.

  • 2.

    Using a sterile round bur and/or a sharp spoon, amputate the coronal pulp.

  • 3.

    Clean canal walls with moistened sterile cotton pellet.

  • 4.

    Apply pressure with a moist sterile cotton pellet on the pulp stump to control hemorrhage.

  • 5.

    Disinfect the pulp wound and cavity with 2% chlorhexidine gluconate.

  • 6.

    MTA, BA, or calcium hydroxide is laid over the pulp stump to a thickness of 2–3 mm.

Vital Pulp Therapy on Immature Teeth

For cases of open apexes, maintaining the pulp vital is essential for the development of the root and maturation of the whole tooth. According to the American Association of Endodontists glossary, apexogenesis is defined as a vital pulp therapy procedure performed to encourage continued physiologic development and formation of the root end. The term is frequently used to describe therapy performed to encourage the continuation of this process. The term, maturogenesis , was recently introduced by Weisleder and Benitez and defined as physiologic root development not restricted to the apical segment. The continued deposition of dentin occurs throughout the length of the root, providing greater strength and resistance to fracture. Patel and Cohenca also presented a case that demonstrates the use of MTA as a direct pulp capping material for the purpose of continued maturogenesis of the root. Clinical and radiographic follow-up demonstrated a vital pulp and physiologic root development in comparison with the contralateral tooth. MTA can be considered as an effective material for vital pulp therapy, with the goal of maturogenesis.

Treatment of Nonvital Immature Teeth

Apexification is defined as a method of inducing a calcified barrier in a root with an open apex or the continued apical development of an incompletely formed root in teeth with necrotic pulp.

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Oct 29, 2016 | Posted by in General Dentistry | Comments Off on Vital Pulp Therapy
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