The healing of the traumatized dental pulp following capping.
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In reviewing the various studies concerning the direct pulp capping procedure in primary teeth, using rigid criteria for case selection and procedure appears to insure a significant amount of success. It is acknowledged that vital primary pulp tissue is capable of healing without resorting to complete pulpectomy, although statistically direct pulp capping has been found to be less successful in primary teeth than indirect pulp therapy or coronal amputation (pulpotomy). To achieve success for direct pulp capping in primary teeth, the considerations involve: selecting teeth with minimal or no clinical signs of pulpal inflammation; or pretreating the carious tooth with a sedative restoration before excavating the caries; disinfecting the cavity floor; enlarging the actual exposure, and flushing out dentinal debris with mild solutions; controlling bleeding by not allowing a clot to form; placing a hard-set, CaOH material over the exposure, followed by a fast-setting, zinc oxide-eugenol cement to achieve a hermetic seal; and lastly, placing a stainless steel crown to minimize microleakage and prevent a fractured or defective restoration. These procedural steps can hardly ensure complete success in direct pulp capping of a primary tooth; but, based on the many cited investigations in this review, a significant amount of success can be expected without resorting more frequently to invasive techniques. Surely the evidence presented leading to the feasibility of direct pulp capping in primary teeth merits further investigations, before dogmatically rejecting this procedure of pulp therapy.
PURPOSE: The importance of pulp capping variables which mediate pulp repair activities and dentin bridge formation following pulp exposure are not well understood. Consequently, the aim of this study was to investigate the effects of pulp capping variables on tertiary dentin bridge formation. MATERIALS AND METHODS: Calcium hydroxide [Ca(OH)2], resin-modified glass-ionomer (RMGI) and resin-based composite (RBC) were used to restore pulp exposures prepared in 161 nonhuman primate teeth, according to ISO usage guidelines. Teeth were collected from between 7 and 720 days to observe the pulp repair activities leading to dentin bridge formation. Bacteria were detected using McKays stain. Pulp activity was categorized histomorphometrically using ISO standards, and analyzed statistically using ANOVA statistics. RESULTS: The pulp capping variables in order of their relationship to dentin bridge area, from the most important to the least important were: time elapsed since pulp capping (P = 0.0009), pulp capping materials (P = 0.0252), bacterial microleakage (P = 0.0358) and area of operative debris in the dentin bridge (0.0362). A further 10 pulp capping variables were found to be less important. Relationships between pulp capping materials, operative debris, tunnel defects, bacterial microleakage, inflammation and dentin bridge formation were observed. Bacteria contaminated 18.6% of RBC, 22.2% of RMGI and 47.0% of Ca(OH)2 capped pulps.
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Forty adult male Sprague-Dawley rats were divided into two equal groups, control (Group 1) and experimental (Group 2). Group 2 received 100 mg of dl-alpha-tocopherol acetate (vitamin E) twice weekly by the oral route. After 2 weeks the animals in both groups were subjected to pulp exposures that were capped with zinc oxide and eugenol and to pulp exposures that were left open. The oral administration of 100 mg dl-alpha-tocopherol acetate in the Group 2 animals was continued for periods of 1 day to 4 weeks after the operative procedures. The animals were killed 1 day, 3 days, and 1, 2, and 4 weeks after the procedures. The most severe, prolonged, and extensive pulpal disease was seen in both groups when the pulp exposure was left open to the oral flora. The most favorable repair and healing results took place after 1, 2, and 4 weeks in the Group 2 animals in pulp exposures covered with zinc oxide and eugenol.
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Air abrasion is regaining popularity especially in the area of pediatric dentistry due to its ease of use and its advantages. Due to the lost of tactile information, while using this technique, there is an increased risk for pulpal exposure. On the other hand, Ca(OH)2 medicament has been proven to induce dentin bridge formation, but an adequate sealing seems to be even more important that the capping material used. The purpose of this study was two fold: to assess the pulpal response after pulpal exposure by air abrasion and to evaluate the healing potential after using Ca(OH)2 medicament or Liner Bond II as a capping agent. Two hundred sixteen teeth from mixed-bred dogs were used in this study. The teeth were divided into three groups, A) pulpal exposure by air-abrasion followed by sealing of the cavity with Liner Bond II, B) pulpal exposure by air-abrasion and Ca(OH)2 pulp capping and C) pulpal exposure by high-speed followed by air-abrasion and Ca(OH)2 pulp capping as a control group. The animals were sacrificed after 7, 14, 30 and 60 days and a histopathological evaluation was undertaken. After applying Analysis of Variance to compare the groups, it was observed that at earlier observation periods, the inflammatory criteria near the exposure site were different among the groups. As time elapsed, the inflammation was resolved in the pulp tissue, however, the odontoblastic layer and the dentin bridge formation had a highly statistically significant difference (p<0.001) among the various groups at all observation periods. In addition, a positive correlation was observed between the organization of the odontoblastic layer and the dentin bridge formation mainly after 30 days. It could be concluded that dentin bridge formation could be achieved with the use of Ca(OH) or Liner Bond II as capping agent with an adequate sealing. However, the formation is delayed especially when Liner Bond II is used as capping agent.
The purpose of this study was to observe the basic morphology and determine the chemical composition of neodentinal bridges adjacent white mineral trioxide aggregate (WMTA) when used as a direct pulp capping material. The experimental procedures were performed on six intact dogs' teeth. The pulps were exposed and cavities were filled with WMTA. After 2 weeks, neodentinal bridge formation was evaluated by scanning electron microscope (SEM) of cross-sections of the specimens and electron probe microanalysis (EPMA) of the pulpal surfaces. Results of SEM observation showed that the most characteristic reaction of pulp cells was the intimate connection of cell processes and secreted extracellular fibres with the crystals of the pulp capping material. Results of EPMA indicated that the mineralisation of neodentinal bridge formation occurred progressively from the periphery to the central area. Based on these results, it appears that WMTA has the potential to be used as a direct pulp capping material during vital pulp therapy.
BACKGROUND: A great deal of controversy exists regarding the reliability of capping the inflamed pulp. In particular, the use of calcium hydroxide as a capping agent has come into question. In this study, hard tissue barrier formation after inflamed pulps were capped directly or after partial pulpotomy was compared with calcium hydroxide or bonded resin and with no additional seal or an IRM surface seal. Seventy teeth in five dogs were used. Ten untreated teeth were used as negative controls. In 60 teeth, pulpal inflammation was induced by preparing a cavity close to the pulp and sealing a cotton pellet soaked in plaque in it for 1 to 2 weeks. The cavities were then re-entered and extended to expose the pulps. MATERIALS AND METHODS: In half the teeth (n = 30) a partial pulpotomy was performed and in the other half (n = 30) pulpal treatment was performed on the superficial exposed pulp. Both pulpal treatment groups received the same restorative procedures: (1) calcium hydroxide + amalgam + IRM surface seal; (2) OptiBond Solo, Prodigy with IRM surface seal; or (3) OptiBond Solo, Prodigy without IRM surface seal. The presence, absence, and quality of a hard tissue barrier were evaluated histologically. RESULTS: The calcium hydroxide groups were statistically superior to all other groups. The IRM surface seal resulted in significantly better healing. Although there was no statistically significant difference between direct pulp capping and partial pulpotomy with the numbers in this study, power statistics indicated that in clinical practice a partial pulpotomy would be preferable. CLINICAL SIGNIFICANCE The results of this study suggest that a partial pulpotomy, calcium hydroxide medicament, and a bacteria-tight coronal restoration represent a viable technique for capping the inflamed pulp.
Bone sialoprotein (BSP), an osteogenic protein (OP), mixed with a carrier, was implanted in the pulp of rat first upper molars (OP group). Cavities were prepared with dental burs and pulp perforation was carried out by pressure with the tip of a steel probe. After 8, 14, and 30 days, the rats were killed and the pulps of the OP group were compared with (1) a sham group (S group), (2) a group where the carrier was implanted alone (C group), and (3) capping with calcium hydroxide (Ca group). After 8 days, a few inflammatory cells were seen, mostly located at the pulp surface near the perforation. In the Ca group, a dentin bridge started to form, in contrast to the other groups. After 15 days, globular structures were seen in the pulps of the S and C groups. A reparative osteodentin bridge isolated the pulp from the cavity in the Ca group. Variable reactions were seen in the OP group, with some evidence of cell and matrix alignments or plugs of osteodentin in continuity with an inner layer of reparative dentin. After 30 days, irregular osteodentin formation was observed in the pulps of the S and C groups, with a tendency for globular structures to merge, but with interglobular spaces filled by pulp remnants. In the Ca group, osteodentin was observed in the mesial part of the pulp chamber. In the BSP-implanted group, the osteogenic protein stimulated the formation of a homogeneous dentin-like deposit occupying most of the mesial part of the pulp. Apparently, BSP stimulates the differentiation of cells which secrete an organized extracellular matrix more efficiently than any other capping material used so far. Altogether, the results reported here support that bone sialoprotein displays novel bioactive properties and is capable of stimulating in 1 month's time the development of a thick reparative dentinal tissue in the pulp, occluding the perforation and filling the mesial third of the pulp chamber.
Exposure of the dental pulp, through a caries lesion, accidentally during routine cavity preparation, or as a result of tooth fracture, is a clinical reality that requires optimal treatment. The potential for healing by formation of a dentinal bridge is good, provided that the pulp is not inflamed. Calcium hydroxide has a long history of inducing dentinal bridge formation to promote successful healing. Resin composites are emerging as alternative materials for pulp capping, but healing is slower, and relatively little clinical experience is available for analysis. The prognosis for healing is poor after exposure of an inflamed pulp. Pulpotomy should be considered to create a wound in an uninflamed location. If an exposure is expected through a caries lesion, stepwise excavation of the carious dentin should be considered to allow healing of the dentin and pulp prior to the final excavation of the carious dentin.
IGF1 (Insulin Growth Factor, 1) was intentionally applied onto pulp tissues, aiming to provoque a dentine regeneration process through the stimulation of the dentinoblasts' potententials. 72 cavities were hence performed on rabbit molars, intentionally exposing the dental pulp. Different concentrations of IGF1 were then applied; The histo and anatomo-pathological observations showed persistent vitality of the pulp without any sign of necrosis, even 6 weeks after the IGF1 application. Dentinoblasts layers (as an indication of the regeneration activity) were counted, according to a pre-established protocol, at days 7, 14, 22, 28 and 42. The type of the applied IGF1, was carefully selected to be "Binding Protein Resistant" (IGF-BPR), so to avoid any inhibition of the IGF1 action by the endogenous binding proteins (Hochscheid and coll). The results were conclusive in indicating the IGF1 as an efficient dental pulp capping product.
During odontogenesis, amelogenins from the preameloblasts are translocated to differentiating odontoblasts in the dental papilla, suggesting that amelogenins may be associated with odontoblast changes during development. In the present study, we have explored the effects of enamel matrix derivative (EMD) on the healing of a pulpal wound. Coronal pulp tissue of permanent maxillary premolars of miniature swine were exposed through buccal class V cavities. The exposed pulp was capped with EMD. The contralateral teeth served as controls and were capped with a calcium hydroxide paste (Dycal). The cavities were sealed with glass-ionomer cement. After 2 and 4 weeks, the histology of the teeth was analyzed. In the EMD-treated teeth, large amounts of newly formed dentin-like hard tissue with associated formative cells outlined the pulpal wound separating the cavity area from the remaining pulp tissue. Inflammatory cells were present in the wound area but not subjacent to the newly formed hard tissue. Morphometric analysis showed that the amount of hard tissue formed in EMD-treated teeth was more than twice that of the calcium-hydroxide-treated control teeth (p < 0.001), suggesting that EMD is capable of promoting reparative processes in the wounded pulp more strongly than is calcium hydroxide.
The aim of this study was to investigate the response of human pulp tissue to a dentin bonding agent, Scotchbond Multi-Purpose Plus (SMPP), in exposed class V cavities. Sixteen human premolar teeth were mechanically exposed. Ten pulps were capped with SMPP and six teeth were capped with Dycal. The cavities were filled with a composite. After 40 days, the teeth were extracted and processed for histologic evaluation. Of the 10 teeth capped with SMPP, eight showed moderate chronic inflammation, one was severely inflamed, and one pulp had no to slight inflammation. None of the teeth capped with SMPP showed dentin bridge formation. Of the six teeth capped with Dycal, three exhibited incomplete dentin bridges associated with no to slight inflammation, and three showed no to slight inflammation, without formation of dentin bridges. Direct capping with Dycal with subsequent sealing with SMPP may show favorable results in pulp tissue. SMPP may cause inflammatory changes when applied directly to exposed pulp tissue.
The treatment of an undeveloped (immature) tooth with a carious exposure has been reported extensively in the literature. The main objective of treatment is to provide vital pulp therapy to allow continued development of root dentin in the hope that the root will attain full maturity. A case report is presented that illustrates root development (maturogenesis), not just closure of the apex (apexogenesis). A direct pulp cap was performed after a carious pulp exposure using calcium hydroxide with iodoform paste. The crown was restored with a glass ionomer/composite resin cement.
AIM: The purpose of this study was to collect quantitative information about the numbers and dentine bridge secretory activity of odontoblast-like cells following dental pulp exposure. METHODOLOGY: The numbers and secretory activity of odontoblast-like cells were measured histomorphometrically between 7 days and 2 years in 161 pulp-exposed nonhuman primate teeth. The area of dentine bridges and the dimensions of cavity preparations were measured. The density of odontoblast-like cells and subjacent reorganizing tissue cells were measured beneath dentine bridge formation. The presence of operative dentine debris and tunnel defects in bridges was noted. Pulp inflammation was categorized according to ISO standards. Bacteria were detected using McKay's stain. RESULTS: The area of dentine bridges was mediated by the density and secretory activity of odontoblast-like cells over time. The cell density of subjacent reorganizing tissue was found to be strongly associated with that of odontoblast-like cells. Bacterial microleakage was found to impede dentine bridge secretion by odontoblast-like cells. CONCLUSIONS: Pulp reparative activity occurs naturally beneath capping materials in the absence of bacterial microleakage. The outcome of pulp-capping treatments could be beneficially influenced by concentrating attention on limiting the width of pulp exposure, minimizing pulp injury by limiting the creation of operative debris and placing materials which prevent bacterial microleakage.
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This study has shown that pulp capping of traumatic exposures with Dycal will stimulate dentine formation, with complete bridging adjacent to the material in seven out of eight teeth 1 month later. The success rate at 3 months was similar, with regular dentine being formed under the initial irregular dentine barrier. Dentine bridging was not found 3 months after pulp capping with MPC, although some reparative dentine had been formed. The coronal pulp was usually partially necrotic and inflamed, although the extent of each was not related. Large amounts of MPC were found in the pulp at some distance from the exposure but were not necessarily associated with inflammation or necrosis. In view of the lack of bridge formation and the presence of inflammation and necrosis, these results do not support the manufacturer's claim that MPC is an effect preparation for capping exposed pulps. This study underlines the importance of biologic testing of new materials prior to commercial distribution, for what may appear similar may not produce the same therapeutic effect.