[Treatment strategies for deep caries].

Deep caries occurs when caries progresses to the deep dentin layer, and further progression has the risk of pulp exposure, which may affect pulp vitality and tooth longevity. Currently, there are no objective standards for the diagnosis of deep caries. In addition, traditional therapy for deep caries emphasizes complete debridement of the decayed tissue, resulting in an incremental high risk of pulp exposure. There are different views on how to deal with the remaining dentin after caries removal, and root canal treatment is often adopted directly after pulp exposure. In recent years, due to advances in dental pulp biology, bioactive pulp-capping materials, and clinical evidence-based medicine, the principle of deep caries treatment has shifted to pulp protection. Based on the latest international research progress, evidence-based medicine and expert consensus, we present a series of advancements in this article, including the terminology of deep caries, pathological changes and defense mechanisms of the pulp close to the deep caries, treatment principles of deep caries, technical strategies for carious tissues removal, and the decision-making of treatment protocols after pulp exposure, with the aim of enhancing the understanding of deep caries among dentists, as well as providing a reference for the clinical diagnosis and treatment of deep caries.

Vital Pulp Therapy of Young First Permanent Molars: A Retrospective Study on Radiographic Findings 24 Months Post-treatment.

PURPOSE: With success rates comparable to that of root canal treatment, vital pulp therapy (VPT) has gained clinical interest and has been used in the management of young permanent teeth with inflamed pulps. The aim of the present study was to retrospectively evaluate the radiographic success of VPT in young first permanent molars 24 months post-treatment and correlate findings with tooth and treatment-related characteristics. MATERIALS AND METHODS: Dental records of all patients with first permanent molars which received VPT in the Department of Paediatric Dentistry (National and Kapodistrian University of Athens) were retrieved. Demographic characteristics and data regarding the treatment performed were recorded. Patients' radiographs were evaluated at 6, 12 and 24 months post-treatment by two qualified paediatric dentists blinded regarding the treatment performed. Radiographic success, reasons for failure and continuation of root development were evaluated. Differences were tested using the Χ2 and Student's t-test, and possible correlations were determined by calculating the odds ratio. RESULTS: Overall radiographic success rate at 24 months was 77%, ranging between 50% for direct pulp capping and 92% for full pulpotomy. Differences were not statistically significant. Continuation of root development was recorded in almost 1/3 of the teeth and completion in almost 1/5. No statistically significant association was recorded between the outcome and any tooth and treatment-related variables. CONCLUSION: VPT seems to be a reliable option in the long term for the treatment of deep carious lesions in young permanent molars.

Evaluation of dentinogenesis inducer biomaterials: an in vivo study.

When exposure of the pulp to external environment occurs, reparative dentinogenesis can be induced by direct pulp capping to maintain pulp tissue vitality and function. These clinical situations require the use of materials that induce dentin repair and, subsequently, formation of a mineralized tissue. OBJECTIVE: This work aims to assess the effect of tricalcium silicate cements and mineral trioxide aggregate cements, including repairing dentin formation and inflammatory reactions over time after pulp exposure in Wistar rats. METHODOLOGY: These two biomaterials were compared with positive control groups (open cavity with pulp tissue exposure) and negative control groups (no intervention). The evaluations were performed in three stages; three, seven and twenty-one days, and consisted of an imaging (nuclear medicine) and histological evaluation (H&E staining, immunohistochemistry and Alizarin Red S). RESULTS: The therapeutic effect of these biomaterials was confirmed. Nuclear medicine evaluation demonstrated that the uptake of 99mTc-Hydroxymethylene diphosphonate (HMDP) showed no significant differences between the different experimental groups and the control, revealing the non-occurrence of differences in the phosphocalcium metabolism. The histological study demonstrated that in mineral trioxide aggregate therapies, the presence of moderate inflammatory infiltration was found after three days, decreasing during follow-ups. The formation of mineralized tissue was only verified at 21 days of follow-up. The tricalcium silicate therapies demonstrated the presence of a slight inflammatory infiltration on the third day, increasing throughout the follow-up. The formation of mineralized tissue was observed in the seventh follow-up day, increasing over time. CONCLUSIONS: The mineral trioxide aggregate (WhiteProRoot®MTA) and tricalcium silicate (Biodentine™) present slight and reversible inflammatory signs in the pulp tissue, with the formation of mineralized tissue. However, the exacerbated induction of mineralized tissue formation with the tricalcium silicate biomaterial may lead to the formation of pulp calcifications.

Evaluation of dentinogenesis inducer biomaterials: an in vivo study

Abstract When exposure of the pulp to external environment occurs, reparative dentinogenesis can be induced by direct pulp capping to maintain pulp tissue vitality and function. These clinical situations require the use of materials that induce dentin repair and, subsequently, formation of a mineralized tissue. Objective: This work aims to assess the effect of tricalcium silicate cements and mineral trioxide aggregate cements, including repairing dentin formation and inflammatory reactions over time after pulp exposure in Wistar rats. Methodology: These two biomaterials were compared with positive control groups (open cavity with pulp tissue exposure) and negative control groups (no intervention). The evaluations were performed in three stages; three, seven and twenty-one days, and consisted of an imaging (nuclear medicine) and histological evaluation (H&E staining, immunohistochemistry and Alizarin Red S). Results: The therapeutic effect of these biomaterials was confirmed. Nuclear medicine evaluation demonstrated that the uptake of 99mTc-Hydroxymethylene diphosphonate (HMDP) showed no significant differences between the different experimental groups and the control, revealing the non-occurrence of differences in the phosphocalcium metabolism. The histological study demonstrated that in mineral trioxide aggregate therapies, the presence of moderate inflammatory infiltration was found after three days, decreasing during follow-ups. The formation of mineralized tissue was only verified at 21 days of follow-up. The tricalcium silicate therapies demonstrated the presence of a slight inflammatory infiltration on the third day, increasing throughout the follow-up. The formation of mineralized tissue was observed in the seventh follow-up day, increasing over time. Conclusions: The mineral trioxide aggregate (WhiteProRoot®MTA) and tricalcium silicate (Biodentine™) present slight and reversible inflammatory signs in the pulp tissue, with the formation of mineralized tissue. However, the exacerbated induction of mineralized tissue formation with the tricalcium silicate biomaterial may lead to the formation of pulp calcifications

Dental pulp exposure, periapical inflammation and suppurative osteomyelitis of the jaws in juvenile Baltic grey seals (Halichoerus grypus grypus) from the late 19th century.

The systematic analysis of museum collections can provide important insights into the dental and skeletal pathology of wild mammals. Here we present a previously unreported type of dental defect and related skull pathology in five juvenile Baltic grey seals that had been collected in the course of a seal culling program along the Danish coast in 1889 and 1890. All five skulls exhibited openings into the pulp cavities at the crown tips of all (four animals) or two (one animal) canines as well as several incisors and (in one animal) also some anterior premolars. The affected teeth showed wide pulp cavities and thin dentin. Pulp exposure had caused infection, inflammation, and finally necrosis of the pulp. As was evidenced by the extensive radiolucency around the roots of the affected teeth, the inflammation had extended from the pulp into the periapical space, leading to apical periodontitis with extensive bone resorption. Further spreading of the inflammation into the surrounding bone regions had then caused suppurative osteomyelitis of the jaws. The postcanine teeth of the pathological individuals typically had dentin of normal thickness and, except for one specimen, did not exhibit pulp exposure. The condition may have been caused by a late onset of secondary and tertiary dentin formation that led to pulp exposure in anterior teeth exposed to intense wear. Future investigations could address a possible genetic causation of the condition in the studied grey seals.

Long-term survival of different deep dentin caries treatments: A 5-year clinical study.

OBJECTIVE: The aim of this in-vivo study was to evaluate the long-term clinical survival of different deep dentin caries treatment options. MATERIALS AND METHODS: : In total, 391 patients with at least one permanent tooth with clinically diagnosed deep dentin caries were inspected. Two hundred and fourteen patients were examined at recall visits. Inclusion criteria were teeth with deep caries lesions with pulp vitality but absence of spontaneous pain and periapical alterations. The subjects received either stepwise removal (SWR), complete caries removal (CCR), or direct pulp capping (DPC). The radiological and clinical exams were performed after a mean observation time of 62 months. Success was defined as pulp sensitivity to vitality test and absence of periapical lesions as well as a clinical symptom. Data were statistically analyzed using Kaplan-Meier and log-rank (Mantel-Cox) tests (α = 0.05). RESULTS: Of the total 214 patients evaluated, 126 received SWR, 88 received CCR, and 67 received DPC treatment. One hundred and twenty-seven restorations were amalgam and 141 were composite. The mean observation period was 62 months. Survival rates were 85.7%, 90.9%, and 59.7% for SWR, CCR, and DPC, respectively (P = 0.001). Success rates of amalgam restorations (86.6%) were similar to composite restorations (83%), and both were found to be successful (P = 0.401). CONCLUSION: SWR treatment should be considered to preserve pulp vitality of deep dentin lesions instead of CCR or DPC. CLINICAL RELEVANCE: SWR method for deep dentin caries management had acceptable results over 5 years.

Changes in the radicular pulp-dentine complex in healthy intact teeth and in response to deep caries or restorations: A histological and histobacteriological study.

INTRODUCTION: The present study reported the histological events that occurred in the radicular pulp of human mature teeth in the presence of medium/deep untreated caries lesions, and those teeth with restorations or direct pulp capping, with particular emphasis on the morphology of the canal wall dentine and the odontoblast layer. METHODS: Sixty-two teeth with medium/deep caries lesions, extensive restorations or after application of a direct pulp capping procedure were obtained from 57 subjects. Fourteen intact mature teeth served as controls. Stained serial sections were examined for the pulp conditions of the coronal pulp. The teeth were classified as those with pulpal inflammation, or those with healed pulps. Histological changes that occurred in the roots at the pulp-dentine junction were investigated in detail. RESULTS: All teeth (100%) in the experimental group showed pathologic changes in the radicular pulp, with varying amounts of tertiary dentine on the canal walls and absence of odontoblasts. These changes were identified from different portions of the canal wall surface. Non-adherent calcifications in the pulp tissue were observed in more than half of the specimens. Changes that deviate from classically-perceived histological relationships of the pulp-dentine complex were also observed in the radicular pulps of 33.7% of the control teeth. CONCLUSION: When challenged by bacteria and bacterial by-products invading dentinal tubules, odontoblasts in the radicular pulp may undergo cell death, possibly by apoptosis. This phenomenon may be caused by progressive root-ward diffusion of bacterial by-products, cytokines or reactive oxygen species through the pulp connective tissue. CLINICAL SIGNIFICANCE: Although the vitality of the dental pulp in teeth with deep dentinal caries may be maintained with direct pulp capping or pulpotomy, the repair tissue that is formed resembles mineralised fibrous connective tissues more than true tubular dentine.

Transient receptor potential vanilloid 4 (TRPV4) expression on the nerve fibers of human dental pulp is upregulated under inflammatory condition.

OBJECTIVE: Transient receptor potential vanilloid 4 (TRPV4) has been considered as a mechano-, thermo- and osmo-receptor. Under inflammatory conditions in dental pulp, teeth can become sensitive upon exposure to a variety of innocuous stimuli. The objective of the present study was to investigate the expression of the TRPV4 channel on nerve fibers in human dental pulp of non-symptomatic and symptomatic teeth associated with inflammatory conditions. DESIGN: Dental pulp from extracted human permanent teeth was processed for fluorescence immunohistochemistry. Ten asymptomatic (normal) and 10 symptomatic (symptoms associated with pulpitis) teeth were used in this study. Nerve fibers were identified by immunostaining for a marker, protein gene product 9.5, and the cells were counterstained with 4',6-diamidino-2-phenylindole. An anti-TRPV4 antibody was used to trace TRPV4 expression. RESULTS: TRPV4 expression was co-localized with the nerve fiber marker. Immunoreactivity for TRPV4 was more intense (p < 0.05) in the nerves of symptomatic teeth than those of normal teeth. The number of co-localization spots was increased significantly (p < 0.05) in the dental pulp of symptomatic teeth compared with that of asymptomatic (normal) teeth. CONCLUSIONS: There is expression of TRPV4 channels on the nerve fibers of human dental pulp. Our findings suggest upregulation of TRPV4 expression under inflammatory conditions in the pulp. The upregulation of TRPV4 channels may be associated with the exaggerated response of dental pulp to innocuous mechanical, thermal and osmotic stimuli under inflammatory conditions.

Age-related morphological, histological and functional changes in teeth.

Throughout lifetime, the teeth are continuously exposed to numerous chemical and physical impacts, which cause the wear of the dental hard tissues, gingival recession and other oral changes with sometimes subsequent problems. Age-related wear of tooth surfaces reduces the dental enamel thickness and exposes deeper layers of enamel, which have different physical and chemical properties than the surface enamel. Gingival recession is the main causal factor of root caries and dentine hypersensitivity. Age-related changes in dentine include the formation of secondary dentine and the reduction in tubular lumen diameter (dentine sclerosis), which lead to a reduction in the volume of the pulp chamber. In addition to the reduction in the volume of pulp chamber, changes to the dental pulp also include dental pulp calcifications. The age-related physiological changes to the teeth should be carefully distinguished from pathological changes, especially when they induce pain or a negative impact on the oral health-related quality of life (OHRQoL) of the older individuals. Therefore, regular oral examinations coupled with early preventive measures should aim at maintaining oral health until old age.

Pulpal Tissue Inflammatory Reactions after Experimental Pulpal Exposure in Mice.

INTRODUCTION: The purpose of this study was to establish a stable experimental mice pulpal inflammatory model and to evaluate inflammatory reactions of pulpal tissue after pulpal exposure. METHODS: Pulpal inflammation was induced in 80 C57BL/6 mice by occlusal exposure of the pulp of the maxillary first molar. The mice were sacrificed randomly at 0, 1, 6, 12, 24, 48, and 72 hours after pulpal exposure. Mice without pulpal exposure served as controls. Maxillary teeth were obtained and prepared for histologic analyses and real-time polymerase chain reaction analyses. RESULTS: As the duration of pulpal exposure increases, the inflammatory reaction is exacerbated. Within 6 to 12 hours after pulpal exposure, pulp tissues experienced red blood cell extravasation to the destruction of the odontoblast layer. After 24 hours, necrosis was observed in the pulpal tissue; until 72 hours, necrosis spread to the whole coronal pulpal tissue, and a large number of inflammatory cells were found in the radicular pulpal tissue. The results of histomorphologic scores have the same trend; samples from the 72-hour group possessed the highest score followed by samples from other groups (P < .01). The expression levels of inflammatory cytokines increased over the 72 hours, and there was a high rate of inflammatory cytokine expression at 6 and 12 hours after pulpal exposure. CONCLUSIONS: Our study represents a stable mice model for studying pulpal inflammation in vivo. Mouse pupal inflammation progresses rapidly, with dramatic changes evident in just a few hours.

Pulpal Responses to Direct Capping with Betamethasone/Gentamicin Cream and Mineral Trioxide Aggregate: Histologic and Micro-Computed Tomography Assessments.

INTRODUCTION: This clinical trial was conducted to evaluate the response of human dental pulp to direct capping with betamethasone/gentamicin (BG) cream and mineral trioxide aggregate (MTA). We hypothesized that the results of direct pulp capping with a topical BG combination would be similar to or better than those with MTA. METHODS: Thirty-six human first premolar teeth scheduled for orthodontic extraction were randomly divided into 4 groups: BG1 group (n = 9), BG cream with 2-week follow-up; BG2 group (n = 10), BG cream with 8-week follow-up; MTA1 group (n = 8), MTA with 2-week follow-up; and MTA2 group (n = 9), MTA with 8-week follow-up. Teeth were extracted and evaluated at respective time intervals. Micro-computed tomography scanning and histologic analyses were performed for all specimens. Pulp pathology (inflammation, pulp abscesses, and pulp necrosis) and reparative reaction (formation of dentin bridges) were recorded. RESULTS: Both BG cream and MTA resulted in significantly better pulpal responses at 8 weeks than at 2 weeks. Dentin bridge formation was significantly thicker in the MTA group at 8 weeks than in any other group (P < .05). Inflammation was of the acute type in all groups; no statistically significant differences in the distribution of inflammatory cells were found among the groups. Pulpal abscesses and/or necrosis were observed more often in teeth capped with BG than with MTA. CONCLUSIONS: Direct pulp capping with both BG cream and MTA was associated with dentin bridge formation. MTA resulted in a significantly better pulpal response, with less inflammation and a thicker dentin bridge at 8 weeks.

Randomized controlled clinical trial of the 24-months survival of composite resin restorations after one-step incomplete and complete excavation on primary teeth.

OBJECTIVE: This randomized clinical trial aimed to compare the 24-months survival of composite restorations in primary molars after partial caries removal (PCR) and total caries removal (TCR). METHODS: Forty-eight children aged 3-8 years with at least one molar with a deep carious lesion were included (PCR; n=66; TCR; n=54). For PCR, excavation was stopped when dentine with a leathery consistency was achieved; in the TCR group, total absence of carious tissue was confirmed using a blunt-tipped probe. Pulpotomy was performed in cases of pulp exposure. Success was assessed by modified USPHS criteria with Alpha and Bravo scores recorded as success. RESULTS: Pulp exposure occurred in 1 and 15 of the teeth treated with PCR and TCR respectively (p<0.01). The restorations survival rate after 24 months was 66% (PCR) and 86% (TCR) (p=0.03). When teeth that received pulpotomy were analyzed separately, the survival rate was 92% (p=0.09). PCR performed in occlusoproximal restorations demonstrated the lowest success rate (p=0.002). PCR increases 2.90 times the probability of having a restorative failure compared to TCR (p=0.03), after adjusting for cavity type. When pulp exposure and restoration failure were considered as the outcome, there was no significant difference between the two groups (p=0.10) with success rates of 64% (PCR) and 61% (TCR). CONCLUSION: Collectively, deciduous teeth submitted to PCR prevented pulp exposure and, consequently, more invasive treatments; otherwise, PCR yielded lower longevity for composite restoration compared to TCR, suggesting that PCR restorations need to be followed over time, especially when multi-surface restorations are involved. CLINICAL SIGNIFICANCE: Composite restorations on carious remaining tissue require monitoring over time, especially those performed in more than one surface. Even if the restorations present shortcomings over the time, the majority of them are subject to repair, allowing more conservative approaches for teeth with deep caries lesions.

Osseous characteristics of mice lacking cannabinoid receptor 2 after pulp exposure.

INTRODUCTION: Endogenous cannabinoid compounds are involved in many physiological processes, including bone metabolism. Cannabinoid receptor 2 (CB2) plays a role in modulating bone density, but published research results are conflicting. Furthermore, the specific role of CB2 in inflammation-induced bone resorption and craniofacial bone density has not been reported. The objective of this study was to assess the role of CB2 in dental pulp exposure-induced periapical bone loss and mandibular bone density. METHODS: Adult female wild-type (WT) and CB2 homozygous knockout (KO) mice were used. Pulp exposures were created unilaterally in the mandibular first molars, and the pulp was left exposed to the oral cavity to induce periapical lesion formation. Mandibles were harvested 26 days after pulp exposure. Mandibular bone mineral density and periapical lesion volume were assessed using micro-computed tomographic imaging. RESULTS: Periapical lesion volume measured on the mesial root of the pulp-exposed first molar was significantly less in CB2 KO than WT mice (P < .05). No significant difference was detected between KO and WT mice in the size of the PDL space measured on the mesial root of the contralateral intact first molar. CB2 KO mice exhibited greater mandibular bone density than WT mice (P < .05). CONCLUSIONS: CB2 plays a role in mandibular bone metabolism. Increased bone density in CB2 KO mice may contribute to the smaller periapical lesion size observed after pulp exposure in KO compared with WT mice. Additional experiments are needed to further elucidate the function of CB2 and clinical implications of cannabinoids on bone and periapical pathosis.

Blood profile and histology in oral infections associated with diabetes.

INTRODUCTION: We aimed to investigate the relationship between blood profile and histologic findings in both apical periodontitis (AP) and periodontal disease (PD) associated with diabetes. METHODS: Wistar rats (N = 80) were assigned to the following 8 groups: control, AP, PD, AP associated with PD, diabetes, diabetes with AP, diabetes with PD, and diabetes with AP and PD. Diabetes mellitus (DM) was induced with streptozotocin, AP was induced by exposure to the oral environment, and PD was induced using periodontal ligature. After 30 days, blood samples were collected, and the rats were euthanized. Subsequently, the maxillae were processed for light microscopy. Hematologic examinations were conducted to determine the total number of erythrocytes and leukocytes, erythrocyte constant, and blood glucose level. One-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at P < .05. RESULTS: A significant correlation was found between the histologic findings and blood parameters. CONCLUSIONS: In conclusion, diabetes accelerated the development and progression of AP and PD in the rats and caused an increase in the average erythrocyte volume as well as the leukocyte and neutrophil counts. Oral infections increase the total number of leukocytes, the number of neutrophils and lymphocytes, and blood glucose concentrations in DM rats.

Is hard tissue formation in the dental pulp after the death of the primary odontoblasts a regenerative or a reparative process?

OBJECTIVES: Conceptually, two types of tertiary dentine may be produced in response to caries and environmental irritations: "reactionary dentine" that is secreted by existing primary odontoblasts and "reparative dentine", formed after the death of the odontoblasts by proliferation and differentiation of progenitor cells into odontoblast-like cells. Because histologic evidence for tubular dentine generated by newly differentiated odontoblast-like cells is lacking in human teeth, the present study examined pulpal cellular changes associated with caries/restorations, in the presence or absence of pulpal exposures. METHODS: Ninety-six extracted human teeth were histologically processed and serial sectioned for light microscopy: 65 contained untreated enamel/dentine caries; 20 were heavily restored and 11 had carious exposures managed by direct pulp-capping. RESULTS: Sparsely distributed, irregularly arranged dentinal tubules were identified from the tertiary dentine formed in teeth with unexposed medium/deep caries and in restored teeth; those tubules were continuous with the tubules of secondary dentine; in some cases, tubules were absent. The palisade odontoblast layer was reduced to a single layer of flattened cells. In direct pulp-capping of pulp exposures, the defects were repaired by the deposition of an amorphous dystrophic calcified tissue that resembled pulp stones more than dentine, sometimes entrapping pulpal remnants. This atubular hard tissue was lined by fibroblasts and collagen fibrils. CONCLUSIONS: Histological evidence from the present study indicates that reparative dentinogenesis cannot be considered as a regenerative process since the so-formed hard tissue lacks tubular features characteristic of genuine dentine. Rather, this process represents a repair response that produces calcified scar tissues by pulpal fibroblasts. CLINICAL SIGNIFICANCE: Formation of hard tissue in the dental pulp after the death of the primary odontoblasts has often been regarded by clinicians as regeneration of dentine. If the objective of the clinical procedures involved is to induce healing, reduce dentine hypersensitivity, or minimise future bacteria exposure, such procedures may be regarded as clinical success. However, current clinical treatment procedures are not adept at regenerating physiological dentne because the tissues formed in the dental pulp are more likely the result of repair responses via the formation of calcified scar tissues.

Iloprost up-regulates vascular endothelial growth factor expression in human dental pulp cells in vitro and enhances pulpal blood flow in vivo.

INTRODUCTION: Prostacyclin (PGI2) is a biomolecule capable of enhancing angiogenesis and cellular proliferation. METHODS: We investigated the influence of a PGI2 analogue (iloprost) on dental pulp revascularization in vitro and in vivo by using human dental pulp cells (HDPCs) and a rat tooth injury model, respectively. Iloprost stimulated the human dental pulp cell mRNA expression of vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), and platelet-derived growth factor (PDGF) in a significant dose-dependent manner. This mRNA up-regulation was significantly inhibited by pretreatment with a PGI2 receptor antagonist and forskolin (a protein kinase A activator). In contrast, a protein kinase A inhibitor significantly enhanced the iloprost-induced mRNA expression of VEGF, FGF-2, and PDGF. Pretreatment with a fibroblast growth factor receptor inhibitor attenuated the VEGF, FGF-2, and PDGF mRNA expression, indicating opposing regulatory mechanisms. RESULTS: The effect of iloprost on the dental pulp was investigated in vivo by using a rat molar pulp injury model. The iloprost-treated group exhibited a significant increase in pulpal blood flow at 72 hours compared with control. CONCLUSIONS: The present study indicates that iloprost may be a candidate agent to promote neovascularization in dental pulp tissue, suggesting the potential clinical use of iloprost in vital pulp therapy.

Histopathological condition of the remaining tissues after endodontic infection of rat immature teeth.

INTRODUCTION: Recently, case reports have shown that immature teeth diagnosed with necrotic pulp and periapical periodontitis can be repaired through a regenerative endodontic procedure. True regeneration depends on the presence of stem cells in the remaining vital tissues. The aim of this study was to evaluate the histologic condition of the pulp tissue, root apical papilla, and periapical tissues after inducing endodontic infection in immature rat teeth for different periods. METHODS: This study evaluated 18 first upper rat molars (36 roots). Periapical lesions were induced and were confirmed radiographically, and the animals were divided into 3 groups according to the days of pulp exposure for endodontic infection induction: 30, 60, and 90 days. Histologic analysis was performed in 5 different areas (ie, cervical, middle, and apical root canal thirds; the apical papilla; and the periapex surrounding the apical papilla). RESULTS: At 30 days, one third of the specimens still showed vital but intensely inflamed pulp tissue in the apical third and vital apical papilla with varying degrees of inflammation. After 60 days, the results were similar with respect to the apical pulp tissue and apical papilla. Completely necrotic pulp tissue in the space canal and vital apical papilla were observed in about 67% of the cases after 90 days. CONCLUSIONS: Vital pulp tissue was observed in the apical third until 60 days and in the vital apical papilla until 90 days of infection in a rat model.

Absent in melanoma 2 (AIM2) in rat dental pulp mediates the inflammatory response during pulpitis.

INTRODUCTION: In recent years, the inflammasome has been determined to play an important role in inflammatory diseases. However, the role of the inflammasome in pulpitis remains unclear. Absent in melanoma 2 (AIM2) is a type of inflammasome that recognizes cytosolic double stranded DNA and forms a caspase-1-activating inflammasome with apoptosis-associated speck-like protein containing a caspase activating recruiting domain. In this study, we determined whether AIM2 was expressed in pulp cells and defined the role of AIM2 in the initiation of inflammation within the dental pulp. METHODS: In the in vivo study, the right maxillary molars from male adult Sprague-Dawley rats (250-350 g) were exposed to the pulp. In the in vitro study, the pulp cells isolated from the mandibular incisors of the Sprague-Dawley rats (2 weeks) were conventionally cultured. Immunofluorescence staining was used to determine the expression and distribution of AIM2 in the rat dental pulp tissues and cells in the presence or absence of inflammatory stimulation. Western blotting and real-time polymerase chain reaction were performed to determine whether there was a correlation between AIM2 expression levels and inflammation both in vivo and in vitro. RESULTS: In healthy dental pulp tissues and cells, AIM2 was only detected in the odontoblast layer. Stimulation significantly increased AIM2 expression in both the dental pulp tissues and cultured cells. The mRNA and protein levels of AIM2 were significantly up-regulated in response to inflammatory stimulation in a dose-dependent manner. Moreover, we also found that AIM2 expression correlated with interleukin-1 levels. These results reveal a direct relationship between the AIM2 inflammasome and pulpitis. CONCLUSIONS: Our study demonstrates that AIM2 is expressed in dental pulp tissues and mediates the inflammatory response during pulpitis. Therapeutic interventions aimed at reducing AIM2 expression may be beneficial in the treatment of pulpitis.

The influence of different therapeutic modalities and platelet rich plasma on apexogenesis: a preliminary study in monkeys.

BACKGROUND: Traumatic injuries of permanent teeth with incomplete root formation are frequent during childhood. Adequate therapy is important for the further destiny of teeth with damaged pulp. OBJECTIVES: To evaluate the effect of pulpotomy and high pulpotomy on the pulp and on root development, and the effect of platelet rich plasma (PRP) with hydroxyapatite (HAP) as a carrier and hydroxyapatite alone on apexogenesis. MATERIAL AND METHODS: The study included eight monkeys (Cercopithecus aethiops) in which high pulpotomies were performed on the mandibular lateral incisors and canines, and pulpotomies were performed on the mandibular central incisors and premolars. The materials used in the study were commercial HAP (Apatec®, Stomygen) and PRP (prepared at the Torlak Institute of Immunology and Virology, Belgrade, Serbia.). Histological and radiological evaluations were done six months after the treatment. RESULTS: Considering the differences between HAP+PRP treated teeth in the pulpotomy group and teeth in the high pulpotomy group, two times more root growth retardation was observed in the high pulpotomy group. In the high pulpotomy group, root growth retardation was less common in HAP+PRP treated teeth (42.9%) than in HAP treated teeth (50%). In the pulpotomy group, retardation of root development was also less common in HAP+PRP treated teeth (25%) compared to HAP treated teeth (50%). There were differences between the pulpotomy and high pulpotomy groups, but without statistical significance. CONCLUSIONS: The application of endogenous growth factors in conjunction with the preservation of dental pulp vitality can result in a good outcome for pulp therapy of injured teeth, which means successfully completed apexogenesis.

Different treatment protocols for different pulpal and periapical diagnoses of 72 cracked teeth.

INTRODUCTION: The treatment plan for cracked teeth depends on the extent of the crack. A tooth with an extensive crack of long duration may be more likely to require root canal treatment. The purpose of this study was to analyze the characteristics of cracked teeth and to assess the outcome of different treatment protocols depending on the pulpal and periapical diagnoses. METHODS: Seventy-two of 476 crown-restored teeth were diagnosed as cracked teeth. The location of the cracked teeth, age and sex of the patients, restoration materials, a diagnosis of pulp and apex, and the periodontal probing depth were analyzed. Cracked teeth were treated by different treatment protocols depending on the pulpal and periapical diagnoses. RESULTS: Mandibular first molars (27.8%) were the most frequently involved teeth followed by maxillary first molars (25%), maxillary second molars (22.2%), and mandibular second molars (19.4%). The most frequently involved ages were 40-49 and 50-59 years. Cracks occurred mainly in nonbonded restorations such as gold (26.4%) and amalgam (12.5%), and 48.6% of cracks were found in intact teeth. In this study, 60 teeth (83.3%) were treated with root canal treatment before being restored with a permanent crown, and only 12 teeth (16.7%) remained vital and were restored with a permanent crown without root canal treatment. The proportion of teeth treated with root canal treatment increased along with a deep periodontal probing depth corresponding to the crack. The prognosis was less favorable in cracked teeth with a deep probing depth. CONCLUSIONS: In this study, the proportion of root canal treatment in the cracked teeth was higher than other studies. Many patients are referred to an endodontist in a university hospital after a long time has passed since the symptom started. Early recognition can help to avoid the propagation of a crack into the pulp chamber or subgingival level. Furthermore, it is important to investigate factors related to cracked teeth and develop different treatment protocols for different pulpal and periapical diagnoses.