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.

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.

[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.

Cytokines as diagnostic markers of pulpal inflammation.

AIM: To measure and compare the levels of the cytokines IL-2, IL-6, IL-8, IL-10, TNF-α and IFN-γ in pulpal blood from irreversible pulpitis, asymptomatic caries exposure and normal pulps. METHODOLOGY: Blood was obtained from pulp exposure sites using cotton pellets. Twenty-five samples were obtained from normal teeth, 40 from asymptomatic caries-exposed pulps and 43 from irreversible pulpitis teeth. Cytokine levels were determined by high-sensitivity ELISA. Data were statistically analysed using Kruskal-Wallis and Mann-Whitney U-tests. RESULTS: Significantly higher levels (P < 0.05) of IL-6, IL-8, IL-10, TNF-α and IFN-γ were detected in caries-exposed pulps and irreversible pulpitis as compared to normal teeth. IL-2 and IL-10 levels were significantly higher (P < 0.05) in caries-exposed pulps as compared to irreversible pulpitis, whilst IL-8 was significantly higher (P < 0.001) in irreversible pulpitis as compared to caries-exposed teeth. Most interestingly, IL-6/IL-10 and IL-8/IL-10 ratios were significantly higher (P < 0.001) in irreversible pulpitis compared with both caries-exposed and normal teeth. CONCLUSION: Levels of IL-8 and the ratios of IL-6/IL-10 and IL-8/IL-10 have the potential to be indicators of pulpal inflammation in caries exposure cases. Cytokine estimation in pulpal blood may help in the diagnosis of pulpal inflammation.

Pulpal and periapical response after restoration of deep cavities in dogs' teeth with Filtek Silorane and Filtek Supreme XT systems.

OBJECTIVE: This study evaluated, histopathologically, the pulpal and periapical response to a silorane-based resin (Filtek Silorane) and a methacrylate-based nanoparticle resin (Filtek Supreme XT) in deep cavities in dogs, having zinc oxide and eugenol-based cement (ZOE) as a control. METHODS: The tooth/bone blocks were collected after 10 and 90 days and processed for microscopic analysis of the dentin, pulp, and periapical tissues using a score system. Data were analyzed statistically by Kruskal-Wallis and Dunn post-test (α=0.05). RESULTS: At 10 days, the pulp, connective tissue, and periodontal ligament showed normal characteristics. No resorption areas were observed. Both resins caused significantly less (p<0.05) periapical and pulpal inflammatory response than ZOE. At 90 days, for all materials, the connective pulp tissue was healthy and dense, with a normal blood vessel system. The apical and periapical region had normal structure and thickness. CONCLUSIONS: The use of the Filtek Silorane and the Filtek Supreme XT resins caused no adverse pulpal and periapical reactions after restoration of deep dentin cavities in vivo.

Regenerative capability of dental pulp cells after crown fracture.

The purpose of this study was to evaluate the characteristics of dental pulp cells for tissue engineering derived from the fractured incisal portion of tooth crowns. Thirty Sprague-Dawley rats were used for histological and immunohistochemical analysis of nestin protein expression and to measure levels of mRNAs encoding osteocalcin, osteopontin, bone sialoprotein (BSP), dentin sialoprotein (DSP), heat shock protein (HSP) 27, vascular endothelial growth factor (VEGF), ATP-binding cassette transporter G2 (ABCG2), nestin, and p57(Kip2) . Odontoblasts at the incisal portion in the control group were oriented in a regular pattern, but those in the experimental group were randomly stratified. Immunohistochemically, only a few odontoblasts were positive for nestin at the incisal portion in the experimental group at 2 days. Some cells in the inner area in the control group were positive for nestin, but nestin-positive cells in the experimental group at the incisal portion were not observed. The mRNA expression for osteogenic or odontogenic markers in the experimental group was higher than in the control group. HSP27 mRNA expression in the experimental group at 2 days was higher than in the control group and in the experimental group at 7 days. mRNA expression of stem cell markers, such as ABCG2 and nestin, in the experimental group tended to decrease compared with the control. In conclusion, this study demonstrates that dental pulp stem cells derived from fractured teeth differentiate to osteogenic or odontogenic cells.

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.

Biodentine(TM) induces TGF-ß1 release from human pulp cells and early dental pulp mineralization.

AIM: To assess the ability of a recently developed tricalcium silicate-based cement (Biodentine™) to induce reparative dentine synthesis and to investigate its capacity to modulate pulp cells TGF-ß1 secretion. METHODOLOGY: Biodentine™ was directly applied onto the dental pulp in an entire human tooth culture model. After various culture periods, the interaction of the material with dental pulp tissue was analysed on tissue sections. The effect of increasing surface area of this material on TGF-ß1 secretion was investigated on pulp cell cultures and compared with that of MTA, calcium hydroxide and Xeno(®) III adhesive resin. After performing artificial injuries on pulp cell cultures, the materials eluates were added for 24 h and then TGF-ß1 secretion was quantified by ELISA. Controls were performed by incubating intact cells with the culture medium, while injured cells TGF-ß1 level was used as the baseline value. RESULTS: Biodentine™ induced mineralized foci formation early after its application. The mineralization appeared under the form of osteodentine and expressed markers of odontoblasts. Biodentine™ significantly increased TGF-ß1 secretion from pulp cells (P < 0.03) independently of the contact surface increase. This increase was also observed with calcium hydroxide and MTA, but not with the resinous Xeno(®) III. The statistical analysis showed statistically significant differences between capping materials and the resinous Xeno(®) III (P < 0.001). CONCLUSIONS: When Biodentine™ was applied directly onto the pulp, it induced an early form of reparative dentine synthesis, probably due to a modulation of pulp cell TGF-ß1 secretion.

Pulpal progenitors and dentin repair.

Mesenchymal stem cells are present in the dental pulp. They have been shown to contribute to dentin-like tissue formation in vitro and to participate in bone repair after a mandibular lesion. However, their capacity to contribute efficiently to reparative dentin formation after pulp lesion has never been explored. After pulp exposure, we have identified proliferative cells within 3 zones. In the crown, zone I is near the cavity, and zone II corresponds to the isthmus between the mesial and central pulp. In the root, zone III, near the apex, at a distance from the inflammatory site, contains mitotic stromal cells which may represent a source of progenitor cells. Stem-cell-based strategies are promising treatments for tissue injury in dentistry. Our experiments focused on (1) location of stem cells induced to leave their quiescent state early after pulp injury and (2) implantation of pulp progenitors, a substitute for classic endodontic treatments, paving the way for pulp stem-cell-based therapies.

[An index for untreated severe caries]. / Een index voor onbehandelde ernstige cariës.

Hardly any data are available on the clinical consequences of untreated severe caries, because there is no method to quantify the prevalence of oral conditions resulting from untreated caries. In the Philippines, an index was developed which records for (the location of) each tooth whether caries has reached the dental pulp, whether ulceration is present in the surrounding soft tissues due to sharp edges of fragments of a tooth lost due to caries, or whether a fistula or abscess is present. By adding the index to the existing Decayed Missing Filled Tooth index, insight is provided on the extent and the consequences of untreated caries and research may be carried out on its possible impact on the general health and wellbeing of national populations.

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.

Occurrence and causing stimuli of postoperative sensitivity in composite restorations.

Despite improvements in composite treatments over the past decade, postoperative sensitivity still remains a problem. Therefore, this clinical study evaluated the appearance of postoperative sensitivity after composite treatments and the stimuli that may have caused it. A total of 600 teeth in 231 patients was included in this study. All treatments were performed by dental students working under close supervision following standard procedures and using the bonding system Optibond FL and the nanofilled composite Ceram X. At baseline (visit 1), the restorations were grouped according to the following criteria: use of anesthesia, use of a rubber dam, indication for the restoration treatment, cavity class and clinical dimension of the cavity. After approximately two weeks (at visit 2), all the restorations were assessed and failure was defined if one of the following criteria occurred: a negative reaction to the vitality test, postoperative pain from masticatory forces or reported postoperative sensitivity by the patient. The reported postoperative sensitivity was specified with a visual analogue scale into hot/cold-sensitivity, sweet/soursensitivity, sharp/dull-sensitivity, spontaneous sensitivity and blistering/stinging-sensitivity. Failure was observed in 6% of the restorations. The statistical analysis showed that the clinical cavity depth turned out to be the only factor to have a significant influence on the appearance of postoperative sensitivity: caries profunda showed a four times higher risk of failure, while cavities with pulp exposure had a 14 times higher failure risk compared to restorations that were localized in the dentin. With regard to the type of sensitivity, no patients reported sensitivity to sweet/sour; most of them described their sensitivity as sharp/dull.

Undetected microscopic pulp exposures in deep class II cavities.

Exposure of the pulp may act as a great insult during preparations, so this study investigated the probability of clinically undiagnosed pulp microexposures. The axial wall of 30 deep class II preparations in human premolars were searched for any microexposure after extraction. Seven teeth (23.7 percent) showed some kind of exposure. It is concluded that approximately 1/5 of class II preparations with the RDT less than 0.5mm may have a pulpal microexposure.

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.

Pathological investigation of caries and occlusal pulpar exposure in donkey cheek teeth using computerised axial tomography with histological and ultrastructural examinations.

Post-mortem examination of 16 donkey cheek teeth (CT) with caries (both peripheral and infundibular) and pulpar exposure were performed using computerised axial tomography (CAT), histology and scanning electron microscopy. CAT imaging was found to be useful to assess the presence and extent of caries and pulp exposure in individual donkey CT. Histology identified the loss of occlusal secondary dentine, and showed pulp necrosis in teeth with pulpar exposure. Viable pulp was present more apically in one exposed pulp horn, with its occlusal aspect sealed off from the exposed aspect of the pulp horn by a false pulp stone. Scanning electron microscopy showed the amelo-cemental junction to be a possible route of bacterial infection in infundibular cemental caries. The basic pathogenesis of dental caries in donkeys appears very similar to its description in other species.

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.

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.

Formation of dentin-like particles in dentin defects above exposed pulp by controlled release of fibroblast growth factor 2 from gelatin hydrogels.

The induction of dentin formation on exposed dental pulp is a major challenge in research on the regeneration of the dentin-pulp complex. We examined the effects of fibroblast growth factor 2 (FGF2), which was delivered in either a collagen sponge (noncontrolled release) or incorporated into gelatin hydrogels (controlled release), on the formation of dentin in exposed rat molar pulps. During the early phase of pulp wound healing, pulp cell proliferation and invasion of vessels into dentin defects above exposed pulp were induced in both groups. In the late phase, the induction of dentin formation was distinctly different between the 2 types of FGF2 release. The noncontrolled release of free FGF2 from collagen sponge induced excessive reparative dentin formation in the residual dental pulp, although dentin defects were not noted. In contrast, controlled release of FGF2 from gelatin hydrogels induced the formation of dentin-like particles with dentin defects above exposed pulp. These results suggest the possibility of a novel therapeutic approach for dentin-pulp complex by controlled release of bioactive FGF2.

Equivalency study of histological responses to complete or partial pulpotomies in inflamed baboon immature first permanent molars.

UNLABELLED: Partial pulpotomy is an accepted treatment for traumatised incisor teeth with exposed pulps. Clinical studies in humans suggest that this may also be an acceptable technique for carious exposed pulps in molar teeth, but objective histological evidence to support this perception is lacking. OBJECTIVE: To compare histological responses to complete or partial pulpotomies of inflamed pulps in immature baboon first permanent molar teeth. METHODS: An experimental study in the baboon (Papio ursinus). Pulpitis was induced with fresh Streptococcus mutans placed into occlusal cavities with a small pulpal exposure in 34 first permanent molars of 9 juvenile baboons. After 14 days a pulpotomy, either complete or partial, was performed on the same molars in contra-lateral quadrants using calcium hydroxide covered with IRM and amalgam. After 90 days specimens were harvested and examined under the light microscope with the examiner blind to the treatment. RESULTS: Reaction frequencies in the complete and partial pulpotomy teeth were: dentine bridges 9/16 and 10/16, viable pulp in root canals 10/16 and 13/18, peri-apical abscesses 3/13 and 4/13. Fisher's exact probability test showed no statistically significant rates between the groups. CONCLUSIONS: Complete or partial pulpotomy of inflamed pulps in immature baboon first permanent molars produced comparable reactions.

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.