International endodontic journal最新文献

Aim: This study aimed to investigate the effects of copaiba oil-resin on induced apical periodontitis in rats.

Methodology: A total of 24 male Wistar rats were divided equally into three groups (eight animals each): control (C), apical periodontitis (AP) and apical periodontitis with copaiba administration (AP + COP). The AP was induced by exposing the pulp chambers of the mandibular first molars to the oral environment. The openings were maintained for 28 days to allow lesion development. The AP + COP group received systemic administration of 200 mg/kg of copaiba oil-resin via intragastric gavage during the final 7 days of the AP induction period. The rats were then euthanised, and their hemimandibles were subjected to histopathological analysis to assess tissue preservation, histochemical staining with picrosirius red to evaluate collagen content, and microcomputed tomography to assess lesion volume and bone quality parameters. Statistical analyses were performed using a one-way ANOVA, followed by Tukey's post hoc test for parametric data and the Kruskal-Wallis test for nonparametric data. The results are expressed as mean and standard error of the mean for parametric tests, and median and interquartile deviation for the nonparametric test.

Results: The findings showed that copaiba oil-resin reduced lesion volume compared to the untreated group (p = 0.0261), as well as reducing the space between the bone trabeculae found in the AP group (p = 0.0063). Additionally, copaiba oil-resin preserved the collagen fibres, which were more degraded in the untreated group (p = 0.0009). Histopathological analysis showed that copaiba oil-resin reduced tissue damage, preserving a significant area of alveolar bone surrounding the lesion.

Conclusions: These results indicate that copaiba oil resin has a promising adjunct therapeutic potential to reduce the bone loss caused by apical periodontitis and contribute to the maintenance of quality in the remaining bone.

Aims: To investigate the phase changes of bismuth oxide in contact with sodium hypochlorite responsible for tooth discolouration.

Methodology: Bismuth oxide (monoclinic α-phase; C) was mixed with sodium hypochlorite at 20°C, 37°C, and 60°C (B20, B37, B60) for a period of 24 weeks with weekly refreshing of solutions. The products were imaged by scanning electron and optical microscopy and characterized by thermographic analysis (TGA), phase analysis by X-ray diffraction (XRD) using Bragg Brentano geometry and Pilatus detector, infrared spectroscopy (FT-IR), and X-ray absorption fine structure (XAFS).

Results: The interaction of bismuth oxide with sodium hypochlorite resulted in a change in microstructure and colour. The thermographic assessment showed a change in mass (5%-10% weight change) and colour reversal to the yellow bismuth oxide at ~450°C. Phase changes dependent on temperature were demonstrated with δ-bismuth oxide, sodium bismuthate and bismuth oxychloride formed as by-products at the different temperatures.

Conclusions: The δ-phase bismuth oxide formation led to the material darkening which will cause tooth discolouration in a clinical setting. Due to the phase changes, the material chemistry after the interaction is different from that of the material placed in the tooth. The by-products of the reaction have not been tested for use in patients. It is recommended to ban the use of bismuth oxide from dental materials and other clinical use due to its instability. The clinical guidance for endodontic treatment needs to be changed to reflect this.

Introduction: This study aimed to validate a commonly used in vitro methodology of testing the performance of the EALs. For that, clinical data obtained from teeth already scheduled for extraction were used to compare the accuracy and precision of an EAL in determining the position of the apical foramen in both clinical and laboratory settings using micro-CT imaging.

Methods: In a clinical setting, the working length of 11 canals was established using the Root ZX II apex locator. Subsequently, these teeth were extracted and imaged with and without the file in place using micro-CT technology. In vitro measurements of the working length were then obtained in these same teeth using an alginate model and new micro-CT scans were performed. Datasets were co-registered and the accuracy and precision of both in vivo and in vitro models were compared by measuring the distance from the file tip to a tangential line crossing the foramen margins, with a tolerance level of ±0.5 mm. Statistical comparisons were performed using Friedman post hoc Related Samples Sign and Bland-Altman tests with a significance level set at 5%.

Results: Statistical analysis revealed no significant difference between the accuracy (p = 0.368) and precision (p = 0.761) measurements obtained in both in vivo and in vitro conditions. Additionally, the Bland-Altman analysis revealed an agreement between in vivo and in vitro methods (p > 0.05).

Conclusions: The in vitro methodology using freshly mixed alginate demonstrated consistent accuracy and precision in identifying the position of the apical foramen, when compared to in vivo measurements.

Aim: The aim of this study was to compare pulp survival following selective caries removal (SCR) and full pulpotomy treatment in teeth with extensive caries over 3 years.

Methodology: This two-arm, exploratory randomised controlled trial included vital mature permanent teeth with extensive primary or secondary caries diagnosed radiographically as being at least 75% or more into the thickness of dentine, without clinical signs of symptomatic irreversible pulpitis or radiographic evidence of a periapical lesion. Carious teeth were randomly allocated to receive either SCR or full pulpotomy. All teeth were reviewed clinically and radiographically at 6 months, 1 year, and 3 years post-treatment. Log-rank tests and Cox proportional hazards regressions were used to compare the outcomes of SCR and pulpotomy, adjusting for clustering using a robust variance estimator. Cost-effectiveness analysis was carried out using the healthcare system and societal perspectives. Significance level was set at 5%.

Results: At 3 years, 44/58 teeth (75.9%) in the SCR group and 37/55 teeth (67.3%) in the full pulpotomy group were reviewed. A total of 13 teeth in the SCR group (29.5%) and 4 teeth in the pulpotomy group (10.8%) required further intervention with root canal treatment (RCT) or extraction (p = 0.039). Survival rates were 74% for SCR and 89% for pulpotomy (p = 0.041). Overall, 79.0% of teeth treated with either SCR or pulpotomy survived without requiring further intervention over the 3-year period. In this study with more than two-thirds of the enrolled teeth classified as extremely deep lesions, pulpotomy was more cost-effective than SCR in the management of extensive caries above a willingness-to-pay threshold of $917 and $928 to avoid one tooth extraction or RCT from the healthcare system and societal perspective, respectively.

Conclusion: Full pulpotomy demonstrated greater effectiveness than SCR in avoiding further intervention over a 3-year period in teeth with extensive caries, of which the majority were extremely deep lesions. Further long-term studies and broader health economic evaluations are warranted to guide clinical decision-making and policy development.

Trial registration: ClinicalTrials.gov identifier: NCT04672070.

Aim: To assess whether there was an additive antimicrobial effect between calcium hydroxide (Ca(OH)₂) and sodium hypochlorite (NaOCl) in an inter-visit root canal dressing.

Methodology: Patients presenting with a single-rooted tooth with pulpal necrosis and asymptomatic apical periodontitis were included in this randomised controlled single-center clinical superiority trial with two parallel arms. Teeth were instrumented using a rotary file system and irrigated with 3% NaOCl. Subsequently, the root canals were dressed with a Ca(OH)₂ slurry that was prepared from pure Ca(OH)₂ powder mixed with either 3% NaOCl (test group) or physiological saline solution (control group). Microbial samples were obtained after accessing the root canal, after chemo-mechanical preparation, and after the root canal dressing with the test or control slurries. A periapical fluid sample was collected after the root canal dressing removal. Samples were transferred to the microbiology lab immediately and assessed for anaerobic growth. The levels of MMP-9 were measured using a specific enzyme-linked immunosorbent assay. Negative to positive growth ratios were compared between groups using Fisher's exact test. Colony-forming units (CFUs) between and within groups and MMP-9/total protein were compared using non-parametric tests, p < 0.05.

Results: From the 110 patients recruited for this study, 48 were available for all three sampling procedures in the test (NaOCl) and 50 in the control (saline) group. All canals showed anaerobic growth initially. Chemo-mechanical instrumentation significantly reduced CFU counts (p < 0.001), yet all canals remained growth-positive. After dressing with Ca(OH)₂/NaOCl, 19 of the 48 (40%) root canals were free of growth, compared to 3 of 50 (6%) in the Ca(OH)₂/saline group (p < 0.001). MMP-9/TP levels in the periapical fluid were similar when root canals were dressed with Ca(OH)₂ slurries mixed with NaOCl or saline (p > 0.05).

Conclusions: Placing a combined NaOCl/Ca(OH)₂ dressing significantly reduced the microbial load in the root canals of teeth with primary apical periodontitis compared to a conventional slurry prepared with saline solution, without causing any apparent inflammatory response in the periapical tissues.

Trial registeration: CTRI/2020/10/028484 (Clinical Trials Registry India).

Background: There is a strong association between root canal curvatures and iatrogenic complications during root canal treatment.

Introduction: This study compared the curvature of mesiobuccal (MB) and mesiolingual (ML) canals in mandibular first molars between sagittal and coronal planes using cone-beam computed tomography.

Methods: Two hundred mesial roots (400) canals from a Brazilian subpopulation were analysed. Curvature angles were measured in sagittal and coronal planes using Schneider's and Weine's methods, while curvature radii were calculated geometrically. The prevalence of S-shaped canals was also recorded. Curvature severity was classified according to the American Association of Endodontists Case Difficulty Assessment form, EndoApp, and modified versions incorporating curvature and radius. The influence of the angle measurement method and radius on case complexity was evaluated. Statistical analyses were performed using t-tests and chi-squared tests, with significance set at p ≤ 0.05.

Results: Sagittal planes showed significantly greater angles and smaller radii than coronal planes. Weine's method yielded consistently higher angles and smaller radii than Schneider's. Severe single curvatures (≥ 30°) were more frequent in sagittal planes, whereas S-shaped canals were more prevalent in coronal planes. MB was more often classified as higher difficulty than ML canals. Incorporating radius into the classification systems generally shifted cases towards greater severity.

Conclusions: Sagittal planes revealed more severe single curvatures, whereas coronal planes showed a higher prevalence of S-shaped canals. Weine's method resulted in greater curvature severity than Schneider's. Inclusion of radius increased case severity grading. These findings highlight the importance of considering both measurement method and projection plane in endodontic treatment planning and research.

Background: Inflammatory radicular cysts (IRCs) arise from periapical granulomas (PGs). IRCs originate from Malassez epithelial remnants (ERMs), which can proliferate under specific biological stimuli. Although ERMs are common within PGs, only a subset of lesions evolves into IRCs, suggesting that specific molecular and immunoregulatory mechanisms govern this selective transformation.

Objectives: Molecular mechanisms and cellular signalling pathways modulating the epithelial proliferation of the ERM represent an inflexion point in the progression from PG to IRC. The objective of this review is to analyse the mechanisms and pathways involved in uncontrolled ERM proliferation, intending to elucidate why only a subset of epithelium-containing PGs progress to IRCs.

Methods: A systematic literature search was conducted across MEDLINE (PubMed), Web of Science and Scopus from inception to July 2025. Sixty-one articles met the inclusion criteria for narrative analysis and synthesis.

Results: ERM proliferation emerges from a coordinated interplay between immune, stromal and epithelial compartments. Fibroblast growth factor-7 (FGF-7/KGF) activates the FGFR2-IIIb-MAPK/PI3K-AKT pathways, maintaining homeostasis of ERM proliferation. Transforming growth factor-β (TGF-β1/β2) and Smad2/3 signalling sustain epithelial quiescence. IGF-BP-6 sequesters bioavailable insulin growth factor (IGF-II), avoiding mitogenic signalling. Proteolytic cleavage of IGF-BP-6 releases bioactive IGF-II, enhancing ERM pathological proliferation. Intense AP upregulates epidermal growth factor (EGF) and its receptor (EGF-R), promoting uncontrolled ERM proliferation. IL-1β antagonises TGF-β/Smad2 suppression through NF-κB (p65) activation. IL-6 promotes pathological ERM proliferation and migration via classic and trans-signalling. Persistent M1 macrophage polarisation and Th1/Th17 dominance reinforce this microenvironment. Activated dendritic cells potentiate T-cell responses and cytokine release.

Conclusion: Not all PGs progress to IRCs because cystic transformation requires the convergence of epithelial, stromal and immune thresholds that override ERM quiescence. This review proposes an integrative theoretical model that redefines ERMs as dynamic, inflammation-responsive progenitors whose activation depends on immune-epithelial cross-talk rather than infection alone. By delineating specific biomarker clusters-epithelial, immune/co-stimulatory and stromal/remodelling-this work proposes a mechanistic framework capable of predicting lesion behaviour. It may establish the foundation for molecularly guided diagnosis and the rational design of targeted therapeutic strategies aimed at preventing or reversing cystic transformation, ultimately bridging molecular insight with clinical endodontic practice.

Aim: Due to the lack of a predictable and noninvasive method for distinguishing different types of apical periodontitis, it is difficult to estimate the actual prognosis of periapical cysts and the effectiveness of nonsurgical treatment for them. This pilot study aimed to establish a diagnostic model to differentiate periapical cysts and nonperiapical-cyst lesions based on parameters derived from magnetic resonance imaging (MRI).

Methodology: Before endodontic microsurgery, MRI scans were performed for the patients with periapical lesions, including T2-weighted images (T2WI), noncontrast-enhanced T1-weighted images (T1WI), diffusion-weighted imaging (DWI) and contrast-enhanced T1-weighted images (T1WI + C). Sixteen parameters were collected, and thirteen derived parameters were calculated. The patients were divided into training and validation cohorts according to time order. The histopathological results were gold standards. Univariate, multivariate regression and multicollinearity analyses were used to filter variables and select predictors. Multivariate logistic regression was applied to develop the nomogram. Discrimination and calibration were evaluated by bootstrapping with 1000 resamples.

Results: Eighty-four patients underwent MRI examinations followed by endodontic surgeries. Lesion length, enhanced area and enhanced-to-lesion area ratio were independent predictors for the diagnosis of periapical cysts. Area under the receiver operating characteristic (ROC) curve (AUC) of the training cohort was 0.861. Sensitivity and specificity based on ROC curves were 80.6% and 75.9%, respectively. The calibration curve of the nomogram was close to the ideal diagonal line. Decision curve analysis indicated positive net benefit in the model. The validation cohort proved the reliability of the prediction nomogram (AUC: 0.930; sensitivity: 81.8%; specificity: 76.9%).

Conclusion: The findings indicated that the proposed nomogram reliably identified periapical cysts through multiparameter MRI. The length of the lesion, enhanced area and enhanced-to-lesion area ratio were important variables for diagnosing periapical cysts. Multiparameter MRI was implicated as an efficient and noninvasive method to differentiate periapical lesions.

Trial registration: The study is registered on the Chinese Clinical Trial Registry website (ChiCTR2000035273).

Aim: The success of vital pulp treatment (VPT) has been linked to the release of growth factors (GFs) from the dentine matrix, which stimulate dental pulp stem cell (DPSC) activities. Ethylenediaminetetraacetic acid (EDTA) is a commonly used chelating agent that induces the release of GFs bound in the dentine matrix. A 7% Maleic acid (MA) solution has been shown to have better smear layer removal capability and less cytotoxicity compared with 17% EDTA. However, no study has evaluated the effect of 7% MA on the release of GFs from circumpulpal dentine and subsequent DPSC behaviour. This study aimed to evaluate the effect of 17% EDTA and 7% MA conditioning of circumpulpal dentine on the release of transforming growth factor-β1 (TGF-β1), as well as the DPSC activities.

Methodology: Dentine slices treated with phosphate-buffered saline (PBS) acted as the control, while the experimental groups comprised 17% EDTA and 7% MA. The release of TGF-β1 was quantified using ELISA following treatment with the experimental solutions. DPSC proliferation was evaluated with the MTT assay, cell migration was assessed through scratch wound and transwell migration assays. Osteogenic differentiation potential of DPSCs was verified using Alizarin Red staining and an alkaline phosphatase (AP) activity assay.

Results: 7% MA induced the highest release of TGF-β1 compared with 17% EDTA and PBS (p < 0.001). 7% MA at 1/1000 dilution significantly increased DPSC proliferation compared with 17% EDTA and PBS (p < 0.001). The scratch wound healing and transwell migration assays demonstrated superior DPSC migration in the 7% MA compared with the 17% EDTA group (p < 0.001). Alizarin Red staining and quantification indicated the highest formation of mineralized nodules in the 7% MA compared with the 17% EDTA group (p < 0.0001). The AP activity assay showed similar enzyme activity in 7% MA and 17% EDTA treated samples.

Conclusions: Within the limitations of this study 7% MA performed better than 17% EDTA in promoting TGF-β1 release from dentine, as well as increased DPSC responses related to cell proliferation, migration, and mineralisation. These findings indicate that 7% MA may be a promising dentine conditioning agent during VPT procedures.