IMPORTANCE:A well-formed dentin bridge isolates irritants and prevents bacterial penetration into the remaining pulp tissue, which is essential for pulp regeneration. The existing literature on promoting reparative dentin formation mostly focuses on the effects of pulp-capping materials but lacks investigations into the underlying mechanisms. OBJECTIVE:To identify potential targets for enhancing reparative dentin formation as well as the epigenetic mechanisms underlying these effects. DESIGN:Laboratory-based study combining multi-omics sequencing, epigenetic assays, in vitro FK506-binding protein 51 (FKBP5) knockdown or overexpression experiments, and in vivo validation using rat pulp injury models and nude mouse subcutaneous transplantation models. SETTING:Laboratory-based in vitro and in vivo study. PARTICIPANTS:N/A. INTERVENTION(S) OR EXPOSURE(S):Dental pulp stem cells (DPSCs) were exposed to odontogenic differentiation induction or Lipopolysaccharide (LPS) stimulation. FKBP5 knockdown and overexpression were conducted using lentiviral vectors. In vivo validation was performed using a rat dental pulp injury model and a nude mouse subcutaneous transplantation model combining FKBP5 knockdown or overexpressed DPSCs with treated dentin matrix. Histone acetylation was modulated using dCas9-p300 targeting or pharmacological treatment with suberoylanilide hydroxamic acid (SAHA) or C646. MAIN OUTCOME(S) AND MEASURE(S):FKBP5 expression, mineralized nodule formation, alkaline phosphatase (ALP) activity, odontogenic marker expression, inflammatory cytokine expression, FKBP5 promoter chromatin accessibility, promoter methylation, H3K9ac/H3K27ac enrichment, reparative dentin formation and collagen formation were assessed. RESULTS:FKBP5 was upregulated during odontogenic differentiation induction and highly expressed in human pulpitis tissues and injured rat pulps. Overexpression of FKBP5 promoting reparative dentin formation, collagen synthesis and mineralization (dentin sialophosphoprotein and dentin matrix protein 1 expressions). Down-regulation of inflammatory factors Interleukin-1β and Interleukin-8 also contributed to the process of pulp repair. H3K9ac and H3K27ac, rather than DNA methylation, were enriched at the FKBP5 promoter, enhancing chromatin accessibility and FKBP5 transcription. SAHA enhanced H3K9ac and H3K27ac and the expression of FKBP5 near the injury site. The newly-formed reparative dentin was upregulated and pulp inflammation was suppressed with the application of SAHA. CONCLUSIONS AND RELEVANCE:FKBP5 facilitated reparative dentin and neoplastic collagen synthesis at the injury site while mitigating inflammation. Histone acetylation H3K9 and H3K27 were the mechanism that modulated differentiation effects of FKBP5.

PURPOSE:To develop a newly designed root-extended overlay (REO) for adolescents' permanent mandibular first molars (M1Ms) with a 4-wall defect and to analyze the stress distribution of REOs using finite element analysis (FEA). METHODS:A post-endodontic M1M was 3D reconstructed from Cone-Beam Computed Tomography, and the model was then modified to simulate a 4-wall defect located 2 mm above the enamel-dentinal junction. Subsequently, REOs with 0-2 mm distal root extensions were designed using Ti-6Al-4V (3D printed), lithium disilicate (IPS e.max Press), and composite resin. In FEA, vertical (400 N) and lateral (225 N) loads were applied to evaluate the maximum von Mises stress (mVMS) and principal stress. RESULTS:Ti-6Al-4V, lithium disilicate, and composite resin exhibited similar stress distribution. Under vertical loading, the 2-mm group showed the highest mVMS in the restorations. Additionally, the 2-mm group exhibited the minimal tensile stress in the alveolar bone. The 2-mm group with Ti-6Al-4V minimized tensile stress in the cement layer and tooth structure under lateral loading. CONCLUSIONS:The REO design was feasible for M1Ms with a 4-wall defect. The stress distribution of 3D printed Ti-6Al-4V was comparable to that of lithium disilicate. A 2-mm root extension exhibited optimal stress distribution across the restoration, cement layer, tooth structure, and periodontal tissues. This optimized stress distribution may reduce root fracture, debonding, and periodontal overload, supporting long-term preservation of mandibular first molars during occlusal and craniofacial development.

Background:Periodontal diseases are associated with complex interactions among inflammatory responses, microbial dysbiosis, and clinical periodontal parameters. However, the relationships among inflammatory biomarkers, microbial biomarkers, and clinical parameters in gingival crevicular fluid (GCF) remain to be further clarified. Objective:To explore the interactions among inflammatory biomarkers, microbial biomarkers, and clinical parameters in gingival crevicular fluid in periodontal diseases. Design:In this cross-sectional study, GCF and subgingival plaque were collected from healthy, gingivitis, and periodontitis participants. Levels of fibrinogen, fibrin (measured as fibrin degradation products (FDP)), Interleukin (IL)-1β, IL-17, Matrix metallopeptidase (MMP)8, and MMP9 were measured by enzyme-linked immunosorbent assay. The subgingival microbiome was analyzed using 16S rRNA gene sequencing. Results:Among all biomarkers, fibrinogen was the most sensitive biomarker detected in GCF. Levels of fibrinogen were higher in the gingivitis (p = 0.024) and periodontitis (p = 0.002) groups than in the healthy group. Positive correlations were found between fibrinogen and numerous subgingival microorganisms, such as Tannerella forsythia, Treponema denticola, Porphyromonas gingivalis, and Filifactor alocis. Fibrinogen was the only GCF marker that could differentiate between healthy and gingivitis individuals. Fibrinogen and its combination with specific subgingival microorganisms may be potential markers indicating gingivitis and periodontitis. Conclusions:Compared with IL-1β, IL-17, MMP8 and MMP9, fibrinogen in GCF demonstrated distinct associations with clinical parameters and subgingival microbiome in periodontal diseases.

Accurate identification of oral bacteria is essential for assessing oral and systemic diseases. Conventional phenotyping methods and molecular biology techniques exhibit limitations, including low sensitivity and operational complexity. Here, we present a terahertz (THz) scattering scanning near-field optical microscopy (s-SNOM) strategy enabling single-bacterium discrimination among multiple oral species. Eight bacterial genera and five Streptococcus species were investigated. Simultaneous acquisition of terahertz near-field images and intensity-height curves allowed the extraction of attenuation parameters (K, A1) and morphological parameters (height, area). Correlation analysis revealed that K and A1 were significantly distinct between rod and coccus, showing inverse relationships with the height and area. Using these four parameters, machine learning models, including Random Forests (RF), Gaussian Process Classification (GPC), and Support Vector Machines (SVM), achieved accurate bacterial differentiation, successfully classifying 23 genus-level pairs (82% achieving 100% accuracy) and 6 Streptococcus species pairs (60% at 100% accuracy) within the current data set. THz imaging effectively visualized bacterial morphology, while machine learning validated the discriminative power of combined parameters. Furthermore, an interactive Shiny-based predictor integrating RF, GPC, and SVM models was developed for real-time demonstration of bacterial classification outputs. Among these, RF exhibited the highest proficiency in classifying Streptococcus aureus, GPC excelled with Limosilactobacillus reuteri and Porphyromonas gingivalis, while SVM was effective for P. gingivalis. This study demonstrates a label-free, high-precision strategy for rapid, single-cell-level identification of oral bacteria using THz near-field nanoscopy, offering a promising platform for microbial diagnostics and biosensing.

Against the backdrop of the"Healthy China 2030"strategy and the advancement of the"Three Reductions and Three Healthinesses"initiative,the oral health issues of obese children have received significant attention.Research has shown that obese children generally have poorer oral health,with significantly higher rates of dental caries,gingivitis,dental malocclusion,and dental trauma compared to children of normal weight.This paper proposes multidimensional measures to improve oral health in obese children,using the"Three Reductions and Three Healthinesses"as the core framework:"reducing salt,oil,and sugar"can lower the risk of oral diseases at the source,while the coordinated promotion of"oral health,healthy body weight,and bone health"can create synergy between oral and overall health.Future efforts will leverage multidisciplinary collaboration,artificial intelligence,and"Internet Plus"technologies to establish a health education system that integrates communities,schools,and families.Implementing tiered management and targeted prevention will enhance both oral and overall health among obese children,contributing to the strategic goals of"Healthy China".

Severely damaged molars pose significant challenges in restorative dentistry. Conventional methods, such as resin composite restorations, often fail to provide sufficient fracture resistance, marginal integrity, and sealing, leading to frequent failures and secondary caries. This study aims to compare the mechanical properties and marginal integrity of 3D-printed Ti-6Al-4V root-extended endocrowns with direct resin composite restorations in molars with 4-wall defects. Forty-two extracted third molars were randomly assigned to a 3D-printed Ti-6Al-4V root-extended endocrown group (n = 21) or a nanohybrid resin composite group (n = 21). All specimens underwent thermocycling. Fracture resistance was evaluated in eight specimens per group using vertical loading. Microleakage was assessed by methylene blue staining, and marginal integrity was evaluated by SEM. Micro-CT was performed on endocrown specimens without visible failure to detect internal microcracks. The endocrown group showed a significantly higher fracture resistance than the resin group (4682 ± 981 N vs. 1334 ± 615 N, P < 0.05). No catastrophic failures occurred in the endocrown group, whereas the resin group exhibited multiple failure modes. Lower microleakage scores and fewer marginal defects were observed in the endocrown group (P < 0.05). Micro-CT revealed limited microcracks in two endocrown specimens, and marginal gaps remained within clinically acceptable limits. The study innovatively designs a 3D-printed Ti-6Al-4V root-extended endocrown, combining the structural advantages of endocrowns and post-core restorations. In our study, the 3D-printed Ti-6Al-4V root-extended endocrowns exhibited markedly enhanced fracture resistance, diminished microleakage, improved marginal integrity in comparison to the direct resin restorations, hence endorsing their application for molars with severe defect.

Emerging evidence indicates that oral microbes are closely related to gastric microbes and gastric lesions, including gastric atrophy, intestinal metaplasia and gastric cancer (GC). Helicobacter pylori is a key pathogen involved in GC. However, the increasing prevalence of H. pylori-negative GC and gastric dysbiosis in GC patients emphasize the potential role of other microbial factors. In this review, we discussed the current evidence about the relationship between the oral–gastric microbial axis and oral and gastric health. Epidemiologic evidence indicates that poor oral hygiene is related to greater GC risk. Multiple oral-associated microbes are enriched in the stomach of GC patients. Once colonizing the stomach, oral-associated microbes Streptococcus anginosus and Prevotella melaninogenica, are involved in gastric inflammation or carcinogenesis. Microbial metabolites such as lactate, nitrite, and acetaldehyde promote malignant transformation. The stomach, as a checkpoint of microbial transmission in the digestive tract, is of great importance since the link between oral microbes and intestinal diseases has been emphasized. Still, new technologies and standardized metrics are necessary to identify potential pathogenetic microbes for GC and the core microbiota, interactions, richness, colonization, location and effect (CIRCLE). In the future, oral microbes could be candidates for noninvasive indicators to predict gastric diseases.

This study identifies autophagy-pyroptosis crosstalk as a driver of periodontal pathogenesis and suggests ATG7 as a preliminary, context-dependent modulator.

Geriatric oral health care encounters significant challenges with the increase in the proportion of older individuals. Age-related changes in the dentition, muscles, and joints result in a decline in objective masticatory function, subjective restoration requirements, and acceptability among the elderly population, with individual variations influenced by systemic health. Considering functional requirements, the adaptability of stomatognathic and systemic health conditions, health economics and other factors, the authors believe that it should not be limited to the conventional "one-to-one" strategy for replacing missing teeth in geriatric prosthodontics. There is an urgent need for a precise and adaptable restoration strategy that is more suitable for older individuals. The proposal of a new concept of functional tooth loss updates the minimal restoration standards for elderly patients and establishes the theory of age-friendly functional restoration. Based on the restoration strategy of functional tooth loss, this paper proposes a new concept termed "age-friendly functional restoration of the stomatognathic system", which integrates treatment considerations including endodontics, periodontology, mucosa, muscles, temporomandibular joint, and systemic health. Efforts should be made in four areas as follows. Firstly, the "assessment of accessible function" should be enhanced by considering the interrelationship between stomatognathic and systemic health. Secondly, the "evaluation of appropriate function" is supposed to be optimised in view of subjective needs and objective evaluation of the stomatognathic system. Moreover, the "formulation of treatment plans" needs to be accomplished with the aid of assistive technologies, such as artificial intelligence, to accurately exert appropriate functional restoration. Lastly, the "management and maintenance of health" is likely to be strengthened through follow-ups, propaganda and education, and preventive healthcare, so as to improve quality of life and ultimately achieve healthy ageing among older individuals.

Appropriate dental pulp repair is based on effective control of inflammation and involves the regeneration of dental pulp nerves, blood vessels (soft tissue), and dentin (hard tissue). Limited evidence has shown how to modulate the uncertainty due to individual variability in dental pulp repair. NRG1, a cytokine modulating nerve injury and repair, was intricately associated with the outcome of pulp repair. Yet, its mobilization in spontaneous pulp repair had individual variability. The study further explored the role of NRG1 during pulp repair as well as an epigenetic way to modulate NRG1 through histone acetylation to enhance pulp repair. Overexpression of NRG1 exhibited the effects of anti-inflammation and integrated regeneration of soft and hard tissue, by inhibiting pro-inflammatory factors IL-1β, IL-8, and promoting the expressions of DSPP, DMP1 (dentin regeneration), and nestin (nerve regeneration). Moreover, restricted H3K9 and H3K27 acetylation correlated with NRG1 expression in pulp repair both temporally and spatially, showing individual variability as well. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor, enhanced H3K9ac and H3K27ac, which dramatically activated NRG1, suppressed pulp inflammation, and facilitated soft and hard tissue regeneration. In summary, targeting histone acetylation with HDAC inhibitors may be an effective approach to promote pulp repair by activating NRG1.

Aim or purpose: Aging impacts both oral health and skeletal muscle, but the associations between oral diseases and sarcopenia remain understudied, especially in low-income regions, prompting this study to investigate their connection and explore potential mediators. Materials and methods: Data were extracted from the 2021-2022 follow-up of the West China Health and Aging Trend study. Assessments included questionnaires, oral examinations, muscle strength tests, physical performance tests, and routine blood tests. Logistic regression analyses were used to assess the oral-sarcopenia nexus. Mediation analyses were evaluated using the bootstrap method. Results: Among 532 adults aged 60 years and older, 75.6% were identified as having ≥20 remaining natural teeth (NRT), 25.8% were found with a number of functional tooth loss (NFTL) >16, and 50.4% experienced possible sarcopenia. After adjusting for confounding factors (including gender, household type, health insurance, pension, education, and living arrangements), older people with NRT ≥20 had a 50% lower risk of possible sarcopenia than those with NRT <20, mediated through chewing impairment (6.0%), immune-inflammation (5.4%), and AST/ALT ratio (8.4%). Conversely, those with NFTL >16 had a 95% higher risk of possible sarcopenia versus NFTL ≤16 counterparts, mediated by chewing impairment (6.1%), platelet-to-lymphocyte ratio (4.9%), and AST/ALT ratio (10.4%). Conclusions: These findings underscore the critical need for incorporating oral health interventions into aged care systems, particularly in low-income communities, so as to potentially reduce sarcopenia risks by addressing chewing capacity, systemic inflammation, and liver function through multidisciplinary strategies.

To investigate site-specific subgingival microbiota by precise probing depth (PD) and their associations with clinical parameters across periodontal states. Participants included healthy-periodontium (n = 20), gingivitis (n = 20) and periodontitis (n = 20). 218 subgingival biofilm samples were collected from PD-based-sites, including health (n = 60), gingivitis (n = 64) and periodontitis (n = 94). Samples further categorized as unstable (PD = 1–3 mm, gingivitis) and dysbiosis (PD ≥ 4 mm, periodontitis). Full-length 16 S rRNA sequencing was performed using third-generation technology. Selenomonas sputigena (S. sputigena), Filifactor alocis (F. alocis), Aggregatibacter segnis (A. segnis), Prevotella intermedia (P. intermedia), Campylobacter gracilis (C. gracilis), Porphyromonas gingivalis (P. gingivalis) positively correlated with clinical parameters—bleeding on probing, modified gingival index, plaque index and PD. Haemophilus parainfluenzae (H. parainfluenzae) negatively correlated with clinical parameters. Microbiota in gingivitis (PD = 4 mm) resembled with periodontitis deep-sites (PD ≥ 4 mm). Periodontitis (PD ≥ 4 mm) showed a dysbiotic microbial profile, where P. gingivalis, P. intermedia and F. alocis were key taxa. Positive correlations with clinical parameters encompassed F. alocis, P. intermedia, C. gracilis, P. gingivalis, etc., while H. parainfluenzae showed negative relations. Gingivitis (PD = 4 mm) exhibited a microbiota resembled the PD ≥ 4 mm of periodontitis. Gingivitis pseudopockets (PD = 4 mm) may exhibited periodontitis-like microbiota, suggesting that such sites should be monitored as early risk indicators for disease progression.

Aim: Autophagy is involved in human apical periodontitis (AP). However, it is not clear whether autophagy is protective or destructive in bone loss via the receptor activator of nuclear factor-kappa B ligand (RANKL)/RANK/osteoprotegerin (OPG) axis. This study aimed to investigate the involvement of autophagy via the RANKL/RANK/OPG axis during the development of AP in an experimental rat model. Methodology: Twenty-four female Sprague-Dawley rats were divided into control, experimental AP (EAP) + saline, and EAP + 3-methyladenine (An autophagy inhibitor, 3-MA) groups. The control group did not receive any treatment. The EAP + saline group and the EAP + 3-MA group received intraperitoneal injections of saline and 3-MA, respectively, starting 1 week after the pulp was exposed. Specimens were collected for microcomputed tomography (micro-CT) scanning, histological processing, and immunostaining to examine the expression of light chain 3 beta (LC3B), RANK, RANKL, and OPG. Data were analysed using one-way analysis of variance (p < .05). Results: Micro-CT showed greater bone loss in the EAP + 3-MA group than in the EAP + saline group, indicated by an elevated trabecular space (Tb.Sp) (p < .05). Inflammatory cell infiltration was observed in the EAP + saline and EAP + 3-MA groups. Compared with EAP + saline group, the EAP + 3-MA group showed weaker expression of LC3B (p < .01) and OPG (p < .05), more intense expression of RANK (p < .01) and RANKL (p < .01), and a higher RANKL/OPG ratio (p < .05). Conclusion: Autophagy may exert a protective effect against AP by regulating the RANKL/RANK/OPG axis, thereby inhibiting excessive bone loss.

ABSTRACT The gastric microbial community plays a fundamental role in gastric cancer (GC), and the two main anatomical subtypes of GC, non-cardia and cardia GC, are associated with different risk factors ( Helicobacter pylori for non-cardia GC). To decipher the different microbial spatial communities of GC, we performed a multicenter retrospective analysis to characterize the gastric microbiota in 223 GC patients, including H. pylori -positive or -negative patients, with tumors and paired adjacent normal tissues, using third-generation sequencing. In the independent validation cohort, both dental plaque and GC tumoral tissue samples were collected and sequenced. The prevalence of H. pylori and oral-associated bacteria was verified using fluorescence in situ hybridization (FISH) assays in GC tumoral tissues and matched nontumoral tissues. We found that the vertical distribution of the gastric microbiota, at the upper, middle, and lower third sites of GC, was likely an important factor causing microbial diversity in GC tumor tissues. The oral-associated microbiota cluster, which included Veillonella parvula , Streptococcus oralis , and Prevotella intermedia , was more abundant in the upper third of the GC. However, H. pylori was more abundant in the lower third of the GC and exhibited a significantly high degree of microbial correlation. The oral-associated microbiota module was co-exclusive with H. pylori in the lower third site of the GC tumoral tissue. Importantly, H. pylori -negative GC patients with oral-associated gastric microbiota showed worse overall survival, while the increase in microbial abundance in H. pylori -positive GC patients showed no difference in overall survival. The prevalence of V. parvula in both the dental plaque and GC tissue samples was concordant in the independent validation phase. We showed that the oral-associated species V. parvula and S. oralis were correlated with overall survival. Our study highlights the roles of the oral-associated microbiota in the upper third of the GC. In addition, oral-associated species may serve as noninvasive screening tools for the management of GC and an independent prognostic factor for H. pylori -negative GCs. IMPORTANCE Our study highlights the roles of the oral-associated microbiota in the upper third of gastric cancer (GC).We showed that the oral-associated species Veillonella parvula and Streptococcus oralis were correlated with overall survival. In addition, oral-associated species may serve as noninvasive screening tools for the management of GC and an independent prognostic factor for Helicobacter pylori -negative GCs.

Autophagy is involved in human apical periodontitis (AP). However, it is not clear whether autophagy is protective or destructive in bone loss via the receptor activator of nuclear factor-κB ligand (RANKL)/RANK/osteoprotegerin (OPG) axis. This study aimed to investigate the involvement of autophagy via the RANKL/RANK/OPG axis during the development of AP in an experimental rat model. Twenty-four female Sprague–Dawley rats were divided into control, experimental AP (EAP) + saline, and EAP + 3-methyladenine (An autophagy inhibitor, 3-MA) groups. The control group did not receive any treatment. The EAP + saline group and the EAP + 3-MA group received intraperitoneal injections of saline and 3-MA, respectively, starting 1 week after the pulp was exposed. Specimens were collected for microcomputed tomography (micro-CT) scanning, histological processing, and immunostaining to examine the expression of light chain 3 beta (LC3B), RANK, RANKL, and OPG. Data were analysed using one-way analysis of variance ( p  < .05). Micro-CT showed greater bone loss in the EAP + 3-MA group than in the EAP + saline group, indicated by an elevated trabecular space (Tb.Sp) ( p  < .05). Inflammatory cell infiltration was observed in the EAP + saline and EAP + 3-MA groups. Compared with EAP + saline group, the EAP + 3-MA group showed weaker expression of LC3B ( p  < .01) and OPG ( p  < .05), more intense expression of RANK ( p  < .01) and RANKL ( p  < .01), and a higher RANKL/OPG ratio ( p  < .05). Autophagy may exert a protective effect against AP by regulating the RANKL/RANK/OPG axis, thereby inhibiting excessive bone loss.

Dental caries, associated with plaque biofilm, is highly prevalent and significantly burdens public health. Streptococcus mutans is the main cariogenic bacteria that adheres to the tooth surface and forms an abundant extracellular polysaccharide matrix (EPS) as a cariogenic biofilm scaffold. S. mutans RNase III-encoding gene (rnc) and a putative chromosome segregation protein-encoding gene (smc) are potentially associated with EPS production. In addition, complex interactions between S. mutans and other oral microorganisms synergistically or antagonistically affect the cariogenicity. Commensal streptococci suppress the growth of cariogenic pathogens, whereas Candida albicans mediates the formation of cariogenic biofilm through aggregation and dual-species biofilm formation with S. mutans. However, label-free detection of cariogenic microbial interactions with the EPS matrix is still challenging during laboratory investigations. Herein, we hypothesized that the S. mutans rnc-smc operon affects EPS production and aimed to observe streptococci, S. mutans, and S. mutans-C. albicans using terahertz scanning near-field optical microscopy (THz s-SNOM). The light in the 0.1- to 0.3-THz frequency range interacted with the sample through a nano-probe tip by a point-by-point scanning process. Additional noise reduction of the original image was achieved by a dual kernel Gaussian filter. The monospecies of streptococci, S. mutans smc/rnc mutants, and the dual-species of S. mutans-C. albicans were scanned by THz s-SNOM. This technique provided terahertz near-field scanning images of S. mutans smc/rnc mutants, streptococci, and dual-species of S. mutans-C. albicans. Additional analysis of the original images potentially revealed the structures of the strains, such as cell diameters and cell wall thickness. In conclusion, the results suggested that the S. mutans rnc-smc operon regulates EPS production. Furthermore, this novel label-free detection of a THz near-field scanning technique had the potential to observe the morphologies of bacterial cells and EPS matrix.

OBJECTIVEThe purpose of the systematic review is to verify the presence of PANoptosis in periodontitis based on the published literatures studying cell death in periodontitis.MATERIALS AND METHODSWe conducted a comprehensive review of literature studying the types of cell death in vitro cellular experiments, in vivo rodent studies and clinical studies from three major databases: PubMed, Scopus, and Web of Science. The present systematic review was recorded in the PROSPERO database, under registration number CRD42022383456.RESULTSIn total, 51 articles were included in this study. Our analysis of in vitro cell models revealed that pyroptosis, necroptosis, and apoptosis could be induced by periodontal pathogens in macrophages, fibroblasts, stem cells, and periodontal ligament cells. Furthermore, three types of cell death were detected in in vivo rodent periodontitis models. Clinical studies on human periodontitis tissue specimens and gingival crevicular fluid (GCF) showed that some key proteins related to pyroptosis, necroptosis, and apoptosis were elevated in periodontitis.CONCLUSIONSVarious studies have established similar in vivo and in vitro models with three modes of death detected under the same conditions, revealing complex interactions between different types of cell death pathways in periodontitis and the potential for PANoptosis to occur in periodontitis.

Objective: A practical visual detection method was established to detect Porphyromonas gingivalis (P. gingivalis) by employing a combination of recombinase polymerase amplification and lateral flow strips (RPA-LF) assay, designed for conducting point-of-care testing in clinical settings.Methods: Primers and probes targeting the P. gingivalis pepO gene were designed. The RPA-LF assay was established by optimising reaction temperature and time, determining the limit of detection (LOD). The specificity of the method was determined by assessing its cross-reactivity with deoxyribonucleic acid from 23 pathogenic bacteria. Finally, the clinical samples from healthy controls (n = 30) and individuals with periodontitis (n = 31) were analysed. The results were compared with those obtained using real-time polymerase chain reaction (PCR).Results: The optimal reaction temperature and time were 39 degrees C and 12 min. The method exhibited a LOD at 6.40 x 10-4 mu g/mL and demonstrated high specificity and sensitivity during cross-reactivity assessment. The RPA-LF assay achieved a P. gingivalis detection rate of 84 % in individuals with periodontitis and 3 % in healthy controls. The results were consistent with those obtained through real-time PCR.Conclusion: An RPA-LF assay was developed for detecting P. gingivalis, characterised by its high sensitivity, high specificity, simple operational procedure, and rapid reaction time.

BACKGROUND:Treating the coronal dens invaginatus (CDI) with pulp infection commonly involves the removal of invagination, which increases the risk of perforation and fracture, and compromises the tooth structure. Minimally invasive endodontic management of CDI is highly recommended. This report describes two cases of type II CDI with the application of personalized templates.CASE PRESENTATION:Two cases of type II CDI, affecting the main root canal in a maxillary canine and a lateral incisor, were diagnosed. A guided endodontics (GE) approach was applied. Cone-beam computed tomography and intraoral scans were imported and aligned in a virtual planning software to design debridement routes and templates. The MICRO principle (which involves the aspects of Mechanical (M) debridement, Irrigation (I), Access cavities (C), Rectilinear routes (R), and Obstruction (O)) was proposed for designing optimal debridement routes for future applications. The templates were innovatively personalized and designed to preserve the tooth structure maximally while effectively debriding the root canal. Root canal treatment with supplementary disinfection was then performed. The follow-up of the two patients revealed favorable clinical and radiographic outcomes.CONCLUSIONS:The GE approach could be a feasible method for preserving healthy dental structure while effectively debriding the root canal, thereby achieving successful and minimally invasive endodontic treatment for CDI.

ABSTRACT Gastric precancerous lesions are thought to be precursors in the occurrence and development of gastric cancer through Correa's cascade. Recent studies have investigated the association between the oral microbiome and gastric precancerous lesions. However, there has yet to be a comprehensive synthesis review of the existing literature on the relationship between oral microbiome and gastric precancerous lesions. A systematic review was conducted to characterize the literature on the association between oral microbiome and gastric precancerous lesions. The studies show that oral microbiome is dynamic in individuals with gastric precancerous lesions. Oral-derived microorganisms were colonized in the gastric precancerous lesions. Interactions between oral and gastric microbiomes affect the response of the host immunity. The abnormal proliferation of oral-associated microorganisms may be linked to the reduction of gastric acid. The present review supports the potential association between oral microbiome and gastric precancerous lesions. However, the interactions are complex and multifaceted, which require further investigation.