Search Results (2,757)

During pregnancy, hormonal, metabolic, and immunological changes influence the composition and function of maternal microbial communities. Increasing evidence suggests that the maternal microbiota—particularly in the vaginal, gut, and oral environments—plays a significant role in maintaining pregnancy homeostasis and supporting fetal development. In healthy pregnancies, the vaginal microbiota is typically dominated by Lactobacillus species, which help maintain a low vaginal pH and protect against ascending infections. However, disruption of this balance (vaginal dysbiosis) has been associated with obstetrical complications such as intrauterine infection and preterm birth. Similarly, the maternal gut microbiota undergoes trimester-specific changes that contribute to metabolic adaptations required for fetal growth, while alterations in microbial composition have been linked to metabolic disorders including gestational diabetes mellitus and preeclampsia. Changes in oral microbiota and periodontal disease have also been associated with adverse pregnancy outcomes through systemic inflammatory pathways and potential microbial translocation to the placenta. Recent advances in sequencing technologies have improved the understanding of host–microbiome interactions in pregnancy, although the existence of a placental microbiome remains controversial. Overall, maternal microbiota plays an important role in pregnancy physiology, and its dysregulation may contribute to obstetrical complications. Understanding these mechanisms may facilitate the development of microbiome-based diagnostic and therapeutic strategies in maternal–fetal medicine. Full article

Chronic periapical periodontitis is a persistent inflammatory disease characterized by progressive bone destruction around the tooth apex. Manual radiographic detection of these lesions is subjective and time-consuming, highlighting the need for automated diagnostic tools. This paper presents a unified deep learning framework for joint tooth segmentation and periapical lesion detection in panoramic radiographs. Our approach employs a joint process: first, a deep learning model identifies and segments individual teeth according to standard dental numbering systems, while a second one detects periapical lesions within the tooth regions obtained from the segmentation outputs in the first stage. The framework incorporates an advanced loss function (Powerful IoU v2) to improve bounding-box regression accuracy and a spatial association mechanism to map detected lesions to specific teeth based on geometric overlap analysis. Our proposed tooth segmentation model achieves an mAP@50 of 97.7% and a mean Dice coefficient of 93.5%, while the periapical lesion detector reaches an mAP@50 of 91.9%. Furthermore, our region-of-interest approach yields a 3.49× computational speedup, averaging 0.1589 s per radiograph when compared to full-image processing. Trained exclusively on open-source datasets, this reproducible framework achieves explicit tooth-to-lesion mapping, providing an efficient and practical tool for periapical lesion screening. Full article

Dental calculus is a highly prevalent oral condition in dogs and is widely recognized as an important risk factor for gingival inflammation and periodontal disease. Effective strategies for its prevention and treatment remain limited, highlighting the significance of exploring novel mechanisms underlying its formation. Neutrophil extracellular traps (NETs), a key component of innate immunity, have been found in various diseases. To investigate the relationship between NETs and canine dental calculus formation, NET-associated markers were assessed in the oral cavities of dogs with dental calculus and healthy controls. Based on previously published full-length 16S rRNA amplicon sequencing data of canine dental calculus, Porphyromonas gulae was selected as a candidate NET-inducing bacterium for subsequent validation experiments. Subsequent neutrophil stimulation experiments were conducted to explore the effects of NETs and related factors on dental calculus formation. Collectively, our findings demonstrate the presence of NETs within canine dental calculus and reveal that P. gulae present in canine dental calculus is capable of inducing NET formation. The level of myeloperoxidase–DNA complex in gingival crevicular fluid was significantly elevated in dogs with dental calculus. NETs promoted aggregation and microcrystal formation from calcium and phosphate ions under both physiological and supersaturated concentrations. By adhering to the surface of dental calculus, NETs facilitated calculus accumulation. This effect showed positive correlation with neutrophil counts and administration frequency, but was independent of the concentration of administered calcium and phosphate solutions. IL-1β promoted the formation of aggregated NETs but did not enhance calculus accumulation. DNase I inhibited this process by degrading NET-DNA. In conclusion, dental calculus and the calculus-inhabiting P. gulae could stimulate oral neutrophils to release NETs, which participate in and facilitate the initial formation, aggregation, and subsequent accumulation of canine dental calculus. Full article

Dental diseases have long been taught and treated as separate entities: cariology, operative dentistry, endodontics, and periodontology, each working within its own boundaries. However, increasing biological and clinical evidence suggests that this classified view does not fully reflect how disease progresses in the mouth. Instead, dental disease should be understood as a continuum within the interconnected tooth–pulp–periodontium complex. This review provides current evidence showing how dental caries can serve as the starting point of a process that can progress through pulpitis and apical periodontitis and eventually affect surrounding periodontal tissues. Caries is now widely known as a biofilm-driven and host-influenced condition shaped by ecological imbalance rather than specific pathogens alone. As lesions penetrate deeper into dentin, the structure becomes more permeable, permitting diffusion of microbial metabolites and signaling molecules toward the pulp. This initiates a multifaceted inflammatory reaction within the pulp tissue. At this stage, pulpitis becomes a critical turning point, where the outcome depends on microbial load, lesion activity, host response, and quality of clinical intervention. If the disease is not well controlled, it may lead to pulp necrosis, allowing infection to spread beyond the root canal and initiate periapical inflammation. Through anatomical pathways such as apical foramina and lateral canals, these processes can extend further, sometimes resembling or overlapping with periodontal disease. This overlap creates diagnostic challenges, as conventional tests may not always distinguish between conditions. A structured, pathway-based diagnostic approach is therefore essential. From a treatment perspective, this continuum model highlights early intervention, minimally invasive care, preservation of pulp vitality when possible, and maintenance of a strong coronal seal. Ultimately, stronger integration across dental disciplines can improve diagnosis, guide treatment decisions, support long-term tooth preservation, and promote unified dental education. This article presents a narrative review supported by a structured literature search and proposes a clinically actionable framework that extends established endodontic–periodontal concepts upstream to include caries initiation and restorative modulation. Full article

Background: The upper gastrointestinal (GI) tract is a complex environment characterized by sharp physicochemical gradients. While the oral microbiome is a major source of microbial seeding for downstream organs, it remains unclear how these communities correlate and diverge across different anatomical sites. This study provides a high-resolution re-analysis of a comprehensive multi-site dataset to delineate the microbial architecture and ecological signatures along the oral–upper GI axis. Method: Human oral, esophageal, gastric mucosal, and gastric juice microbiome sequencing data were retrieved from the publicly available National Center for Biotechnology Information (NCBI) BioProject PRJNA1049979 database. Using these publicly available 16S rRNA sequencing data, we performed an integrated ecological analysis. Microbial diversity, taxonomic composition, and niche-specific community structures were evaluated using Quantitative Insights Into Microbial Ecology 2 (QIIME2) and R-based tools, including linear discriminant analysis effect size (LEfSe) and phylogenetic mapping. Results: The esophageal microbiome showed significantly greater richness and evenness than the oral cavity and stomach. Beta diversity analysis demonstrated clear compositional separation between oral and downstream upper GI communities, whereas gastric samples, particularly gastric juice, showed greater heterogeneity. Although major phyla were shared across sites, their relative abundances differed markedly. Oral samples were enriched with periodontal-associated taxa, including Porphyromonas, Prevotella, Alloprevotella, and Fusobacterium. In contrast, gastric mucosal samples were enriched with Akkermansia muciniphila and Helicobacter pylori, whereas gastric juice was characterized by Sarcina ventriculi, Fusobacterium periodonticum, and Clostridium perfringens. These findings indicate both taxonomic continuity and pronounced site-specific ecological divergence along the oral–upper GI axis. Conclusion: The oral cavity, esophagus, stomach, and gastric juice share a common microbial framework but exhibit distinct community restructuring driven by local environmental selection. This study provides a detailed ecological view of the oral–upper GI microbiome and highlights the importance of site-specific microbial organization in upper GI health and disease. Full article

The 2018 classification of periodontal and peri-implant diseases introduced a multidimensional diagnostic framework integrating staging, grading, and disease extent, representing a major advance over earlier severity-based systems. By incorporating structural destruction, treatment complexity, spatial distribution, and estimated risk of progression, the classification aimed to support more individualized and biologically informed diagnosis. However, increasing clinical application has revealed interpretive challenges, particularly in cases where different components of the system appear discordant. This perspective examines these challenges through a conceptual and clinical lens, focusing on the distinction between focal severity and overall disease burden in staging, the biological meaning of disease distribution, the interpretation of tooth loss as a historical rather than current indicator of disease status, and the need to differentiate between observed progression and risk-based modifiers in grading. Rather than reflecting deficiencies of the classification itself, these discordances are understood as a consequence of applying categorical systems to a biologically heterogeneous and temporally dynamic disease. A biologically grounded interpretive hierarchy is proposed, prioritizing observed tissue behavior and realized tissue destruction over probabilistic risk indicators while integrating structural parameters, historical outcomes, and susceptibility modifiers within their appropriate conceptual roles. This approach enhances diagnostic coherence and supports a more phenotype-oriented interpretation of periodontal disease. Full article

Periodontal disease is driven by a dysbiotic subgingival microbiota enriched in anaerobic pathogens, and novel antimicrobial strategies are needed to complement conventional therapy. This pilot study assessed changes in the subgingival microbiota following diode laser-activated indocyanine green-based treatment (EmunDo) using 16S rDNA amplicon sequencing of paired samples collected before and after therapy. Microbiome analysis revealed compositional shifts across all taxonomic levels, with reductions in disease-associated genera including Porphyromonas, Treponema, Fretibacterium, and Prevotella, and relative increases in taxa more commonly associated with periodontal health, such as Streptococcus, Actinomyces, and Haemophilus. Functional prediction further suggested treatment-associated variation in metabolic categories. Overall microbial richness was preserved between groups. These findings suggest that EmunDo treatment was associated with a restructuring of the subgingival microbiota toward a less dysbiotic profile, warranting further investigation in larger controlled studies using higher-resolution approaches such as shotgun metagenomics. Full article

Periodontal disease remains one of the leading causes of tooth loss worldwide, highlighting the need for effective regeneration of alveolar bone, periodontal ligament, and cementum. The structural complexity and unique biological behavior of these tissues have historically posed significant challenges for clinical regeneration strategies. The primary therapeutic approach used is guided bone regeneration; however, it has certain limitations, such as morbidity, low structural integrity and dimensional stability. Recent advances in 3-dimensional (3D) bioprinting have made it possible to fabricate customized scaffolds with precise architecture and spatial organization that closely mimic normal periodontal structures. The incorporation of multifunctional nanocomposite biomaterials and nanoparticles further enhances the performance of the scaffolds by increasing mechanical strength, bioactivity and controlling degradation rates. These advanced scaffolds function as dynamic microenvironments that support cell adhesion, proliferation and differentiation, ultimately promoting tissue regeneration. Furthermore, their multifunctional properties allow for the controlled release of growth factors, anti-inflammatory and antimicrobial agents, as well as the incorporation of stem cells and bioactive molecules that facilitate angiogenesis. This review investigates and critically evaluates modern approaches for the regeneration of periodontal tissues through scaffolds, biomaterials and 3D bioprinting technologies, as well as to assess their effectiveness compared to established clinical practices. Full article

Background: The association between oral health and gastrointestinal (GI) cancers has been primarily investigated within a periodontitis-centered framework. However, the potential contribution of cumulative oral disease burden, including dental caries and apical pathology, remains insufficiently explored. The Decayed, Missing, and Filled Teeth (DMFT) index reflects lifetime exposure to oral microbial dysbiosis and chronic inflammation. Methods: This retrospective exploratory study included patients with GI cancers referred for perioperative oral screening and management at a tertiary care center between 2015 and 2025. Oral health was evaluated using the DMFT index, periodontal probing depth, and radiographically diagnosed apical periodontitis. Age-stratified DMFT and periodontal parameters were compared with national reference data, while apical periodontitis prevalence was descriptively assessed. Results: Patients with GI cancers demonstrated higher DMFT values than national averages across most adult age groups. The prevalence of periodontal pockets (≥4 mm and ≥6 mm) was also elevated. Apical periodontitis was common, affecting 46.3% of patients, with some age groups exceeding 50%. Overall, these findings indicate oral disease clustering with coexisting chronic oral conditions. Conclusions: Patients with GI cancers exhibit substantial oral disease burden, including increased caries experience, periodontal pathology, and apical lesions. These findings suggest that the oral–gastrointestinal cancer relationship may extend beyond a periodontitis-centered paradigm, and that cumulative oral disease burden—including cariogenic processes—may represent an underrecognized component of this axis. The DMFT index may serve as a surrogate marker of lifelong oral inflammatory exposure. While causal relationships cannot be established, this study provides a basis for future mechanistic and longitudinal investigations. Full article

Salivary aldehyde dehydrogenases (ALDHs), particularly ALDH3A1, are increasingly recognized as potential contributors to oral defense against aldehyde-associated stress at the oral–environment interface. Unlike freely secreted salivary enzymes, measurable salivary ALDH activity primarily reflects intracellular and vesicle-associated enzymes derived from salivary gland epithelial cells, oral mucosal cells, immune cells, and exfoliated cellular components. Within the oral exposome, ALDHs expressed in oral epithelial and salivary gland tissues participate in the detoxification of reactive aldehydes, while salivary ALDH activity may serve as an indicator of local aldehyde-detoxification capacity and tissue redox status. Beyond aldehyde metabolism, emerging evidence suggests that ALDH-associated pathways are linked to redox regulation, epithelial stress adaptation, inflammatory signaling, and tissue repair through NAD(P)⁺-dependent processes and stress-responsive networks such as Nrf2 and SIRT1. This review provides a saliva-focused synthesis of ALDH biology, emphasizing isoform-specific functions and the potential importance of ALDH3A1 in oral epithelial defense. Altered salivary ALDH activity has been reported in association with oral conditions including periodontitis, oral lichen planus, radiation-induced salivary dysfunction, and oral squamous cell carcinoma (OSCC). Genetic factors, particularly ALDH2 polymorphisms, together with environmental exposures and microbial dysbiosis, may further influence aldehyde burden and oral disease susceptibility. Although current evidence supports the biological relevance of salivary ALDHs, their utility as clinical biomarkers or therapeutic targets remains investigational and requires further mechanistic and clinical validation. Full article

Background and Objectives: This study aims to evaluate the recent literature on the oral–gut connection in the context of periodontal disease, emphasizing the significance of systemic risk associated with chronic inflammation. This review explores whether chronic inflammation resulting from periodontal disease can induce systemic conditions through alterations in the gut microbiome and whether periodontal treatment may contribute to overall health improvement. Materials and Methods: A systematic database search was performed using pre-established search strategies. Searches were conducted in three databases between 1 and 20 October 2025. A total of 578 articles were screened for eligibility based on inclusion and exclusion criteria. Two authors agreed on the selection process used. The methodological quality of the included studies was assessed using the Newcastle–Ottawa scale and the Risk of Bias 2 Tool. Results: Eleven studies were considered eligible for inclusion in the review. The gut microbiome is similar to the oral microbiome in patients with periodontitis. Gut microbial shifts may drive systemic inflammation and metabolic dysfunction. Tooth loss and gum disease are linked to alterations in the gut bacteria, potentially compromising the intestinal barrier permeability. In contrast, the presence of natural teeth may prevent oral–gut bacterial transmission. Changes in the gut microbiota are correlated with improvements in periodontal status after non-surgical periodontal therapy. Conclusions: The evidence presented in this review supports an association between periodontitis, oral–gut microbial alterations, and systemic inflammatory conditions. However, most available studies are observational, limiting causal inference. Targeted modulation of the gut microbiome may represent a promising area for future research, but its clinical applicability remains inconclusive. Full article

Bone loss in the maxillofacial region arises from multiple causes, including periodontal disease, trauma, surgical procedures, infection, congenital anomalies, and cancer. Traditional treatment relies on bone grafting, either alone or in combination with biomaterials. Advances in tissue engineering have introduced synthetic or natural scaffolds to mimic the mineralized bone matrix. Natural scaffolds offer excellent biocompatibility and similarity to native tissue but often lack sufficient mechanical strength and exhibit poor degradation rates. Synthetic scaffolds provide tunable porosity and mechanical stability; however, their biological inertness makes them poor sources of osteogenic signaling. A key factor in the success of any scaffold is its interaction with the host immune system. Upon implantation, the innate immune response is initiated, with neutrophils and macrophages being the first cells to contact the scaffold. Macrophage polarization toward proinflammatory (M1) or anti-inflammatory (M2) phenotypes determines whether the microenvironment favors inflammation or remodeling. The adaptive immune response also plays a critical role: T and B lymphocytes may promote tolerance and integration through Th2/Treg pathways and antibody-mediated regulation, or they may trigger chronic inflammation and rejection through Th1/Th17 activation. This review examines the natural and synthetic materials used for bone remodeling and their biological properties. It then outlines the sequence of immune events occurring from the moment a scaffold is implanted to its potential integration or failure. Finally, this study highlights the relevance of cellular models and in vitro assays for the early evaluation of immunogenicity and biocompatibility, which are essential for optimizing scaffold design and improving outcomes in maxillofacial bone regeneration. Full article

Background/Objectives: Although gingivitis is the most common oral disease in children, periodontitis accompanied by alveolar bone resorption may develop in patients with severe congenital neutropenia. However, no reports to date have focused on changes in the alveolar bone of these patients during long-term follow-up. Case Summary: A girl aged 8 years and 5 months who developed leukemia due to severe neutropenia was admitted to the hospital and referred to the pediatric dentistry department for oral care. Panoramic radiographs at the first visit revealed significant alveolar bone resorption and mobility in the remaining deciduous teeth. We provided oral care, and the patient later underwent a hematopoietic stem cell transplant. No oral mucositis was observed. Measurement of alveolar bone thickness in the anterior and posterior regions revealed that the ratio increased as the patient’s systemic condition improved, showing a relative increase in alveolar bone thickness in the posterior region. Conclusions: Although this report is descriptive and observational, the patient’s alveolar bone loss with severe congenital neutropenia improved as the patient’s systemic condition improved. In addition, improvement of alveolar bone loss was observed along with systemic recovery and tooth eruption. Full article

Hydrogel scaffolds have emerged as instructive microenvironments for craniofacial tissue regeneration, moving beyond passive cell carriers toward platforms that regulate cell fate, vascularization, immune remodeling, and tissue-specific architecture. This review synthesizes hydrogel-associated strategies across dental pulp, periodontal ligament, gingival, bone marrow, jawbone, endothelial, oral mucosal, induced pluripotent stem cell (iPSC), extracellular vesicle (EV), exosome, secretome, and acellular systems. The evidence indicates that craniofacial hydrogel performance is governed by reciprocal interactions among biological source, scaffold composition, matrix mechanics, spatial architecture, mineral or ionic signaling, growth factor delivery, vesicle-mediated communication, and inflammatory niche modulation. Mineralized and ion-releasing hydrogels most consistently supported osteogenesis and bone repair, whereas extracellular matrix (ECM)-mimetic, peptide, collagen, fibrin, gelatin methacryloyl (GelMA), alginate, hyaluronic acid (HA), and chitosan-based systems enabled pulp–dentin, periodontal, peri-implant, oral mucosal, and soft-tissue reconstruction. Responsive, antimicrobial, antioxidant, conductive, and immunomodulatory hydrogels further expanded the field by targeting diseased microenvironments rather than regeneration alone. Despite strong preclinical evidence, translation remains limited by heterogeneity in scaffold formulations, biological sources, analytical endpoints, defect models, and long-term functional validation. Future progress will require standardized characterization, tissue-specific design criteria, clinically relevant large-animal models, scalable cell-free technologies, and integrated assessment of regeneration, immunity, vascularization, innervation, mechanics, and safety. Full article

Background/Objectives: Systemic diseases such as diabetes mellitus and hepatitis C virus infection are increasingly recognized as important modifiers of oral health. However, their combined impact, as well as the role of behavioral confounders such as smoking, remains insufficiently explored. This study aimed to evaluate oral health parameters in patients with diabetes and/or hepatitis C virus infection, to investigate the prevalence of oral mucosal conditions, and to identify independent predictors of xerostomia, with particular emphasis on glycemic control and smoking. Methods: A cross-sectional study was conducted on 66 patients, including 33 systemically affected individuals and 33 healthy controls. Clinical parameters included the number of teeth, tooth mobility, bleeding on brushing, xerostomia, and oral lichen planus. Glycemic control was defined by using glycated hemoglobin thresholds (controlled < 7%, uncontrolled ≥ 7%). Statistical analyses included non-parametric tests, Spearman correlation, and multivariate logistic regression. Results: Patients with diabetes exhibited significantly fewer teeth (p = 0.001), increased tooth mobility (p = 0.001), and a higher prevalence of gingival bleeding (p = 0.042). Hepatitis C virus infection was strongly associated with oral lichen planus (p = 0.009). Xerostomia was more prevalent in hepatitis C virus infection patients, but in multivariate analysis, smoking emerged as the only independent predictor (OR = 5.73; p = 0.014). Glycemic control was not independently associated with xerostomia after adjustment. Conclusions: Diabetes primarily influences periodontal destruction, while hepatitis C virus infection is associated with mucosal pathology. Smoking plays a dominant role in xerostomia and may confound associations attributed to systemic disease. These findings highlight the importance of integrated oral-systemic assessment and behavioral risk management. Full article