Pathogenesis Of Periodontitis Research Articles

Role of CD86 on granulocyte in mediating the effect of Genus Roseburia on periodontitis.

This study aimed to explore the causal link between the gut microbiota and periodontitis, and to delineate and quantify the intermediary role of immune cells, so as to provide new insights into the pathogenesis, prevention and treatment of periodontitis. We employed a two-sample Mendelian randomization (MR) approach to analyze the genetic predictors of gut microbiota composition (covering 412 gut microbiota taxa and functions) and periodontitis (involving 4,784 cases and 272,252 controls) derived from genome-wide association study (GWAS) datasets. A subsequent two-step MR analysis was conducted to evaluate the extent to which immune cell traits (encompassing 731 immune cell characteristics) mediate the influence of gut microbiota on periodontitis risk. Our analysis implicated nine gut microbiota taxa as causal factors in periodontitis susceptibility (p < 0.05). Notably, the Genus Roseburia was identified as exerting a protective effect against periodontitis, partially mediated through the upregulation of CD86 expression on granulocytes, with an 8.15% mediation effect observed. Our findings establish a causal relationship between the gut microbiota and periodontitis, highlighting the protective role of Roseburia against this condition. A notable proportion of this protective effect is mediated via the upregulation of CD86 on granulocytes. It can provide new ideas for the pathogenesis, prevention and treatment for periodontitis through exploring the causal link between the gut microbiota and periodontitis, and describing and quantifying the intermediary role of immune cells.

Pathogenic Mechanisms That May Link Periodontal Disease and Type 2 Diabetes Mellitus-The Role of Oxidative Stress.

Given the posited role of oxidative stress in the pathogenesis of both periodontitis and type 2 diabetes mellitus (T2DM), it may also serve as a link between these highly prevalent chronic inflammatory diseases. This view is supported by an ample body of evidence indicating that the severity and progression of periodontitis is in part driven by diabetes, while periodontal infection may hinder the attainment of adequate glycemic control in diabetic patients. Thus, this review focuses on the potential synergistic interactions along the oxidative stress-inflammation pathway characterizing both conditions. Because periodontitis and T2DM share the same risk factors and compromise patients' quality of life, to develop effective strategies for combatting both conditions, their mutual influence needs to be explored.

Role of CRISPR-Cas systems in periodontal disease pathogenesis and potential for periodontal therapy: A review.

Clustered regularly interspaced short palindromic repeats (CRISPRs) are DNA sequences capable of editing a host genome sequence. CRISPR and its specific CRISPR-associated (Cas) protein complexes have been adapted for various applications. These include activating or inhibiting specific genetic sequences or acting as molecular scissors to cut and modify the host DNA precisely. CRISPR-Cas systems are also naturally present in many oral bacteria, where they aid in nutrition, biofilm formation, inter- and intraspecies communication (quorum sensing), horizontal gene transfer, virulence, inflammation modulation, coinfection, and immune response evasion. It even functions as an adaptive immune system, defending microbes against invading viruses and foreign genetic elements from other bacteria by targeting and degrading their DNA. Recently, CRISPR-Cas systems have been tested as molecular editing tools to manipulate specific genes linked with periodontal disease (such as periodontitis) and as novel methods of delivering antimicrobial agents to overcome antimicrobial resistance. With the rapidly increasing role of CRISPR in treating inflammatory diseases, its application in periodontal disease is also becoming popular. Therefore, this review aims to discuss the different types of CRISPR-Cas in oral microbes and their role in periodontal disease pathogenesis and precision periodontal therapy.

Associations between exposure to brominated flame retardants and periodontitis in U.S. adults

BackgroundIncreasing evidence has shown that environmental factors play a crucial role in the pathogenesis of periodontitis. Humans are simultaneously exposed to a variety of environmental brominated flame retardants (BFRs). However, the relationship between BFRs in periodontitis remains unclear. This study aimed to investigate the overall association between BFRs and periodontitis in a nationally representative US population and to further identify important chemicals. MethodsData from 3322 NHANES participants from 2009 to 2016 were used. Serum BFRs were registered, including PBDE-28, PBDE-47, PBDE-85, PBDE-99, PBDE100, PBDE-153, PBDE-154, PBDE-183, PBDE-209 and PBB-153. Survey weighted generalized logistic regression models, restricted cubic splines (RCS) were conducted to assess single BFRs exposure with periodontitis. Meanwhile, weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR) were used to evaluate the overall association of BFRs mixtures with periodontitis and to identify significant chemicals. ResultsA total of 3322 participants were included in the study, of whom 1795 had periodontitis. After adjusting for potential confounders, multiple logistic regression analysis revealed significant positive associations between serum levels of PBDE-28, PBDE-47, PBDE-85, PBDE-99, PBDE-100, PBDE-154, PBDE-183, and PBB-153 and the risk of periodontitis (all P < 0.05). A dose-response relationship was observed for many of these BFRs, with higher quantiles associated with an increased risk of periodontitis. WQS regression identified PBDE-183 (38.60%), PBDE-153 (21.20%), PBDE-209 (14.40%), and PBDE-99 (11.90%) as the BFRs with the largest weights contributing to the overall mixture effect on periodontitis risk. BKMR analysis further supported the positive association between serum BFRs and periodontitis, with most individual BFRs showing a positive trend, except for PBDE-153. Restricted cubic spline analysis revealed a generally increasing probability of periodontitis with increasing concentrations of BFRs, albeit with some nonlinear patterns for certain compounds. ConclusionIn conclusion, this study provides compelling evidence of a significant association between exposure to brominated flame retardants (BFRs) and an increased risk of periodontitis in a nationally representative sample of U.S. adults. Elevated serum levels of several BFRs, including PBDE-28, PBDE-47, PBDE-85, PBDE-99, PBDE-100, PBDE-154, PBDE-183, and PBB-153, were found to be positively associated with periodontitis, exhibiting a dose-response relationship.

Association between the Composite Dietary Antioxidant Index and periodontitis in US adults: a cross-sectional analysis.

The pathogenesis of periodontitis may be related to host-mediated inflammatory and immune responses caused by accumulation of oral microbial plaque. Nutrients have anti-inflammatory and pro-inflammatory capabilities. Dietary intake of antioxidants and micronutrients is associated with the inflammatory burden of the diet. The Composite Dietary Antioxidant Index (CDAI) is a composite index for assessing the antioxidant properties of a diet and the relationship with periodontitis is unclear. The aim of this study was to investigate the relationship between periodontitis and CDAI. The study was a cross-sectional design and included 7471 participants from the National Health and Nutrition Examination Survey (NHANES) 2009-2014 database. Participants were divided into experimental and control groups according to the relevant criteria, where the control group consisted of participants with no/mild periodontitis (including 3646 participants) and the experimental group consisted of participants with moderate/severe periodontitis (including 3825 participants). First, baseline characteristics 22 of the two groups of participants were compared. Weighted logistic regression analyses was used to explore the relationship between periodontitis and CDAI. And the linear relationship between the two was assessed using restricted cubic spline. Finally, subgroup analyses was used to assess model stability. Differences between the two groups of participants were statistically significant in age, gender, race, education, ratio of household income to poverty(PIR), body mass index(BMI), smoking status, drinking status, and prevalence of diabetes. CDAI, as a continuous variable, was not found to be significantly associated with periodontitis. The CDAI was converted to categorical variables according to quartile. In model1, participants in the second and third quartile groups had a lower risk of developing periodontitis compared with participants in the lowest quartile group(OR(95%CI):0.81(0.681,0.963),P&#61;0.021;OR(95%CI):0.811(0.691,0. 951),P&#61;0.014;respectively). In model2, participants in the second, third, and fourth quartile groups had a lower risk of developing periodontitis compared to the lowest quartile group(OR(95%CI):0.803(0.66,0.978),P&#61;0.0349;OR(95%CI):0.753( 0.632, 0.897),P&#61;0.0028;OR(95%CI):0.753(0.617,0.92),P&#61;0.0083;respectively). There was a non-linear relationship between CDAI and periodontitis (p non-linearity &#61; 0.0055), with the inflection point occurring at a CDAI equal to 0.6342. There is a nonlinear relationship 44 between CDAI and periodontitis in US adults. However, further prospective studies are still needed to validate our results.

Identification of cross-talk pathways and PANoptosis-related genes in periodontitis and Alzheimer's disease by bioinformatics analysis and machine learning.

Periodontitis (PD), a chronic inflammatory disease, is a serious threat to oral health and is one of the risk factors for Alzheimer's disease (AD). A growing body of evidence suggests that the two diseases are closely related. However, current studies have not provided a comprehensive understanding of the common genes and common mechanisms between PD and AD. This study aimed to screen the crosstalk genes of PD and AD and the potential relationship between cross-talk and PANoptosis-related genes. The relationship between core genes and immune cells will be analyzed to provide new targets for clinical treatment. The PD and AD datasets were downloaded from the GEO database and differential expression analysis was performed to obtain DEGs. Overlapping DEGs had cross-talk genes linking PD and OP, and PANoptosis-related genes were obtained from a literature review. Pearson coefficients were used to compute cross-talk and PANoptosis-related gene correlations in the PD and AD datasets. Cross-talk genes were obtained from the intersection of PD and AD-related genes, protein-protein interaction(PPI) networks were constructed and cross-talk genes were identified using the STRING database. The intersection of cross-talk and PANoptosis-related genes was defined as cross-talk-PANoptosis genes. Core genes were screened using ROC analysis and XGBoost. PPI subnetwork, gene-biological process, and gene-pathway networks were constructed based on the core genes. In addition, immune infiltration on the PD and AD datasets was analyzed using the CIBERSORT algorithm. 366 cross-talk genes were overlapping between PD DEGs and AD DEGs. The intersection of cross-talk genes with 109 PANoptosis-related genes was defined as cross-talk-PANoptosis genes. ROC and XGBoost showed that MLKL, DCN, IL1B, and IL18 were more accurate than the other cross-talk-PANoptosis genes in predicting the disease, as well as better in overall characterization. GO and KEGG analyses showed that the four core genes were involved in immunity and inflammation in the organism. Immune infiltration analysis showed that B cells naive, Plasma cells, and T cells gamma delta were significantly differentially expressed in patients with PD and AD compared with the normal group. Finally, 10 drugs associated with core genes were retrieved from the DGIDB database. This study reveals the joint mechanism between PD and AD associated with PANoptosis. Analyzing the four core genes and immune cells may provide new therapeutic directions for the pathogenesis of PD combined with AD.

Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets.

Chronic inflammatory processes in the oral mucosa and periodontitis are common disorders caused by microflora and microbial biofilms. These factors activate both the innate and adaptive immune systems, leading to the production of pro-inflammatory cytokines. Cytokines are known to play a crucial role in the pathogenesis of gingivitis and periodontitis and have been proposed as biomarkers for diagnosis and follow-up of these diseases. They can activate immune and stromal cells, leading to local inflammation and tissue damage. This damage can include destruction of the periodontal ligaments, gingiva, and alveolar bone. Studies have reported increased local levels of pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta), tumor necrosis factor (TNF), IL-6, IL-17, and IL-23, in patients with periodontitis. In experimental models of periodontitis, TNF and the IL-23/IL-17 axis play a pivotal role in disease pathogenesis. Inactivation of these pro-inflammatory pathways through neutralizing antibodies, genetic engineering or IL-10 function has been demonstrated to reduce disease activity. This review discusses the role of cytokines in gingivitis and periodontitis, with particular emphasis on their role in mediating inflammation and tissue destruction. It also explores new therapeutic interventions that offer potential for research and clinical therapy in these chronic inflammatory diseases.

TFEB alleviates periodontitis by activating autophagy and inhibiting inflammation

Periodontitis is a chronic inflammatory oral disease that impaired the tooth-supporting apparatus, including gingival tissue destruction and alveolar bone resorption. The initiation of periodontitis is linked to the presence of oral bacteria, particularly P. gingivalis within pathogenic biofilms. Here, we demonstrated the central role of the autophagy regulator Transcription Factor EB (TFEB) in orchestrating autophagy activation and modulating the host immune response against P. gingivalis in periodontitis. Upregulation of TFEB expression at the protein level and heightened nuclear localization occurred during the progressive stages of periodontitis. Functionally, TFEB overexpression emerges as a potent alleviator of periodontitis-associated phenotypes, operating through the activation of autophagy and the inhibition of the NF-κB pathway in both in vivo and in vitro models. In addition, TFEB knockdown exacerbates the inflammatory response by upregulating pro-inflammatory cytokines. The dual regulatory role of TFEB in governing both autophagy and inflammatory responses unveils novel insights into periodontitis pathogenesis, positioning TFEB as a promising therapeutic target for periodontitis intervention.

Omentin-1 attenuates lipopolysaccharide-induced inflammation and osteogenic differentiation in periodontal ligament stem cells and reduces M1 macrophages polarization through repressing endoplasmic reticulum stress

Periodontitis is featured as the periodontium’s pathologic destruction caused by the host’s overwhelmed inflammation. Omentin-1 has been reported to be aberrantly downregulated in patients with periodontitis, but the specific regulation of Omentin-1 during the pathogenesis of periodontitis remains unclear. In this study, human periodontal ligament stem cells (hPDLSCs) were stimulated by lipopolysaccharide (LPS) from Porphyromonas gingivalis to establish an in vitro inflammatory periodontitis model. hPDLSCs were treated with recombinant human Omentin-1 (250, 500 and 750 ng/mL) for 3 h before LPS stimulation. Results revealed that Omentin-1 significantly inhibited LPS-induced inflammation in hPDLSCs through reducing the production of proinflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6) and downregulating the expression of Cox2 and iNOS. Meanwhile, Omentin-1 significantly enhanced alkaline phosphatase (ALP) activity and Alizarin red-stained area, accompanied by increasing expression osteogenic markers BMP2, OCN and Runx2, confirming that Omentin-1 restores osteogenic differentiation in LPS-induced hPDLSCs. In addition, the conditioned medium (CM) from LPS-induced hPDLSCs was harvested to culture macrophages, which resulted in macrophage polarization towards M1, while CM from Omentin-1-treated hPDLSCs reduced M1 macrophages polarization and elevated M2 polarization. Furthermore, Omentin-1 also inhibited LPS-triggered endoplasmic reticulum (ER) stress in hPDLSCs, and additional treatment of the ER stress activator tunicamycin (TM) partially reversed the functions of Omentin-1 on inflammation, osteogenic differentiation and macrophages polarization. In summary, Omentin-1 exerted a protective role against periodontitis through inhibiting inflammation and enhancing osteogenic differentiation of hPDLSCs, providing a novelty treatment option for periodontitis.

Identification and Validation of Aging- and Endoplasmic Reticulum Stress-Related Genes in Periodontitis Using a Competing Endogenous RNA Network.

Periodontitis is a multifactorial chronic inflammatory disease that destroy periodontium. Apart from microbial infection and host immune responses, emerging evidence shows aging and endoplasmic reticulum stress (ER stress) play a key role in periodontitis pathogenesis. The aim of this study is to identify aging-related genes (ARGs) and endoplasmic reticulum stress-related genes (ERGs) in periodontitis. Data were obtained from the Gene Expression Omnibus (GEO), Human Ageing Genomic Resources (HAGR) and GeneCards databases to identify differentially expressed mRNAs/miRNAs/lncRNAs (DEmRNAs/DEmiRNAs/DElncRNAs), ARGs and ERGs, respectively. We used the MultiMiR database for the reverse prediction of miRNAs and predicted miRNA-lncRNA interactions using the STARBase database. Afterwards, we constructed a mRNA-miRNA-lncRNA ceRNA network. A total of 10 hub genes, namely LCK, LYN, CXCL8, IL6, HCK, IL1B, BTK, CXCL12, GNAI1 and FCER1G, and 5 DEmRNAs-ARGs-ERGs were then discovered. Further, weighted gene co-expression network analysis (WGCNA) and single sample gene set enrichment analysis (ssGSEA) were performed to explore co-expression modules and immune infiltration respectively. Finally, we used transmission electron microscope (TEM), inverted fluorescence microscopy, quantitative real-time polymerase chain reaction (qRT-PCR) and Western Blot to verify the bioinformatic results in periodontal ligament stem cells (PDLSCs) infected with Porphyromonas gingivalis (P. gingivalis). The experimental results broadly confirmed the accuracy of bioinformatic analysis. The present study established an aging- and ER stress-related ceRNA network in periodontitis, contributing to a deeper understanding of the pathogenesis of periodontitis.

ETIOPATHOGENETIC ASPECTS OF SYNTROPY AND MUTUAL BURDEN IN THE PATHOLOGY OF THE GASTROINTESTINAL TRACT AND THE DISEASES OF THE ORAL CAVITY

The purpose of the work is to study the main etiopathogenetic mechanisms of development and peculiarities of the clinical course in the comorbidity of diseases of the oral cavity and pathology of the gastrointestinal tract by analyzing the results of scientific research published in modern scientific publications.Material and methods. Search, systematization, elaboration and analysis of scientific works of domestic and foreign authors, which present the modern results of research on etiopathogenesis and peculiarities of the clinical course in comorbidity of diseases of the oral cavity and gastrointestinal tract, with the involvement of search engines Google Scholar, PubMed and other electronic resources. The bibliosematic and analytical methods are used in the research.Results. The problem of syntropies, the basis of which is the association of etiological and pathogenetic factors of certain diseases, is an actual problem in modern medicine. The analysis of data from modern scientific literary sources proves that the development and progression of periodontal and oral mucosa diseases depends not only on the influence of local factors but also is a reaction to the influence of pathogenic factors that arise as a result of diseases of the gastrointestinal tract.Steady persistence of microflora in certain areas of the digestive tract can complicate the course of dental and gastrointestinal diseases. A gradual change in the properties of representatives of the conditionally pathogenic group of microorganisms, their association with specific diseases of the oral cavity and gastrointestinal tract indicates their role in the pathogenesis of many diseases. Mechanisms of free radical damage to cellular structures and changes in humoral and cellular immunity are important common links in the pathogenesis of periodontal and gastrointestinal tract diseases. The development of an imbalance of the endocrine system and psycho-emotional stress has a significant impact on the process of mutual burden of diseases of the gastrointestinal tract and oral cavity.Conclusion. Тoday considerable factual material has been accumulated regarding the understanding of common mechanisms of etiopathogenesis and syntropy of diseases of the oral cavity and pathology of the gastrointestinal tract. This knowledge makes it possible to develop effective comprehensive measures for the diagnosis, prevention and treatment of both diseases of the oral cavity and diseases of the gastrointestinal tract, taking into account the mutual burden of these pathologies.

Association between proton pump inhibitors use and the severity of periodontal disease and peri-implantitis: a systematic review.

This systematic review investigates the probable effect of proton pump inhibitor (PPI) use on the severity of periodontal disease and peri-implantitis and implant survival. We conducted a literature search in PubMed, Scopus, and Cochrane Central Library up to April 2024. Two review authors independently screened the title and abstracts and then the full texts of retrieved studies. Observational and clinical trial studies that assessed the association between PPIs use and periodontal disease severity and peri-implantitis or implant survival were included. Data extraction from the included studies was done by two reviews independently. Of 940 studies initially retrieved from online searching, 7 research met the inclusion criteria. Three studies examined periodontitis, while four focused on peri-implantitis and implant longevity. On the contrary, evidence regarding the impact of PPIs use on peri-implantits and implant survival is conflicting. Therefore, more well-designed RCTs are warranted to come to a definite conclusion. Since proton pump inhibitors alter the gut microbiome, and affect bone, plus the pathogenesis and etiology of periodontal disease are affected by bacteria within the periodontal pocket, it is hypothesized that they may affect periodontal pathogenesis.

The PerioGene North Study Uncovers Serum Proteins Related to Periodontitis

The sequalae of periodontitis include irreversible degradation of tooth-supporting structures and circulatory spread of inflammatory mediators. However, the serum protein profile in periodontitis is not well described, which is partly attributable to the limited number of studies based on large and well-characterized periodontitis cohorts. This study aims to identify novel, circulating inflammation-related proteins associated with periodontitis within the PerioGene North case-control study, which includes 478 cases with severe periodontitis and 509 periodontally healthy controls. The serum concentrations of high-sensitivity C-reactive protein (hs-CRP) and a panel of 45 inflammation-related proteins were analyzed using targeted proteomics. A distinguishable serum protein profile was evident in periodontitis cases. The protein pattern could separate cases from controls with a sensitivity of 0.81 and specificity of 0.81 (area under the curve = 0.87). Adjusted levels for hs-CRP and 24 of the 45 proteins were different between cases and controls. High levels of hs-CRP and matrix metalloproteinase–12, and low levels of epidermal growth factor (EGF) and oxidized low-density lipoprotein receptor 1 (OLR-1) were detected among the cases. Furthermore, the levels of C-C motif chemokine–19, granulocyte colony-stimulating factor–3 (CSF-3), interleukin-7 (IL-7), and hs-CRP were significantly higher in cases with a high degree of gingival inflammation. The levels of CSF-3 and tumor necrosis factor ligand superfamily member–10 TNFSF-10 were higher in cases with many deep periodontal pockets. The PerioGene North study includes detailed clinical periodontal data and uncovers a distinct serum protein profile in periodontitis. The findings of lower EGF and OLR-1 among the cases are highlighted, as this has not been presented before. The role of EGF and OLR-1 in periodontitis pathogenesis and as possible future biomarkers should be further explored.

Potential Roles of Long Non-coding RNAs in the Pathogenesis of Periodontitis: Inflammation Response, Immune Infiltration, Collagen Fibers Synthesis, and Bone Remodeling.

It is evident that long non-coding RNAs (lncRNAs) are implicated in the pathogenesis of periodontitis. However, the detailed functional mechanisms remain unknown. This study aimed to elucidate the pathogenic mechanisms of lncRNAs in periodontitis by investigating their regulation of protein-coding gene expression. Human Gingival Fibroblasts-1 (HGF-1) were stimulated with 5 μg/mL of Lipopolysaccharide (LPS) for 24 hours to construct the periodontitis cell model. qRTPCR and western blot analyses were carried out to determine mRNA and protein levels of genes induced by LPS or involved in the inflammatory response. Cytokine levels and inflammatory proteins were assayed using ELISA. Transcriptome sequencing and analysis were conducted to reveal the expression signatures of lncRNAs. DESeq2 (v1.4.5) was used to analyze differentially expressed genes. Gene function enrichment was carried out using Phyper. AnimalTFDB v3.0 was used to analyze transcription factors involved in the pathogenesis of periodontitis. Prot\ein domains and families of the target proteins were identified based on the Pfam protein family database. In LPS-treated HGF-1 cells, we detected the secretion of TNF-α and IL-1β, along with the production of MDA and ROS, indicating that LPS significantly triggered inflammatory responses and oxidative stress in HGF-1 cells. A total of 15,295 lncRNAs were detected in both the control (ConT) and LPS-treated groups. We selected 10 significantly differentially co-expressed lncRNA-coding genes (MIR222HG, SNHG15, SNHG12, URS00005F6AA3, URS00009C153E, URS0000D57D7F, URS00019A4688, URS00019AF240, URS00019C6526, and URS0001A00B79) as potential biomarkers for diagnosing the progression of periodontitis. An interaction network consisting of 2 lncRNA- encoding genes (MIR222HG and SNHG15) and protein-encoding genes (CBX5, NUPR1, CHAC1, and MAB21L3) may be involved in the pathogenesis of periodontitis. The ceRNA network analysis revealed the differentially expressed lncRNAs to be involved in inflammatory response, immune infiltration, collagen fiber synthesis, and bone remodeling in LPS-induced periodontitis. This study has identified pivotal molecules implicated in the pathogenesis of periodontitis, including those involved in inflammation regulation, collagen fiber synthesis, and bone remodeling. Our findings may contribute to explaining how lncRNAs participate in the pathological process of periodontitis.

Interlinked Pathways: Exploring the Bidirectional Impacts of Periodontitis and Metabolic Syndrome.

Metabolic syndrome (MBS) and periodontitis are distinct conditions with overlapping and unique risk factors. Periodontitis is a chronic destructive disease of the periodontium, driven by alterations in the host immune-inflammatory response to virulent periodontal pathogens. MBS is characterized by various abnormalities, including visceral abdominal obesity, dyslipidemia (low high-density lipoprotein (HDL) and high triglyceride (TG) levels), hypertension, and hyperglycemia. These factors collectively increase the risk of atherosclerotic cardiovascular disease (CVD) and diabetes. Several pro-inflammatory mediators are involved in the pathogenesis of periodontitis and MBS, and the deleterious bidirectional effects of these mediators exacerbate the severity and progression of both conditions. This comprehensive review focuses on the intricate relationship between MBS and periodontitis. Specifically, it explores the pathophysiological mechanisms of each disease component of MBS and its impact on periodontitis, and vice versa.

Periodontitis promotes hepatocellular carcinoma in Stelic Animal model (STAM) mice

Periodontitis is a prevalent oral inflammatory disease that leads to alveolar bone loss and may exert an adverse impact on systemic health. Periodontal disease may be associated with hepatocellular carcinoma (HCC); however, the mechanism of such an association is unknown. In this study, Stelic Animal model (STAM) mice, a model of nonalcoholic steatohepatitis (NASH)-HCC, were induced to develop periodontitis and subjected to histopathological and immunological analyses. HCC progression was greater in STAM mice with experimental periodontitis compared with that in STAM mice without experimental periodontitis. Tumor necrosis factor-α (TNFα), matrix metalloproteinase-9 (MMP9), collagen 1, and angiopoietin-like protein 2 (ANGPTL2) gene expression was significantly increased in the liver of the periodontitis group. ANGPTL2 was previously reported to be involved in the pathogenesis of periodontitis, and HCC and ANGPTL2 protein tended to be more abundant in the pocket epithelium of STAM mice with experimental periodontitis than in control STAM mice. ANGPTL2 levels in the serum of STAM mice with experimental periodontitis tended to be higher than in control STAM mice. Our results indicate that ANGPTL2 is produced in chronically inflamed periodontal tissue and then travels to the liver via the bloodstream where it accumulates to promote the progression of hepatocellular carcinoma.

Effect of toxins from different periodontitis-associated bacteria on human platelet function.

Periodontitis is caused by a dysbiosis of oral bacteria resulting in alveolar bone destruction and teeth loss. The role of platelets in pathogenesis of periodontitis is a subject of research. The release of toxins from periodontitis-associated bacteria may influence platelet function and contribute to the modulation of hemostatic or inflammatory responses. Therefore, we explored platelet function upon exposure to defined toxins: leukotoxin A from Aggregatibacter actinomycetemcomitans (LtxA), a synthetic version of the C14-Tri-LAN-Gly peptide from Fusobacterium nucleatum (C14), and lipopolysaccharides from Porphyromonas gingivalis (LPS). Light transmission aggregometry was performed after the addition of toxins to platelet-rich plasma in different doses. Flow cytometry was used to identify inhibitory effects of toxins by measuring phosphorylation of the vaso-dilator-stimulated phosphoprotein or to identify activating effects by the detection of CD62P expression. The release of chemokines derived from washed platelets was determined by immunoassays. Collagen-induced threshold aggregation values were diminished upon incubation with LtxA and C14, accompanied with an increase of vaso-dilator-stimulated phosphoprotein (VASP) phosphorylation, indicating platelet inhibition. In contrast, LPS did not affect aggregation but slightly enhanced CD62P expression under co-stimulation with low-dose thrombin pointing to slight platelet activation. The three toxins did not relevantly influence the secretion of chemokines. Although weak, the investigated toxins differently influenced human platelet function. LtxA and C14 mediated inhibitory effects, whereas LPS contributed to a slight activation of platelets. Further analysis of specific cellular responses mediated by bacterial toxins may render novel targets and suggestions for the treatment of periodontitis.

Periodontal Tissue Homoeostasis, Immunity, the Red Complex Pathogens, and Dysbiosis: Unraveling the microRNA Effect.

microRNAs are a family of small, non-coding RNA molecules that can regulate the translation of messenger RNAs (mRNAs). Numerous miRNAs have been proposed as potential indicators for periodontal disease, and their regulation might serve as a potent means of restricting the disease process. MiRNAs act as important immune system regulators that promote the production of many cytokines, including interferon (IFN), tumour necrosis factor (TNF), and IL-1as well as RANK. Investigations pertaining to the use of specific miRNAs as therapeutic agents are underway. They can influence a variety of regulatory organs and target several genes. Additionally, distinct components of the same expression pathway can be controlled by combining miRNAs and their antagonists. In recent years, many miRNA delivery methods have been created for therapeutic applications. Studies pertaining to the role of miRNAs in periodontal disease pathogenesis may pave the way for the use of miRNAs as biomarkers of periodontal disease. A complete understanding of the role of miRNA in periodontal disease and its mechanism of action can pave the way towards therapeutic strategies that can reduce or even prevent the progression of periodontal diseases.

Unravelling the intricacies of Porphyromonas gingivalis: virulence factors, lifecycle dynamics and phytochemical interventions for periodontal disease management.

Porphyromonas gingivalis is a gram-negative anaerobic bacterium recognized for its pivotal role in the pathogenesis of periodontal diseases. This review covers an overview of the virulence factors and lifecycle stages of P. gingivalis, with a specific focus on attachment and colonization, biofilm formation, growth and multiplication, dormancy survival and dissemination. Additionally, we explore the significance of inter-bacterial cross-feeding within biofilms. Furthermore, we discuss potential phytochemical-based strategies to target P. gingivalis, including the use of curcumin, apigenin, quercetin and resveratrol. Understanding the virulence factors and lifecycle stages of P. gingivalis, along with the promising phytochemical-based interventions, holds promise for advancing strategies in periodontal disease management and oral health promotion.

Is There a Relationship Between the Dietary Inflammatory Index and Clinical Attachment Loss in Patients with Periodontitis?

Objective The pathogenesis of periodontal diseases is partially driven by oxidative stress. However, studies on the relationship between periodontitis and the inflammatory load of diet are still insufficient. Therefore, this study aimed to examine the relationship between the diet’s inflammatory load and periodontitis and clinical attachment loss (CAL). Methods This cross-sectional study included 119 participants diagnosed with periodontitis according to the 1999 classification. The dietary inflammatory index (DII) was calculated using three-day food consumption records and divided into quartiles (Q1, Q2, and Q3). Body mass index (BMI) was calculated as weight and height (kg/m2). Clinical attachment loss (CAL) score was determined, and the patients were grouped with those CAL scores as 7 < CAL and ≥7 CAL. Results Of the 119 patients with periodontitis, aged 46.24 ± 12.84 years, 45.3% were found to have an anti-inflammatory diet profile (n = 54). When the daily energy and nutrient intake of individuals were examined, it was found that the intake of omega-3 fatty acids (p = 0.004), black tea (p = 0.021), and green pepper (p = 0.029) was higher in those with CAL < 7 compared to those with CAL ≥ 7. There was no relationship between the patients’ DII and CAL values. Daily energy, protein, fiber, vitamin A, vitamin E, folic acid, Fe, Zn, and Mg intake in patients with an anti-inflammatory diet in Q1 were higher than in Q2 and Q3 (p < 0.001). Conclusion This study found no relationship between DII levels and CAL scores. However, it was observed that periodontitis patients following an anti-inflammatory diet had higher intakes of omega-3 fatty acids, vitamins A, E, and C, as well as zinc and magnesium which are nutrients known to be effective against inflammation. These patients also had CAL scores below 7. Therefore, reducing the inflammatory load of the diet may prevent the development of periodontitis, and further research in this regard would be beneficial.