Probiotics, active microorganisms benefiting human health, currently serve as nutritional supplements and clinical treatments. Periodontitis, a chronic infectious oral disease caused by Porphyromonas gingivalis (P. gingivalis), activates the host immune response to release numerous proinflammatory cytokines. Here, we aimed to clarify Leuconostoc mesenterica (L. mesenteroides) LVBH107 probiotic effects based on the inhibition of P. gingivalis activities while also evaluating the effectiveness of an in vitro P. gingivalis lipopolysaccharide-stimulated RAW 264.7 cell-based inflammation mode. L. mesenteroides LVBH107 survived at acid, bile salts, lysozyme, and hydrogen peroxide conditions, auto-aggregated and co-aggregated with P. gingivalis, exhibited strong hydrophobicity and electrostatic action, and strongly adhered to gingival epithelial and HT-29 cells (thus exhibiting oral tissue adherence and colonization abilities). Moreover, L. mesenteroides LVBH107 exhibited sensitivity to antibiotics erythromycin, doxycycline, minocycline, ampicillin, and others (thus indicating it lacked antibiotic resistance plasmids), effectively inhibited P. gingivalis biofilm formation and inflammation (in vitro inflammation model), reduced the secretion of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and inflammatory mediators (NO and PGE₂), and decreased the expression levels of inflammation related genes. Thus, L. mesenterica LVBH107 holds promise as a probiotic that can inhibit P. gingivalis biofilm formation and exert anti-inflammatory activity to maintain oral health.

Toxicity assessment of Caenorhabditis elegans Cu-Ls Nz with laccase-like activity.

Introduction: Periodontitis and inflammatory bowel disease are chronic inflammatory diseases with shared epidemiological, biological, and therapeutic associations. Given the similarities in their pathogenic factors, this study hypothesized that mesalazine, a key treatment agent for inflammatory bowel disease, could also be effective in managing periodontitis.Methods: The antimicrobial effect of mesalazine on Porphyromonas gingivalis was investigated in vitro, including observations of morphological changes on the surface of P. gingivalis. Additionally, the impact of mesalazine on both the formation and established plaque biofilms was examined. The antimicrobial mechanism was elucidated by assessing the expression of P. gingivalis virulence genes and by determining the disruptive effect on P. gingivalis cell membranes. An in vivo rat model of periodontitis was constructed to evaluate mesalazine’s efficacy and its influence on the periodontal bacterial flora in the context of periodontitis.Results and discussion: Our results demonstrated that mesalazine concentrations ranging from 0.5 to 2 mg/mL significantly inhibited P. gingivalis proliferation over 72 h. Flow cytometry revealed a marked reduction in the number of viable cells following mesalazine treatment. At the nanometer scale, mesalazine induced crumpling and rupture of the P. gingivalis surface, compromising cell membrane integrity. Mesalazine not only suppressed the formation of plaque biofilms by P. gingivalis and polymicrobial communities but also disrupted pre-existing biofilms. The data also suggested that mesalazine could disrupt the integrity of the P. gingivalis cell membrane and inhibit the expression of virulence factors. An animal model of periodontitis in rats was successfully constructed in vivo. Mesalazine treatment inhibited alveolar bone resorption, alleviated inflammation of periodontal tissues, and improved the composition of the periodontal flora to a healthier state. This study establishes that mesalazine can treat periodontitis through modulation of the periodontal flora and its anti-inflammatory properties, thus broadening its classical therapeutic applications.

Oral mucosal disease (OMD) is a public health challenge globally, but the epidemiological findings in older adults have been inconsistent in China. Thus, this meta-analysis was carried out to explore the prevalence of OMD and its moderating factors in this population. An electronic literature search was conducted of both international (PubMed, PsycINFO, and EMBASE) and Chinese (China National Knowledge Infrastructure and WanFang) databases from inception to November 1, 2019. The Der–Simonian and Laird random effects model was used to synthesize the prevalence of OMD and its 95% confidence intervals (95% CI). Twenty-four studies covering 23,653 older adults were included. The pooled prevalence of OMD was 23% (95% confidence interval: 17.9%–29.0%) Subgroup analyses and meta-analysis revealed that the prevalence of OMD was significantly associated with the reporting sampling, year of publication, and survey (all p values <0.05). This meta-analysis found that the prevalence of OMD among older adults in mainland China was significantly high. Early detection and effective intervention of OMD in older adults have public health and clinical importance.

Background: Oral squamous cell carcinoma (OSCC) is one of the most common oral malignancies, which can occur in any part of the mouth and is highly malignant. DNA Methylation is an epigenetic modification of the genome, which is involved in key cellular processes and has a crucial impact on the occurrence, development, invasion and metastasis of tumors. In this study, we conducted a comprehensive analysis of DNA methylation characteristics in OSCC with the aim of identifying potential diagnostic epigenetic biomarkers and exploring possible mechanisms of methylation’s influence on OSCC. Methods: In this study, genome-wide DNA methylation analysis was performed using Infinium Methylation EPIC arrays, including tumor tissue and adjacent non-tumor tissue from 12 OSCC patients. Differential methylation probes and regions (DMP/DMR) were identified for gene function analysis. Characteristic DMPs and genes were screened according to the specific situation, and OSCC-targeted methylation data from 25 patients in the validation cohort were used to further validate the differential methylation levels of our selected genes. Finally, the expression levels of methylated genes in OSCC were verified by combining RNA-Seq data with quantitative real-time polymerase chain reaction (qRT-PCR). Results: There were 277,805 DMPs in OSCC tumor tissue. Hypermethylated DMP accounted for 37.4% of all DMPs and hypomethylated DMPs was 62.6%. Functional pathway analysis showed that it was mainly related to passive transmembrane transporter activity, cancer proteoglycan and PI3K-Akt signaling pathway. The methylation level of ZNF880 was emphatically verified in the verification cohort, and the results showed that there was high methylation in ZNF880 in the verification cohort. Subsequently, through RNA-Seq data and qRT-PCR, it was confirmed that the expression of ZNF880 in OSCC tissues was significantly lower than that in normal tissues. This verified the correlation between the high methylation of ZNF880 and gene expression. Conclusions: This study comprehensively reveals changes in genome-wide DNA methylation patterns in OSCC, indicating that abnormal hypermethylation of the ZNF880 gene plays a catalytic role in the pathogenesis of OSCC.