Heteroaggregation and deposition behaviors of carboxylated nanoplastics with different types of clay minerals in aquatic environments: Important role of calcium(II) ion-assisted bridging.

The widespread utilization of plastic products ineluctably leads to the ubiquity of nanoplastics (NPs), causing potential risks for aquatic environments. Interactions of NPs with mineral surfaces may affect NPs transport, fate and ecotoxicity. This study aims to investigate systematically the deposition and aggregation behaviors of carboxylated polystyrene nanoplastics (COOH-PSNPs) by four types of clay minerals (illite, kaolinite, Na-montmorillonite, and Ca-montmorillonite) under various solution chemistry conditions (pH, temperature, ionic strength and type). Results demonstrate that the deposition process was dominated by electrostatic interactions. Divalent cations (i.e., Ca2+, Mg2+, Cd2+, or Pb2+) were more efficient for screening surface negative charges and compressing the electrical double layer (EDL). Hence, there were significant increases in deposition rates of COOH-PSNPs with clay minerals in suspension containing divalent cations, whereas only slight increases in deposition rates of COOH-PSNPs were observed in monovalent cations (Na+, K+). Negligible deposition occurred in the presence of anions (F-, Cl-, NO3-, CO32-, SO42-, or PO43-). Divalent Ca2+ could incrementally facilitate the deposition of COOH-PSNPs through Ca2+-assisted bridging with increasing CaCl2 concentrations (0-100 mM). The weakened deposition of COOH-PSNPs with increasing pH (2.0-10.0) was primarily attributed to the reduce in positive charge density at the edges of clay minerals. In suspensions containing 2 mM CaCl2, increased Na+ ionic strength (0-100 mM) and temperature (15-55 ◦C) also favored the deposition of COOH-PSNPs. The ability of COOH-PSNPs deposited by four types of clay minerals followed the sequence of kaolinite > Na-montmorillonite > Ca-montmorillonite > illite, which was related to their structural and surface charge properties. This study revealed the deposition behaviors and mechanisms between NPs and clay minerals under environmentally representative conditions, which provided novel insights into the transport and fate of NPs in natural aquatic environments.

Vitamin intake and periodontal disease: a meta-analysis of observational studies.

OBJECTIVE: A meta-analysis was performed to assess the epidemiological correlation between dietary intake of various types of vitamin intake and the risk of periodontal disease. METHODS: A comprehensive computerized search was conducted in eight databases, namely PubMed, Web of Science, Embase, Cochrane Library, China Biology Medicine Disc, CNKI, VIP, and WanFang Database, and a random effect model was applied to combine pooled odds ratio (ORs) with corresponding 95% confidence intervals (CIs) of the included studies, and the sensitivity analysis was performed to explore the impact of a single study on the comprehensive results. RESULTS: We finally included 45 effect groups from 23 observational studies, with a total number of study participants of 74,488. The results showed that higher levels of vitamin A (OR: 0.788, 95% CI: 0.640-0.971), vitamin B complex (OR: 0.884, 95% CI: 0.824-0.948), vitamin C (OR: 0.875, 95% CI: 0.775-0.988), vitamin D (OR: 0.964, 95% CI: 0.948-0.981), and vitamin E (OR: 0.868, 95% CI: 0.776-0.971) intake all were negatively correlated with periodontal disease. After removing each study, leave-one-out sensitivity analysis indicated no significant change in the overall results of any of the five meta-analyses. CONCLUSIONS: The results from this meta-analysis demonstrated a negative association between high-dose vitamin A, vitamin B complex, vitamin C, vitamin D, and vitamin E consumption and the likelihood of developing periodontal disease, revealing the significant role of vitamins in preventing periodontal disease.

IL-10 secreting B cells regulate periodontal immune response during periodontitis.

Periodontitis is a disease caused by periodontopathogens and is characterized by periodontal inflammation and alveolar bone resorption. As has been proven, host immune responses incite the development and progression of periodontitis. The present study sought to establish B10 cell functions and mechanisms in regulating host immunity during periodontitis. Periodontopathogen-specific B10 cells were purified and then injected into recipients to create the adoptive transfer models. We compared inflammatory cytokines and regulatory T (Treg)/Th17 cell expression in a healthy, normal model, an experimental periodontitis model, and experimental periodontitis model adoptively transferred with B10 cells. Compared with experimental periodontitis animals, our results showed that transfer of B10 cells alleviated alveolar bone resorption (P < 0.05) by reducing periodontal osteoclastogenesis (P < 0.05). Additionally, we found that B10 cell transfer into the experimental periodontitis ones resulted in increased IL-10 (P < 0.05), but decreased IL-17 (P < 0.05) and receptor activator for nuclear factor κB ligand (RANKL) (P < 0.05) gene and protein expression in local lesions. Moreover, adoptive transfer of B10 cells reduced the proportion of Th17 cells (P < 0.05) in the gingiva. The results of our study confirmed that B10 cells can modulate local host immune responses and prevent inflammatory damage of alveolar bone by reducing pro-inflammatory cytokine expression and decreasing local proliferation of Th17 cells.

Improved RANKL expression and osteoclastogenesis induction of CD27+CD38- memory B cells: A link between B cells and alveolar bone damage in periodontitis.

BACKGROUND AND OBJECTIVE: Periodontitis is a bacteria-induced disease that often leads to alveolar bone damage. Its mechanisms were considered to be complicated, involving an imbalance of the formation and resorption of bone. We sought to disclose the antibody-independent function of B cells during periodontitis. MATERIAL AND METHODS: Production of receptor activator for nuclear factor-κB ligand (RANKL) by total lymphocytes or sorted B-cell subsets in gingiva from healthy or experimental periodontitis animals was examined by flow cytometry, real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. To define the effects of lymphocytes or B-cell subsets on osteoclastogenesis induction, bone marrow mononuclear cells were culture in culture medium of lymphocytes or cocultured with B-cell subsets. Osteoclasts were enumerated by tartrate-resistant acid phosphatase staining. Constituent ratio of B-cell subsets in healthy or experimental periodontitis was also detected by flow cytometry. RESULT: Gingiva B cells produce more RANKL and support more osteoclastogenesis than T and other lymphocytes, and this potential improved in periodontitis. Memory B cells (CD27+CD38-) decreased their percentage in periodontitis. Memory B cells have the highest propensity for RANKL production. Remarkably, memory B cells from periodontitis animals expressed significantly more RANKL compared to healthy controls. Memory B cells supported osteoclast differentiation in vitro in a RANKL-dependent manner, and the number of osteoclasts was higher in cultures with memory B cells from periodontitis animals than in those derived from healthy ones. Other B-cell subsets have limited impact on osteoclast formation. CONCLUSION: Findings of this study further disclose the roles of B cells engaged in periodontal immunomodulation and reveal the considerable importance of memory B cells in alveolar bone homeostasis and their likely contribution to alveolar bone destruction in periodontitis.

Soluble RANKL Cleaved from Activated Lymphocytes by TNF-α-Converting Enzyme Contributes to Osteoclastogenesis in Periodontitis.

Host immune responses play a key role in promoting bone resorption in periodontitis via receptor activator of NF-κB ligand (RANKL)-dependent osteoclastogenesis. Both membrane-bound RANKL (mRANKL) expressed on lymphocytes and soluble RANKL (sRANKL) are found in periodontal lesions. However, the underlying mechanism and cellular source of sRANKL release and its biological role in periodontitis are unclear. TNF-α-converting enzyme (TACE) is reported to cleave the following: 1) precursor TNF-α with release of mature, soluble TNF-α and 2) mRANKL with release of sRANKL. Both soluble TNF-α and sRANKL are found in the periodontitis lesion, leading to the hypothesis that TACE expressed on lymphocytes is engaged in RANKL shedding and that the resulting sRANKL induces osteoclastogenesis. In the current study, upon stimulating PBLs with mitogens in vitro, RANKL expression, sRANKL secretion, and TACE expression were all upregulated. Among the four putative mRANKL sheddases examined in neutralization assays, TACE was the only functional sheddase able to cleave mRANKL expressed on PBL. Moreover, PBL culture supernatant stimulated with mitogens in the presence of anti-TACE Ab or anti-RANKL Ab showed a marked reduction of osteoclastogenesis from osteoclast precursors, indicating that TACE-mediated sRANKL may possess sufficient osteoclastogenic activity. According to double-color confocal microscopy, B cells expressed a more pronounced level of RANKL and TACE expression than T cells or monocytes in periodontally diseased gingiva. Conditioned medium of patients' gingival lymphocyte culture increased in vitro osteoclastogenic activity, which was suppressed by the addition of anti-TACE Ab and anti-RANKL Ab. Therefore, TACE-mediated cleavage of sRANKL from activated lymphocytes, especially B cells, can promote osteoclastogenesis in periodontitis.

Adsorption of metals on aged microplastics in intensive mariculture areas: Aggravating the potential ecological risks to marine organisms.

Field determination of the metal adsorption capacity of microplastics (MPs) by using a passive sampler had been done in typical subtropical mariculture area in China. The adsorption of eight metals (Fe, Mn, Cu, Zn, As, Pb, Cr and Cd) by five types of MPs (low-density polyethylene, polypropylene, polystyrene, poly(ethylene terephthalate) and poly(vinyl chloride) (PVC) was compared, including metal types, mariculture types (cage and longline culture), metal residue content in ambient environment, polymer types and particle sizes of MPs. The results showed that Cu, Zn, As, Cd, Pb and Cr in the mariculture environment were contaminated compared with the quality criteria. The concentrations of these six metals adsorbed on five MPs increased linearly with those in seawater. More enriched Cu and As in MPs in marine cage culture than in longline culture, due to the obvious endogenous pollution emissions for the artificial diets, fish medicine and disinfectants. Aged PVC with more cracks and pores showed higher metal adsorption capacity than any other polymers. MPs with a smaller size range of 50-74 µm tended to accumulate higher amounts of metals than those with a larger size range of 74-178 µm, consisting with the surface characteristics of MPs. The significant positive relationship between the concentrations of nutrients in seawater and the adsorption amounts of Cu, Zn and As on MPs implies that the eutrophication would promote their pollution. Based on the ecological risk assessment, the occurrence of MPs could aggravate the potential risk of metals to marine organisms in intensive mariculture areas. This is the first time to reveal the impacts of the adsorption of metals on aged MPs on the potential ecological risks of metals to organisms under the realistic environmental condition.

Digital measurement of deciduous tooth dimensions in China: A cross-sectional survey.

OBJECTIVE: Crown dimensions data of deciduous teeth hold anthropological, forensic, and archaeological value. However, such information remains scarce for the Chinese population. This multi-center study aimed to collect a large sample of deciduous crown data from Chinese children using three-dimensional measurement methods and to analyze their dimensions. DESIGN: A total of 1592 children's deciduous dentition samples were included, and the sample size was distributed according to Northeast, North, East, Northwest, Southwest and South China. Digital dental models were reconstructed from plaster dental models. Independent sample t test, paired t test, principal component analysis (PCA), and factor analysis (FA) were used to analyze the tooth crown dimensions. RESULT: 18,318 deciduous teeth from 1592 children were included. Males exhibited slightly larger values than females. The range of sexual dimorphism percentages for each measurement was as follows: mesiodistal diameter (0.40-2.08), buccolingual diameter (0.13-2.24), and maxillogingival diameter (0.48-3.37). The FA results showed that the main trend of crown dimensions changes was the simultaneous increase or decrease in mesiodistal diameter, buccolingual diameter and maxillogingival diameter in three directions. CONCLUSION: This is the first large-scale survey of deciduous tooth crown dimensions in China, which supplements the data of deciduous tooth measurement and provides a reference for clinical application.

Porphyromonas gingivalis infection-associated periodontal bone resorption is dependent on receptor activator of NF-κB ligand.

Porphyromonas gingivalis is one of the oral microorganisms associated with human chronic periodontitis. The purpose of this study is to determine the role of the receptor activator of nuclear factor-κB ligand (RANKL) in P. gingivalis infection-associated periodontal bone resorption. Inbred female Rowett rats were infected orally on four consecutive days (days 0 to 3) with 1 × 10(9) P. gingivalis bacteria (strain ATCC 33277). Separate groups of rats also received an injection of anti-RANKL antibody, osteoprotegerin fusion protein (OPG-Fc), or a control fusion protein (L6-Fc) into gingival papillae in addition to P. gingivalis infection. Robust serum IgG and salivary IgA antibody (P < 0.01) and T cell proliferation (P < 0.05) responses to P. gingivalis were detected at day 7 and peaked at day 28 in P. gingivalis-infected rats. Both the concentration of soluble RANKL (sRANKL) in rat gingival tissues (P < 0.01) and periodontal bone resorption (P < 0.05) were significantly elevated at day 28 in the P. gingivalis-infected group compared to levels in the uninfected group. Correspondingly, RANKL-expressing T and B cells in rat gingival tissues were significantly increased at day 28 in the P. gingivalis-infected group compared to the levels in the uninfected group (P < 0.01). Injection of anti-RANKL antibody (P < 0.05) or OPG-Fc (P < 0.01), but not L6-Fc, into rat gingival papillae after P. gingivalis infection resulted in significantly reduced periodontal bone resorption. This study suggests that P. gingivalis infection-associated periodontal bone resorption is RANKL dependent and is accompanied by increased local infiltration of RANKL-expressing T and B cells.

Oral mucosal diseases and psychosocial factors: progress in related neurobiological mechanisms.

The aetiology of oral mucosal diseases, such as recurrent aphthous ulcer (RAU), oral lichen planus (OLP) and burning mouth syndrome (BMS), involves many factors, and it remains difficult for clinicians to effectively relieve disease symptoms and formulate coping strategies. With the rapid development of psychology, the role of mental and psychological factors in RAU, OLP and BMS has gradually attracted researchers attention, but the specific mechanism has not been completely determined. This narrative review describes the potential neurobiological mechanism of oral mucosal diseases and detailed psychological factors after introducing relevant research into psychological factors and oral mucosal diseases. Future research strategies and innovations needed to understand and treat oral mucosal diseases and psychological factors, as well as how to prevent oral mucosal diseases by regulation of the neuroendocrine system, are also discussed.

Exosomal miR-205-5p derived from periodontal ligament stem cells attenuates the inflammation of chronic periodontitis via targeting XBP1.

INTRODUCTION: Chronic periodontitis (CP) is an inflammatory periodontal disease with high incidence and complex pathology. This research is aimed to investigate the function of exosomal miR-205-5p (Exo-miR-205-5p) in CP and the underlying molecular mechanisms. METHOD: Exo-miR-205-5p was isolated from miR-205-5p mimics-transfected periodontal ligament stem cells (PDLSCs), and subsequently cocultured with lipopolysaccharide (LPS)-induced cells or injected into LPS-treated rats. The mRNA expression of inflammatory factors and Th17/Treg-related factors were measured by quantitative real-time PCR. The contents of inflammatory factors and the percentages of Th17/Treg cells were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. Besides, the target relation between miR-205-5p and X-box binding protein 1 (XBP1) was explored. RESULTS: MiR-205-5p was downregulated in LPS-induced PDLSCs and corresponding exosomes. Exo-miR-205-5p inhibited inflammatory cell infiltration, decreased the production of TNF-α, IL-1ß, and IL-6, and decreased the percentage of Th17 cells in LPS-treated rats. In addition, XBP1 was a target of miR-205-5p. Overexpression of XBP1 weakened the effects of Exo-miR-205-5p on inhibiting inflammation and regulating Treg/Th17 balance in LPS-induced cells. CONCLUSIONS: Exo-miR-205-5p derived from PDLSCs relieves the inflammation and balances the Th17/Treg cells in CP through targeting XBP1.

Advances in the prevention and treatment of Alzheimer's disease based on oral bacteria.

With the global population undergoing demographic shift towards aging, the prevalence of Alzheimer's disease (AD), a prominent neurodegenerative disorder that primarily afflicts individuals aged 65 and above, has increased across various geographical regions. This phenomenon is accompanied by a concomitant decline in immune functionality and oral hygiene capacity among the elderly, precipitating compromised oral functionality and an augmented burden of dental plaque. Accordingly, oral afflictions, including dental caries and periodontal disease, manifest with frequency among the geriatric population worldwide. Recent scientific investigations have unveiled the potential role of oral bacteria in instigating both local and systemic chronic inflammation, thereby delineating a putative nexus between oral health and the genesis and progression of AD. They further proposed the oral microbiome as a potentially modifiable risk factor in AD development, although the precise pathological mechanisms and degree of association have yet to be fully elucidated. This review summarizes current research on the relationship between oral bacteria and AD, describing the epidemiological and pathological mechanisms that may potentially link them. The purpose is to enrich early diagnostic approaches by incorporating emerging biomarkers, offering novel insights for clinicians in the early detection of AD. Additionally, it explores the potential of vaccination strategies and guidance for clinical pharmacotherapy. It proposes the development of maintenance measures specifically targeting oral health in older adults and advocates for guiding elderly patients in adopting healthy lifestyle habits, ultimately aiming to indirectly mitigate the progression of AD while promoting oral health in the elderly.

Identification of Key Gene Targets for Periodontitis Treatment by Bioinformatics Analysis.

Background: Periodontitis is considered to be the leading cause of tooth loss in adults, and it interacts with some serious systemic diseases. Periodontal basic therapy is the cornerstone of periodontal disease treatment and long-term maintenance and has a positive impact on the treatment of systemic diseases. Aim: To explore the potential gene targets of periodontitis therapies by bioinformatics method. Methods: We analyzed the expression database (GSE6751) downloaded from the Gene Expression Omnibus (GEO) with weighted gene coexpression network analysis (WGCNA) to confirm the functional gene modules. Pathway enrichment network analyses the key genes in functional modules and verified the candidate genes from the samples in peripheral blood sources of GSE43525. Moreover, we confirmed the expression of target protein in the periodontal tissues of experimental periodontitis-afflicted mice using western blotting. Results: The functional gene modules were found to have biological processes, and ARRB2, BIRC3, CD14, DYNLL1, FCER1G, FCGR1A, FCGR2B, FGR, HCK, and PRKCD were screened as candidates' genes in functional modules. The 921 DEG from GSE43525 and 418 DEG is from the green module of GSE6751 and identified AMICA1, KDELR1, DHRS7B, LMNB1, CTSA, S100A12, and FCGR1A as target genes. Finally, FCGR1A (CD64) was confirmed as the key gene that affects periodontal treatment. Western blot analysis showed an increasing trend in the expression level of FCGR1A protein in the periodontal tissues of experimental periodontitis mice compared to normal mice. Conclusions: FCGR1A (CD64) may be a key gene target for periodontal therapy in patients with periodontitis and other systemic diseases.

[Expression of B cell activation factor and correlation analysis in patients of systemic lupus erythematosus and its correlation with periodontitis].

PURPOSE: To detect the level of B cell activating factor (B - cell activating factor of the TNF family, BAFF) in the serum of patientes suffering from systemic lupus erythematosus (SLE) with periodontitis, and analyze the relationship between the expression of BAFF with periodontitis and SLE. METHODS: According to the inclusion criteria, patients visiting the Department of Stomatology and Rheumatology, Shengjing Hospital Affiliated to China Medical University were selected, including 19 patients in the periodontitis group(P group), 22 in the systemic lupus erythematosus group (SLE group), 24 in the systemic lupus erythematosus combined with periodontitis group(SLE+P group), and 20 in the healthy control group(H group). The general information, periodontal probing depth (PD), clinical attachment loss (CAL), gingival sulcus bleeding index(SBI) were collected. Serum samples of patients in each group were collected, and BAFF content was determined by Elisa. Rheumatic and immunological indexes of subjects in SLE group and SLE+P group were determined, and the correlation between BAFF content and periodontal indexes was analyzed. SPSS 20.0 software package was used for statistical analysis. RESULTS: CAL in P+SLE group was significantly higher than that in P group(P＜0.05). Serum BAFF concentrations in SLE+P group, SLE group and P group were significantly higher than those in the healthy control group (P＜0.05). Serum BAFF concentration in SLE+P group was significantly higher than that in SLE group(P＜0.05). ESR, SLEDAI and disease duration in SLE+P group were significantly higher than those in SLE group (P＜0.05). The expression level of BAFF in serum was positively correlated with CAL and SBI(P＜0.01). The expression level of BAFF in serum was positively correlated with PD(P＜0.05). There was significant positive correlation between serum BAFF level and duration of disease and hormone use(P＜0.01). Serum BAFF level was positively correlated with C3 (P＜0.05). CONCLUSIONS: SLE has certain correlation with periodontitis, and serum BAFF in SLE patients with periodontitis is significantly increased.BAFF may be associated with the development of SLE and periodontitis.

[Environmental Process, Effects and Risks of Emerging Contaminants in the Estuary-Coastal Environment].

Human activities and global climate change have contributed substantially to the input of land-sourced pollutants into the aquatic environment, especially for emerging or newly identified contaminants, such as microplastics, emerging persistent organic pollutants, pharmaceuticals, and personal care products. The prevalence and toxicity of these emerging pollutants has raised continued concern for the health and safety of the public worldwide. A review of sources, distribution, interfacial transport processes of microplastics, per-and polyfluorinated compounds, antibiotics, and endocrine-disrupting chemicals and factors that influence their environmental behavior in the estuary-coastal environment have been included. The adverse ecological effects and health risks of these emerging contaminants to humans were also reviewed. Lastly, the direction of future research was provided regarding the environmental behavior of multiple emerging pollutants in the coastal environment and the health risks resulting from their interactions, supporting the prevention and control of marine pollution and the healthy development of the marine economy.

Antibody to receptor activator of NF-κB ligand ameliorates T cell-mediated periodontal bone resorption.

Activated T and B lymphocytes in periodontal disease lesions express receptor activator of NF-κB ligand (RANKL), which induces osteoclastic bone resorption. The objective of this study was to evaluate the effects of anti-RANKL antibody on periodontal bone resorption in vitro and in vivo. Aggregatibacter actinomycetemcomitans outer membrane protein 29 (Omp29) and A. actinomycetemcomitans lipopolysaccharide (LPS) were injected into 3 palatal gingival sites, and Omp29-specific T clone cells were transferred into the tail veins of rats. Rabbit anti-RANKL IgG antibody or F(ab')2 antibody fragments thereof were injected into the palatal sites in each rat (days -1, 1, and 3). Anti-RANKL IgG antibody significantly inhibited soluble RANKL (sRANKL)-induced osteoclastogenesis in vitro, in a dose-dependent manner, but also gave rise to a rat antibody response to rabbit IgG in vivo, with no significant inhibition of periodontal bone resorption detected. Lower doses (1.5 and 0.15 µg/3 sites) of F(ab')2 antibody were not immunogenic in the context of the experimental model. Periodontal bone resorption was inhibited significantly by injection of the anti-RANKL F(ab')2 antibody into gingivae. The sRANKL concentrations for the antibody-treated groups were decreased significantly compared to those for the untreated group. Osteoclasts on the alveolar bone surface were also diminished significantly after antibody injection. Gingival sRANKL concentration and bone loss showed a significant correlation with one another in animals receiving anti-RANKL F(ab')2 antibody. These results suggest that antibody to RANKL can inhibit A. actinomycetemcomitans-specific T cell-induced periodontal bone resorption by blockade and reduction of tissue sRANKL, providing an immunological approach to ameliorate immune cell-mediated periodontal bone resorption.

[Preliminary study on the correlation between IL-6,IL-33, and IL-10 and periodontitis and rheumatoid arthritis].

PURPOSE: To determine the expression levels of interleukin-6(IL-6), interleukin-33 (IL-33) and interleukin-10 (IL-10) in gingival crevicular fluid in patients with periodontitis and rheumatoid arthritis, and to investigate the correlation between IL-6, IL-33, IL-10 and periodontitis and rheumatoid arthritis. METHODS: According to the inclusion criteria, patients who were admitted to the Department of Stomatology and Rheumatology and Immunology of Shengjing Hospital of China Medical University were selected, including 21 patients with periodontitis (PD group), 21 patients with rheumatoid arthritis (RA group), and 24 patients with periodontitis combined with rheumatoid arthritis (PD+RA group), 24 healthy patients (H group). General information for each subject was recorded including periodontal probing depth (PPD), clinical attachment loss (CAL), and gingival sulcus bleeding index (SBI). Samples of gingival crevicular fluid were collected from each group, and the contents of IL-6, IL-33 and IL-10 in gingival crevicular fluid were determined by ELISA, and the correlation between IL-6, IL-33, IL-10 and periodontal clinical indicators was analyzed. SPSS 20.0 software package was used to analyze the date. RESULTS: The expression level of IL-6 in PD+RA group was significantly higher than that in H group, PD group and RA group (P<0.05). The content of IL-33 in PD group, RA group and PD+RA group was significantly higher than that in H group (P<0.05), while the content of IL-33 in PD+RA group was significantly higher than that in RA group (P<0.05). The expression level of IL-10 in the RA group was significantly higher than that in the H group, the PD group and the PD+RA group (P<0.05). PPD in PD group was positively correlated with the contents of IL-6 and IL-33 (r=0.62, 0.43), SBI, PPD and CAL in PD+RA group were positively correlated with the contents of IL-33 (r=0.69, 0.58, 0.55). CONCLUSIONS: The levels of IL-6 and IL-33 in gingival crevicular fluid of patients with periodontitis accompanied by rheumatoid arthritis are significantly increased, while the contents of IL-10 are significantly decreased, suggesting that IL-6, IL-33 and IL-10 play an important role in the occurrence and development of periodontitis and rheumatoid arthritis.

Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice.

Periodontitis is the second most common oral disease affecting tooth-supporting structures. The tissue damage is mainly initiated by the excessive secretion of proinflammatory cytokines by immune cells. Macrophages are a type of antigen-presenting cells that influence the adaptive immunity function. We used a unique set of cytokines, i.e., a combination of IL-4, IL-13, and IL-10, to stimulate macrophages into a subset of M2 polarization cells that express much higher levels of ARG-1, CD206, and PDL-2 genes. The cells' anti-inflammatory potential was tested with mixed-lymphocyte reaction assay, which showed that this subset of macrophages could increase IL-2 secretion and suppress IL-17, IL-6, and TNF-α secretion by splenocytes. The gram-negative bacterial species Porphyromonas gingivalis was used to initiate an inflammatory process in murine periodontal tissues. In the meantime, cell injection therapy was used to dampen the excessive immune reaction and suppress osteoclast differentiation during periodontitis. Maxilla was collected and analyzed for osteoclast formation. The results indicated that mice in the cell injection group exhibited less osteoclast activity within the periodontal ligament region than in the periodontitis group. Moreover, the injection of M2 macrophages sustained the regulatory population ratio. Therefore, the M2 macrophages induced under the stimulation of IL-4, IL-13, and IL-10 combined had tremendous immune modulation ability. Injecting these cells into local periodontal tissue could effectively alleviate the symptom of periodontitis.

[Detection and significance of IL-6 and TNF-α in patients with Graves disease and periodontitis].

PURPOSE: To investigate the expression of IL-6 and TNF-α in gingival crevicular fluid (GCF) and serum of patients with Graves' disease(GD) and periodontitis (CP), and to analyze the correlation between Graves' disease and periodontitis. METHODS: One hundred and twenty subjects were selected and divided into 4 groups: 30 healthy participants as the control group, 30 patients with CP, 30 patients with GD, and 30 patients with GD and CP. The serum and GCF level of IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA), and clinical periodontal parameters including probing depth (PD), clinical attachment level (CAL) and sulcus bleeding indexes (SBI) were examined. The date was analyzed with SPSS19.0 software package. RESULTS: The concentration of IL-6 and TNF-α in serum and GCF of patients with GD+CP group was significantly higher than that in CP group and GD group (P<0.05). The level of IL-6 and TNF-α in serum and GCF of patients in GD+CP group and GD group was positively correlated with FT3 and FT4 (P<0.05), and the correlation between GD+CP group was significantly higher than that in GD group. CONCLUSIONS: The level of IL-6 and TNF-α in GD+CP group were significantly higher than those in CP group and GD group, indicating that there is an interaction between periodontitis and Graves' disease in immune mechanism.

Switched memory B cells promote alveolar bone damage during periodontitis: An adoptive transfer experiment.

Periodontitis is a bacteria-induced disease that often leads to alveolar bone damage. We sought to determine the role and mechanism of switched memory B cells in alveolar bone destruction during periodontitis. Sensitized B cells were sorted and cultured, then their expression of receptor activator for nuclear factor-κB ligand (RANKL), interleukin-6 (IL-6), and interleukin-12 (IL-12) was detected. Using these cells, we prepared adoptive transfer models in which we induced periodontitis. We found that switched memory B cells produced more RANKL in terms of both protein and mRNA levels than other subpopulations. Switched memory B cells expressed more IL-6 and IL-12 mRNA than other subpopulations, but differences in respective protein levels were not significant. Moreover, we found that switched memory B cell transfer resulted in increased alveolar bone loss and periodontal osteoclastogenesis. Moreover, switched memory B cell transfer increased the proportion of Th1 and Th17 cells as well as the expression of RANKL, osteoprotegerin (OPG), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-1ß, IL-6, IL-17A in gingiva, and cervical lymph nodes (CLNs). The outcomes of the present study indicate that switched memory B cells regulate alveolar bone homeostasis via enhancing cytokine expression and increasing proliferation of Th1 and Th17 cells.

IL-35 may maintain homeostasis of the immune microenvironment in periodontitis.

T lymphocyte cells, including regulatory T (Treg) and T helper 17 cells, have important roles in the human periodontium. However, the basis for Treg cytokine expression in various compartments of the periodontium remains unclear. The aim of the present study was to investigate the expression of interleukin (IL)-35 in the peripheral blood mononuclear cells (PBMCs) and periodontal tissues of patients with chronic periodontitis (CP), with a view to understanding its role in this disease, and ultimately providing improved treatments. Peripheral blood, periodontal tissues and gingival crevicular fluids (GCFs) were collected from patients with CP or impacted teeth, the latter serving as healthy controls. The expression levels of IL-35 subunit mRNAs in PBMCs and periodontal tissues were determined using reverse transcription-quantitative polymerase chain reaction, while the IL-35 protein expression in GCFs and sera was quantified by ELISA. The relative expression of IL-35 subunit mRNAs in the affected tissues of patients with CP was significantly higher compared with that in samples from healthy controls (P<0.05). The mean concentration of IL-35 protein in the GCFs and sera of patients with periodontitis was also significantly higher compared with that in samples from healthy controls (P<0.001). IL-35 protein and periodontal clinical indicators were negatively correlated. It was hypothesized that the increased level of IL-35 plays a protective role in periodontal disease by maintaining immune system homeostasis and dampening the inflammatory response, and highlights IL-35 as a potential new therapy for the treatment of periodontitis.