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BACKGROUND: Lipocalin-2 (LCN-2) is an osteokine that suppresses appetite, stimulates insulin secretion, regulates bone remodeling, and is induced by proinflammatory cytokines. The aim of this work was to investigate the participation of LCN-2 in periodontitis associated with type 2 diabetes (T2D) by evaluating alveolar bone loss, glycemic control, inflammation, and femur fragility. METHODS: A murine model of periodontitis with T2D and elevated LCN-2 concentration was used. Functional LCN-2 inhibition was achieved using an anti-LCN-2 polyclonal antibody, and isotype immunoglobulin G was used as a control. The alveolar bone and femur were evaluated by micro-CT. Glucose metabolism was determined. Tumor necrosis factor (TNF-α) and receptor activator of nuclear factor kappa-B ligand (RANKL) levels in alveolar bone lysates were quantified using ELISA, and serum cytokines were quantified using flow cytometry. A three-point bending test was performed in the femur, and RANKL levels were measured in femur lysates using ELISA. RESULTS: Functional inhibition of LCN-2 in T2D-periodontitis mice decreased alveolar bone loss in buccal and palatal surfaces and preserved the microarchitecture of the remaining bone, decreased TNF-α and RANKL in alveolar bone, reduced hyperglycemia, glucose intolerance, and insulin resistance, and increased insulin production through improving the functionality of pancreatic ß cells. Furthermore, this inhibition increased serum free-glycerol levels, decreased serum interleukin (IL)-6, increased serum IL-4, and reduced femur fragility and RANKL expression in the femur. CONCLUSIONS: LCN-2 participates in periodontitis associated with T2D. Inhibiting its function in mice with T2D and periodontitis improves pancreatic ß-cell function, and glucose metabolism and decreases inflammatory cytokines and bone-RANKL levels, which results in the preservation of femoral and alveolar bone microarchitecture. PLAIN LANGUAGE SUMMARY: In this study, we explored the role of a bone protein known as lipocalin-2 (LCN-2) in the connection between periodontitis and type 2 diabetes (T2D). Periodontitis is a destructive gum and alveolar bone disease. LCN-2 levels are increased in both T2D and periodontitis. Using a mouse model of T2D with periodontitis, we examined how blocking LCN-2 function affected various aspects of these two diseases. We found that this inhibition led to significant improvements. First, it reduced alveolar bone loss and preserved bone structure by decreasing local inflammation and bone resorption. Second, it improved glucose and lipid metabolism, leading to better blood-sugar control and decreased insulin resistance. Blocking the functions of LCN-2 also decreased systemic inflammation throughout the body and strengthened bone integrity. Overall, our results suggest that LCN-2 plays a crucial role in the periodontitis associated with T2D. By inhibiting LCN-2 function, we were able to improve pancreatic function, improve glucose metabolism, reduce inflammation, and enhance bone health. Targeting LCN-2 could be a promising strategy for the harmful effects of T2D and periodontitis.

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This study presents an in vitro analysis of the bactericidal and cytotoxic properties of hybrid films containing nickel oxide (NiO) and nickel ferrite (NiFe2O4) nanoparticles embedded in polypropylene (PP). The solvent casting method was used to synthesize films of PP, PP@NiO, and PP@NiFe2O4, which were characterized by different spectroscopic and microscopic techniques. The X-ray diffraction (XRD) patterns confirmed that the small crystallite sizes of NiO and NiFe2O4 NPs were maintained even after they were incorporated into the PP matrix. From the Raman scattering spectroscopy data, it was evident that there was a significant interaction between the NPs and the PP matrix. Additionally, the Scanning Electron Microscopy (SEM) analysis revealed a homogeneous dispersion of NiO and NiFe2O4 NPs throughout the PP matrix. The incorporation of the NPs was observed to alter the surface roughness of the films; this behavior was studied by atomic force microscopy (AFM). The antibacterial properties of all films were evaluated against Pseudomonas aeruginosa (ATCC®: 43636™) and Staphylococcus aureus (ATCC®: 23235™), two opportunistic and nosocomial pathogens. The PP@NiO and PP@ NiFe2O4 films showed over 90% bacterial growth inhibition for both strains. Additionally, the effects of the films on human skin cells, such as epidermal keratinocytes and dermal fibroblasts, were evaluated for cytotoxicity. The PP, PP@NiO, and PP@NiFe2O4 films were nontoxic to human keratinocytes. Furthermore, compared to the PP film, improved biocompatibility of the PP@NiFe2O4 film with human fibroblasts was observed. The methodology utilized in this study allows for the production of hybrid films that can inhibit the growth of Gram-positive bacteria, such as S. aureus, and Gram-negative bacteria, such as P. aeruginosa. These films have potential as coating materials to prevent bacterial proliferation on surfaces.

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Inequalities in oral health are influenced by the social strata of the population. Few studies have focused on the multitude of factors related to social development as indicators of living conditions and periodontal health status. The aim of this study is to evaluate the association between self-reported periodontal conditions and the Social Development Index (SDI). A cross-sectional validated questionnaire was carried out among 1294 Mexican adults. Descriptive statistics and multivariate logistic regression models were used to identify the best predictors of self-reported periodontal conditions. Bone loss reporting was used as a proxy for the presence of periodontal disease. We found that higher global scores on the SDI and quality and available space in the home (QASH) increase the probability of having bone loss. Global SDI (OR = 7.27) and higher QASH (OR = 3.66) were indeed the leading societal factors related to periodontal disease. These results have pointed out how SDI and its indicators, in particular QASH, can be used to further explore inequities related to privileged access to dental care in the context of periodontal diseases.

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(1) Dental caries, periodontitis, or peri-implantitis are commensal infections related to oral biofilm former bacteria. Likewise, magnesium oxide nanoparticles (MgO-NPs) were studied to introduce them to the antibacterial properties of a few microorganisms. Considering this, the purpose of the present investigation was to determine the antibacterial properties of MgO-NPs on representative oral strains. (2) Methods: MgO-NPs with a cubic crystal structure were obtained by magnesium hydroxide mechanical activation. After synthesis, the MgO-NPs product was annealed at 800 °C (2 h). The MgO-NPs obtained were tested against ten oral ATCC strains at ten serial concentrations (1:1 20.0-0.039 mg/mL per triplicate) using the micro-broth dilution method to determine the minimal inhibitory concentration (MIC) or minimal bactericidal concentration (MIB). Measures of OD595 were compared against each positive control with a Student's t-test. Viability was corroborated by colony-forming units. (3) Results: The polycrystalline structure had an average size of 21 nm as determined by X-ray diffraction and transmission electron microscopy (high resolution). Antimicrobial sensitivity was observed in Capnocytophaga gingivalis (MIB/MIC 10-5 mg/mL), Eikenella corrodens (MIB 10 mg/mL), and Streptococcus sanguinis (MIB 20 mg/mL) at high concentrations of the MgO-NPs and at lower concentrations of the MgO-NPs in Actinomyces israelii (MIB 0.039 mg/mL), Fusobacterium nucleatum subsp. nucleatum (MIB/MIC 5-2.5 mg/mL), Porphyromonas gingivalis (MIB 20 mg/mL/MIC 2.5 mg/mL), Prevotella intermedia (MIB 0.625 mg/mL), Staphylococcus aureus (MIC 2.5 mg/mL), Streptococcus mutans (MIB 20 mg/mL/MIC 0.321 mg/mL), and Streptococcus sobrinus (MIB/MIC 5-2.5 mg/mL). (4) Conclusions: The MgO-NPs' reported antibacterial properties in all oral biofilm strains were evaluated for potential use in dental applications.

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(1) Background: Probiotics can be considered a non-invasive periodontal monotherapy for the modulation of microbiota when periodontal treatment is not accessible. The aim was to evaluate the ability of Lactobacillus reuteri Prodentis as monotherapy to modulate periodontal parameters and subgingival biofilm dysbiosis. (2) Methods: A 30-year-old patient with periodontitis was followed longitudinally after one month of daily consumption of L. reuteri Prodentis (T0). Periodontal measurements and microbial identification by Checkerboard DNA−DNA hybridization of 40 bacteria were compared between baseline (T0) and 30 days (T1) or 90 days (T2), using the Kruskal−Wallis (KW) and Mann−Whitney U (MW) tests. (3) Results: Low values of pocket depth, attachment level, dental plaque, gingival erythema (GE), and suppuration were observed at T0 vs. T1, with the clinical improvement of GE (p < 0.05, MW) and the recovery of tooth 46 fistulation. T1 vs. T0 comparisons showed lower levels (Lev) or proportions (Prop) of Parvimonas micra (Lev: p < 0.05, MW; Prop: p < 0.01, MW) and Streptococcus gordonii (Prop: p < 0.05, MW), and a predominance (Lev/Prop) of Actinomyces odontolyticus and Streptococcus mitis; lower levels and proportions of P. micra, Eubacterium saburreum, Porphyromonas gingivalis, and Tannerella forsythia were observed in tooth 46 (T1/T2 vs. T0). (4) Conclusions: Under monotherapy with L. reuteri Prodentis, periodontal measurements of the patient were maintained, with selective changes in the subgingival microbiota that were proportional to the time of probiotic administration, with any additional periodontal treatment.

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Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. High blood pressure in particular, continues to increase throughout the global population at an increasingly fast pace. The relationship between arterial hypertension and periodontitis has been recently discussed in the context of its origins and implications. Particularly relevant is the role of the periodontal microbiome linked to persistent local and systemic inflammation, along with other risk factors and social determinants of health. The present protocol will investigate/assess the association between periodontal disease and its microbiome on the onset of hypertension, within a cohort from Mexico City. One thousand two hundred twelve participants will be studied during a 60-month period. Studies will include analysis of periodontal conditions, sampling and sequencing of the salivary and subgingival microbiome, interviews on nutritional and lifestyle habits, social determinants of health, blood pressure and anthropometric measurements. Statistical associations and several classic epidemiology and machine learning approaches will be performed to analyze the data. Implications for the generation of public policy-by early public health interventions or epidemiological surveillance approaches-and for the population empowerment-via the establishment of primary prevention recommendations, highlighting the relationship between oral and cardiovascular health-will be considered. This latter set of interventions will be supported by a carefully planned science communication and health promotion strategy. This study has been registered and approved by the Research and Ethics Committee of the School of Dentistry, Universidad Nacional Autónoma de México (CIE/0308/05/2019) and the National Institute of Genomic Medicine (CEI/2020/12). The umbrella cohort was approved by the Institutional Bioethics Committee of the National Institute of Cardiology-Ignacio Chavez (INC-ICh) under code 13-802.

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BACKGROUND: Type-2-Diabetes (T2D) and Periodontitis are major inflammatory diseases. However, not much is known about the specific subgingival microbiota in Mexicans with diabetes and metabolic dysbiosis. The aim of this study was to describe the subgingival microbiota of Mexicans with T2D and the different periodontal and metabolic conditions, through "Checkerboard" DNA-DNA hybridization. METHODS: Subjects were divided into two groups-periodontal-health (PH) (PH_non-T2D; n = 59, PH_T2D; n = 14) and generalized-periodontitis (GP) (GP_non-T2D; n = 67, GP_T2D; n = 38). Obesity (BMI ≥ 30 kg/m2) and serum levels of glycated-hemoglobin (HbA1c), total-lipids, triglycerides, total-cholesterol, high-density-lipids, and low-density-lipids were measured for the T2D individuals. Subgingival microbial identification was processed for 40 species through DNA-probes. RESULTS: Subjects with T2D harbored significantly higher mean total levels (PH: p < 0.001, and GP_NS), a lower proportion of "red" complex (GP: p < 0.01), a higher proportion of "yellow" (GP; p < 0.001), and "orange" (GP; p < 0.01) complex than the non-T2D. GP_T2D individuals exhibited a greater proportion of putative-species-Campylobacter gracilis and S. constellatus (p < 0.001), and Parvimonas micra and Prevotella nigrescens (p < 0.01), than GP_non-T2D. T2D individuals with HbA1c > 8% had presented significantly higher mean pocket-depth and higher levels of G. morbillorum (p < 0.05) and those with obesity or dyslipidemia harbored higher levels, prevalence, or proportion of Streptococcus sp., Actinomyces sp., and Capnocytophaga sp. CONCLUSIONS: T2D individuals harbored a particular microbial profile different to non-T2D microbiota. Metabolic control was related to dysbiosis of microbiota-HbA1c>8% related to periodontitis and obesity or dyslipidemia with the predominance of saccharolytic bacteria, irrespective of their periodontal condition.

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