Periodontal Disease and Preterm Delivery: Influences of Campylobacter rectus Infection on Placental Innate Immunity

Preterm delivery (PTD) is the major cause of neonatal mortality/ morbidity in the world. PTD pathogenesis can be initiated by multiple mechanisms; however inflammation is the most crucial step that leads to membrane weakening, placental rupture and early uterine contraction initiation. Maternal infections are believed to account for most of preterm delivery cases (25-40%), and uterine infections have been reported to be the leading cause of PTD. Vaginal microorganisms are capable of reaching the fetal membranes and inducing local proinflammatory response (chorioamnionitis) that ultimately results in PTD. Nonetheless, the treatment of symptomatic and/or asymptomatic uterine infections during pregnancy has revealed contradictory results in decreasing PTD rates. It has been speculated that other pathogens may come from different untreated focal infections in the body that reach the uterus through hematogenous dissemination and infect the maternal-fetal interface. In particular, Campylobacter rectus is a Gram negative anaerobe harbored in periodontitis-associated oral biofilms that has shown the competence to translocate to the fetoplacental unit and operate as a potential fetal infectious agent eliciting prematurity. Moreover, a number of clinical studies have found an association between periodontitis and preterm delivery. Maternal periodontitis has been found to be associated with increased risk for fetal exposure to periodontal pathogens in PTD cases. Yet, the underlying biological mechanisms sustaining preterm delivery onset after C. rectus infection remain largely unknown. This dissertation hypothesized that C rectus induces a placental innate inflammatory response mediated by Toll-like receptors (TLRs). Our experimental data on animal models have demonstrated C. rectus ability to disseminate from distant sites of infection, to induce a local placental inflammatory response along with a fetal intrauterine growth restriction phenotype, and to upregulate TLR-4 expression in placental trophoblasts after infection. The experimental results here presented demonstrated the importance of TLRs in mediating proinflammatory phenotype both in vitro (human trophoblastic cell line) and in vivo (murine) infection models in response to C. rectus infection. Taken together, the results here presented will elucidate in part the maternal/fetal biological mechanisms leading to PTD in humans, bringing new insights, theories and health policies into the preterm delivery field

Systemic Th17 response in the presence of periodontal inflammation

The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology. Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis. Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4+CD161+) cells and Th17IL23R+ (CD4+CD161+IL-23R+) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the “enriched population” (50,000 events for each). Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266). Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis

Cannabinoids in Periodontology: Where Are We Now?

INTRODUCTION: Cannabinoids are a well-documented treatment modality for various immune and inflammatory diseases, including asthma, chronic obstructive pulmonary disease, Crohn\u27s disease, arthritis, multiple sclerosis, and a range of neurodegenerative conditions. However, limited information is available regarding the therapeutic potential of cannabinoids in treating periodontal disease. OBJECTIVE: The objective of this study is to analyze the current evidence on the antibacterial and immunomodulatory effects of cannabis and its role in the healing and regeneration processes within periodontal tissues. RESULTS: This review discusses the potential role of cannabinoids in restoring periodontal tissue homeostasis. CONCLUSIONS: The examination of the endocannabinoid system and the physiological effects of cannabinoids in the periodontium suggests that they possess immunomodulatory and antibacterial properties, which could potentially promote proper tissue healing and regeneration

Periodontal treatment effects on endothelial function and cardiovascular disease biomarkers in subjects with chronic periodontitis: protocol for a randomized clinical trial

Abstract Background Periodontal disease (PD) is an infectious clinical entity characterized by the destruction of supporting tissues of the teeth as the result of a chronic inflammatory response in a susceptible host. It has been proposed that PD as subclinical infection may contribute to the etiology and to the pathogenesis of several systemic diseases including Atherosclerosis. A number of epidemiological studies link periodontal disease/edentulism as independent risk factor for acute myocardial infarction, peripheral vascular disease, and cerebrovascular disease. Moreover, new randomized controlled clinical trials have shown an improvement on cardiovascular surrogate markers (endothelial function, sICAM, hsPCR level, fibrinogen) after periodontal treatment. Nonetheless, such trials are still limited in terms of external validity, periodontal treatment strategies, CONSORT-based design and results consistency/extrapolation. The current study is designed to evaluate if periodontal treatment with scaling and root planning plus local delivered chlorhexidine improves endothelial function and other biomarkers of cardiovascular disease in subjects with moderate to severe periodontitis. Methods/Design This randomized, single-blind clinical trial will be performed at two health centers and will include two periodontal treatment strategies. After medical/periodontal screening, a baseline endothelium-dependent brachial artery flow-mediated dilatation (FMD) and other systemic surrogate markers will be obtained from all recruited subjects. Patients then will be randomized to receive either supragingival/subgingival plaque cleaning and calculus removal plus chlorhexidine (treatment group) or supragingival plaque removal only (control group). A second and third FMD will be obtained after 24 hours and 12 weeks in both treatment arms. Each group will consist of 49 patients (n = 98) and all patients will be followed-up for secondary outcomes and will be monitored through a coordinating center. The primary outcomes are FMD differences baseline, 24 hours and 3 months after treatment. The secondary outcomes are differences in C-reactive protein (hs-CRP), glucose serum levels, blood lipid profile, and HOMA index. Discussion This RCT is expected to provide more evidence on the effects of different periodontal treatment modalities on FMD values, as well as to correlate such findings with different surrogate markers of systemic inflammation with cardiovascular effects. Trial registration number ClinicalTrials.gov Identifier: NCT00681564

Disruption of Immune Homeostasis in Human Dendritic Cells via Regulation of Autophagy and Apoptosis by

As fundamental processes of immune homeostasis, autophagy, and apoptosis must be maintained to mitigate risk of chronic inflammation and autoimmune diseases. Periodontitis is a chronic inflammatory disease characterized by oral microbial dysbiosis, and dysregulation of dendritic cell (DC) and T cell responses. The aim of this study was to elucidate the underlying mechanisms by which the oral microb

Systemic Antibiotic Therapy Reduces Circulating Inflammatory Dendritic Cells and Treg-Th17 Plasticity in Periodontitis

Periodontitis (PD) is a common dysbiotic inflammatory disease that leads to local bone deterioration and tooth loss. PD patients experience low-grade bacteremias with oral microbes implicated in the risk of heart disease, cancer, and kidney failure. Although Th17 effectors are vital to fighting infection, functional imbalance of Th17 effectors and regulatory T cells (Tregs) promote inflammatory diseases. In this study, we investigated, in a small pilot randomized clinical trial, whether expansion of inflammatory blood myeloid dendritic cells (DCs) and conversion of Tregs to Th17 cells could be modulated with antibiotics (AB) as part of initial therapy in PD patients. PD patients were randomly assigned to either 7 d of peroral metronidazole/amoxicillin AB treatment or no AB, along with standard care debridement and chlorhexidine mouthwash. 16s ribosomal RNA analysis of keystone pathoge

Antisépticos orales para la disminución del riesgo de transmisión del COVID-19 : bases biológicas

La descontaminación oral ha sido incluida en casi todas las publicaciones que relacionan el COVID-19 con la práctica odontológica. Esto se fundamenta en la presencia del coronavirus SARS-CoV-2 en la saliva y en la alta posibilidad de contagio en forma de aerosoles. La recomendación del uso de antisépticos orales específicos, en los diferentes protocolos que las asociaciones científicas han publicado a nivel mundial, se basa en los resultados de investigaciones realizadas para estudiar la prevención de otras patologías virales, así como en algunas causadas por bacterias. El objetivo de la presente revisión es establecer la base biológica para el uso de antisépticos orales, con el fin de disminuir la carga viral en la saliva y como mecanismo para prevenir la transmisión del SARS-CoV-2. En este trabajo, se recoge información sobre la naturaleza de la enfermedad, cómo se expresan los receptores de entrada en tejidos (haciendo énfasis en la cavidad oral) y su relevancia en la infección (carga viral en la saliva, rutas de infección y una posible participación de los aerosoles en la transmisión), para que, junto con la mecánica de acción y la potencial capacidad virucida de cada antiséptico, se implemente su uso para disminuir el riesgo de transmisión, tanto en el consultorio como en los protocolos de higiene oral diarios.ColgateBogot

Oral Pathobiont Activates Anti-Apoptotic Pathway, Promoting both Immune Suppression and Oncogenic Cell Proliferation.

Chronic periodontitis (CP) is a microbial dysbiotic disease linked to increased risk of oral squamous cell carcinomas (OSCCs). To address the underlying mechanisms, mouse and human cell infection models and human biopsy samples were employed. We show that the \u27keystone\u27 pathogen Porphyromonas gingivalis, disrupts immune surveillance by generating myeloid-derived dendritic suppressor cells (MDDSCs) from monocytes. MDDSCs inhibit CTLs and induce FOXP3 + 

Ex vivo validation of magnetically actuated intravascular untethered robots in a clinical setting

Intravascular surgical instruments require precise navigation within narrow vessels, necessitating maximum flexibility, minimal diameter, and high degrees of freedom. Existing tools often lack control during insertion due to undesirable bending, limiting vessel accessibility and risking tissue damage. Next-generation instruments aim to develop hemocompatible untethered devices controlled by external magnetic forces. Achieving this goal remains complex due to testing and implementation challenges in clinical environments. Here we assess the operational effectiveness of hemocompatible untethered magnetic robots using an ex vivo porcine aorta model. The results demonstrate a linear decrease in the swimming speed of untethered magnetic robots as arterial blood flow increases, with the capability to navigate against a maximum arterial flow rate of 67 mL/min. The untethered magnetic robots effectively demonstrate locomotion in a difficult-to-access target site, navigating through the abdominal aorta and reaching the distal end of the renal artery