scholarly journals Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

2021 ◽  
Vol 11 ◽  
Author(s):  
Qingsong Jiang ◽  
Yuxi Zhao ◽  
Yusen Shui ◽  
Xuedong Zhou ◽  
Lei Cheng ◽  
...  
Keyword(s):  
Late Onset ◽  
Neutrophil Recruitment ◽  
Neutrophil Extracellular Trap ◽  
Periodontal Pocket ◽  
Junctional Epithelium ◽  
Periodontal Pathogens ◽  
Inflammatory Reactions ◽  
Periodontal Tissues ◽  
Microbial Invasion ◽  
Excessive Activation

Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

scholarly journals INVESTIGATION OF SPECIES COMPOSITION OF MICROFLORA IN PERIODONTAL POCKETS IN PATIENTS WITH GENERALIZED PERIODONTITIS AND METABOLIC SYNDROME

2021 ◽  
Vol 21 (3) ◽  
pp. 147-150
Author(s):  
T.A. Hlushchenko
Keyword(s):  
Metabolic Syndrome ◽  
Periodontal Disease ◽  
Species Composition ◽  
Periodontal Diseases ◽  
Oral Microbiome ◽  
Periodontal Pathogens ◽  
Periodontal Tissues ◽  
The Metabolic Syndrome ◽  
Microbial Invasion ◽  
Rank One

Among dental diseases, periodontal diseases rank one of the leading places and are considered as the most pressing issues of modern dentistry. The presence of concomitant somatic pathology, in particular, cardiovascular, endocrinological, autoimmune diseases is an important factor that considerably determines the course and prognosis of periodontal disease. Metabolic syndrome is regarded as an urgent social and medical issue due to its high prevalence among the general population and its contribution to the development and progression of cardiovascular disease. The number of reports and scientific interest in the metabolic syndrome has grown up significantly in recent years, but despite the significant number of studies, the oral microbiome in patients with periodontal disease and underlying metabolic syndrome is still remaining insufficiently studied. The aim of this work was to investigate the species composition of the microflora in periodontal pockets and the frequency of excretion of certain types of microorganisms in the acute generalized periodontitis in patients with metabolic syndrome. A microbiological study was performed in 30 people with metabolic syndrome and generalized periodontitis, who formed the main group, and in 30 people with generalized periodontitis without endocrinological pathology, who formed a comparison group. The results of microbiological examination indicate pathological changes in the oral microbiome in the patients with metabolic syndrome demonstrating a predominance of periodontal pathogens. It can be assumed that the components of the metabolic syndrome can initiate and support microbial invasion thus resulting in the inflammatory reaction of periodontal tissues. There is a similarity between pathogenetic mechanisms of metabolic syndrome and periodontal disease that lead to the impairment of all types of metabolism: protein, lipid, mineral, carbohydrate. As a consequence, this contributes to the progressive destruction of oral tissues. The obtained data enable to suggest the dependence between the presence of the patient's metabolic syndrome and the development of intensive damage to periodontal tissues.

scholarly journals Neutrophils Orchestrate the Periodontal Pocket

2021 ◽  
Vol 12 ◽  
Author(s):  
Ljubomir Vitkov ◽  
Luis E. Muñoz ◽  
Janina Schoen ◽  
Jasmin Knopf ◽  
Christine Schauer ◽  
...  
Keyword(s):  
Regional Differences ◽  
Late Onset ◽  
Neutrophil Extracellular Trap ◽  
Periodontal Pocket ◽  
Oral Microbiota ◽  
Tooth Surfaces ◽  
Molecular Patterns ◽  
Neutrophil Response ◽  
Stimulation Of

The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show “healthy” oral microbiota pattern, but a high diversity depending on culture, diets, regional differences, age, social state etc. These findings relativise the aetiological role of the dysbiosis in periodontitis. Furthermore, many late-onset periodontitis traits cannot be explained by dysbiosis; e.g. age-relatedness, attenuation by anti-ageing therapy, neutrophil hyper-responsiveness, and microbiota shifting by dysregulated immunity, yet point to the crucial role of dysregulated immunity and neutrophils in particular. Furthermore, patients with neutropenia and neutrophil defects inevitably develop early-onset periodontitis. Intra-gingivally injecting lipopolysaccharide (LPS) alone causes an exaggerated neutrophil response sufficient to precipitate experimental periodontitis. Vice versa to the surplus of LPS, the increased neutrophil responsiveness characteristic for late-onset periodontitis can effectuate gingiva damage likewise. The exaggerated neutrophil extracellular trap (NET) response in late-onset periodontitis is blameable for damage of gingival barrier, its penetration by bacteria and pathogen-associated molecular patterns (PAMPs) as well as stimulation of Th17 cells, resulting in further neutrophil activation. This identifies the dysregulated immunity as the main contributor to periodontal disease.

scholarly journals The Role of Neutrophil Extracellular Traps in Periodontitis

2021 ◽  
Vol 11 ◽  
Author(s):  
Jingyi Wang ◽  
Yucong Zhou ◽  
Biao Ren ◽  
Ling Zou ◽  
Bing He ◽  
...  
Keyword(s):  
Immune Response ◽  
Late Onset ◽  
Neutrophil Extracellular Traps ◽  
Polymorphonuclear Neutrophils ◽  
Inflammatory Factors ◽  
Periodontal Pathogens ◽  
Growth Environment ◽  
Periodontal Tissues ◽  
Extracellular Traps ◽  
Periodontal Bacteria

Periodontitis is a chronic, destructive disease of periodontal tissues caused by multifaceted, dynamic interactions. Periodontal bacteria and host immunity jointly contribute to the pathological processes of the disease. The dysbiotic microbial communities elicit an excessive immune response, mainly by polymorphonuclear neutrophils (PMNs). As one of the main mechanisms of PMN immune response in the oral cavity, neutrophil extracellular traps (NETs) play a crucial role in the initiation and progression of late-onset periodontitis. NETs are generated and released by neutrophils stimulated by various irritants, such as pathogens, host-derived mediators, and drugs. Chromatin and proteins are the main components of NETs. Depending on the characteristics of the processes, three main pathways of NET formation have been described. NETs can trap and kill pathogens by increased expression of antibacterial components and identifying and trapping bacteria to restrict their spread. Moreover, NETs can promote and reduce inflammation, inflicting injuries on the tissues during the pro-inflammation process. During their long-term encounter with NETs, periodontal bacteria have developed various mechanisms, including breaking down DNA of NETs, degrading antibacterial proteins, and impacting NET levels in the pocket environment to resist the antibacterial function of NETs. In addition, periodontal pathogens can secrete pro-inflammatory factors to perpetuate the inflammatory environment and a friendly growth environment, which are responsible for the progressive tissue damage. By learning the strategies of pathogens, regulating the periodontal concentration of NETs becomes possible. Some practical ways to treat late-onset periodontitis are reducing the concentration of NETs, administering anti-inflammatory therapy, and prescribing broad-spectrum and specific antibacterial agents. This review mainly focuses on the mechanism of NETs, pathogenesis of periodontitis, and potential therapeutic approaches based on interactions between NETs and periodontal pathogens.

scholarly journals CLINICAL COURSE OF PERIODONTAL DISEASES IN PATIENTS WITH POSTMENOPAUSAL OSTEOPOROSIS TREATED WITH BISPHOSPHONATES

2021 ◽  
Vol 11 (2) ◽  
pp. 118-122
Author(s):  
Marietta Sukhorukikh ◽  
Marina Kozlova ◽  
Ekaterina Gorbatova ◽  
Larisa Dzikovitskaya ◽  
Alexey Bashtovoy
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Clinical Course ◽  
Periodontal Diseases ◽  
Prolonged Treatment ◽  
Tablet Form ◽  
Inflammatory Reactions ◽  
Periodontal Tissues ◽  
Dental Examination ◽  
Probe System

The aim of the study was to assess the state of the clinical course of periodontal diseases in patients with postmenopausal osteoporosis (OP), depending on the long-term oral administration of various groups of bisphosphonates (BP). The study included 120 women aged 55–65 years with postmenopausal OP for at least three years who took complex antiosteoporetic therapy, including BP in tablet form. The dental examination included an examination of the oral cavity, the study of the pH of the oral fluid, the hygienic state of the mouth (the "Florida Probe" system). According to the results of the study, it was revealed that prolonged treatment of BP in tablets can provoke the development of inflammatory reactions in periodontal tissues. This phenomenon is associated with a shift in the pH of saliva to the acidic side, at which its buffer properties change.

scholarly journals Periodontitis-level butyrate-induced ferroptosis in periodontal ligament fibroblasts by activation of ferritinophagy

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Yunhe Zhao ◽  
Jiao Li ◽  
Wei Guo ◽  
Houxuan Li ◽  
Lang Lei
Keyword(s):  
Cell Death ◽  
Periodontal Ligament ◽  
Iron Homeostasis ◽  
Glutathione Depletion ◽  
Periodontal Pocket ◽  
Periodontal Ligament Fibroblasts ◽  
Periodontal Tissues ◽  
Regulated Cell Death ◽  
Long Term Treatment

Abstract Loss of periodontal ligament fibroblasts (PDLFs) is one critical issue for regenerating lost periodontal tissues. A wide variety of regulated cell death pathways, such as apoptosis, pyroptosis, and necroptosis have been proposed in the periodontitis development. The aim of the present study was to explore whether long-term periodontitis-level butyrate may trigger ferroptosis, a newly characterized iron-dependent regulated cell death in PDLFs. Here, we showed that long-term treatment of butyrate, an important short-chain fatty acid in the periodontal pocket, induces the cargo receptor nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy and ferroptosis in PDLFs. Butyrate-induced iron accumulation, reactive oxygen species (ROS) generation, glutathione depletion and lipid peroxidation in PDLFs, and the butyrate-induced ferroptosis can be blocked by the lipid peroxide scavenger ferrostatin-1. The NCOA4-mediated ferritinophagy is dependent on p38/hypoxia inducible factor-1α (HIF-1α) pathway activation as well as Bromodomain-containing protein (BRD) 4 and cyclin-dependent kinase 9 (CDK9) coordination. These lines of evidence provide a new mechanistic insight into the mechanism of loss of PDLFs during periodontitis development, showing that periodontitis-level butyrate disrupted iron homeostasis by activation of NCOA4-mediated ferritinophagy, leading to ferroptosis in PDLFs.

scholarly journals In vitro minocycline activity on superinfecting microorganisms isolated from chronic periodontitis patients

2006 ◽  
Vol 20 (3) ◽  
pp. 202-206 ◽  
Author(s):  
Luciana Fernandes de Oliveira ◽  
Antonio Olavo Cardoso Jorge ◽  
Silvana Soléo Ferreira dos Santos
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Chronic Periodontitis ◽  
Periodontal Pocket ◽  
Dilution Method ◽  
Agar Dilution Method ◽  
Periodontal Pathogens ◽  
Candida Spp ◽  
Systemic Antibiotic Therapy ◽  
Staphylococcus Spp

Chronic periodontitis is the most common type of periodontitis and it is associated with various species of microorganisms. Enteric rods, Pseudomonas, Staphyloccocus and Candida have been retrieved from periodontal pockets of patients with chronic periodontitis and correlated to cases of superinfection. Local or systemic antibiotic therapy is indicated to reinforce the effects of the conventional mechanical therapy. Minocycline has been suggested as one of the most effective drugs against periodontal pathogens. The aim of this work was to evaluate the minimal inhibitory concentration (MIC) of minocycline on superinfecting microorganisms isolated from the periodontal pocket and the oral cavity of individuals with chronic periodontitis. Isolates of Enterobacteriaceae (n = 25), Staphylococcus spp. (n = 25), Pseudomonas aeruginosa (n = 9) and Candida spp. (n = 25) were included in the study. Minimal inhibitory concentrations (MIC) of minocycline were determined using the Müeller-Hinton agar dilution method. Staphylococcus spp. isolates were the most sensitive to minocycline with a MIC of 8 µg/mL, followed by Enterobacteriaceae with a MIC of 16 µg/mL. The concentration of 16 µg/mL inhibited 96% of Candida spp. isolates. The MIC for 88.8% of the isolates of Pseudomonas aeruginosa was 128 µg/mL. A concentration of 1,000 µg/mL was not enough to inhibit 100% of the tested isolates.

scholarly journals Simultaneous Measurement of 25 Inflammatory Markers and Neurotrophins in Neonatal Dried Blood Spots by Immunoassay with xMAP Technology

2005 ◽  
Vol 51 (10) ◽  
pp. 1854-1866 ◽  
Author(s):  
Kristin Skogstrand ◽  
Poul Thorsen ◽  
Bent Nørgaard-Pedersen ◽  
Diana E Schendel ◽  
Line C Sørensen ◽  
...  
Keyword(s):  
Neonatal Screening ◽  
Inflammatory Markers ◽  
Late Onset ◽  
High Capacity ◽  
Dried Blood Spots ◽  
Case Control Studies ◽  
Inflammatory Reactions ◽  
Screening Programs ◽  
Reactive Protein ◽  
Xmap Technology

Abstract Background: Inflammatory reactions and other events in early life may be part of the etiology of late-onset diseases, including cerebral palsy, autism, and type 1 diabetes. Most neonatal screening programs for congenital disorders are based on analysis of dried blood spot samples (DBSS), and stored residual DBSS constitute a valuable resource for research into the etiology of these diseases. The small amount of blood available, however, limits the number of analytes that can be determined by traditional immunoassay methodologies. Methods: We used new multiplexed sandwich immunoassays based on flowmetric Luminex® xMAP technology to measure inflammatory markers and neutrophins in DBSS. Results: The high-capacity 25-plex multianalyte method measured 23 inflammatory and trophic cytokines, triggering receptor expressed on myeloid cells-1 (TREM-1), and C-reactive protein in two 3.2-mm punches from DBSS. It also measured 26 cytokines and TREM-1 in serum. Standards Recovery in the 25-plex method were 90%–161% (mean, 105%). The low end of the working range for all 25 analytes covered concentrations found in DBSS from healthy newborns. Mean recovery of exogenous analytes added at physiologic concentrations in DBSS models was 174%, mean intra- and interassay CVs were 6.2% and 16%, respectively, and the mean correlation between added and measured analytes was r2 = 0.91. In DBSS routinely collected on days 5–7 from 8 newborns with documented inflammatory reactions at birth, the method detected significantly changed concentrations of inflammatory cytokines. Measurements on DBSS stored at −24 °C for >20 years showed that most cytokines are detectable in equal concentrations over time. Conclusions: The method can reliably measure 25 inflammatory markers and growth factors in DBSS. It has a large potential for high-capacity analysis of DBSS in epidemiologic case–control studies and, with further refinements, in neonatal screening.

scholarly journals MICRO BIOLOGY OF PERIODONTAL DISEASE- A REVIEW

2021 ◽  
Vol 5 (6) ◽  
Author(s):  
Jageer Chinna ◽  
Jannat Sharma
Keyword(s):  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Disease Process ◽  
Fusobacterium Nucleatum ◽  
Host Cells ◽  
Bacterial Invasion ◽  
Periodontal Pathogens ◽  
Tissue Destruction ◽  
Campylobacter Rectus ◽  
Periodontal Tissues

Periodontal diseases are inflammatory and destructive diseases of the dentogingival complex associated with specific periodontal pathogens inhabiting periodontal pockets. Periodontal diseases lead to damage of the periodontal tissues supporting the teeth (bone and connective tissue) and affect the quality of life of the affected individuals: poor alimentation, tooth loss, social and financial problems. Although it is generally considered that the disease has multifactorial etiology, data show that some specific Gram-negative microorganisms in the subgingival plaque biofilm play a major role in the initiation and progression of periodontitis. Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia form a consortium in the subgingival biofilm and are regarded as the principal periodontopathogenic bacteria. Other microorganisms that have been implicated as predominant species in the disease process are: Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus migros, Eikenella corrodens. In periodontitis, the initiation of the disease is the colonization of the tissues by these pathogenic species. The next step is bacterial invasion or invasion by pathogenic products into the periodontal tissues, interactions of bacteria or their substances with host cells, and this directly/indirectly causes degradation of the periodontium, resulting in tissue destruction. Keywords: periodontal disease, periodontal pathogens, microbiology.

scholarly journals Host-Microbial Interactions in Systemic Lupus Erythematosus and Periodontitis

2019 ◽  
Author(s):  
L.C. Pessoa ◽  
G. Aleti ◽  
S. Choudhury ◽  
D. Nguyen ◽  
T. Yaskell ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Systemic Inflammation ◽  
Proinflammatory Cytokines ◽  
Lupus Erythematosus ◽  
Microbial Interactions ◽  
Low Grade ◽  
Periodontal Pathogens ◽  
Systemic Lupus ◽  
Periodontal Tissues ◽  
Low Grade Inflammation

AbstractSystemic lupus erythematosus (SLE) is a potentially fatal complex autoimmune disease, that is characterized by widespread inflammation manifesting tissue damage and comorbidities across the human body including heart, blood vessels, joints, skin, liver, kidneys, and periodontal tissues. The etiology of SLE is partially attributed to a deregulated inflammatory response to microbial dysbiosis and environmental changes. In the mouth, periodontal environment provides an optimal niche to assay local dynamic microbial ecological changes in health and disease important to systemic inflammation in SLE subjects. Our aim was to evaluate the reciprocal impact of periodontal subgingival microbiota on SLE systemic inflammation. Ninety-one female subjects were recruited, including healthy (n=31), SLE-inactive (n=29), and SLE-active (n=31). Patients were screened for probing depth (PD), bleeding on probing (BOP), clinical attachment level (CAL), and classified with or without periodontal dysbiosis, periodontitis. Serum inflammatory cytokines were measured by human cytokine panel and subgingival biofilm was examined by DNA-DNA checkerboard. The results showed significant upregulation of proinflammatory cytokines in individuals with SLE when compared to controls. Stratification of subject’s into SLE-inactive (I) and SLE-active (A) phenotypes or periodontitis and non-periodontitis groups provided new insights into SLE pathophysiology. While low-grade inflammation was found in SLE-I subjects, a potent anti-inflammatory cytokine, IL-10 was found to control clinical phenotypes. Out of twenty-four significant differential oral microbial abundances found in SLE, fourteen unique subgingival bacteria profiles were found to be elevated in SLE. Pathogens from periodontal disease sites (Treponema denticola and Tannerella forsythia) showed increase abundance in SLE-A subjects when compared to controls. Cytokine-microbial correlations showed that periodontal pathogens dominating the environment increased proinflammatory cytokines systemically. Deeper clinical attachment loss and periodontal pathogens were found in SLE subjects, especially on SLE-I, likely due to long-term chronic and low-grade inflammation. Altogether, local periodontal pathogen enrichment was positively associated with high systemic inflammatory profiles, relevant to the overall health and SLE disease pathogenesis.

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