scholarly journals Bacterial pathogenesis and mediators in apical periodontitis

2007 ◽  
Vol 18 (4) ◽  
pp. 267-280 ◽  
Author(s):  
José F. Siqueira Jr ◽  
Isabela N. Rôças
Keyword(s):  
Inflammatory Diseases ◽  
Outer Membrane Proteins ◽  
Disease Process ◽  
Lipoteichoic Acid ◽  
Bacterial Pathogenesis ◽  
Apical Periodontitis ◽  
Related Factors ◽  
Therapeutic Measures ◽  
Root Canal System ◽  
Shock Proteins

Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria- and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

scholarly journals EKSPRESI TNF-α DAN CALCINEURIN PADA ASIMTOMATIS APIKAL PERIODONTITIS AKIBAT INDUKSI Enterococcus faecalis

2019 ◽  
Vol 7 (2) ◽  
pp. 74
Author(s):  
Randy Carlos Sietho ◽  
Mandojo Rukmo ◽  
Edhie Arif Prasetyo ◽  
Tamara Yuanita
Keyword(s):  
Enterococcus Faecalis ◽  
Wistar Rat ◽  
Lipoteichoic Acid ◽  
Apical Periodontitis ◽  
Dominant Group ◽  
Gram Positive Bacteria ◽  
Tnf Α ◽  
Molar Teeth ◽  
Root Canal System ◽  
Factor Α

Background. Gram positive bacteria strain are the major cause of endodontic failure as asymptomatic apical periodontitis. One of the dominant group of bacteria is Enterococcus faecalis that still persistent in root canal system post endodontic therapy procedures. This bacteria has lipoteichoic acid on its membrane that can cause induction of cytokines expression such as Tumor Necrosing Factor-α (TNF-α) and Calcineurin Purpose. This experiment to demonstrated asymptomatic apical periodontitis that induced with Enteroccus faecalis produce raising amount of TNF-α and Calcineurin expression cells in pericapical tissue of wistar rat. Method. The upper right molar teeth of the rat was drilled until perforation then exposed by BHIB 10µl (control positive group), E.faecalis 106 CFU in BHIB 10µl (experimental group) and without drilling (control negative group) then observed until 21th days and counting the amount of TNF-α and Calcineurin expression cells. Conclusion.The results show that asymtomatic apical periodontitis that was induced E.faecalis produce increasing amount of TNF-α and Calcineurin expression cells in periapical tissue wistar rat.

scholarly journals FRI0322 INSULIN RESISTANCE IN NON-DIABETES PATIENTS WITH SPONDYLOARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 752.2-753
Author(s):  
J. C. Quevedo-Abeledo ◽  
F. Genre ◽  
J. Rueda-Gotor ◽  
A. Corrales ◽  
V. Hernández-Hernández ◽  
...  
Keyword(s):  
Cell Function ◽  
Inflammatory Diseases ◽  
Univariate Analysis ◽  
Serum Levels ◽  
Β Cell ◽  
Related Factors ◽  
C Peptide ◽  
Related Data ◽  
Β Cell Function ◽  
Beta Coefficient

Background:Insulin resistance (IR) is a state in which a given concentration of insulin is associated with a subnormal glucose response. IR constitutes a major underlying abnormality driving cardiovascular disease in the general population and has been linked to inflammatory diseases. In this sense, several reports have confirmed that inflammation worsens IR and impairs pancreatic β-cell function in inflammatory diseases such as rheumatoid arthritis and systemic lupus erythematosus.Objectives:In this study we aimed to determine the prevalence of IR in patients with spondyloarthritis (SpA) compared to controls, and whether IR can be explained by disease-related features in SpA patients.Methods:Study of 577 subjects, 306 patients diagnosed with SpA according to ASAS criteria and 271 controls. Insulin and C-peptide serum levels, IR and β-cell function (%B) indexes by homeostatic model assessment (HOMA2), and lipid profiles were assessed in patients and controls. A multivariate regression analysis was performed to evaluate the differences in IR indexes between patients and controls and to determine how IR is associated with disease-related characteristics.Results:SpA patients showed higher serum levels of insulin (8.7 [4.8-15.9] vs. 8.0 [5.7-11.2] uU/ml, p=0.001) and C peptide (1.4 [0.7-2.5] vs. 1.2 [0.7-1.7] ng/ml, p=0.000) than controls in the univariate analysis. Similarly, HOMA2-B% and IR were all significantly higher in SpA patients. These differences were still evident when the comparisons were made after the multivariate analysis had been adjusted for traditional IR-related factors (sex, age, BMI, hypertension, dyslipidemia, smoking and, cholesterol), glucocorticoids intake, insulin and C-peptide. Moreover, HOMA2-B% and HOMA2-IR scores, both calculated with insulin or C-peptide, yielded statistically higher significant values in SpA patients than controls.Classic IR-related factors (age, BMI, waist circumference, hypertension, obesity, dyslipidemia, atherogenic index, and triglycerides), as well as CRP serum levels, were all related, to a greater or lesser degree, with IR and β-cell function. Regarding disease-related data, ASDAS-CRP, BASFI and BASMI scores were positively associated with IR; and BASMI and BASDAI scores were positively related to HOMA2-%B-C peptide. Moreover, the use of NSAID and prednisone were, respectively, positive and negatively related to β-cell function. However, only some of the associations of the univariate analysis were maintained after adjusting for confounders. In this sense, disease duration (beta coefficient 2 [95% CI 1-3], p=0.001) and positivity for HLA-B27 (beta coefficient 30 [95% CI 12-49], p=0.002) were associated with higher β-cell functionality after the multivariate analysis.Conclusion:Patients with SpA have an increased IR compared to controls. SpA disease-related data like disease duration and HLA-B27 are independently associated with β-cell dysfunction.Disclosure of Interests:Juan Carlos Quevedo-Abeledo Speakers bureau: Abbvie, Fernanda Genre: None declared, Javier Rueda-Gotor: None declared, Alfonso Corrales Speakers bureau: Abbvie, Vanessa Hernández-Hernández Speakers bureau: Pfizer, Abbvie, MSD, Natalia Fañanas-Rodríguez: None declared, Bernardo Lavín-Gómez: None declared, delgado frias esmeralda Speakers bureau: Pfizer, Abbvie, MSD, Antonia de Vera-González: None declared, Alejandra Delgado-González: None declared, Laura de Armas-Rillo: None declared, Maria Teresa García-Unzueta: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Iván Ferraz-Amaro Grant/research support from: Pfizer, Abbvie, Speakers bureau: Pfizer, Abbvie, MSD.

scholarly journals Induction of macrophage pyroptosis-related factors by pathogenic E. coli high pathogenicity island (HPI) in Yunnan Saba pigs

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Chunlan Shan ◽  
Shushu Miao ◽  
Chaoying Liu ◽  
Bo Zhang ◽  
Weiwei Zhao ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Inflammatory Diseases ◽  
Pathogenicity Island ◽  
Cell Membrane Permeability ◽  
Inflammatory Factor ◽  
Related Factors ◽  
Membrane Pore ◽  
E Coli ◽  
Caspase 1 ◽  
High Pathogenicity

Abstract Background Pyroptosis plays a pivotal role in the pathogenesis of many inflammatory diseases. The molecular mechanism by which pyroptosis is induced in macrophages following infection with pathogenic E. coli high pathogenicity island (HPI) will be evaluated in our study. Results After infection with the HPI+/HPI− strains and LPS, decreased macrophage cell membrane permeability and integrity were demonstrated with propidium iodide (PI) staining and the lactate dehydrogenase (LDH) assay. HPI+/HPI−-infection was accompanied by upregulated expression levels of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD, with significantly higher levels detected in the HPI+ group compared to those in the HPI− group (P < 0.01 or P < 0.05). HPI+ strain is more pathogenic than HPI− strain. Conclusion Our findings indicate that pathogenic E. coli HPI infection of Saba pigs causes pyroptosis of macrophages characterized by upregulated expression of pyroptosis key factors in the NLRP3/ASC/caspase-1 signaling pathway, direct cell membrane pore formation, and secretion of the inflammatory factor IL-1β and IL-18 downstream of NLRP3 and caspase-1 activation to enhance the inflammatory response.

scholarly journals Role of Serum Amyloid A Protein in Various Diseases with Special Reference to Periodontal and Periapical Inflammation- A Review

2020 ◽  
Author(s):  
Syed Wali Peeran ◽  
Ahmed Elhassan ◽  
Mohammed Zameer ◽  
Syed Nahid Basheer ◽  
Mohammed Mustafa ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Serum Amyloid A ◽  
Inflammatory Diseases ◽  
Apical Periodontitis ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Serum Amyloid A Protein ◽  
Health And Disease ◽  
Periapical Inflammation

Serum Amyloid A (SAA) is an Acute-Phase Protein (APP) produced as an innate nonspecific response to any tissue damage. Hence, it plays a significant role in chronic inflammatory diseases. In particular, SAA levels increase dramatically in chronic periodontitis and chronic apical periodontitis. Recent studies suggest this role of SAA in the pathogenesis of various diseases, including chronic periodontitis and chronic apical periodontitis. Thus, the focus of this review is to sum up the current understanding of the role of SAA in health and disease and to elaborate on possible mechanisms by which SAA could play a role in the pathogenesis of chronic periodontitis and chronic apical periodontitis.

Comparison of anti-microbial efficacy of Calcipex and Metapex in endodontic treatment of chronic apical periodontitis (Preprint)

2020 ◽  
Author(s):  
Momina Anis Motiwala ◽  
Saqib Habib ◽  
Robia Ghafoor ◽  
Seema Irfan
Keyword(s):  
Bacterial Culture ◽  
Apical Periodontitis ◽  
T Test ◽  
Endodontic Treatment ◽  
Microbial Culture ◽  
Routine Procedure ◽  
Canal System ◽  
Colony Forming Unit ◽  
Root Canal System ◽  
Level Of Significance

BACKGROUND Various intracanal medicaments have been used in cases of chronic apical periodontitis for appropriate disinfection of the root canal system to eliminate microbes specially from the inaccessible areas. Caclcium Hydroxide (CH) is the most common intracanal medicament available in various forms, but its effectiveness with or without iodoform using microbial culture is unknown. OBJECTIVE To compare the anti-microbial efficacy of Calcipex and Metapex in endodontic treatment of teeth presenting with chronic apical periodontitis METHODS 60 single rooted teeth of patients with diagnosis of chronic apical periodontitis were selected and the canals were debrided chemo-mechanically. The patients were randomized into two groups: Calcipex and Metapex. The first sample (S1) for bacterial culture was taken before placement of intracanal medicament and the second sample (S2) was taken after 7 days, before final obturation from the canal and sent to lab for culture. Colony Forming Unit (CFU) will be evaluated. Paired t-test will be used to assess difference bet¬ween antimicrobial efficacies within the group of medicaments. Independent sample t-test will be used to assess antimicrobial efficacies between groups. Level of significance will be kept at 0.05. RESULTS The results wil be shared upon completion of study. CONCLUSIONS There is no risk involved in this study as the study is based on routine procedure of endodontic treatment. It will be a benefit for future patients which will help us to decide which intracanal medicament is more effective to use in infected canals. CLINICALTRIAL NCT04336709

Small Heat Shock Proteins in Inflammatory Diseases

2020 ◽  
Author(s):  
V. Sudhakar Reddy ◽  
Trinath Jamma ◽  
G. Bhanuprakash Reddy
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Inflammatory Diseases ◽  
Small Heat Shock Proteins ◽  
Shock Proteins

scholarly journals Designing a multi-epitopic vaccine against the enterotoxigenic Bacteroides fragilis based on immunoinformatics approach

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mahnoor Majid ◽  
Saadia Andleeb
Keyword(s):  
Outer Membrane ◽  
Inflammatory Diseases ◽  
Outer Membrane Proteins ◽  
3D Structure ◽  
Human Microbiome ◽  
Bacteroides Fragilis ◽  
Effective Vaccine ◽  
Vaccine Strategy ◽  
Intestinal Infections ◽  
Normal Human

AbstractEnterotoxigenic Bacteroides fragilis is an enteric pathogen which is described as a causative agent of various intestinal infections and inflammatory diseases. Moreover, various research studies have reported it to be a leading factor in the development of colorectal cancer. As a part of the normal human microbiome, its treatment has become quite a challenge due to the alarming resistance against the available antibiotics. Although, this particular strain of B. fragilis shows susceptibility to few antibiotics, it is pertinent to devise an effective vaccine strategy for its elimination. There is no vaccine available against this pathogen up to date; therefore, we systematically ventured the outer membrane toxin producing proteins found exclusively in the toxigenic B. fragilis through the in-silico approaches to predict a multi-epitopic chimeric vaccine construct. The designed protein constitutes of epitopes which are predicted for linear B cells, Helper and T cells of outer membrane proteins expected to be putative vaccine candidates. The finalized proteins are only expressed in the enterotoxigenic B. fragilis, thus proving them to be exclusive. The 3D structure of the protein was first predicted followed by its refinement and validation via utilizing the bioinformatic approaches. Docking of the designed protein with the TLR2 receptor forecasted apt binding. Upon immune simulation, notable levels were observed in the expression of the immune cells.

scholarly journals Calprotectin in rheumatic diseases

2016 ◽  
Vol 242 (8) ◽  
pp. 859-873 ◽  
Author(s):  
Francesca Ometto ◽  
Lara Friso ◽  
Davide Astorri ◽  
Costantino Botsios ◽  
Bernd Raffeiner ◽  
...  
Keyword(s):  
Rheumatic Diseases ◽  
Potential Role ◽  
Inflammatory Diseases ◽  
Disease Process ◽  
Serum Levels ◽  
Autoimmune Disorders ◽  
High Serum ◽  
Response To Treatment ◽  
Tnf Α ◽  
Activated Monocytes

Calprotectin is a heterodimer formed by two proteins, S100A8 and S100A9, which are mainly produced by activated monocytes and neutrophils in the circulation and in inflamed tissues. The implication of calprotectin in the inflammatory process has already been demonstrated, but its role in the pathogenesis, diagnosis, and monitoring of rheumatic diseases has gained great attention in recent years. Calprotectin, being stable at room temperature, is a candidate biomarker for the follow-up of disease activity in many autoimmune disorders, where it can predict response to treatment or disease relapse. There is evidence that a number of immunomodulators, including TNF-α inhibitors, may reduce calprotectin expression. S100A8 and S100A9 have a potential role as a target of treatment in murine models of autoimmune disorders, since the direct or indirect blockade of these proteins results in amelioration of the disease process. In this review, we will go over the biologic functions of calprotectin which might be involved in the etiology of rheumatic disorders. We will also report evidence of its potential use as a disease biomarker. Impact statement Calprotectin is an acute-phase protein produced by monocytes and neutrophils in the circulation and inflamed tissues. Calprotectin seems to be more sensitive than CRP, being able to detect minimal residual inflammation and is a candidate biomarker in inflammatory diseases. High serum levels are associated with some severe manifestations of rheumatic diseases, such as glomerulonephritis and lung fibrosis. Calprotectin levels in other fluids, such as saliva and synovial fluid, might be helpful in the diagnosis of rheumatic diseases. Of interest is also the potential role of calprotectin as a target of treatment.

scholarly journals Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure

2009 ◽  
Vol 55 (12) ◽  
pp. 2098-2112 ◽  
Author(s):  
Walter E Kelley ◽  
James L Januzzi ◽  
Robert H Christenson
Keyword(s):  
Heart Failure ◽  
Acute Coronary Syndrome ◽  
Respiratory Disease ◽  
Cardiac Troponin ◽  
Inflammatory Diseases ◽  
Disease Process ◽  
Length Of Hospital Stay ◽  
Myocardial Damage ◽  
Coronary Syndrome ◽  
Upper Gastrointestinal

AbstractBackground: Although cardiac troponin (cTn) is a cornerstone marker in the assessment and management of patients with acute coronary syndrome (ACS) and heart failure (HF), cTn is not diagnostically specific for any single myocardial disease process. This narrative review discusses increases in cTn that result from acute and chronic diseases, iatrogenic causes, and myocardial injury other than ACS and HF.Content: Increased cTn concentrations have been reported in cardiac, vascular, and respiratory disease and in association with infectious processes. In cases involving acute aortic dissection, cerebrovascular accident, treatment in an intensive care unit, and upper gastrointestinal bleeding, increased cTn predicts a longer time to diagnosis and treatment, increased length of hospital stay, and increased mortality. cTn increases are diagnostically and prognostically useful in patients with cardiac inflammatory diseases and in patients with respiratory disease; in respiratory disease cTn can help identify patients who would benefit from aggressive management. In chronic renal failure patients the diagnostic sensitivity of cTn for ACS is decreased, but cTn is prognostic for the development of cardiovascular disease. cTn also provides useful information when increases are attributable to various iatrogenic causes and blunt chest trauma.Summary: Information on the diagnostic and prognostic uses of cTn in conditions other than ACS and heart failure is accumulating. Although increased cTn in settings other than ACS or heart failure is frequently considered a clinical confounder, the astute physician must be able to interpret cTn as a dynamic marker of myocardial damage, using clinical acumen to determine the source and significance of any reported cTn increase.

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