scholarly journals The Role of Osteoimmunology in Periodontal Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Rayyan A. Kayal
Keyword(s):  
Periodontal Disease ◽  
Inflammatory Mediators ◽  
Pathological Condition ◽  
Inflammatory Cells ◽  
Innate And Adaptive Immunity ◽  
Tooth Structure ◽  
Continuous State ◽  
Host Defense System ◽  
Bacterial Plaque

Periodontal disease is a pathological condition that involves inflammation of the tooth supporting structures. It occurs in response to the presence of bacterial plaque on the tooth structure. The host defense system, including innate and adaptive immunity, is responsible for combating the pathologic bacteria invading the periodontal tissue. Failure to eradicate the invading pathogens will result in a continuous state of inflammation where inflammatory cells such as lymphocytes, PMNs, and macrophages will continue to produce inflammatory mediators in an effort to destroy the invaders. Unfortunately, these inflammatory mediators have a deleterious effect on the host tissue as well as foreign microbes. One of the effects of these mediators on the host is the induction of matrix degradation and bone resorption through activation of proteases and other inflammatory mediators that activate osteoclasts.

The Role of Toothbrushing in the Prevention and Treatment of Periodontal Disease: Personal Experience of Both Clinical and Experimental Observation for More than Thirty Years

1988 ◽  
Vol 2 (2) ◽  
pp. 204-208 ◽  
Author(s):  
J. Ishikawa
Keyword(s):  
Periodontal Disease ◽  
Personal Experience ◽  
Experimental Studies ◽  
Food Habit ◽  
Tooth Surface ◽  
Treatment And Prevention ◽  
Oral Environment ◽  
Systemic Factors ◽  
Bacterial Plaque

There have been dramatic developments in the theory and therapy of periodontal disease in the last few decades. This paper focuses on the role of toothbrushing in the treatment and prevention of periodontal disease, based on the author's personal experience gained from both clinical and experimental observations for more than 30 years. Even in the recent past, periodontal disease was considered to be untreatable because of various misconceptions regarding its etiology. Attention was concentrated mainly on systemic factors. As a result, periodontallyinvolved teeth were extracted mostly due to lack of technical know-how. The author devoted his primary investigative efforts to systemic factors and found that those were only minimally significant. Later, after using wild and captive monkeys to make extensive experimental studies on local factors, he was convinced that food habit (hard, fibrous, or soft) contributes directly to the etiology of periodontal disease which is restricted in the oral environment itself. Today it is well-established that accumulation of bacterial plaque on the tooth surface is the most important single factor responsible for periodontal disease, and systemic influence can merely modify the condition. Therefore, the accumulated plaque should be mechanically removed by toothbrushing. The essence of mechanical toothbrushing is not only to remove the plaque but also to compensate for the mechanical stimulation of the gingiva (gingival massage), which is lacking with modern soft food. This lecture reviews the effect of methodical toothbrushing obtained from both clinical and experimental studies in animals.

scholarly journals Inflammatory Mediators and Angiogenic Factors in Choroidal Neovascularization: Pathogenetic Interactions and Therapeutic Implications

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
Claudio Campa ◽  
Ciro Costagliola ◽  
Carlo Incorvaia ◽  
Carl Sheridan ◽  
Francesco Semeraro ◽  
...  
Keyword(s):  
Growth Factor ◽  
Choroidal Neovascularization ◽  
Inflammatory Mediators ◽  
Transforming Growth Factor ◽  
Pathological Condition ◽  
Inflammatory Cells ◽  
Angiogenic Factors ◽  
Age Related Macular Degeneration ◽  
Therapeutic Implications ◽  
Age Related

Choroidal neovascularization (CNV) is a common and severe complication in heterogeneous diseases affecting the posterior segment of the eye, the most frequent being represented by age-related macular degeneration. Although the term may suggest just a vascular pathological condition, CNV is more properly definable as an aberrant tissue invasion of endothelial and inflammatory cells, in which both angiogenesis and inflammation are involved. Experimental and clinical evidences show that vascular endothelial growth factor is a key signal in promoting angiogenesis. However, many other molecules, distinctive of the inflammatory response, act as neovascular activators in CNV. These include fibroblast growth factor, transforming growth factor, tumor necrosis factor, interleukins, and complement. This paper reviews the role of inflammatory mediators and angiogenic factors in the development of CNV, proposing pathogenetic assumptions of mutual interaction. As an extension of this concept, new therapeutic approaches geared to have an effect on both the vascular and the extravascular components of CNV are discussed.

scholarly journals Chronic Inflammation as an Immunological Abnormality and Effectiveness of Exercise

Biomolecules ◽  
2019 ◽  
Vol 9 (6) ◽  
pp. 223 ◽  
Author(s):  
Katsuhiko Suzuki
Keyword(s):  
Chronic Inflammation ◽  
Pathological Condition ◽  
Inflammatory Cells ◽  
The Elderly ◽  
Healthy Life ◽  
Daily Lives ◽  
Food Ingredients ◽  
Tissue Degeneration ◽  
Age Related

Reduced levels of physical activity in people’s daily lives cause the development of metabolic syndromes or age-related disorders. Chronic inflammation is now understood to be an underlying pathological condition in which inflammatory cells such as neutrophils and monocyte/macrophages infiltrate into fat and other tissues and accumulate when people become obese due to overeating and/or physical inactivity. Pro-inflammatory mediators such as cytokines that are secreted in excess from inflammatory cells will not only lead to the development of arteriosclerosis when they chronically affect blood vessels but also bring tissue degeneration and/or dysfunction to various organs. Chronic inflammation is also involved in sarcopenia that brings hypofunction in the elderly, dementia, osteoporosis, or cancer and negatively affects many chronic diseases and people’s healthy life expectancy. In this paper, outlines of such studies are introduced in terms of homeostatic inflammation, which occurs chronically due to the innate immune system and its abnormalities, while focusing on the efficacy of exercise from aspects of immunology and oxidative stress. The preventative effects of functional food ingredients in combination with exercise are also introduced and described. The challenges and future directions in understanding the role of exercise in the control of chronic inflammation are discussed.

scholarly journals TO008COMPARATIVE TRANSCRIPTOME AND CO-EXPRESSION NETWORK ANALYSIS REVEALED A POTENTIAL ROLE OF C1QB AND INTERFERON TYPE 1 PATHWAY IN CIRCULATING IMMUNE CELLS OF KIDNEY TRANSPLANTS PATIENTS WITH CHRONIC ANTIBODY MEDIATED REJECTION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Gloria Santoro ◽  
Simona Granata ◽  
Paola Pontrelli ◽  
Mattia Rossi ◽  
Giovanni Gambaro ◽  
...  
Keyword(s):  
Network Analysis ◽  
Mononuclear Cells ◽  
Pathological Condition ◽  
Inflammatory Cells ◽  
Study Groups ◽  
Molecular Diagnostic ◽  
Peripheral Blood Mononuclear ◽  
Antibody Mediated Rejection

Abstract Background and Aims Chronic antibody-mediated rejection (CAMR) is a multifactorial pathological condition that can affect more that 40-50% of kidney allografts. Its clinical evolution is often silent, and this can delay its diagnosis. Although many advances in understanding the biological mechanisms underlying its onset/development, at the moment, no reliable non-invasive diagnostic biomarkers are available in clinic. Method We enrolled 29 patients with biopsy-proven CAMR, 29 stable transplant recipients (controls). Subsequently, the microarray profile of mRNA isolated from peripheral blood mononuclear cells (PBMCs) from 10 randomly selected CAMR patients and 10 controls was evaluated by Agilent technology. For the bioinformatics analysis we employed several statistical algorithms (including ANOVA and Kruskal-Wallis tests adjusted for multiple-tests) and a Weighted Gene Correlation Network Analysis (WGCNA) to select genes biologically associated in co-expressed networks. Results 935 genes resulted differentially expressed between the two study groups, demonstrating the large biological impact of this pathological condition on circulating immune-inflammatory cells. After WGCNA co-expression analysis, a group of genes (enclosed in a single co-expression module, 13 genes) resulted highly discriminating CAMR versus controls (p<.5.2 e-7, FDR<1%). This module included: Interferon-induced transmembrane proteins (IFITM) 2, 3, 4, confirming previous results by our group. However, the top discriminative gene was C1QB (Complement component 1, q subcomponent, B chain, p <000.1), a key element involved in the classical complement pathway. ELISA confirmed the microarray results on the entire patients’ cohort. Conclusion Our study confirmed the role of the type 1 interferon pathway in CAMR and underlined its capability to promote C1QB expression. These effects could contribute to better define the role of innate immunity in CAMR. Finally, C1QB, if validated in a large cohort of patients, could represent a new valuable molecular diagnostic biomarker for this complication.

scholarly journals Tumor Necrosis Factor-αand Interleukin-6: Potential Interorgan Inflammatory Mediators Contributing to Destructive Periodontal Disease in Obesity or Metabolic Syndrome

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Roozbeh Khosravi ◽  
Khady Ka ◽  
Ting Huang ◽  
Saeed Khalili ◽  
Bich Hong Nguyen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Periodontal Disease ◽  
Inflammatory Mediators ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Artery Disease ◽  
Necrosis Factor

Obesity has become a worldwide health burden in the last two decades. Obesity has been associated with increased comorbidities, such as coronary artery disease, diabetes, and destructive periodontal disease. Obesity is also part of a group of risk factors occurring together in an individual, which is referred to as metabolic syndrome. Clinical studies have shown higher risk for destructive periodontal disease in obesity and metabolic syndrome. However, the role of obesity and metabolic syndrome in the onset and development of destructive periodontal disease has not yet been fully understood. In this review, we discuss a working model, which focuses on interorgan inflammation as a common etiological factor for destructive periodontal disease associated with obesity and metabolic syndrome. Specifically, we suggest that elevated levels of tumor necrosis factor-α(TNF-α) or interleukin 6 (IL-6)—both adipokines and known risk factors for destructive periodontal disease—in obesity and metabolic syndrome contribute to the onset and development of destructive periodontal disease. The connections between destructive periodontal disease and systemic conditions, such as obesity or metabolic syndrome, are complex and potentially multidirectional. This review largely focuses on TNF-αand IL-6, inflammatory mediators, as potential common risk factors and does not exclude other biological mechanisms.

scholarly journals THE RELATIONSHIP BETWEEN PERIODONTAL DISEASE (PD) AND CARDIOVASCULAR DISEASE (CVD).

2010 ◽  
Vol 2 (3) ◽  
pp. e2010030 ◽  
Author(s):  
Maurizio Trevisan ◽  
Joan Dorn
Keyword(s):  
Cardiovascular Disease ◽  
Periodontal Disease ◽  
Inflammatory Process ◽  
Pathological Condition ◽  
Clinical Manifestations ◽  
Periodontal Treatment ◽  
Adult Age ◽  
Potential Link ◽  
Infection And Inflammation

The recent focus on the potential link between periodontal and cardiovascular disease (PD and CVD)  is part of the larger renewed interest on the role of infection and inflammation in the etiology of atherosclerosis and its clinical manifestations.  Periodontal Disease is an inflammatory process affecting the periodontium, the tissue that surrounds and supports the teeth . The process usually starts with an inflammatory process of the gum (gingivitis) but it may progress with an extensive involvement of the gum, as well as the periodontal ligament and the bone surrounding the teeth resulting in substantial bone loss. Periodontal disease is a common oral pathological condition in the adult age and represents the leading cause of tooth loss. PD prevalence increases with age and there are estimates that up to 49,000,000 Americans may suffer from some form of gum disease. The gingival plaque associated with PD is colonized by a number of gram-positive and gram-negative bacteria that have been shown to affect the initiation and development of PD and have been associated with the potential etiological role of PD in CVD and other chronic conditions. A potential etiological link between PD and CVD may have important public health implications as both the exposure (PD) and the outcomes (CVD) are highly prevalent in industrialized societies. In situations in which both the exposure and the outcome are highly prevalent even modest associations, like those observed in the studies reporting on the link between PD and CVD outcomes, may have relevance. There are  not  definite data on the effect of periodontal treatment on CVD clinical outcomes (either in primary or secondary prevention) however it should be pointed out that the limited (both in terms of numbers and study design) experimental evidence in humans suggests a possible beneficial effect of periodontal treatment of indices of functional and structural vascular health.

scholarly journals The Immunobiology of Prostanoid Receptor Signaling in Connecting Innate and Adaptive Immunity

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Hedi Harizi
Keyword(s):  
Adaptive Immunity ◽  
Inflammatory Cells ◽  
Cell Interaction ◽  
Membrane Receptors ◽  
Receptor Expression ◽  
Receptor Signaling ◽  
Cell Surface Molecule ◽  
Innate And Adaptive Immunity ◽  
Prostanoid Receptor

Prostanoids, including prostaglandins (PGs), thromboxanes (TXs), and prostacyclins, are synthesized from arachidonic acid (AA) by the action of Cyclooxygenase (COX) enzymes. They are bioactive inflammatory lipid mediators that play a key role in immunity and immunopathology. Prostanoids exert their effects on immune and inflammatory cells by binding to membrane receptors that are widely expressed throughout the immune system and act at multiple levels in innate and adaptive immunity. The immunoregulatory role of prostanoids results from their ability to regulate cell-cell interaction, antigen presentation, cytokine production, cytokine receptor expression, differentiation, survival, apoptosis, cell-surface molecule levels, and cell migration in both autocrine and paracrine manners. By acting on immune cells of both systems, prostanoids and their receptors have great impact on immune regulation and play a pivotal role in connecting innate and adaptive immunity. This paper focuses on the immunobiology of prostanoid receptor signaling because of their potential clinical relevance for various disorders including inflammation, autoimmunity, and tumorigenesis. We mainly discuss the effects of major COX metabolites, PGD2, PGE2, their signaling during dendritic cell (DC)-natural killer (NK) reciprocal crosstalk, DC-T cell interaction, and subsequent consequences on determining crucial aspects of innate and adaptive immunity in normal and pathological settings.

scholarly journals Role of placental inflammatory mediators and growth factors in patients with rheumatic diseases with a focus on systemic sclerosis

Rheumatology ◽  
2020 ◽  
Author(s):  
Francesca Motta ◽  
Veronica Codullo ◽  
Véronique Ramoni ◽  
Stefania Cesari ◽  
Giuseppina Ferrario ◽  
...  
Keyword(s):  
Growth Factors ◽  
Rheumatic Diseases ◽  
Inflammatory Mediators ◽  
Inflammatory Cells ◽  
Obstetric Complications ◽  
Histopathological Analysis ◽  
Increased Risk ◽  
Leucocyte Infiltration ◽  
Hepatocyte Growth

Abstract Objectives Pregnancy in SSc is burdened with an increased risk of obstetric complications. Little is known about the underlying placental alterations. This study aimed to better understand pathological changes and the role of inflammation in SSc placentas. Leucocyte infiltration, inflammatory mediators and atypical chemokine receptor 2 (ACKR2) expression in SSc placentas were compared with those in other rheumatic diseases (ORD) and healthy controls (HC). Methods A case–control study was conducted on eight pregnant SSc patients compared with 16 patients with ORD and 16 HC matched for gestational age. Clinical data were collected. Placentas were obtained for histopathological analysis and immunohistochemistry (CD3, CD20, CD11c, CD68, ACKR2). Samples from four SSc, eight ORD and eight HC were analysed by qPCR for ACKR2 expression and by multiplex assay for cytokines, chemokines and growth factors involved in angiogenesis and inflammation. Results The number of placental CD3, CD68 and CD11 cells was significantly higher in patients affected by rheumatic diseases (SSc+ORD) compared with HC. Hepatocyte growth factor was significantly increased in the group of rheumatic diseases patients (SSc+ORD) compared with HC, while chemokine (C-C motif) ligand 5 (CCL5) was significantly higher in SSc patients compared with ORD and HC. CCL5 levels directly correlated with the number of all local inflammatory cells and higher levels were associated with histological villitis. Conclusions Inflammatory alterations characterize placentas from rheumatic disease patients and could predispose to obstetric complications in these subjects.

scholarly journals Perivascular Inflammation in Pulmonary Arterial Hypertension

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2338
Author(s):  
Yijie Hu ◽  
Leon Chi ◽  
Wolfgang M Kuebler ◽  
Neil M Goldenberg
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Inflammatory Mediators ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Cytokines And Chemokines ◽  
Perivascular Inflammation ◽  
Pulmonary Arterial ◽  
Parenchymal Cells

Perivascular inflammation is a prominent pathologic feature in most animal models of pulmonary hypertension (PH) as well as in pulmonary arterial hypertension (PAH) patients. Accumulating evidence suggests a functional role of perivascular inflammation in the initiation and/or progression of PAH and pulmonary vascular remodeling. High levels of cytokines, chemokines, and inflammatory mediators can be detected in PAH patients and correlate with clinical outcome. Similarly, multiple immune cells, including neutrophils, macrophages, dendritic cells, mast cells, T lymphocytes, and B lymphocytes characteristically accumulate around pulmonary vessels in PAH. Concomitantly, vascular and parenchymal cells including endothelial cells, smooth muscle cells, and fibroblasts change their phenotype, resulting in altered sensitivity to inflammatory triggers and their enhanced capacity to stage inflammatory responses themselves, as well as the active secretion of cytokines and chemokines. The growing recognition of the interaction between inflammatory cells, vascular cells, and inflammatory mediators may provide important clues for the development of novel, safe, and effective immunotargeted therapies in PAH.

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