scholarly journals Resveratrol and Its Analogs as Functional Foods in Periodontal Disease Management

2021 ◽  
Vol 2 ◽  
Author(s):  
Yi Rong Ivan Lim ◽  
Philip M. Preshaw ◽  
Haishu Lin ◽  
Kai Soo Tan
Keyword(s):  
Disease Management ◽  
Inflammatory Response ◽  
Periodontal Disease ◽  
Inflammatory Disease ◽  
Functional Foods ◽  
Chronic Inflammatory Disease ◽  
Oral Microbiome ◽  
Periodontal Treatment ◽  
Potential Utility ◽  
Therapeutic Properties

Periodontitis is a common chronic inflammatory disease driven by the interaction between a dysbiotic oral microbiome and the dysregulated host immune-inflammatory response. Naturally derived nutraceuticals, such as resveratrol and its analogs, are potential adjunctive therapies in periodontal treatment due to their antimicrobial and anti-inflammatory properties. Furthermore, different analogs of resveratrol and the choice of solvents used may lead to varying effects on therapeutic properties. This review presents the current findings and gaps in our understanding on the potential utility of resveratrol and its analogs in periodontal treatment.

scholarly journals Interplay Among the Oral Microbiome, Oral Cavity Conditions, the Host Immune Response, Diabetes Mellitus, and Its Associated-Risk Factors—An Overview

2021 ◽  
Vol 2 ◽  
Author(s):  
Thais de Cássia Negrini ◽  
Iracilda Zeppone Carlos ◽  
Cristiane Duque ◽  
Karina Sampaio Caiaffa ◽  
Rodrigo Alex Arthur
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Immune Response ◽  
Oral Health ◽  
Inflammatory Response ◽  
Oral Cavity ◽  
Periodontal Disease ◽  
Host Immune Response ◽  
Oral Microbiome ◽  
Associated Risk Factors

This comprehensive review of the literature aimed to investigate the interplay between the oral microbiome, oral cavity conditions, and host immune response in Diabetes mellitus (DM). Moreover, this review also aimed to investigate how DM related risk factors, such as advanced age, hyperglycemia, hyperlipidemia, obesity, hypertension and polycystic ovary syndrome (PCOS), act in promoting or modifying specific mechanisms that could potentially perpetuate both altered systemic and oral conditions. We found that poorly controlled glycemic index may exert a negative effect on the immune system of affected individuals, leading to a deficient immune response or to an exacerbation of the inflammatory response exacerbating DM-related complications. Hyperglycemia induces alterations in the oral microbiome since poor glycemic control is associated with increased levels and frequencies of periodontal pathogens in the subgingival biofilm of individuals with DM. A bidirectional relationship between periodontal diseases and DM has been suggested: DM patients may have an exaggerated inflammatory response, poor repair and bone resorption that aggravates periodontal disease whereas the increased levels of systemic pro-inflammatory mediators found in individuals affected with periodontal disease exacerbates insulin resistance. SARS-CoV-2 infection may represent an aggravating factor for individuals with DM. Individuals with DM tend to have low salivary flow and a high prevalence of xerostomia, but the association between prevalence/experience of dental caries and DM is still unclear. DM has also been associated to the development of lesions in the oral mucosa, especially potentially malignant ones and those associated with fungal infections. Obesity plays an important role in the induction and progression of DM. Co-affected obese and DM individuals tend to present worse oral health conditions. A decrease in HDL and, an increase in triglycerides bloodstream levels seem to be associated with an increase on the load of periodontopathogens on oral cavity. Moreover, DM may increase the likelihood of halitosis. Prevalence of impaired taste perception and impaired smell recognition tend to be greater in DM patients. An important interplay among oral cavity microbiome, DM, obesity and hypertension has been proposed as the reduction of nitrate into nitrite, in addition to contribute to lowering of blood pressure, reduces oxidative stress and increases insulin secretion, being these effects desirable for the control of obesity and DM. Women with PCOS tend to present a distinct oral microbial composition and an elevated systemic response to selective members of this microbial community, but the association between oral microbiome, PCOS are DM is still unknown. The results of the studies presented in this review suggest the interplay among the oral microbiome, oral cavity conditions, host immune response and DM and some of the DM associated risk factors exist. DM individuals need to be encouraged and motivated for an adequate oral health care. In addition, these results show the importance of adopting multidisciplinary management of DM and of strengthening physicians-dentists relationship focusing on both systemic and on oral cavity conditions of DM patients.

scholarly journals miR-221 Alleviates the Ox-LDL-Induced Macrophage Inflammatory Response via the Inhibition of DNMT3b-Mediated NCoR Promoter Methylation

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Jinshan Ye ◽  
Yaxi Wu ◽  
Ruiwei Guo ◽  
Wenjun Zeng ◽  
Yanan Duan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Inflammatory Response ◽  
Inflammatory Disease ◽  
Promoter Methylation ◽  
Promoter Region ◽  
Inflammatory Responses ◽  
Chronic Inflammatory Disease ◽  
Expression Levels

Atherosclerosis (AS) is a chronic inflammatory disease, and macrophages play a key role in all phases of AS. Recent studies have shown that miR-221 is a biomarker for AS and stroke; however, the role and mechanism of miR-221 in AS are unclear. Herein, we found that miR-221 and NCoR levels were decreased in ox-LDL-treated THP-1-derived macrophages. In contrast, DNMT3b, IL-6, and TNF-α expression levels were increased under these conditions. Upregulation of miR-221 or NCoR could partially inhibit ox-LDL-induced IL-6 and TNF-α expression. Further studies showed that DNMT3b was a target of miR-221. DNMT3b inhibition also suppressed IL-6 and TNF-α expression and increased NCoR expression in the presence of ox-LDL. Moreover, DNMT3b was involved in ox-LDL-induced DNA methylation in the promoter region of NCoR. These findings suggest that miR-221 suppresses ox-LDL-induced inflammatory responses via suppressing DNMT3b-mediated DNA methylation in the promoter region of NCoR. These results provide a rationale for using intracellular miR-211 as a possible antiatherosclerotic target.

scholarly journals Bacterial sialoglycosidases in Virulence and Pathogenesis

Pathogens ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 39
Author(s):  
Preethi Sudhakara ◽  
Iyappan Sellamuthu ◽  
A. Aruni
Keyword(s):  
Sialic Acid ◽  
Inflammatory Disease ◽  
Drug Targets ◽  
Bacterial Pathogen ◽  
The United States ◽  
Chronic Inflammatory Disease ◽  
Oral Microbiome ◽  
Toll Like Receptor ◽  
Host Defenses ◽  
Sialic Acid Receptor

Human oral microbiome and dysbiotic infections have been recently evidently identified. One of the major reasons for such dysbiosis is impairment of the immune system. Periodontitis is a chronic inflammatory disease affecting the tissues that surround and support the teeth. In the United States., approximately 65 million people are affected by this condition. Its occurrence is also associated with many important systemic diseases such as cardiovascular disease, rheumatoid arthritis, and Alzheimer’s disease. Among the most important etiologies of periodontitis is Porphyromonas gingivalis, a keystone bacterial pathogen. Keystone pathogens can orchestrate inflammatory disease by remodeling a normally benign microbiota causing imbalance between normal and pathogenic microbiota (dysbiosis). The important characteristics of P. gingivalis causing dysbiosis are its virulence factors which cause effective subversion of host defenses to its advantage allowing other pathogens to grow. Some of the mechanisms involved in these processes are still not well-understood. However, various microbial strategies target host sialoglycoproteins for immune dysregulation. In addition, the enzymes that break down sialoglycoproteins and sialoglycans are the “sialoglycoproteases”, resulting in exposed terminal sialic acid. This process could lead to pathogen-toll like receptor (TLR) interactions mediated through sialic acid receptor ligand mechanisms. Assessing the function of P. gingivalis sialoglycoproteases, could pave the way to designing carbohydrate analogues and sialic acid mimetics to serve as drug targets.

Biological Aging and Periodontal Disease: Analysis of NHANES (2001–2002)

2021 ◽  
pp. 238008442199581
Author(s):  
L.M. Nguyen ◽  
J.J. Chon ◽  
E.E. Kim ◽  
J.C. Cheng ◽  
J.L. Ebersole
Keyword(s):  
Periodontal Disease ◽  
Life Span ◽  
Inflammatory Disease ◽  
Host Response ◽  
Chronic Inflammatory Disease ◽  
Bacterial Biofilm ◽  
Noncommunicable Disease ◽  
Health Concern ◽  
Biological Aging ◽  
Race Ethnicity

Introduction: Periodontitis is a chronic inflammatory disease caused by multiple potential contributing factors such as bacterial biofilm infection of the tissues surrounding the teeth and environmental determinants and a dysregulated host response for modifying and resolving the inflammation. Because periodontal disease is a major public health concern with substantial increases in the prevalence and severity in aging populations, previous studies of periodontitis tended to approach the disease as an age-associated outcome across the life span. However, few investigations have considered that, as a chronic noncommunicable disease, periodontitis may not simply be a disease that increases with age but may contribute to more rapid biologic aging. Objectives: Increasing population data supports the potential disconnect between chronological aging and biologic aging, which would contribute to the heterogeneity of aging phenotypes within chronologic ages across populations. Thus, our aim was to test whether periodontal disease affects biological aging across the life span. Methods: The prevalence of periodontitis in the adult US population is a portion of the assessment of the National Health and Nutrition Examination Survey (NHANES), which has been ongoing since 1971 through 2-y cycles sampling populations across the country. We used NHANES 2001–2002 to test the hypothesis that the presence/severity of periodontal disease as an exposure variable would negatively affect telomere length, a measure of biological aging, and that this relationship is modified by factors that also affect the progression of periodontitis, such as sex, race/ethnicity, and smoking. Results: The data demonstrated a significant impact of periodontitis on decreasing telomere lengths across the life span. These differences were modulated by age, sex, race/ethnicity, and smoking within the population. Conclusion: The findings lay the groundwork for future studies documenting broader effects on biological aging parameters as well as potential intervention strategies for periodontitis in driving unhealthy aging processes. Knowledge Transfer Statement: Periodontitis is a chronic inflammatory disease and dysregulated host response. Shortening of telomeres is a reflection of biologic aging. Decreased telomere lengths with periodontitis are seemingly related to chronic infection and persistent local and systemic inflammation. These findings suggest that periodontitis is not simply a disease of aging but may also transmit chronic systemic signals that could affect more rapid biological aging. Clinicians can use this outcome to recognize the role of periodontitis in driving unhealthy aging processes in patients.

scholarly journals Review. The Link between Periodontal Disease, Inflammation and Atherosclerosis — an Interdisciplinary Approach

2017 ◽  
Vol 2 (s1) ◽  
pp. 11-16
Author(s):  
Theodora Benedek
Keyword(s):  
Periodontal Disease ◽  
Arterial Wall ◽  
Immune Reaction ◽  
Interdisciplinary Approach ◽  
Chronic Inflammatory Disease ◽  
Oral Microbiome ◽  
Atheromatous Plaque ◽  
Inflammatory Disorder ◽  
Common Pathway ◽  
Atherosclerotic Lesions

AbstractPeriodontal disease is a chronic inflammatory disease that results from the activity of altered oral microbiome, leading to altered immune reaction, destruction of tissues supporting the teeth, and oral bone loss. This disease is particularly associated with an expressed systemic inflammation, being considered nowadays an inflammatory disorder. At the same time, inflammation has been recognized to play a major role in the development of atherosclerotic lesions. Atheromatous plaque formation is triggered by alterations in the structure of the endothelium, which lead to the expression of adhesion molecules and recruitment of immune cells such as macrophages, in the arterial wall. While the association between periodontal disease, inflammation and cardiovascular diseases has been well established, the causality relation between these three entities has not been demonstrated so far. This review presents the most common advances in understanding the complex link between periodontal disease, inflammation and atherosclerosis, as a common pathway leading to increased cardiovascular risk.

scholarly journals Porphyromonas gingivalis Fimbriae Inhibit Caspase-3-Mediated Apoptosis of Monocytic THP-1 Cells under Growth Factor Deprivation via Extracellular Signal-Regulated Kinase-Dependent Expression of p21 Cip/WAF1

2001 ◽  
Vol 69 (8) ◽  
pp. 4944-4950 ◽  
Author(s):  
Ken Ozaki ◽  
Shigemasa Hanazawa
Keyword(s):  
Growth Factor ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Inflammatory Disease ◽  
Caspase 3 ◽  
Chronic Inflammatory Disease ◽  
Serum Withdrawal ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Growth Factor Deprivation

ABSTRACT Apoptotic regulation of monocytes/macrophages appears to be closely associated with chronic inflammatory reactions. Since it was demonstrated earlier that certain bacterial cell components are involved in apoptotic regulation of these cells, in the present study, we investigated whether the bacterial fimbria, an important cell structure involved in bacterial adherence to host cells, regulates apoptosis of human monocytic THP-1 cells induced under growth factor deprivation. To investigate this point, we used fimbriae ofPorphyromonas gingivalis, a pathogen causing periodontal disease, which is a chronic inflammatory disease. The fimbriae inhibited apoptosis of the cells under growth factor deprivation. This inhibitory action of the fimbriae was completely neutralized by anti-fimbrial antibody. The fimbriae stimulated activation of extracellular signal-regulated kinase (ERK) and expression of cyclin-dependent kinase inhibitor p21 Cip/WAF1 (p21) in the cells. The stimulatory effect of the fimbriae on the expression of the p21 protein was inhibited by treatment with PD98059, a specific inhibitor of ERK. The cell apoptosis was inhibited by treatment with Ac-DEVD-CHO, an inhibitor of caspase-3. The fimbriae inhibited the serum withdrawal-induced cleavage of the caspase-3 proform and poly(ADP-ribose) polymerase, one of the caspase-3 substrates. Furthermore, PD98059 and antisense p21 oligonucleotide blocked the fimbrial inhibition of apoptosis and caspase-3 activation of the cells induced by serum withdrawal. These results show that the bacterial fimbriae inhibited apoptosis of THP-1 cells induced under growth factor deprivation via ERK-dependent expression of p21. The present study suggests that bacterial fimbriae act as potent regulators of chronic inflammatory disease, e.g., periodontal disease, through blocking apoptosis of monocytes/macrophages.

The Biochemical Effects of Non-surgical Periodontal Therapy in Patients with and without Chronic Renal Disease

2017 ◽  
Vol 68 (3) ◽  
pp. 605-607
Author(s):  
Cerasela Dorina Sincar ◽  
Nicoleta Ioanid ◽  
Ioana Rudnic ◽  
Ioana Martu ◽  
Sorina Mihaela Solomon ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Periodontal Disease ◽  
Renal Disease ◽  
Chronic Periodontitis ◽  
Chronic Renal Disease ◽  
Systemic Disease ◽  
Systemic Inflammatory Response ◽  
Periodontal Therapy ◽  
Periodontal Treatment ◽  
Control Group

Recent studies have shown an association between high levels of biomarkers and periodontitis, association which decreases after the periodontal treatment. Because of this association with systemic inflammatory response, chronic periodontitis was recently included as a risk factor for chronic renale disease. Specifically, in this study we hypothesized that a part of chronic inflammatory response observed in patients with chronic renale disease is due to physiopathological reactions caused by the presence of chronic periodontitis, which, during the course of its evolution, induces an increase in the expression of inflammatory markers. Patients were divided into two groups: the first group consisted of patients with chronic renale disease and periodontal disease who were undergoing periodontal treatment (test group) and the second group, control group, composed of patients without any systemic disease, but who experienced moderate to severe chronic periodontitis, also periodontal treated. Blood samples were taken for biochemical analysis at baseline and at 3 months after periodontal therapy. Venous blood was collected in vacuum tubes between 7:00 am and 9:00 am after 12 hours after the last meal. A tube containing EDTA was analyzed for blood following parameters: albumin, uric acid, creatinin, urea. An association between periodontal disease and renale disease is often found in studies using a population where the renale disease is already diagnosed. In these cases, duration of renal end stage and type of topical and systemic treatment administered to patients significantly affect the association. Therefore, we have shown that periodontitis may promote any detectable changes in renal function. Thus, by analogy, in this study the test groups and control groups were compared not only with each other but also comparative analyzes were performed based on the reference values of markers of renal dysfunction. We think it could be plausible existence of a causal link between periodontal disease and chronic renal disease both by glomerular invasion by periodontal pathogens, directly and indirectly through systemic inflammatory effect caused by chronic periodontitis. Success of periodontal therapy reduce systemic inflammatory response and decreases levels of biochemicals markers indicating that this may be an important intervention therapy in patients with chronic renale disease.

Malacoplakia of the Retroperitoneum in a Girl with Systemic Lupus Erythematosus

PEDIATRICS ◽  
1982 ◽  
Vol 70 (2) ◽  
pp. 296-299
Author(s):  
Jahed A. Hamdan ◽  
Mohammed S. Ahmad ◽  
Abdel Rahman Sa'adi
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Case Report ◽  
Inflammatory Response ◽  
Inflammatory Disease ◽  
Lupus Erythematosus ◽  
English Language ◽  
Chronic Inflammatory Disease ◽  
Systemic Lupus ◽  
The Third ◽  
Language Literature

Malacoplakia is a rare chronic inflammatory disease, usually involving the bladder but occasionally affecting other organs. However, only two cases of malacoplakia of the retroperitoneum and ureter have been reported in the English language literature.1,2 Herein, we describe the third case of malacoplakia of the retroperitoneum and ureter in a patient with systemic lupus erythematosus who had been receiving prednisone therapy for two years. Modification by the steroid of phagocytosis and of the normal inflammatory response to bacterial infection, and the systemic lupus erythematosus, may have been of major importance in the genesis of malacoplakia in this patient. CASE REPORT

scholarly journals The Roles of FOXO1 in Periodontal Homeostasis and Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Liang Ren ◽  
Jing Yang ◽  
Jun Wang ◽  
Xuedong Zhou ◽  
Chengcheng Liu
Keyword(s):  
Inflammatory Response ◽  
Periodontal Disease ◽  
Bone Remodeling ◽  
Chronic Inflammatory Disease ◽  
Periodontal Pathogens ◽  
Ros Scavenging ◽  
Cellular Processes ◽  
Periodontal Bacteria ◽  
Forkhead Box ◽  
Signaling Axis

Periodontitis is an oral chronic inflammatory disease that is initiated by periodontal microbial communities and requires disruption of the homeostatic responses. The prevalence of periodontal disease increases with age; more than 70% of adults 65 years and older have periodontal disease. A pathogenic microbial community is required for initiating periodontal disease. Dysbiotic immune-inflammatory response and bone remodeling are characteristics of periodontitis. The transcription factor forkhead box protein O1 (FOXO1) is a key regulator of a number of cellular processes, including cell survival and differentiation, immune status, reactive oxygen species (ROS) scavenging, and apoptosis. Although accumulating evidence indicates that FOXO1 activity can be induced by periodontal pathogens, the roles of FOXO1 in periodontal homeostasis and disease have not been well documented. The present review summarizes how the FOXO1 signaling axis can regulate periodontal bacteria-epithelial interactions, immune-inflammatory response, bone remodeling, and wound healing.

Sign in / Sign up

Export Citation Format

Share Document