scholarly journals Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?

2020 ◽  
Vol 21 (20) ◽  
pp. 7441
Author(s):  
Ruben Aquino-Martinez ◽  
Sundeep Khosla ◽  
Joshua N. Farr ◽  
David G. Monroe
Keyword(s):  
Immune Response ◽  
Dna Damage ◽  
Periodontal Disease ◽  
Bacterial Invasion ◽  
Tissue Destruction ◽  
Disease Etiology ◽  
Gram Negative ◽  
Periodontal Tissues ◽  
Abnormal Accumulation ◽  
Underlying Mechanisms

The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction.

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 Life Below the Gum Line: Pathogenic Mechanisms ofPorphyromonas gingivalis

1998 ◽  
Vol 62 (4) ◽  
pp. 1244-1263 ◽  
Author(s):  
Richard J. Lamont ◽  
Howard F. Jenkinson
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Periodontal Disease ◽  
Regulation Of Gene Expression ◽  
Surface Protein ◽  
Opportunistic Pathogen ◽  
Host Cells ◽  
Transcriptional Level ◽  
Tissue Destruction ◽  
Periodontal Tissues

SUMMARY Porphyromonas gingivalis, a gram-negative anaerobe, is a major etiological agent in the initiation and progression of severe forms of periodontal disease. An opportunistic pathogen, P. gingivalis can also exist in commensal harmony with the host, with disease episodes ensuing from a shift in the ecological balance within the complex periodontal microenvironment. Colonization of the subgingival region is facilitated by the ability to adhere to available substrates such as adsorbed salivary molecules, matrix proteins, epithelial cells, and bacteria that are already established as a biofilm on tooth and epithelial surfaces. Binding to all of these substrates may be mediated by various regions of P. gingivalis fimbrillin, the structural subunit of the major fimbriae. P. gingivalis is an asaccharolytic organism, with a requirement for hemin (as a source of iron) and peptides for growth. At least three hemagglutinins and five proteinases are produced to satisfy these requirements. The hemagglutinin and proteinase genes contain extensive regions of highly conserved sequences, with posttranslational processing of proteinase gene products contributing to the formation of multimeric surface protein-adhesin complexes. Many of the virulence properties of P. gingivalis appear to be consequent to its adaptations to obtain hemin and peptides. Thus, hemagglutinins participate in adherence interactions with host cells, while proteinases contribute to inactivation of the effector molecules of the immune response and to tissue destruction. In addition to direct assault on the periodontal tissues, P. gingivalis can modulate eucaryotic cell signal transduction pathways, directing its uptake by gingival epithelial cells. Within this privileged site, P. gingivalis can replicate and impinge upon components of the innate host defense. Although a variety of surface molecules stimulate production of cytokines and other participants in the immune response, P. gingivalis may also undertake a stealth role whereby pivotal immune mediators are selectively inactivated. In keeping with its strict metabolic requirements, regulation of gene expression in P. gingivalis can be controlled at the transcriptional level. Finally, although periodontal disease is localized to the tissues surrounding the tooth, evidence is accumulating that infection with P. gingivalis may predispose to more serious systemic conditions such as cardiovascular disease and to delivery of preterm infants.

scholarly journals Host Mediators in Gingival Crevicular Fluid: Implications for the Pathogenesis of Periodontal Disease

1992 ◽  
Vol 3 (1) ◽  
pp. 31-60 ◽  
Author(s):  
Ira B. Lamster ◽  
M. John Novak
Keyword(s):  
Immune Response ◽  
Periodontal Disease ◽  
Gingival Crevicular Fluid ◽  
Critical Role ◽  
Arachidonic Acid Metabolite ◽  
Reactive Oxygen Metabolites ◽  
Tissue Destruction ◽  
Crevicular Fluid ◽  
Relationship Of ◽  
The Relationship

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes P-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-la, IL-1β, tumor necrosis factor-a), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1β and TNF-a, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.

scholarly journals THE ROLE OF LEUKOCYTE PROTEINASES IN THE PATHOGENESIS OF INFLAMMATORY PERIODONTAL DISEASES IN PATIENTS WITH METABOLIC SYNDROME SIGNS

2020 ◽  
Vol 16 (1) ◽  
pp. 70-74
Author(s):  
Viktoriya Miroshnichenko ◽  
Alena Kokoreva ◽  
Anastasiya Safonova
Keyword(s):  
Pathogenic Bacteria ◽  
Inflammatory Process ◽  
Periodontal Diseases ◽  
Capillary Endothelium ◽  
Elastic Fibers ◽  
Bacterial Invasion ◽  
Tissue Destruction ◽  
Destructive Effect ◽  
Periodontal Tissues

Subject. Despite the constant efforts of practicing physicians and scientists, the prevalence proportion of inflammatory and destructive periodontal diseases in the world is not subsiding. Previously scientists have examined several different theories on the development of pathological conditions in periodontal tissues, ranging problems from the neurotrophic theory of occurrence to the effect of occlusion injury on periodontal tissues. Theories dealing with the influence of specific and non-specific bacterial plaque have also been studied. None of the theories has become reasonable and single valued. It is believed that the mechanism of the development of the disease is complex, autoimmune, damaging primarily collagen, elastic fibers of the capillary endothelium, gingival ligament and bone tissue. Over the past decade, it has been proven that inflammation in periodontal tissues is initiated and proceeds in response to the introduction of pathogenic bacteria. However, it can be said that not all patients develop an inflammatory response to bacterial invasion. The second important factor in the development and progression of the inflammatory-destructive process is the immune response of a particular individual. Scientists have noted the influence of the non-microbial factor and have come to the conclusion that in the surrounding tissues of the inflamed area there are not only enzymes secreted by bacteria, but also leukocyte proteinases, which in turn are mediators of the tissue destruction. Purpose ― to examine the role of leukocyte proteinases in the pathogenesis of inflammatory periodontal diseases. Methodology. The number of indigenous and foreign literature sources dealing with the study of the role of leukocyte proteinases in the development and maintenance of a destructive inflammatory process has been reviewed by us. Conclusion. The role of the aggressive destructive effect of leukocyte proteinases on periodontal tissues has been analyzed. Leukocyte proteinases are mediators of progressive destruction of connective tissue and can be used as markers to assess the severity of the course and predict the development of the inflammatory process in periodontal tissues.

scholarly journals PERIODONTAL DISEASES AND ATHEROSCLEROSIS (LITERATURE REVIEW)

2019 ◽  
Vol 72 (3) ◽  
pp. 462-465
Author(s):  
Iryna S. Dankevych-Kharchyshyn ◽  
Olena M. Vynogradova ◽  
Natalia V. Malko ◽  
Roman M. Gnid ◽  
Andriana P. Skalat ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Vascular Disease ◽  
Periodontal Diseases ◽  
Disease Diagnosis ◽  
Modern Concept ◽  
Bacterial Invasion ◽  
Periodontal Tissue ◽  
Atherosclerotic Vascular Disease ◽  
Periodontal Tissues ◽  
The Relationship

Introduction: The relationship between periodontal diseases and atherosclerosis is addressed in this article. Both these diseases have an inflammatory basis. Because periodontal disease is a risk factor for developing atherosclerotic vascular disease, diagnosis of the former is important. Particular attention must be paid to patients who have periodontal disease with other risk factors for atherosclerotic vascular disease. Recommendations managing these patients have been made included. The aim: The paper is aimed at familiarization of broad medical public with the presence of the relationship between diseases of periodontal tissues and atherosclerosis. Materials and methods: A thorough comprehensive analysis and generalization of scientific achievements elucidated in the fundamental and periodical publications, relating to diseases of the periodontal tissues and atherosclerosis, has been carried out. Review: The article consists of many researchers regarding the prevalence and intensity of periodontal tissue diseases in people of all ages. Problems associated with the state of periodontal tissues in people under study as dentists and general practitioners. Proven role in the pathogenesis of inflammatory diseases of the periodontal tissues in people with atherosclerosis. In the modern concept of the etiology and pathogenesis of periodontal diseases in people is extremely important role for the immune system and resistance to periodontal bacterial invasion. Analyzed common changes important for pathogenesis of periodontal tissue diseases and atherosclerosis. Conclusions: Consequently, recent studies have shown a clear, directly proportional relationship between periodontal tissue diseases and atherosclerosis, but mechanisms for their development and interaction are not fully disclosed.

Abstract TP85: Impact of Periodontal Disease and -Bacteria on Intracranial Aneurysms

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Shotaro Yoshioka
Keyword(s):  
Periodontal Disease ◽  
Intracranial Aneurysms ◽  
Inflammatory Responses ◽  
Periodontal Diseases ◽  
Gram Negative Bacteria ◽  
Periodontal Pathogens ◽  
Treatment Needs ◽  
Gram Negative ◽  
Periodontal Tissues ◽  
Periodontal Index

Introduction: Periodontal Gram-negative bacteria and their products can initiate inflammatory responses in periodontal tissues with systemic consequences. They are associated with the pathogenesis of atherosclerosis and ischemic stroke. Local inflammation and oxidative stress play a crucial role in the pathophysiology of intracranial aneurysms (IAs). Under the hypothesis that the severity of periodontal disease is associated with the formation and rupture of IAs we assessed which periodontal pathogens contribute to the pathogenesis of IAs. Methods: We enrolled patients with ruptured- (n=5, age 60±11.9) and unruptured IAs (n=13, age 67±6.1) and controls without IAs (n=7, age 58±8.5); their prior informed consent was obtained. The severity of periodontitis was recorded using the community periodontal index (CPI) of the Treatment Needs code. Subgingival plaques (n=23) were evaluated with the quantitative real-time PCR assay to check for the Gram-negative bacteria Aggregatibacter actinomycetemcomitans (Aa), Fusobacterium nucleatum, Treponema denticola, Prevotella intermedia (Pi), Tannerella forsythia, and Porphyromonas gingivalis (Pg). Plasma IgG titers of antibody against Pg, Pi, Aa, and Eikenella corrodens were evaluated by ELISA. Results: The CPI was significantly higher in patients with IAs than the controls (2.7 vs 1.9, p<0.05) and their DNA level of subgingival plaques and their plasma IgG titers of Pg were also higher. Periodontal disease was more severe and the plasma IgG titers of Pg were higher in patients with ruptured- than unruptured IAs, suggesting that Pg is associated not only with the formation but also the rupture of IAs. Conclusions: We present evidence that severe periodontal disease and Pg infection may be involved in the pathophysiology of IAs. The management of periodontal diseases may help to prevent the formation and rupture of IAs.

Localization of Porphyromonas gingivalis and Tannerella Forsythia In vivo and In vitro

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Rajakaruna GA ◽  
◽  
Izumi Y ◽  
Keyword(s):  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Human Body ◽  
Pathogenic Bacteria ◽  
Molecular Mechanisms ◽  
Bacterial Species ◽  
Future Research ◽  
Bacterial Invasion ◽  
Tannerella Forsythia ◽  
Periodontal Tissues

Porphyromonas gingivalis and Tannerella forsythia have been identified as pathogenic bacteria associated with periodontal disease. Also, there are reports describing possible association of periodontal disease with other systemic diseases and some studies have revealed the presence of these bacterial species or their genomic content in sites distal to oral cavity in human body. There have been various studies investigating on possible pathogenic mechanisms that these bacteria device in healthy and disease conditions. Majority of the studies have been focused on possible molecular mechanisms and investigating the end products that are released as a result of bacteria coming into contact with the human tissues/ cells. Up to date only a limited number of studies have visualized direct histo-pathological and cellular events of these bacteria with time lapse information. In this mini review we tried to narrow down our focus on the visualization P. gingivalis and T. forsythia, starting from the oldest possible publications to current advancements, their contribution on understanding the histo-morpho-pathological changes during bacterial invasion, the pros and cons in these methods and how future research should be shaped to reveal the possible translocation of these bacteria from periodontal tissues to distal sites of the human body.

scholarly journals Pyroptosis-Mediated Periodontal Disease

2021 ◽  
Vol 23 (1) ◽  
pp. 372
Author(s):  
Mariane Beatriz Sordi ◽  
Ricardo de Souza Magini ◽  
Layla Panahipour ◽  
Reinhard Gruber
Keyword(s):  
Periodontal Disease ◽  
Virulence Factors ◽  
Tissue Homeostasis ◽  
Host Responses ◽  
Caspase Activation ◽  
Tissue Destruction ◽  
Periodontal Tissues ◽  
Cellular Events ◽  
Pathological Mechanism ◽  
Potential Strategy

Pyroptosis is a caspase-dependent process relevant to the understanding of beneficial host responses and medical conditions for which inflammation is central to the pathophysiology of the disease. Pyroptosis has been recently suggested as one of the pathways of exacerbated inflammation of periodontal tissues. Hence, this focused review aims to discuss pyroptosis as a pathological mechanism in the cause of periodontitis. The included articles presented similarities regarding methods, type of cells applied, and cell stimulation, as the outcomes also point to the same direction considering the cellular events. The collected data indicate that virulence factors present in the diseased periodontal tissues initiate the inflammasome route of tissue destruction with caspase activation, cleavage of gasdermin D, and secretion of interleukins IL-1β and IL-18. Consequently, removing periopathogens’ virulence factors, triggering pyroptosis, is a potential strategy to combat periodontal disease and regain tissue homeostasis.

Awareness of Periodontal Medicine among Medical Students at a Tertiary Care Center

2019 ◽  
Vol 3 (2) ◽  
pp. 66-69
Author(s):  
Junima Rajkarnikar ◽  
Jemish Acharya ◽  
Karnika Yadav
Keyword(s):  
Medical Students ◽  
Periodontal Disease ◽  
Proteolytic Enzymes ◽  
Care Center ◽  
Tertiary Care ◽  
Tertiary Care Center ◽  
Tissue Destruction ◽  
Periodontal Tissues ◽  
The Impact ◽  
Periodontal Medicine

Introduction: Tissue destruction of supporting periodontal tissues is mediated by an overreactive immune inflammatory response to bacteria in the subgingival environment. Tissue destruction in periodontitis occurs by the stimulatory action of pro inflammatory cytokines and proteolytic enzymes released by neutrophils, macrophages, and the action of bone resorption mediators, all of which are being regulated by B and T cells. Periodontitis act as a focus of infection and bacteria metastases through blood stream to various vital organs like heart, lungs, joints and amniotic fluid. Objective: To assess the awareness of periodontal medicine among medical students at a tertiary care center in Kathmandu. Methods: A total of 115 subjects were taken for the present study. Data was collected using a questionnaire which included questions used to assess the knowledge about periodontal diseases and its possible effects on systemic conditions. Results: Out of the total participants, 58 (50.4%) said that periodontal disease was not related to coronary heart diseases. Only 14 (12.2%) had an idea about the association of pre-term birth and periodontitis. While 86 (74.8%) knew the impact of diabetes on periodontium, only 34 (29.6%) said that there was an association between periodontitis and hospital acquired pneumonia. Conclusion: Knowledge about the association of periodontal disease with various systemic conditions is not satisfactory among the various medical students of this hospital.

scholarly journals Periodontal Disease: Linking the Primary Inflammation to Bone Loss

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Adriana Di Benedetto ◽  
Isabella Gigante ◽  
Silvia Colucci ◽  
Maria Grano
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Innate Immune ◽  
Host Cells ◽  
Tissue Destruction ◽  
Innate Response ◽  
Periodontal Tissues ◽  
Local Inflammatory Reaction ◽  
Disease Initiation ◽  
Host Inflammatory Response

Periodontal disease (PD), or periodontitis, is defined as a bacterially induced disease of the tooth-supporting (periodontal) tissues. It is characterized by inflammation and bone loss; therefore understanding how they are linked would help to address the most efficacious therapeutic approach. Bacterial infection is the primary etiology but is not sufficient to induce the disease initiation or progression. Indeed, bacteria-derived factors stimulate a local inflammatory reaction and activation of the innate immune system. The innate response involves the recognition of microbial components by host cells, and this event is mediated by toll-like receptors (TLRs) expressed by resident cells and leukocytes. Activation of these cells leads to the release of proinflammatory cytokines and recruitment of phagocytes and lymphocytes. Activation of T and B cells initiates the adaptive immunity with Th1 Th2 Th17 Treg response and antibodies production respectively. In this inflammatory scenario, cytokines involved in bone regulation and maintenance have considerable relevance because tissue destruction is believed to be the consequence of host inflammatory response to the bacterial challenge. In the present review, we summarize host factors including cell populations, cytokines, and mechanisms involved in the destruction of the supporting tissues of the tooth and discuss treatment perspectives based on this knowledge.

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