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.

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 Nexus between COVID-19 and periodontal disease

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052110026
Author(s):  
Kanchana Sukumar ◽  
Anupama Tadepalli
Keyword(s):  
Periodontal Disease ◽  
Host Cells ◽  
Multifactorial Disease ◽  
Tissue Destruction ◽  
The Past ◽  
Appropriate Care ◽  
Bacterial Stimulation ◽  
Plaque Control ◽  
Disease Understanding ◽  
Pro Inflammatory Cytokines

Over the past several decades, studies have demonstrated the existence of bi-directional relationships between periodontal disease and systemic conditions. Periodontitis is a polymicrobial and multifactorial disease involving both host and environmental factors. Tissue destruction is primarily associated with hyperresponsiveness of the host resulting in release of inflammatory mediators. Pro-inflammatory cytokines play a major role in bacterial stimulation and tissue destruction. In addition, these cytokines are thought to underlie the associations between periodontitis and systemic conditions. Current research suggests that increased release of cytokines from host cells, referred to as the cytokine storm, is associated with disease progression in patients with coronavirus disease 2019 (COVID-19). An intersection between periodontitis and pulmonary disease is biologically plausible. Hence, we reviewed the evidence linking COVID-19, cytokines, and periodontal disease. Plaque control is essential to prevent exchange of bacteria between the mouth and the lungs, reducing the risk of lung disease. Understanding these associations may help identify individuals at high risk and deliver appropriate care at early stages.

scholarly journals Bacterial Cyclic Dinucleotides and the cGAS–cGAMP–STING Pathway: A Role in Periodontitis?

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 675
Author(s):  
Samira Elmanfi ◽  
Mustafa Yilmaz ◽  
Wilson W. S. Ong ◽  
Kofi S. Yeboah ◽  
Herman O. Sintim ◽  
...  
Keyword(s):  
Immune Response ◽  
Periodontal Disease ◽  
Innate Immune ◽  
Host Cells ◽  
Type I Interferons ◽  
Type I ◽  
Vaccine Adjuvants ◽  
Cyclic Dinucleotides ◽  
Sting Pathway

Host cells can recognize cytosolic double-stranded DNAs and endogenous second messengers as cyclic dinucleotides—including c-di-GMP, c-di-AMP, and cGAMP—of invading microbes via the critical and essential innate immune signaling adaptor molecule known as STING. This recognition activates the innate immune system and leads to the production of Type I interferons and proinflammatory cytokines. In this review, we (1) focus on the possible role of bacterial cyclic dinucleotides and the STING/TBK1/IRF3 pathway in the pathogenesis of periodontal disease and the regulation of periodontal immune response, and (2) review and discuss activators and inhibitors of the STING pathway as immune response regulators and their potential utility in the treatment of periodontitis. PubMed/Medline, Scopus, and Web of Science were searched with the terms “STING”, “TBK 1”, “IRF3”, and “cGAS”—alone, or together with “periodontitis”. Current studies produced evidence for using STING-pathway-targeting molecules as part of anticancer therapy, and as vaccine adjuvants against microbial infections; however, the role of the STING/TBK1/IRF3 pathway in periodontal disease pathogenesis is still undiscovered. Understanding the stimulation of the innate immune response by cyclic dinucleotides opens a new approach to host modulation therapies in periodontology.

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.

Porphyromonas gingivalis-Epithelial Cell Interactions in Periodontitis

2006 ◽  
Vol 85 (5) ◽  
pp. 392-403 ◽  
Author(s):  
E. Andrian ◽  
D. Grenier ◽  
M. Rouabhia
Keyword(s):  
Epithelial Cells ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Pathogenic Bacteria ◽  
Current Knowledge ◽  
Oral Bacteria ◽  
Host Cells ◽  
Host Responses ◽  
Tissue Destruction ◽  
Adaptive Ability

Emerging data on the consequences of the interactions between invasive oral bacteria and host cells have provided new insights into the pathogenesis of periodontal disease. Indeed, modulation of the mucosal epithelial barrier by pathogenic bacteria appears to be a critical step in the initiation and progression of periodontal disease. Periodontopathogens such as Porphyromonas gingivalis have developed different strategies to perturb the structural and functional integrity of the gingival epithelium. P. gingivalis adheres to, invades, and replicates within human epithelial cells. Adhesion of P. gingivalis to host cells is multimodal and involves the interaction of bacterial cell-surface adhesins with receptors expressed on the surfaces of epithelial cells. Internalization of P. gingivalis within host cells is rapid and requires both bacterial contact-dependent components and host-induced signaling pathways. P. gingivalis also subverts host responses to bacterial challenges by inactivating immune cells and molecules and by activating host processes leading to tissue destruction. The adaptive ability of these pathogens that allows them to survive within host cells and degrade periodontal tissue constituents may contribute to the initiation and progression of periodontitis. In this paper, we review current knowledge on the molecular cross-talk between P. gingivalis and gingival epithelial cells in the development of periodontitis.

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 Distinct Signaling Pathways Between Human Macrophages and Primary Gingival Epithelial Cells by Aggregatibacter actinomycetemcomitans

Pathogens ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 248 ◽  
Author(s):  
Ellen S. Ando-Suguimoto ◽  
Manjunatha R. Benakanakere ◽  
Marcia P.A. Mayer ◽  
Denis F. Kinane
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inflammatory Responses ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Aggressive Periodontitis ◽  
Host Cells ◽  
Tissue Destruction ◽  
Periodontal Tissues ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells

In aggressive periodontitis, the dysbiotic microbial community in the subgingival crevice, which is abundant in Aggregatibacter actinomycetemcomitans, interacts with extra- and intracellular receptors of host cells, leading to exacerbated inflammation and subsequent tissue destruction. Our goal was to understand the innate immune interactions of A. actinomycetemcomitans with macrophages and human gingival epithelial cells (HGECs) on the signaling cascade involved in inflammasome and inflammatory responses. U937 macrophages and HGECs were co-cultured with A. actinomycetemcomitans strain Y4 and key signaling pathways were analyzed using real-time PCR, Western blotting and cytokine production by ELISA. A. actinomycetemcomitans infection upregulated the transcription of TLR2, TLR4, NOD2 and NLRP3 in U937 macrophages, but not in HGECs. Transcription of IL-1β and IL-18 was upregulated in macrophages and HGECs after 1 h interaction with A. actinomycetemcomitans, but positive regulation persisted only in macrophages, resulting in the presence of IL-1β in macrophage supernatant. Immunoblot data revealed that A. actinomycetemcomitans induced the phosphorylation of AKT and ERK1/2, possibly leading to activation of the NF-κB pathway in macrophages. On the other hand, HGEC signaling induced by A. actinomycetemcomitans was distinct, since AKT and 4EBP1 were phosphorylated after stimulation with A. actinomycetemcomitans, whereas ERK1/2 was not. Furthermore, A. actinomycetemcomitans was able to induce the cleavage of caspase-1 in U937 macrophages in an NRLP3-dependent pathway. Differences in host cell responses, such as those seen between HGECs and macrophages, suggested that survival of A. actinomycetemcomitans in periodontal tissues may be favored by its ability to differentially activate host cells.

scholarly journals HOST PROTEASE INHIBITION BY SPECIFIC PATHOGENS IN PERIODONTAL DISEASE

2018 ◽  
Vol 6 (4) ◽  
pp. 131-137
Author(s):  
Saipriya S ◽  
Vijay Kumar Chava
Keyword(s):  
Periodontal Disease ◽  
Protease Inhibitors ◽  
Gingival Crevicular Fluid ◽  
Critical Role ◽  
Periodontal Pathogens ◽  
Tissue Destruction ◽  
Protease Inhibition ◽  
Periodontal Tissues ◽  
Functional Classes ◽  
Crevicular Fluid

Proteolytic tissue degradation is a typical phenomenon in chronic inflammatory periodontal disease with the uncontrolled release of host and bacterial derived proteases causing self-digestion and tissue destruction. Antimicrobial proteins and peptides constitute a diverse class of host defense molecules that act early to combat invasion and infection with bacteria and other microorganisms and protease inhibitors forms one of the functional classes of antimicrobial peptides.  Plasma protease inhibitors present in gingival crevicular fluid as well as tissues may play a critical role in the protection of periodontal tissues by modulating protease activity, more particularly during active phases. This literature review attempts to highlight the role of host protease inhibitors and their interaction with specific periodontal pathogens in the pathogenesis of periodontal disease.

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