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 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.

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 Is There a Link between COVID-19 Infection, Periodontal Disease and Acute Myocardial Infarction?

Life ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1050
Author(s):  
Ioana-Patricia Rodean ◽  
Carmen-Ioana Biriș ◽  
Vasile-Bogdan Halațiu ◽  
Andrei Modiga ◽  
Luminița Lazăr ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Periodontal Disease ◽  
Plaque Formation ◽  
Atheromatous Plaque ◽  
Tissue Destruction ◽  
Systemic Complications ◽  
Chronic Disorders ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host’s immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal–cardiovascular diseases and COVID-19 infection.

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.

Periodontopathogens: a new view. Systematic review. Part 2

2020 ◽  
Vol 20 (2) ◽  
pp. 160-167
Author(s):  
E. S. Slazhneva ◽  
E. A. Tikhomirova ◽  
V. G. Atrushkevich
Keyword(s):  
Systematic Review ◽  
Periodontal Disease ◽  
Pathogenic Bacteria ◽  
Periodontal Diseases ◽  
Oral Microbiome ◽  
Controlled Trials ◽  
New Paradigm ◽  
Microbial Composition ◽  
Randomized Controlled ◽  
The Past

Relevance. The modern view of periodontitis as a dysbiotic disease that occurs as a result of changes in the microbial composition of the subgingival region is considered in a systematic review.Purpose. To study a new paradigm of development of generalized periodontitis.Materials and methods. Randomized controlled trials (RCTS) were selected for the study, including cluster RCTS, controlled (non-randomized) microbiological and clinical studies of the oral microbiome in adult patients with generalized periodontitis over the past 10 years.Results. The transition from a symbiotic microflora to a dysbiotic pathogenic community triggers the host's inflammatory response, which contributes to the development of periodontal diseases. Modern ideas about periodontal pathogenic bacteria dictate new requirements for the treatment of periodontal diseases. The second part of the review examines the microbial profiles of periodontal disease in various nosological forms, the mechanisms of the immune response and approaches to the treatment of periodontal disease from the perspective of biofilm infection.Conclusions. As follows from modern literature periodontitis is to a certain extent caused by the transition from a harmonious symbiotic bacterial community to a dysbiotic one. Recent scientific studies have shown that not single microorganism is not able to cause disease but the microbial community as a whole leads to the development of pathology.

Salivary Diagnosis - Clinical Uses in Assessing Oral Inflammation

2017 ◽  
Vol 68 (6) ◽  
pp. 1201-1204 ◽  
Author(s):  
Iulia Ioana Stanescu ◽  
Alexandra Totan ◽  
Florentina Rus ◽  
Daniela Miricescu ◽  
Brandusa Mocanu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Periodontal Disease ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Marker ◽  
Clinical Settings ◽  
Tissue Destruction ◽  
Whole Saliva ◽  
Oral Inflammation ◽  
Positive Correlations ◽  
Crevicular Fluid

The past decades demonstrated that saliva and its components represent a remarkable diagnosis fluid with valuable clinical uses for both oral and systemic diseases. At the same time it is well established that oxidative stress is involved in a wide number of pathologies, including periodontitis. The specific aim of the present study which included 50 subjects is to determine if saliva can be used in clinical settings to correlate oxidative stress and tissue destruction markers with the severity of periodontal disease. An important oxidative stress marker - 8-hydroxydesoxyguanosine (8-OHdG) and a collagen degradation marker - beta-crosslaps (b-CTX) were quantified in both saliva and gingival crevicular fluid (GCF) using ELISA kits and were found to be significantly increased in the chronic periodontitis group when compared to respective controls (p[0.05). At the same time positive correlations were observed between whole saliva and gingival crevicular fluid (p[0.05). Significant correlations were also determined between GCF and salivary markers and clinical parameters of periodontal disease. Present results demonstrate that saliva and its components can successfully be used in clinical settings and represents a reliable tool for assessing periodontal disease severity.

scholarly journals Molecular Mechanisms of Periodontal Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 930
Author(s):  
Mikihito Kajiya ◽  
Hidemi Kurihara
Keyword(s):  
Infectious Diseases ◽  
Periodontal Disease ◽  
Molecular Mechanisms ◽  
Alveolar Bone ◽  
Tissue Destruction ◽  
Connective Tissues ◽  
Inflammatory Tissue

Periodontal disease, one of the most prevalent human infectious diseases, is characterized by chronic inflammatory tissue destruction of the alveolar bone and the connective tissues supporting the tooth [...]

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 Morphometric analysis of collagen and inflammatory cells in periodontal disease

2015 ◽  
Vol 72 (3) ◽  
pp. 219-224 ◽  
Author(s):  
Ranko Golijanin ◽  
Bojan Kujundzic ◽  
Zoran Milosavljevic ◽  
Dragan Milovanovic ◽  
Zlatibor Andjelkovic ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Morphometric Analysis ◽  
Plasma Cells ◽  
Relative Proportion ◽  
Inflammatory Cells ◽  
Test System ◽  
Clinical Staging ◽  
Gingival Tissue ◽  
Tissue Destruction ◽  
Immunochemical Method

Background/Aim. Periodontal disease affects gingival tissue and supporting apparatus of the teeth leading to its decay. The aim of this study was to highlight and precisely determine histological changes in the gum tissue. Methods. Gingival biopsy samples from 53 healthy and parodontopathy-affected patients were used. Clinical staging of the disease was performed. Tissue specimens were fixed and routinely processed. Sections, 5 ?m thin, were stained with hematoxylin and eosin, histochemical Van-Gieson for the collagen content, Spicer method for mast-cells and immunochemical method with anti-CD68 and anti-CD38 for the labelling of the macrophages and plasma-cells. Morphometric analysis was performed by a M42 test system. Results. While the disease advanced, collagen and fibroblast volume density decreased almost twice in the severe cases compared to the control ones, but a significant variation was observed within the investigated groups. The mast-cell number increased nearly two times, while the macrophage content was up to three times higher in severe parodontopathy than in healthy gingival tissue. However, the relative proportion of these cells stayed around 6% in all cases. Plasma-cells had the most prominent increase in the number (over 8 times) compared to the control, but again, a variation within investigated groups was very high. Conclusion. Gingival tissue destruction caused by inflammatory process leads to significant changes in collagen density and population of resident connective tissue cells. Although inflammatory cells dominated with the disease advancing, a high variation within the same investigated groups suggests fluctuation of the pathological process. <br><br><font color="red"><b> This article has been corrected. Link to the correction <u><a href="http://dx.doi.org/10.2298/VSP1704391E">10.2298/VSP1704391E</a><u></b></font>

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