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Periodontology 2000 Jun 2022In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low-level systemic inflammation have been... (Review)
Review
In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low-level systemic inflammation have been speculated to play a role. However, the impact of oral microorganisms, such as Porphyromonas gingivalis, on the pathogenesis of Alzheimer disease and the potential causative relationship is still unclear. The present review has critically reviewed the literature by examining the following aspects: (a) the oral microbiome and the immune response in the elderly population, (b) human studies on the association between periodontal and gut microorganisms and Alzheimer disease, (c) animal and in vitro studies on microorganisms and Alzheimer disease, and (d) preventive and therapeutic approaches. Factors contributing to microbial dysbiosis seem to be aging, local inflammation, systemic diseases, wearing of dentures, living in nursing homes and no access to adequate oral hygiene measures. Porphyromonas gingivalis was detectable in post-mortem brain samples. Microbiome analyses of saliva samples or oral biofilms showed a decreased microbial diversity and a different composition in Alzheimer disease compared to cognitively healthy subjects. Many in-vitro and animal studies underline the potential of P gingivalis to induce Alzheimer disease-related alterations. In animal models, recurring applications of P gingivalis or its components increased pro-inflammatory mediators and β-amyloid in the brain and deteriorated the animals' cognitive performance. Since periodontitis is the result of a disturbed microbial homoeostasis, an effect of periodontal therapy on the oral microbiome and host response related to cognitive parameters may be suggested and should be elucidated in further clinical trials.
Topics: Aged; Alzheimer Disease; Animals; Dysbiosis; Humans; Inflammation; Microbiota; Porphyromonas gingivalis
PubMed: 35244967
DOI: 10.1111/prd.12429 -
Frontiers in Cellular and Infection... 2020Periodontal disease is a chronic infectious disease associated with a variety of bacteria, which can cause damage to the periodontal support structure and affect a... (Review)
Review
Periodontal disease is a chronic infectious disease associated with a variety of bacteria, which can cause damage to the periodontal support structure and affect a variety of systemic system diseases such as cancer, cardiovascular disease, diabetes, rheumatoid arthritis, non-alcoholic fatty liver, and Alzheimer's disease. () is the most important pathogenic bacteria for periodontal disease. It can produce outer membrane vesicles (OMVs) and release them into the environment, playing an important role in its pathogenesis. This article focuses on OMVs, reviews its production and regulation, virulence components, mode of action and related diseases, with a view to providing new ideas for the prevention and treatment of diseases related to infections.
Topics: Humans; Periodontal Diseases; Porphyromonas gingivalis; Virulence; Virulence Factors
PubMed: 33585266
DOI: 10.3389/fcimb.2020.585917 -
Archives of Razi Institute Oct 2022Chronic periodontitis is an inflammatory disease of the dental plaque and affects the soft tissues supporting the tooth. It is one of the most practical oral health... (Review)
Review
Chronic periodontitis is an inflammatory disease of the dental plaque and affects the soft tissues supporting the tooth. It is one of the most practical oral health issues across the globe and adversely affects the quality of life. In a neutrophil-mediated action, the inflammatory response to periodontitis destroys the periodontal ligaments, gums, the alveolar bone, and the cementum. Some of the most associated invasive pathogens with periodontitis are , , and . Google Scholar and PubMed were used to search the evidence using key terms like 'periodontitis,' ',' 'Oral Dysbiosis and Periodontitis,' ' and Periodontitis,' etc. Only studies were included reviewing the and its role in periodontitis. It has been observed from several oral pathogens that has received immense attention due to a strong association between and periodontal disease. also disrupts the delicate balance between various members of the oral microbial communities and promotes oral dysbiosis. The dysbiotic state of the oral microbiome is distinct in functional capabilities and shows a higher expression of genes involved in lipopolysaccharide synthesis, energy regulation, and bacterial motility. Certain virulence factors such as gingipains, LPS, and fimbriae also increase the invasion and pathogenicity of . Its presence in the periodontal tissues increases the secretion of numerous pro-inflammatory mediators such as TNF-α, IL-8, and IL-1β, leading to the destruction of soft gingival tissues and ligaments. Early detection of periodontitis and immediate treatment can prevent soft tissue destruction and dentition loss. In conclusion, details about the oral microbiome, oral dysbiosis, and inflammation may offer new therapeutic options in the future, including a personalized approach and the use of combination therapy.
Topics: Dysbiosis; Inflammation; Periodontitis; Porphyromonas gingivalis; Quality of Life; Humans
PubMed: 37123122
DOI: 10.22092/ARI.2021.356596.1875 -
Trends in Microbiology Apr 2021
Topics: Bacteroidaceae Infections; Gingipain Cysteine Endopeptidases; Humans; Porphyromonas gingivalis
PubMed: 33546976
DOI: 10.1016/j.tim.2021.01.010 -
Periodontology 2000 Jun 2022The link between oral health and adverse pregnancy outcomes has been suggested by numerous epidemiological studies. More recent studies indicate the relationship between... (Review)
Review
The link between oral health and adverse pregnancy outcomes has been suggested by numerous epidemiological studies. More recent studies indicate the relationship between severity of periodontal disease and adverse pregnancy outcomes. Two virulence mechanisms are proposed: direct invasion of oral microorganisms or their components into the fetal-placenta unit and inflammatory mediators produced in the oral cavity affecting the fetal-placenta unit. While interventional periodontal therapy still yielded contradictory results, animal studies suggest that maternal supplementation of omega-3 fatty acids protects the fetus by suppressing inflammation as well as bacteria proliferation in the placenta. This article reviews the recent epidemiological, mechanistic, interventional, and therapeutic studies of oral health and adverse pregnancy outcomes.
Topics: Animals; Female; Fusobacterium nucleatum; Humans; Oral Health; Periodontal Diseases; Porphyromonas gingivalis; Pregnancy; Pregnancy Outcome
PubMed: 35244963
DOI: 10.1111/prd.12436 -
Journal of Dental Research May 2023Gingival fibroblasts (GFs) are essential components of the periodontium, which are responsible for the maintenance of tissue structure and integrity. However, the... (Review)
Review
Gingival fibroblasts (GFs) are essential components of the periodontium, which are responsible for the maintenance of tissue structure and integrity. However, the physiological role of GFs is not restricted to the production and remodeling of the extracellular matrix. GFs also act as sentinel cells that modulate the immune response to oral pathogens invading the gingival tissue. As an important "nonclassical" component of the innate immune system, GFs respond to bacteria and damage-related signals by producing cytokines, chemokines, and other inflammatory mediators. Although the activation of GFs supports the elimination of invading bacteria and the resolution of inflammation, their uncontrolled or excessive activation may promote inflammation and bone destruction. This occurs in periodontitis, a chronic inflammatory disease of the periodontium initiated and sustained by dysbiosis. In the inflamed gingival tissue, GFs acquire imprinted proinflammatory phenotypes that promote the growth of inflammophilic pathogens, stimulate osteoclastogenesis, and contribute to the chronicity of inflammation. In this review, we discuss the biological functions of GFs in healthy and inflamed gingival tissue, highlighting recent studies that provide insight into their role in the pathogenesis of periodontal diseases. We also draw parallels with the recently discovered fibroblast populations identified in other tissues and their roles in health and disease. This knowledge should be used in future studies to discover more about the role of GFs in periodontal diseases, especially chronic periodontitis, and to identify therapeutic strategies targeting their pathological interactions with oral pathogens and the immune system.
Topics: Humans; Porphyromonas gingivalis; Inflammation; Gingiva; Chronic Periodontitis; Fibroblasts
PubMed: 36883660
DOI: 10.1177/00220345231151921 -
ACS Nano Nov 2022Periodontitis is a chronic inflammatory disease caused by the interaction of oral microorganisms with the host immune response. (P.g.) acts as a key mediator in...
Periodontitis is a chronic inflammatory disease caused by the interaction of oral microorganisms with the host immune response. (P.g.) acts as a key mediator in subverting the homeostasis of the local immune system. On the one hand, P.g. inhibits phagocytosis and the killing capacity of immune cells. On the other hand, P.g. increases selective cytokine release, which is beneficial to its further proliferation. Here, we prepared a penetrating macrophage-based nanoformulation (MZ@PNM)-encapsulating hydrogel (MZ@PNM@GCP) that responded to the periodontitis microenvironment. MZ@PNM targeted P.g. via the Toll-like receptor complex 2/1 (TLR2/1) on its macrophage-mimicking membrane, then directly killed P.g. through disruption of bacterial structural integrity by the cationic nanoparticles and intracellular release of an antibacterial drug, metronidazole (MZ). Meanwhile, MZ@PNM interrupted the specific binding of P.g. to immune cells and neutralized complement component 5a (C5a), preventing P.g. subversion of periodontal host immune response. Overall, MZ@PNM@GCP showed potent efficacy in periodontitis treatment, restoring local immune function and killing pathogenic bacteria, while exhibiting favorable biocompatibility, all of which have been demonstrated both and .
Topics: Humans; Periodontitis; Porphyromonas gingivalis; Macrophages; Cytokines
PubMed: 36288552
DOI: 10.1021/acsnano.2c05923 -
Periodontology 2000 Jun 2020Atherosclerosis is central to the pathology of cardiovascular diseases, a group of diseases in which arteries become occluded with atheromas that may rupture, leading to... (Review)
Review
Atherosclerosis is central to the pathology of cardiovascular diseases, a group of diseases in which arteries become occluded with atheromas that may rupture, leading to different cardiovascular events, such as myocardial infarction or ischemic stroke. There is a large body of epidemiologic and animal model evidence associating periodontitis with atherosclerotic disease, and many potential mechanisms linking these diseases have been elucidated. This chapter will update knowledge on these mechanisms, which generally fall into 2 categories: microbial invasion and infection of atheromas; and inflammatory and immunologic. With respect to the invasion and infection of atheromas, it is well established that organisms from the subgingival biofilm can enter the circulation and lodge in most distant tissues. Bacteremias resulting from oral interventions, and even oral hygiene activities, are well documented. More recently, indirect routes of entry of oral organisms (via phagocytes or dendritic cells) have been described for many oral organisms, into many tissues. Such organisms include the periodontal pathogens Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Tannerella forsythia, and Fusobacterium nucleatum. Intracellular survival of these organisms with dissemination to distant sites (The Trojan Horse approach) has been described. Their relative contribution to atheroma formation and progression has been studied mainly in experimental research, with results demonstrating that these organisms can invade endothelial cells and phagocytic cells within the atheroma, leading to pathogenic changes and progression of the atheroma lesion. The second category of mechanisms potentially linking periodontitis to atherosclerosis includes the dumping of inflammatory mediators originating from periodontal lesions into the systemic circulation. These inflammatory mediators, such as C-reactive protein, matrix metalloproteinases, fibrinogen, and other hemostatic factors, would further accelerate atheroma formation and progression, mainly through oxidative stress and inflammatory dysfunction. Moreover, direct effects on lipid oxidation have also been described. In summary, the evidence supports the concept that periodontitis enhances the levels of systemic mediators of inflammation that are risk factors for atherosclerotic diseases.
Topics: Aggregatibacter actinomycetemcomitans; Atherosclerosis; Endothelial Cells; Humans; Periodontitis; Porphyromonas gingivalis; Prevotella intermedia
PubMed: 32385879
DOI: 10.1111/prd.12304 -
Gut bacteria identified in colorectal cancer patients promote tumourigenesis via butyrate secretion.Nature Communications Sep 2021Emerging evidence is revealing that alterations in gut microbiota are associated with colorectal cancer (CRC). However, very little is currently known about whether and...
Emerging evidence is revealing that alterations in gut microbiota are associated with colorectal cancer (CRC). However, very little is currently known about whether and how gut microbiota alterations are causally associated with CRC development. Here we show that 12 faecal bacterial taxa are enriched in CRC patients in two independent cohort studies. Among them, 2 Porphyromonas species are capable of inducing cellular senescence, an oncogenic stress response, through the secretion of the bacterial metabolite, butyrate. Notably, the invasion of these bacteria is observed in the CRC tissues, coinciding with the elevation of butyrate levels and signs of senescence-associated inflammatory phenotypes. Moreover, although the administration of these bacteria into Apc mice accelerate the onset of colorectal tumours, this is not the case when bacterial butyrate-synthesis genes are disrupted. These results suggest a causal relationship between Porphyromonas species overgrowth and colorectal tumourigenesis which may be due to butyrate-induced senescence.
Topics: Bacteria; Butyrates; Carcinogenesis; Cellular Senescence; Colorectal Neoplasms; Epithelial Cells; Feces; Gastrointestinal Microbiome; Humans; Intestines; Porphyromonas; RNA, Ribosomal, 16S
PubMed: 34584098
DOI: 10.1038/s41467-021-25965-x -
International Journal of Oral Science Sep 2021Ulcerative Colitis (UC) has been reported to be related to Porphyromonas gingivalis (P. gingivalis). Porphyromonas gingivalis peptidylarginine deiminase (PPAD), a...
Ulcerative Colitis (UC) has been reported to be related to Porphyromonas gingivalis (P. gingivalis). Porphyromonas gingivalis peptidylarginine deiminase (PPAD), a virulence factor released by P. gingivalis, is known to induce inflammatory responses. To explore the pathological relationships between PPAD and UC, we used homologous recombination technology to construct a P. gingivalis strain in which the PPAD gene was deleted (Δppad) and a Δppad strain in which the PPAD gene was restored (comΔppad). C57BL/6 mice were orally gavaged with saline, P. gingivalis, Δppad, or comΔppad twice a week for the entire 40 days (days 0-40), and then, UC was induced by dextran sodium sulfate (DSS) solution for 10 days (days 31-40). P. gingivalis and comΔppad exacerbated DDS-induced colitis, which was determined by assessing the parameters of colon length, disease activity index, and histological activity index, but Δppad failed to exacerbate DDS-induced colitis. Flow cytometry and ELISA revealed that compared with Δppad, P. gingivalis, and comΔppad increased T helper 17 (Th17) cell numbers and interleukin (IL)-17 production but decreased regulatory T cells (Tregs) numbers and IL-10 production in the spleens of mice with UC. We also cocultured P. gingivalis, Δppad, or comΔppad with T lymphocytes in vitro and found that P. gingivalis and comΔppad significantly increased Th17 cell numbers and decreased Treg cell numbers. Immunofluorescence staining of colon tissue paraffin sections also confirmed these results. The results suggested that P. gingivalis exacerbated the severity of UC in part via PPAD.
Topics: Animals; Colitis, Ulcerative; Mice; Mice, Inbred C57BL; Porphyromonas gingivalis; Protein-Arginine Deiminases; Virulence Factors
PubMed: 34593756
DOI: 10.1038/s41368-021-00136-2