-
Advances in Protein Chemistry and... 2020Periodontitis is an infection-driven inflammatory disease, which is characterized by gingival inflammation and bone loss. Periodontitis is associated with various... (Review)
Review
Periodontitis is an infection-driven inflammatory disease, which is characterized by gingival inflammation and bone loss. Periodontitis is associated with various systemic diseases, including cardiovascular, respiratory, musculoskeletal, and reproductive system related abnormalities. Recent theory attributes the pathogenesis of periodontitis to oral microbial dysbiosis, in which Porphyromonas gingivalis acts as a critical agent by disrupting host immune homeostasis. Lipopolysaccharide, proteases, fimbriae, and some other virulence factors are among the strategies exploited by P. gingivalis to promote the bacterial colonization and facilitate the outgrowth of the surrounding microbial community. Virulence factors promote the coaggregation of P. gingivalis with other bacteria and the formation of dental biofilm. These virulence factors also modulate a variety of host immune components and subvert the immune response to evade bacterial clearance or induce an inflammatory environment. In this chapter, our focus is to discuss the virulence factors of periodontal pathogens, especially P. gingivalis, and their roles in regulating immune responses during periodontitis progression.
Topics: Humans; Periodontitis; Porphyromonas gingivalis; T-Lymphocytes; Virulence Factors
PubMed: 32085888
DOI: 10.1016/bs.apcsb.2019.12.001 -
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 -
Inflammatory Bowel Diseases Jul 2023One of the prospective sequelae of periodontal disease (PD), chronic inflammation of the oral mucosa, is the development of inflammatory gastrointestinal (GI) disorders... (Review)
Review
One of the prospective sequelae of periodontal disease (PD), chronic inflammation of the oral mucosa, is the development of inflammatory gastrointestinal (GI) disorders due to the amplification and expansion of the oral pathobionts. In addition, chronic inflammatory diseases related to the GI tract, which include inflammatory bowel disease (IBD), can lead to malignancy susceptibility in the colon of both animals and humans. Recent studies suggest that dysbiosis of the oral microbiota can alter the microbial composition in relative abundance or diversity of the distal gut, leading to the progression of digestive carcinogenesis. The link between PD and specific GI disorders is also closely associated with the migration and colonization of periodontal pathogens and the subsequent microbe-reactive T cell induction within the intestines. In this review, an in-depth examination of this relationship and the accessibility of different mouse models of IBD and PD may shed light on the current dogma. As such, oral microbiota dysbiosis involving specific bacteria, including Fusobacterium nucleatum and Porphyromonas gingivalis, can ultimately lead to gut malignancies. Further understanding the precise mechanism(s) of the oral-gut microbial axis in PD, IBD, and colorectal cancer pathogenesis will be pivotal in diagnosis, prognosis, and future treatment.
Topics: Animals; Mice; Humans; Dysbiosis; Prospective Studies; Periodontal Diseases; Gastrointestinal Diseases; Inflammatory Bowel Diseases; Porphyromonas gingivalis
PubMed: 36527679
DOI: 10.1093/ibd/izac241 -
Gut Microbes 2022Intratumor microbiome shapes the immune system and influences the outcome of various tumors. (), the keystone periodontal pathogen, is highly epidemically connected...
Intratumor microbiome shapes the immune system and influences the outcome of various tumors. (), the keystone periodontal pathogen, is highly epidemically connected with pancreatic cancer (PC). However, its causative role and the underlining mechanism in promoting PC oncogenesis remain unclear. Here, we illustrated the landscape of intratumor microbiome and its bacterial correlation with oral cavity in PC patients, where presented both in the oral cavity and tumor tissues. When exposed to , tumor development was accelerated in orthotopic and subcutaneous PC mouse model, and the cancerous pancreas exhibited a neutrophils-dominated proinflammatory tumor microenvironment. Mechanistically, the intratumoral promoted PC progression via elevating the secretion of neutrophilic chemokines and neutrophil elastase (NE). Collectively, our study disclosed the bacterial link between periodontitis and PC, and revealed a previously unrecognized mechanism of in PC pathophysiology, hinting at therapeutic implications.
Topics: Animals; Carcinogenesis; Cell Transformation, Neoplastic; Gastrointestinal Microbiome; Humans; Leukocyte Elastase; Mice; Neutrophils; Pancreas; Periodontitis; Porphyromonas gingivalis; Tumor Microenvironment
PubMed: 35549648
DOI: 10.1080/19490976.2022.2073785 -
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 -
Journal of Translational Medicine Sep 2022In the last decades, the ortho-aesthetic-functional rehabilitation had significant advances with the advent of implantology. Despite the success in implantology... (Review)
Review
In the last decades, the ortho-aesthetic-functional rehabilitation had significant advances with the advent of implantology. Despite the success in implantology surgeries, there is a percentage of failures mainly due to in loco infections, through bacterial proliferation, presence of fungi and biofilm formation, originating peri-implantitis. In this sense, several studies have been conducted since then, seeking answers to numerous questions that remain unknown. Thus, the present work aims to discuss the interaction between host-oral microbiome and the development of peri-implantitis. Peri-implantitis was associated with a diversity of bacterial species, being Porphiromonas gingivalis, Treponema denticola and Tannerella forsythia described in higher proportion of peri-implantitis samples. In a parallel role, the injury of peri-implant tissue causes an inflammatory response mediated by activation of innate immune cells such as macrophages, dendritic cells, mast cells, and neutrophils. In summary, the host immune system activation may lead to imbalance of oral microbiota, and, in turn, the oral microbiota dysbiosis is reported leading to cytokines, chemokines, prostaglandins, and proteolytic enzymes production. These biological processes may be responsible for implant loss.
Topics: Cytokines; Dental Implants; Humans; Microbiota; Peptide Hydrolases; Peri-Implantitis; Porphyromonas gingivalis; Prostaglandins
PubMed: 36138430
DOI: 10.1186/s12967-022-03636-9 -
Periodontology 2000 Jun 2022Oral and esophageal squamous cell carcinomas harbor a diverse microbiome that differs compositionally from precancerous and healthy tissues. Though causality is yet to... (Review)
Review
Oral and esophageal squamous cell carcinomas harbor a diverse microbiome that differs compositionally from precancerous and healthy tissues. Though causality is yet to be definitively established, emerging trends implicate periodontal pathogens such as Porphyromonas gingivalis as associated with the cancerous state. Moreover, infection with P. gingivalis correlates with a poor prognosis, and P. gingivalis is oncopathogenic in animal models. Mechanistically, properties of P. gingivalis that have been established in vitro and could promote tumor development include induction of a dysbiotic inflammatory microenvironment, inhibition of apoptosis, increased cell proliferation, enhanced angiogenesis, activation of epithelial-to-mesenchymal transition, and production of carcinogenic metabolites. The microbial community context is also relevant to oncopathogenicity, and consortia of P. gingivalis and Fusobacterium nucleatum are synergistically pathogenic in oral cancer models in vivo. In contrast, oral streptococci, such as Streptococcus gordonii, can antagonize protumorigenic epithelial cell phenotypes induced by P. gingivalis, indicating functionally specialized roles for bacteria in oncogenic communities. Consistent with the notion of the bacterial community constituting the etiologic unit, metatranscriptomic data indicate that functional, rather than compositional, properties of the tumor-associated communities have more relevance to cancer development. A consistent association of P. gingivalis with oral and orodigestive carcinoma could have diagnostic potential for early detection of these conditions that have a high incidence and low survival rates.
Topics: Animals; Carcinoma, Squamous Cell; Fusobacterium nucleatum; Humans; Microbiota; Mouth Neoplasms; Porphyromonas gingivalis; Tumor Microenvironment
PubMed: 35244980
DOI: 10.1111/prd.12425 -
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