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Representative images of P. gingivalis staining in the gingival tissue of interdental papillae. (a) H & E stained section of the gingival epithelium, showing the approximate region (boxed area) where P. gingivalis was detected by immunostaining (right panel). White arrow points to a P. gingivalis positive area (pseudocolored green) in the gingival epithelial layer that is also shown in the magnified inset. White arrowhead points to an autofluorescent red blood cell present in the section. (b) H & E stained section of the subgingival connective tissue matrix, boxed region indicates approximate location of where P. gingivalis positive subgingival capillaries were detected (white arrow, pseudocolored green) that is also included in the top magnified inset. The white arrowhead points to an autofluorescent red blood cell present in the section. Transillumination was used to demarcate tissue architecture and nuclei were stained with DAPI (blue). Scale bars are 50 μm
Source publication
Objective: Microvascular dysfunction is a feature of periodontal disease. P. gingivalis, one of the most common oral bacteria present in gingival tissue biofilms, has also been identified in the gingival capillaries of patients with chronic periodontitis. We sought to determine the effect of P. gingivalis W83 infection on microvascular endothelium...
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Citations
... While subgingival instrumentation is crucial for periodontal therapy, its effectiveness in eradicating periodontal pathogens is not always guaranteed. This is due to the bacteria's ability to escape mechanical debridement by burrowing into soft tissues or taking refuge in hard-to-access anatomical structures, such as dentinal tubuli, furcations, or deep infrabony defects [13][14][15][16][17]. ...
Caries and periodontitis are the most prevalent oral diseases worldwide. Major factors contributing to the development of these oral conditions include poor oral hygiene, dental biofilm formation, high carbohydrates diet, smoking, other systemic diseases, and genetic factors. Various preventive measures have been established to mitigate the risk of caries and periodontal disease development. The present review aims to discuss the role of the probiotics Lactobacillus rhamnosus and Lactobacillus plantarum in the prevention and treatment of caries and periodontal diseases. The study was conducted in accordance with PRISMA guidelines and was registered on PROSPERO. The search involved PubMed, Web of Science, and Scopus and considered the PICO format. Studies were screened by two reviewers independently, and disagreements were solved by consensus with a third reviewer. Data extraction included details about the type of probiotics, strains, and purpose of administration. A total of 15 RCTs were included, of which just 1 was about tooth cavities. Overall, 87% of the included studies were good-quality papers regarding the Jadad Scale. Several studies agreed on the potential of probiotics L. rhamnosus and L. plantarum, both alone and combined, to prevent and improve clinical outcomes in caries and periodontal treatments, weaker evidence is provided for the microbiological benefit.
... Here are some cardiovascular conditions that may be affected by Porphyromonas gingivalis, such as atherosclerosis, myocardial infarction, stroke and endocarditis. Porphyromonas gingivalis, can potentially affect cardiovascular diseases through various mechanisms (12,13). First of all, Porphyromonas gingivalis can induce a localized (15). ...
Background
Periodontitis (PD) and cardiovascular diseases (CVD) rank among the most prevalent pathologies worldwide, and their correlation has been a subject of prolonged investigation. Numerous studies suggest shared etiological factors; however, a definitive causal connection remains unestablished. The objective of this study was to employ bibliometric and visual analyses in order to comprehensively examine the overarching characteristics, focal areas of research, and prospective trends pertaining to the PD-CVD relationship.
Methods
We sourced articles, reviews, and online publications on PD- and CVD- research from the Web of Science Core Collection (WoSCC) spanning from January 1, 1993, to May 15, 2023. A triad of analytical tools (R-Bibliometrix, VOSviewer 1.6.19, and CiteSpace 6.2.R3) were utilized to facilitate collaboration network analysis, co-citation analysis, co-occurrence analysis, and citation burst detection.
Results
Out of the 1,116 publications that fulfilled the eligibility criteria in the WoSCC database, the comprehensive characteristics analysis divulged a sustained growth trend in publication frequency. In the cluster analysis of reference co-citation and keyword co-occurrence, prominent themes such as “periodontitis”, “cardiovascular diseases”, “inflammation”, “ Porphyromonas gingivalis ”, and “atherosclerosis” consistently emerged. Contemporary topics such as “peri-implantitis,” “COVID-19”, “cardiovascular risk factors,” and “endocarditis” were pinpointed as burgeoning research hotspots.
Conclusion
Based on this bibliometric study, in the field of association studies between PD and CVD, the etiologic mechanisms of both diseases have been intensively studied in the last three decades. Periodontal pathogens might serve as potential initiating factors linking PD and CVD. Inflammation may constitute a significant etiological factor shared by both diseases. Several emerging topics, such as COVID-19 and peri-implantitis, exhibit promising potential. This exhaustive overview casts light on pivotal research arenas, augmenting the field's understanding and stimulating further scholarly investigations.
... 89 Expression of ICAM-1, an adhesion receptor, on human microvascular endothelial cells has been shown to facilitate Pg invasion. [89][90][91][92][93] Increased invasion would enhance speed of disease progression, as observed in Stat6VT mice and SvP. 94,95 Past studies have categorised patients as having aggressive or chronic periodontitis. ...
Objective:
The aim of this research was to investigate the role of the cornified epithelium, the outermost layer of the oral mucosa, engineered to prevent water loss and microorganism invasion, in severe forms of periodontitis (stage III or IV, grade C).
Methods:
Porphyromonas gingivalis, a major periodontal disease pathogen, can affect cornified epithelial protein expression through chronic activation of signal transducer and activator of transcription 6 (Stat6). We used a mouse model, Stat6VT, that mimics this to determine the effects of barrier defect on P gingivalis-induced inflammation, bone loss, and cornified epithelial protein expression, and compared histologic and immunohistologic findings with tissues obtained from human controls and patients with stage III and IV, grade C disease. Alveolar bone loss in mice was assessed using micro-computerised tomography, and soft tissue morphology was qualitatively and semi-quantitatively assessed by histologic examination for several proteins, including loricrin, filaggrin, cytokeratin 1, cytokeratin 14, a proliferation marker, a pan-leukocyte marker, as well as morphologic signs of inflammation. Relative cytokine levels were measured in mouse plasma by cytokine array.
Results:
In the tissues from patients with periodontal disease, there were greater signs of inflammation (rete pegs, clear cells, inflammatory infiltrates) and a decrease and broadening of expression of loricrin and cytokeratin 1. Cytokeratin 14 expression was also broader and decreased in stage IV. P gingivalis-infected Stat6VT mice showed greater alveolar bone loss in 9 out of 16 examined sites, and similar patterns of disruption to human patients in expression of loricrin and cytokeratins 1 and 14. There were also increased numbers of leukocytes, decreased proliferation, and greater signs of inflammation compared with P gingivalis-infected control mice.
Conclusions:
Our study provides evidence that changes in epithelial organisation can exacerbate the effects of P gingivalis infection, with similarities to the most severe forms of human periodontitis.
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... P. gingivalis not only enters and survives in ECs mediated by ICAM-1 but also releases from ECs and infects neighboring cells (194,195). Repeated stimulation with P. gingivalis increases the expression of pro-inflammatory molecules (IL-6, MCP-1, GM-CSF) and vasoconstrictor molecules (Ang II) in ECs, increases monocyte adhesion to the endothelium and inhibits endothelial diastolic function (67). Similarly, a systemic Th1-type immune response occurred in mice immunized with P. gingivalis antigen, increasing the sensitivity of ECs to AngII and exacerbating the inhibition of endothelial diastolic function (196). ...
Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the “dominant flora” in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.
... As plaque accumulation and gingival inflammation allow periopathogens to enter the systemic circulation [110], it may increase the risk of developing medical conditions [111,112]. These mechanisms involve the increased vascular permeability and damage of the oral epithelium caused by periopathogens [113]. A dysregulated immune system and the contributing role of impaired barriers play an important role in pathogenesis of ACI [114,115]. ...
It has been suggested that molecular pathological mechanisms responsible for periodontitis can be linked with biochemical alterations in neurodegenerative disorders. Hypothetically, chronic systemic inflammation as a response to periodontitis plays a role in the etiology of cognitive impairment. This study aimed to determine whether periodontitis (PDS) is a risk factor for age-related cognitive impairment (ACI) based on evidence of clinical studies. A comprehensive, structured systematic review of existing data adhering to the Preferred Reporting Items for Systematic Review and Meta Analyses (PRISMA) guidelines was carried out. Five electronic databases, PubMed, Embase, Scopus, Web of Science, and Cochrane, were searched for key terms published in peer-reviewed journals until January 2021. The Newcastle–Ottawa scale was used to assess the quality of studies and risk of bias. The primary and residual confounders were explored and evaluated. A meta-analysis synthesizing quantitative data was carried out using a random-effects model. Seventeen clinical studies were identified, including 14 cohort, one cross-sectional, and two case-control studies. Study samples ranged from 85 to 262,349 subjects, with follow-up between 2 and 32 years, and age above 45 years, except for two studies. The findings of studies suggesting the PDS-ACI relationship revealed substantial differences in design and methods. A noticeable variation related to the treatment of confounders was observed. Quality assessment unveiled a moderate quality of evidence and risk of bias. The subgroups meta-analysis and pooled sensitivity analysis of results from seven eligible studies demonstrated overall that the presence of PDS is associated with an increased risk of incidence of cognitive impairment (OR = 1.36, 95% CI 1.03–1.79), particularly dementia (OR = 1.39, 95% CI 1.02–1.88) and Alzheimer’s disease (OR = 1.03 95% CI 0.98–1.07)). However, a considerable heterogeneity of synthesized data (I2 = 96%) and potential publication bias might affect obtained results. While there is a moderate statistical association between periodontitis and dementia, as well as Alzheimer’s disease, the risk of bias in the evidence prevents conclusions being drawn about the role of periodontitis as a risk factor for age-related cognitive impairment.
... A study by Li et al. showed that lectin-type oxidized LDL receptor 1 (LOX-1) plays a key role in P. gingivalis-induced migration and adhesion of monocytes to human EC [58]. Moreover, in an in vivo and in vitro study by Reyes et al., it was found that P. gingivalis infection led to microvascular EC damage and that invasion of these cells via intercellular adhesion molecule 1 [ICAM-1] (anti-ICAM-1 antibodies reduced P. gingivalis invasion in EC) may be important for microbial persistence within tissues [59]. Periodontal pathogens are characterized by the ability to directly infect vascular endothelial cells (EC) [60]. ...
Atherosclerotic cardiovascular disease (ASCVD) and periodontal disease (PD) are global health problems. High frequency of ASCVD is associated with the spread of many risk factors, including poor diet, sedentary lifestyle, diabetes, hyperlipidemia, obesity, smoking, hypertension, chronic kidney disease, hypertension, hyperhomocysteinemia, hyperuricemia, excessive stress, virus infection, genetic predisposition, etc. The pathogenesis of ASCVD is complex, while inflammation plays an important role. PD is a chronic, multifactorial inflammatory disease caused by dysbiosis of the oral microbiota, causing the progressive destruction of the bone and periodontal tissues surrounding the teeth. The main etiological factor of PD is the bacteria, which are capable of activating the immune response of the host inducing an inflammatory response. PD is associated with a mixed microbiota, with the evident predominance of anaerobic bacteria and microaerophilic. The “red complex” is an aggregate of three oral bacteria: Tannerella forsythia Treponema denticola and Porphyromonas gingivalis responsible for severe clinical manifestation of PD. ASCVD and PD share a number of risk factors, and it is difficult to establish a causal relationship between these diseases. The influence of PD on ASCVD should be treated as a factor increasing the risk of atherosclerotic plaque destabilization and cardiovascular events. The results of observational studies indicate that PD significantly increases the risk of ASCVD. In interventional studies, PD treatment was found to have a beneficial effect in the prevention and control of ASCVD. This comprehensive review summarizes the current knowledge of the relationship between PD and ASCVD.
... In the AS initial stage, P. gingivalis can introduce ECs to internalize it and begin autophagy, which was utilized in transporting bacteria or/and toxins. In in vitro experiments, P. gingivalis invaded ECs through ICAM-1-mediated endocytosis (134). After that, EC autophagy induced by P. gingivalis provides a replicative niche where bacteria survive and replicate while suppressing apoptosis (135). ...
Atherosclerosis (AS), one of the most common types of cardiovascular disease, has initially been attributed to the accumulation of fats and fibrous materials. However, more and more researchers regarded it as a chronic inflammatory disease nowadays. Infective disease, such as periodontitis, is related to the risk of atherosclerosis. Porphyromonas gingivalis (P. gingivalis), one of the most common bacteria in stomatology, is usually discovered in atherosclerotic plaque in patients. Furthermore, it was reported that P. gingivalis can promote the progression of atherosclerosis. Elucidating the underlying mechanisms of P. gingivalis in atherosclerosis attracted attention, which is thought to be crucial to the therapy of atherosclerosis. Nevertheless, the pathogenesis of atherosclerosis is much complicated, and many kinds of cells participate in it. By summarizing existing studies, we find that P. gingivalis can influence the function of many cells in atherosclerosis. It can induce the dysfunction of endothelium, promote the formation of foam cells as well as the proliferation and calcification of vascular smooth muscle cells, and lead to the imbalance of regulatory T cells (Tregs) and T helper (Th) cells, ultimately promoting the occurrence and development of atherosclerosis. This article summarizes the specific mechanism of atherosclerosis caused by P. gingivalis. It sorts out the interaction between P. gingivalis and AS-related cells, which provides a new perspective for us to prevent or slow down the occurrence and development of AS by inhibiting periodontal pathogens.
... P. gingivalis fimbria and LPS also support monocyte to migrate and infiltrate into endothelial cells, which differentiate monocyte into pro-inflammatory macrophages [16,17]. More recently, P. gingivalis W83 strain was reported to invade into dermal microvascular cells via Intercellular Adhesion Molecule 1 (ICAM-1) and inhibit the formation of vascular networks [18]. Autoantibody against citrullinated proteins is considered an important pathological base of rheumatoid arthritis (RA). ...
Extracellular vesicles (EVs) have been recognized as a universal method of cellular communications and are reportedly produced in bacteria, archaea, and eukaryotes. Bacterial EVs are often called "Outer Membrane Vesicles" (OMVs) as they were the result of a controlled blebbing of the outer membrane of gram-negative bacteria such as Porphyromonas gingivalis (P. gingivalis). Bacterial EVs are natural messengers, implicated in intra- and inter-species cell-to-cell communication among microorganism populations present in microbiota. Bacteria can incorporate their pathogens into OMVs; the content of OMVs differs, depending on the type of bacteria. The production of distinct types of OMVs can be mediated by different factors and routes. A recent study highlighted OMVs ability to carry crucial molecules implicated in immune modulation, and, nowadays, they are considered as a way to communicate and transfer messages from the bacteria to the host and vice versa. This review article focuses on the current understanding of OMVs produced from major oral bacteria, P. gingivalis: generation, characteristics, and contents as well as the involvement in signal transduction of host cells and systemic diseases. Our recent study regarding the action of P. gingivalis OMVs in the living body is also summarized.
... According to several studies, oral bacterial can enter the systemic circulation [12], especially in patients with gingival inflammation and multiple dental interventions [13]. At the same time, the presence of bacteremia has been shown to influence the appearance and progression of atheromatosis in animals [14] and humans [15], with studies showing invasion of the endothelium in vitro [16]. ...
Background
Periodontal disease, a frequent oral health problem, is connected with cardiovascular morbidity and mortality. This study aimed to assess the unstimulated saliva flow rate and saliva pH as markers of the severity of periodontal disease in patients with cardiovascular disease.
Material/Methods
A cohort of 155 patients (78 men and 77 women, aged 30–92 years) was included, and a structured questionnaire obtained information about their health status, oral healthcare behaviors, and eating habits. An oral examination was performed to assess periodontal status and presence of dental calculus. The unstimulated whole salivary flow rate and salivary pH were measured. An oral hygienization was performed, and 3 months later, salivary flow rate and pH were reevaluated.
Results
A severe form of periodontal disease was found in 22.4% of patients. Disease severity was strongly correlated with low pH values (6.25 in stage IV periodontal disease), lower salivary flow rate (0.28 mL/min), smoking, poor oral hygiene habits and obesity, with no significant differences by sex. We observed a significant increase of pH (up to 6.30±0.17) in patients with severe periodontal disease (P=0.001) and salivary flow rate values (0.29±0.07 mL/min; P=0.014) 3 months after oral hygienization. There was a strong association between the severity of periodontal disease and presence of cardiovascular disease (P=0.001).
Conclusions
Our study suggests that the decrease of salivary flow rate and pH level might be associated with the severity of periodontal disease.
