Effect of <i>Porphyromonas gingivalis</i> lipopolysaccharide on calcification of human umbilical artery smooth muscle cells co-cultured with human periodontal ligament cells

Li, Jing; Deng, Jing; Shang, Shuxian; Liu, Guirong; Song, Wan; Sun, Peng; Jiang, Wenjing; Pan, Keqing

doi:10.3892/etm.2021.10087

Cited by 5 publications

(6 citation statements)

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“…P. gingivalis LPS promoted calcification in VSMCs co-cultured with human periodontal ligament cells. This study indicates that the calcification effect is not only derived from the stimulation of P. gingivalis LPS, but also the secretion of various pro-inflammatory factors by P. gingivalis LPS-stimulated human periodontal ligament cells ( 252 ). This study somewhat mimics the in vivo environment in which periodontitis and cardiovascular disease coexist.…”

Section: Immune Mechanism Of P Gingivalis To Promo...mentioning

confidence: 81%

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Ruan

Guan²,

Qi³

et al. 2023

Front. Immunol.

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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.

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Section: Immune Mechanism Of P Gingivalis To Promo...mentioning

confidence: 81%

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Ruan

Guan²,

Qi³

et al. 2023

Front. Immunol.

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“… 43 Evidence from in vitro cell culture studies suggests that P. gingivalis infection accelerates phosphate-induced calcification of vascular smooth muscle cells 22 and that P. gingivalis lipopolysaccharide increases alkaline phosphatase activity and upregulates the expression of genes involved in calcification to stimulate calcification. 44 In addition, it has been shown that P. gingivalis invasiveness is enhanced after high-glucose treatment, and vascular calcification can be initiated by stimulating autocrine regulation of bone morphogenetic protein 4 in aortic smooth muscle cells. 21 P. gingivalis infection elicits an inflammatory response in the host, which is in line with the definition of periodontitis as a chronic inflammatory disease.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that periodontal pathogens can be detected in the blood of patients with coronary heart disease, and it is hypothesised that periodontal pathogens can spread through the blood to other parts of the body, where they may enhance inflammatory processes, leading to the development or aggravation of atherosclerosis 43. Evidence from in vitro cell culture studies suggests that P. gingivalis infection accelerates phosphate-induced calcification of vascular smooth muscle cells22 and that P. gingivalis lipopolysaccharide increases alkaline phosphatase activity and upregulates the expression of genes involved in calcification to stimulate calcification 44. In addition, it has been shown that P. gingivalis invasiveness is enhanced after high-glucose treatment, and vascular calcification can be initiated by stimulating autocrine regulation of bone morphogenetic protein 4 in aortic smooth muscle cells 21 .…”

Section: Discussionmentioning

confidence: 99%

Unravelling the link between periodontitis and abdominal aortic calcification in the US adult population: a cross-sectional study based on the NHANES 2013–2014

et al. 2023

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ObjectiveWe aimed to explore the association between periodontitis and abdominal aortic calcification (AAC) among a nationally representative sample of US adults.DesignCross- sectional study.SettingThe National Health and Nutrition Examination Survey (2013–2014).ParticipantsA total of 2149 participants aged 40 years or older who have complete information for periodontitis and AAC assessment test were included in this study.Primary and secondary outcome measuresAAC scores can be accurately identified on lateral spine images obtained by dual-energy X-ray absorptiometry, and both the AAC-24 and AAC-8 semiquantitative scoring tools were used for AAC evaluation. Linear regression analysis was used to investigate the relationship between periodontitis and the AAC-8 and AAC-24 scores. Multivariate logistic regression models and reported ORs were used to examine the relationship between periodontitis and AAC.ResultsThe prevalence of severe periodontitis combined with severe AAC was 8.49%–8.54%. According to the AAC-8 and AAC-24 score classifications, patients with severe periodontitis had higher odds of severe AAC (AAC-8 score ≥3: (OR: 2.53; 95% CI 1.04 to 6.17) and AAC-24 score >6: (OR: 3.60; 95% CI 1.48 to 8.78)). A positive association between mild–moderate periodontitis and severe AAC was found only when the AAC-24 score was applied (OR: 2.25; 95% CI 1.24 to 4.06). In the subgroup analyses, the likelihood ratio test showed no multiplicative interaction (all p value for interaction >0.05).ConclusionsThe findings showed that periodontitis is associated with an increased risk of severe AAC in the US population aged 40 years and older; this requires further large-scale prospective studies for confirmation.

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“…Furthermore, studies in mice have shown that P. gingivalis infection adversely affects the myocardium and promotes cardiomyocyte apoptosis [ 160 , 161 ]. Moreover, in vitro studies have shown that P. gingivalis LPS stimulates vascular calcification by affecting the expression of the osteogenic gene [ 162 ]. In another in vitro study, it was suggested that infecting primary human aortic endothelial cells with P.gingivalis can cause significant changes in the endothelial glycogen synthase kinase-3 beta, endothelial nitric oxide synthase, tetrahydrobiopterin, and nuclear factor erythroid 2–related factor pathways, which may lead to impaired vascular relaxation [ 163 ].…”

Section: Clinical Implication Of Periodontal Infections Caused By ...mentioning

confidence: 99%

Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery Diseases

Aleksijević

Škrlec

et al. 2022

Pathogens

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Porphyromonas gingivalis is a gram-negative, anaerobic bacterium that lives in the oral cavity. It is an integral part of the oral microbiome, which includes more than 500 types of bacteria. Under certain circumstances, as a consequence of virulence factors, it can become very destructive and proliferate to many cells in periodontal lesions. It is one of the causative agents present extremely often in dental plaque and is the main etiological factor in the development of periodontal disease. During various therapeutic procedures, P. gingivalis can enter the blood and disseminate through it to distant organs. This primarily refers to the influence of periodontal agents on the development of subacute endocarditis and can facilitate the development of coronary heart disease, atherosclerosis, and ischemic infarction. The action of P. gingivalis is facilitated by numerous factors of virulence and pathogenicity such as fimbriae, hemolysin, hemagglutinin, capsules, outer membrane vesicles, lipopolysaccharides, and gingipains. A special problem is the possibility of biofilm formation. P. gingivalis in a biofilm is 500 to 1000 times less sensitive to antimicrobial drugs than planktonic cells, which represents a significant problem in the treatment of infections caused by this pathogen.

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Effect of Porphyromonas gingivalis lipopolysaccharide on calcification of human umbilical artery smooth muscle cells co-cultured with human periodontal ligament cells

Cited by 5 publications

References 37 publications

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Porphyromonas gingivalis regulates atherosclerosis through an immune pathway

Unravelling the link between periodontitis and abdominal aortic calcification in the US adult population: a cross-sectional study based on the NHANES 2013–2014

Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery Diseases

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