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

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      Pathogens
      MDPI AG

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          Abstract

          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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          Most cited references178

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          Microbial complexes in subgingival plaque

          Journal of Clinical Periodontology, 25(2), 134-144
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            Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulum

            Autophagy is the engulfment of cytosol and organelles by double-membrane vesicles termed autophagosomes. Autophagosome formation is known to require phosphatidylinositol 3-phosphate (PI(3)P) and occurs near the endoplasmic reticulum (ER), but the exact mechanisms are unknown. We show that double FYVE domain–containing protein 1, a PI(3)P-binding protein with unusual localization on ER and Golgi membranes, translocates in response to amino acid starvation to a punctate compartment partially colocalized with autophagosomal proteins. Translocation is dependent on Vps34 and beclin function. Other PI(3)P-binding probes targeted to the ER show the same starvation-induced translocation that is dependent on PI(3)P formation and recognition. Live imaging experiments show that this punctate compartment forms near Vps34-containing vesicles, is in dynamic equilibrium with the ER, and provides a membrane platform for accumulation of autophagosomal proteins, expansion of autophagosomal membranes, and emergence of fully formed autophagosomes. This PI(3)P-enriched compartment may be involved in autophagosome biogenesis. Its dynamic relationship with the ER is consistent with the idea that the ER may provide important components for autophagosome formation.
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              The oral microbiota: dynamic communities and host interactions

              The dynamic and polymicrobial oral microbiome is a direct precursor of diseases such as dental caries and periodontitis, two of the most prevalent microbially induced disorders worldwide. Distinct microenvironments at oral barriers harbour unique microbial communities, which are regulated through sophisticated signalling systems and by host and environmental factors. The collective function of microbial communities is a major driver of homeostasis or dysbiosis and ultimately health or disease. Despite different aetiologies, periodontitis and caries are each driven by a feedforward loop between the microbiota and host factors (inflammation and dietary sugars, respectively) that favours the emergence and persistence of dysbiosis. In this Review, we discuss current knowledge and emerging mechanisms governing oral polymicrobial synergy and dysbiosis that have both enhanced our understanding of pathogenic mechanisms and aided the design of innovative therapeutic approaches for oral diseases.
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                Author and article information

                Contributors
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                Journal
                PATHCD
                Pathogens
                Pathogens
                MDPI AG
                2076-0817
                October 2022
                October 11 2022
                : 11
                : 10
                : 1173
                Article
                10.3390/pathogens11101173
                36297228
                bb6eeb59-c7c3-46df-b1c1-dfcc7847a48c
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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