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Where Cancer and Bacteria Meet
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Alexandra Merlos, Ricardo Perez-Tomás, José López-López, Miguel Viñas
In this context, infectious agents, mostly bacteria, influence cancer emergence and progression [34] but do not induce cancer directly. For example, long-term infection of oral cancer cells by P. gingivalis leads to the increased expression of the malignant stem cell markers CD44 and CD133 and exacerbates the tumorigenic properties of infected versus noninfected cancer cells [35]. Moreover, P. gingivalis is a noncanonical activator of β-catenin, inducing the disassociation of the β-catenin destruction complex by gingipain-dependent proteolytic processing. β-Catenin activation in epithelial cells by P. gingivalis may thus contribute to a proliferative phenotype [36]. A relationship between other oral bacteria, such as the above-mentioned F. nucleatum, and cancer has also been proposed on the basis of the observed stimulation of human OSCC proliferation and the expression of key molecules involved in tumorigenesis [37].
Bacterial Infections of the Oral Cavity
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
P. S. Manoharan, Praveen Rajesh
P. gingivalis are observed as black colonies in culture on blood agar plates. Burdon in 1928 has grouped such black/brown colony-forming organisms as Bacteroides melanogenicum. Deeper pockets have shown presence of serotype I, whereas II and III are isolated commonly from shallow pockets and gingivitis (Dahlen, 1993) In the Bacteroides group, the P. gingivalis group are saccharolytic (i.e., breaking down sugar products to produce energy), whereas P. intermedia and P. melanogenica are sacharolytic. P. gingivalis group of microorganisms are found to produce collagenase, hydrogen sulfide, indole, proteases (including those which breakdown immunoglobulins), gingipain, hemolysins, endotoxin, ammonia, and fatty acids. P. gingivalis inhibits polymorphonuclear leucocytes to diapedise through epithelium, and it has been demonstrated to influence production and destruction of cytokines by mammalian cells. Its absence in healthy gum or gingivitis and its presence in an advanced and destructive form of periodontal disease where there is increased pocket depth indicate its aggressiveness, behavior, and nutritional source. Immunization using hemagglutinin B, capsular polysaccharide, heat shock protein, gingipain R, and the active sites of RgpA and Kgp proteinases have found to reduce alveolar bone loss in mouse models. And their action was found to raise the level of specific antibodies to P. gingivalis antigens.
Subgingival microbiome at different levels of cognition
Published in Journal of Oral Microbiology, 2023
Nele Fogelholm, Jaakko Leskelä, Muhammed Manzoor, Jacob Holmer, Susanna Paju, Kaija Hiltunen, Hanna-Maria Roitto, Riitta Kt Saarela, Kaisu Pitkälä, Maria Eriksdotter, Kåre Buhlin, Pirkko J Pussinen, Päivi Mäntylä
Although experimental and clinical studies suggest an interconnection between oral dysbiotic microbiota related to common oral diseases, such as caries and periodontal diseases, and brain health/cognitive function, robust evidence is still lacking [10,11]. The oral microbiome comprises many organisms, which can induce inflammatory conditions in vulnerable individuals, such as older adults and immunocompromised people. Those inflammatory conditions can develop in several extra-oral tissues, including the brain, causing infection-induced neuroinflammation and gradual cognitive decline. In an animal study, neurodegenerative features in brain tissue, including fewer number of intact neuronal cells, were evident after repeated oral application of Porphyromonas gingivalis/gingipain, which suggests a role of oral pathogen in the development of neuropathology [12]. P. gingivalis and/or its bacterial components have been identified in post-mortem brain specimens from Alzheimer disease (AD) patients suggesting the evasion of oral pathogens to the brain [13,14]. Also, Treponema denticola has been identified from brain samples by molecular and immunological techniques [15], and serum antibody IgG levels to Fusobacterium nucleatum, Prevotella intermedia [16] and Actinomyces naeslundii [17] have been associated with declining cognition. Another proposed mechanism of oral-brain connection is via the communication of systemic inflammation to the brain induced by bacteraemia [18].
Possible effects of Porphyromonas gingivalis on the blood–brain barrier in Alzheimer’s disease
Published in Expert Review of Anti-infective Therapy, 2021
Periodontitis is mainly regarded as an infection. Although a number of bacteria can be recovered from this disease, the keystone pathogen is believed to be P. gingivalis [6–8]. The ulcerated epithelium in periodontal pockets, typical of periodontitis, enables easy access for this bacterium and its lipopolysaccharide (LPS), proteases (gingipains) and other virulence factors [9], as well as inflammatory products to the blood circulation. In periodontitis, bacteriemias can occur repeatedly during the day [10]. Interestingly, positive blood cultures were significantly higher (p = 0.05) for tooth extraction cases with periodontitis (79.40%) than for tooth extraction cases without periodontitis (56.50%) [11]. The periodontal microbiota may also reach the brain through the trigeminal nerve, circumventricular organs, perivascular spaces and olfactory unsheathing cells acting as Trojan horses [12]. Although combined antibiotic therapy has been found effective in animal models of AD, antibacterial drugs are not being widely investigated in AD patients [13]. However, inhibition of gingipain reduced established P. gingivalis brain infection, blocked Aβ1-42 production, diminished neuroinflammation, and rescued hippocampal neurons [14]. Therefore, gingipain inhibitors may be valuable for treating P. gingivalis brain colonization and neurodegeneration in AD.
Synergistic effects of D-arginine, D-methionine and D-histidine against Porphyromonas gingivalis biofilms
Published in Biofouling, 2021
Zhenyang Zhang, Baosheng Li, Qing Cai, Shuwei Qiao, Dan Wang, Heling Wang, Huiyan Zhang, Yalan Yang, Weiyan Meng
The red complex is a group of bacteria that are categorized together based on their association with severe forms of periodontal disease (Holt and Ebersole 2005). P. gingivalis is a Gram-negative, black-pigmented anaerobic bacterium, which is one of the three members of the red complex. Once incorporated into biofilms, P. gingivalis can colonize subgingivally and contact surrounding tissues directly. Then, it secretes lipopolysaccharides, peptidoglycans, gingipains and other virulence factors, thereby stimulating the host’s innate immune response, producing inflammatory factors such as IL-6, IL-8, INF-γ, and TNF-α, and resulting in tissue necrosis (Giacaman et al. 2009; Benedyk et al. 2016). Furthermore, gingipain could enable P. gingivalis to escape the host defense system by degrading antimicrobial peptides (Palm et al. 2015). In general, P. gingivalis has been proven to be an important pathogen causing peri-implantitis or periodontitis, thus eradicating its biofilm phenotype is crucial for the elimination of its toxicological effects.