Bacterial Infections of the Oral Cavity
K. Balamurugan, U. Prithika in Pocket Guide to Bacterial Infections, 2019
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.
Where Cancer and Bacteria Meet
Ananda M. Chakrabarty, Arsénio M. Fialho in Microbial Infections and Cancer Therapy, 2019
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].
Porphyromonas gingivalis laboratory strains and clinical isolates exhibit different distribution of cell surface and secreted gingipains
Published in Journal of Oral Microbiology, 2021
Christine A. Seers, A. Sayeed M. Mahmud, N. Laila Huq, Keith J. Cross, Eric C. Reynolds
The involvement of gingipains in the pathogenicity of P. gingivalis has made gingipains promising drug targets for the treatment of P. gingivalis-associated diseases including destructive periodontal disease [30–32]. However, the characteristics of gingipain activities and cell distribution (that is whether the proteinases remain membrane associated or are released into the environment) has not been studied for a range of clinical isolates. Here we have determined the cell-associated and soluble (vesicle-free) gingipain proteinase activities of a panel of global P. gingivalis clinical isolates. We demonstrate widely varied relative proteinase activities between the isolates, particularly in the distribution between cell-associated and soluble forms released into the environment.
A Dual Zinc plus Arginine formulation attenuates the pathogenic properties of Porphyromonas gingivalis and protects gingival keratinocyte barrier function in an in vitro model
Published in Journal of Oral Microbiology, 2020
Amel Ben Lagha, Ying Yang, Harsh M. Trivedi, James G. Masters, Daniel Grenier
The oral epithelium creates a physical protective barrier between the underlying connective tissue and invasive periodontal pathogens and their toxic products in the oral environment, and thus plays an active role in the maintenance of periodontal health [8,9]. The intercellular tight junctions, which are composed of specialized transmembrane proteins that regulate transepithelial permeability, are the primary cellular determinant of epithelial barrier integrity and function [10]. P. gingivalis has developed different strategies to compromise the structural and functional integrity of the oral epithelium. Using specific gingipain inhibitors and gingipain-deficient mutants of P. gingivalis, Groeger et al. [11] provided evidence that these proteolytic enzymes are involved in the degradation of cell-to-cell junctions and the disruption of the epithelial barrier. Once the integrity of the oral epithelium is disrupted, P. gingivalis, along with other periodontal pathogens, can reach deeper connective tissues and trigger a marked pro-inflammatory response that modulates tissue destruction. Bacteria and their toxins can also enter the bloodstream, migrate to extra-oral sites, and cause systemic complications [12,13]. Taken the above into consideration, conditions or substances with the ability to attenuate the P. gingivalis-mediated destructive process or to promote the oral epithelial barrier integrity may be of high interest for maintaining or recovering oral health.
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.
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