Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Ji, Sang-Hoon; Choi, Youngok

doi:10.1111/jre.12248

Cited by 114 publications

(107 citation statements)

References 180 publications

(297 reference statements)

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“…Invasion of periodontal pathogens into periodontal tissues is an important step that can initiate periodontal diseases [18]. Gingival epithelium is the first cell layer that bacteria in subgingival biofilms have to pass through in order to invade into the deeper parts of periodontal tissues.…”

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis suppresses invasion of Fusobacterium nucleatum into gingival epithelial cells

Jung

Jun

Choi

2017

Journal of Oral Microbiology

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Invasion of periodontal pathogens into periodontal tissues is an important step that can cause tissue destruction in periodontal diseases. Porphyromonas gingivalis is a keystone pathogen and its gingipains are key virulence factors. Fusobacterium nucleatum is a bridge organism that mediates coadhesion of disease-causing late colonizers such as P. gingivalis and early colonizers during the development of dental biofilms. The aim of this study was to investigate how P. gingivalis, in particular its gingipains, influences the invasion of coinfecting F. nucleatum into gingival epithelial cells. When invasion of F. nucleatum was analyzed after 4 h of infection, invasion of F. nucleatum was suppressed in the presence of P. gingivalis compared with during monoinfection. However, coinfection with a gingipain-null mutant of P. gingivalis did not affect invasion of F. nucleatum. Inhibition of PI3K reduced invasion of F. nucleatum. P. gingivalis inactivated the PI3K/AKT pathway, which was also dependent on gingipains. Survival of intracellular F. nucleatum was promoted by P. gingivalis with Arg gingipain mutation. The results suggest that P. gingivalis, in particular its gingipains, can affect the invasion of coinfecting F. nucleatum through modulating intracellular signaling of the host cells.

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Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis suppresses invasion of Fusobacterium nucleatum into gingival epithelial cells

Jung

Jun

Choi

2017

Journal of Oral Microbiology

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“…Thus, TRPV4‐associated epithelial cell‐cell junctions appear to play an important role in human oral mucosal epithelia. It is well known that bacteria and their components can intrude into the junctional epithelium, which increase neutrophil penetration and enhance periodontal inflammation . Impaired epithelial cell‐cell contact via TRPV4 may lead to more serious vulnerability of periodontal tissues to bacteria or mechanical stresses and aggravate periodontal inflammation.…”

Section: Discussionmentioning

confidence: 99%

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

Kitsuki

Yoshimoto

Aijima

et al. 2019

J of Periodontal Research

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Background and Objective As the interface between the oral cavity and the teeth, the junctional epithelial barrier is critical for gingival defense. The junctional epithelium is subject to mechanical stresses from biting force or external insults such as bacterial attacks, but little is known about the effects of mechanical stimuli on epithelial functions. Transient receptor potential vanilloid 4 (TRPV4) functions as a mechanosensitive nonselective cation channel. In the present study, based on marked expression of TRPV4 in the mouse junctional epithelium, we aimed to clarify the putative links between TRPV4 and junctional complexes in the junctional epithelium. Methods and Results Histological observations revealed that the junctional epithelium in TRPV4‐deficient (TRPV4−/−) mice had wider intercellular spaces than that in wild‐type (TRPV4+/+) mice. Exogenous tracer penetration in the junctional epithelium was greater in TRPV4−/− mice than in TRPV4+/+ mice, and immunoreactivity for adherens junction proteins was suppressed in TRPV4−/− mice compared with TRPV4+/+ mice. Analysis of a mouse periodontitis model showed greater bone volume loss in TRPV4−/− mice compared with TRPV4+/+ mice, indicating that an epithelial barrier deficiency in TRPV4−/− mice may be associated with periodontal complications. Conclusion The present findings identify a crucial role for TRPV4 in the formation of adherens junctions in the junctional epithelium, which could regulate its permeability. TRPV4 may be a candidate pharmacological target to combat periodontal diseases.

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“…The degradation of the soft and hard tissues of the periodontium results from both the colonization of tooth surfaces by certain Gram-negative anaerobic bacteria, such as Aggregatibacter actinomycetemcomitans 2,3) and Porphyromonas gingivalis 4) , and the host response to its accumulation 5) . In dental plaque, lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria induces the production of bone-absorbing cytokines, such as interleukin (IL)-1, IL-6, interferon (IFN)-α, and tumor necrosis factor (TNF)-α [6][7][8] , and of prostaglandin E2 (PGE2) 9) .…”

Section: Introductionmentioning

confidence: 99%

JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

Han

Lee

2017

J Dent Hyg Sci

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Bacterial infection and smoking are an important risk factors involved in the development and progression of periodontitis. However, the signaling mechanism underlying the host immune response is not fully understood in periodontal lesions. In this study, we determined the expression of janus kinase (JAK)/signal transducer and activator of transcription (STAT) on Porphyromonas gingivalis lipopolysaccharide (LPS)-and nicotine-induced cytotoxicity and the production of inflammatory mediators, using osteoblasts. The cells were cultured with 5 mM nicotine in the presence of 1 μg/ml LPS. Cell viability was determined using MTT assay. The role of JAK on inflammatory mediator expression and production, and the regulatory mechanisms involved were assessed via enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot analysis. LPS-and nicotine synergistically induced the production of cyclooxgenase-2 (COX-2) and prostaglandin E2 (PGE2) and increased the protein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and PGE2 as well as the expression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-6 in LPS-and nicotine-stimulated osteoblasts. These results suggest that JAK/STAT is closely related to the LPS-and nicotine-induced inflammatory effects and is likely to regulate the immune response in periodontal disease associated with dental plaque and smoking.

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Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Cited by 114 publications

References 180 publications

Porphyromonas gingivalis suppresses invasion of Fusobacterium nucleatum into gingival epithelial cells

Porphyromonas gingivalis suppresses invasion of Fusobacterium nucleatum into gingival epithelial cells

Enhanced junctional epithelial permeability in TRPV4‐deficient mice

JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

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