Chronic Inflammatory Gingival and Periodontal Disease

Page, Roy C.; Engel, L. David; Narayanan, A. Sampath; Clagett, James

doi:10.1001/jama.1978.03290060047012

Cited by 45 publications

(26 citation statements)

References 4 publications

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“…This subsequently leads to damage to the surrounding gingival tissues and supporting structures of the tooth. It varies in severity from reversible gingivitis to severe irreversible periodontitis, where the periodontal ligaments and alveolar bone are destroyed [28]. Despite our ability to easily prevent this disease with oral hygiene measures, it remains one of the most prevalent diseases in the world, with nearly half of adults in the USA developing periodontitis [29].…”

Section: Periodontal Disease: An Uncontrolled Ganglandmentioning

confidence: 99%

Fungi at the Scene of the Crime: Innocent Bystanders or Accomplices in Oral Infections?

Delaney

Kean

Short

et al. 2018

Curr Clin Micro Rpt

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Purpose of Review Over the last decade, microbiome studies have enhanced our knowledge and understanding of the polymicrobial nature of oral infections. Recently, profiling of the fungal microbiome has expanded our conventional understanding of oral ecology, revealing the critical importance of yeasts within this complex microbiome. This review aims to explore our current appreciation of interkingdom interactions in oral disease. Recent Findings There is a growing evidence base of interactions and pathogenic synergy and antagonism with bacterial species within oral disease. Recent studies have helped to develop our knowledge of how Candida albicans, alongside bacteria such as Porphyromonas gingivalis, Streptococcus mutans, Staphylococcus aureus, Enterococcus faecalis, and Lactobacillus species, influence overall pathogenicity. Summary Clinical and experimental evidence makes a compelling case for a role for C. albicans in a number of oral infections, though whether its role is an active accomplice or passive bystander remains to be determined.

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Section: Periodontal Disease: An Uncontrolled Ganglandmentioning

confidence: 99%

Fungi at the Scene of the Crime: Innocent Bystanders or Accomplices in Oral Infections?

Delaney

Kean

Short

et al. 2018

Curr Clin Micro Rpt

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“…9 Periodontitis is one of the most widespread inflammatory diseases, characterized by gingival bleeding, periodontal pocket formation, destruction of connective tissue attachment, and alveolar bone resorption. 13,14 Many studies have demonstrated that atherosclerosis and periodontitis are associated and possibly causally linked. [15][16][17][18][19] Therefore, it is possible that periodontitis augments the effects of obesity on atherosclerosis.…”

mentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n ¼ 24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factora (TNF-a), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic b-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-a were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

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“…A rapid increase of ATP concentration in the extracellular environment is a danger signal which alerts immune cells of an impending threat, and mobilizes a rapid inflammatory response to clear invading pathogens. Exacerbated host inflammatory response against plaque bacteria lead to hallmark features of periodontal disease including gingival inflammation, pocket formation, tissue damage, and alveolar bone loss (Page et al, 1978). Presence of ATP in the extracellular environment has been shown to exacerbate periodontitis.…”

Section: Introductionmentioning

confidence: 99%

The Danger Signal Extracellular ATP Is an Inducer of Fusobacterium nucleatum Biofilm Dispersal

Ding

Tan

2016

Front. Cell. Infect. Microbiol.

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Plaque biofilm is the primary etiological agent of periodontal disease. Biofilm formation progresses through multiple developmental stages beginning with bacterial attachment to a surface, followed by development of microcolonies and finally detachment and dispersal from a mature biofilm as free planktonic bacteria. Tissue damage arising from inflammatory response to biofilm is one of the hallmark features of periodontal disease. A consequence of tissue damage is the release of ATP from within the cell into the extracellular space. Extracellular ATP (eATP) is an example of a danger associated molecular pattern (DAMP) employed by mammalian cells to elicit inflammatory and damage healing responses. Although, the roles of eATP as a signaling molecule in multi-cellular organisms have been relatively well studied, exogenous ATP also influences bacteria biofilm formation. Since plaque biofilms are continuously exposed to various stresses including exposure to the host damage factors such as eATP, we hypothesized that eATP, in addition to eliciting inflammation could potentially influence the biofilm lifecycle of periodontal associated bacteria. We found that eATP rather than nutritional factors or oxidative stress induced dispersal of Fusobacterium nucleatum, an organism associated with periodontal disease. eATP induced biofilm dispersal through chelating metal ions present in biofilm. Dispersed F. nucleatum biofilm, regardless of natural or induced dispersal by exogenous ATP, were more adhesive and invasive compared to planktonic or biofilm counterparts, and correspondingly activated significantly more pro-inflammatory cytokine production in infected periodontal fibroblasts. Dispersed F. nucleatum also showed higher expression of fadA, a virulence factor implicated in adhesion and invasion, compared to planktonic or biofilm bacteria. This study revealed for the first time that periodontal bacterium is capable of co-opting eATP, a host danger signaling molecule to detach from biofilms. Our results further showed that dispersed F. nucleatum possessed distinct virulence characteristics compared to their biofilm and planktonic counterparts.

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Chronic Inflammatory Gingival and Periodontal Disease

Cited by 45 publications

References 4 publications

Fungi at the Scene of the Crime: Innocent Bystanders or Accomplices in Oral Infections?

Fungi at the Scene of the Crime: Innocent Bystanders or Accomplices in Oral Infections?

Effects of periodontitis on aortic insulin resistance in an obese rat model

The Danger Signal Extracellular ATP Is an Inducer of Fusobacterium nucleatum Biofilm Dispersal

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