Expression of ICAM‐1 and E‐selectin in gingival tissues of smokers and non‐smokers with periodontitis

Rezavandi, Kia; Palmer, Richard; Odell, Edward; Scott, Darren M.; Wilson, Ron

doi:10.1046/j.0904-2512.2001.joptest.doc.x

Cited by 80 publications

(84 citation statements)

References 47 publications

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“…In addition, all plaque samples from diseased sites also induced increased the TLR4-dependent expression of E-selectin in endothelial cells. This strong activation of E-selectin in disease is corroborated by a body of work demonstrating increase detection of this leukocyte extravasation molecule in inflamed tissues of chronic periodontitis patients (26). The clinical associations with clinical measurements described here agree with a previous study investigating supragingival plaque stimulation of TLR4 and TLR2 (27).…”

Section: Discussionsupporting

confidence: 80%

Subgingival Plaque in Periodontal Health Antagonizes at Toll-Like Receptor 4 and Inhibits E-Selectin Expression on Endothelial Cells

Gümüş

Nizam

et al. 2016

Infect Immun

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The ability of the subgingival microbial community to induce an inappropriate inflammatory response ultimately results in the destruction of bone and gingival tissue. In this study, subgingival plaque samples from both healthy and diseased sites in the same individual were obtained from adults with chronic periodontitis and screened for their ability to either activate Toll-like receptor 2 (TLR2) or TLR4 and to antagonize TLR4-specific activation by agonist, Fusobacterium nucleatum LPS. Subgingival plaque from diseased sites strongly activated TLR4, whereas matched plaque samples obtained from healthy sites were significantly more variable, with some samples displaying strong TLR4 antagonism, while others were strong TLR4 agonists when combined with F. nucleatum LPS. Similar results were observed when TLR4 dependent E-selectin expression by endothelial cells was determined. These results are the first to demonstrate TLR4 antagonism from human plaque samples and demonstrate that healthy but not diseased sites display a wide variation in TLR4 agonist and antagonist behavior. The results have identified a novel characteristic of clinically healthy sites and warrant further study on the contribution of TLR4 antagonism in the progression of a healthy periodontal site to a diseased one.

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Section: Discussionsupporting

confidence: 80%

Subgingival Plaque in Periodontal Health Antagonizes at Toll-Like Receptor 4 and Inhibits E-Selectin Expression on Endothelial Cells

Gümüş

Nizam

et al. 2016

Infect Immun

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“…37 As an attempt to determine the mechanisms involved in smoking modulation of the periodontal tissues, in vitro and in vivo studies have investigated the impact of cigarette compounds, including nicotine and cotinine, on the periodontal tissues. In general, nicotine has been reported to adversely affect proliferation, attachment and chemotaxis of periodontal ligament cells, and induce pro-inflammatory cytokine production by human gingival fibroblasts synergistically with lipopolysaccharide from Escherichia coli and P. gingivalis.…”

Section: Biological Effects and Eventsmentioning

confidence: 99%

Smoking and periodontal tissues: a review

et al. 2012

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The impact of smoking on general health has been widely studied and is directly related to several important medical problems including cancer, low birth weight, and pulmonary and cardiovascular disease. In the past 25 years, there has also been an increasing awareness of the role of cigarette consumption in oral health problems such as periodontal disease. Smoking is considered the major risk factor in the prevalence, extent and severity of periodontal diseases. This article will discuss the available evidence and provide the reader with an overview of the impact of smoking and its cessation on the pathogenesis and treatment of periodontal diseases.

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“…Zoals eerder vermeld kan roken de klinische verschijnselen van ontsteking reduceren. De verminderde bloeding wordt veroorzaakt doordat er minder bloedvaten aanwezig zijn in de ontstoken gebieden (Rezavandi et al, 2002). Dit heeft tevens tot gevolg dat er minder zuurstof naar de weefsels gaat en misschien ook minder makkelijk afvalproducten kunnen worden afgevoerd.…”

Section: Effect Van Roken Op De Afweerunclassified

19 Modificerende factoren: diabetes, roken en stress

Bruyn¹,

Velden²

2009

Parodontologie

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Parodontitis is een multifactoriele aandoening waarvan wordt verondersteld dat deze start als een door plaque veroorzaakte gingivitis. Epidemiologisch gezien is er een duidelijke relatie tussen de mate van mondhygiëne en de ernst van de parodontitis. Er is echter een aanzienlijke variatie in de populatie. Er zijn mensen die vatbaar zijn voor parodontitis en al op jeugdige leeftijd ernstige parodontitis kunnen ontwikkelen. Daar tegen over zijn er mensen die zeer resistent zijn. Deze verschillen zijn gedeeltelijk toe te schrijven aan de hoeveelheid plaque en de aanwezigheid van paropathogene bacteriën daarin, de mate waarin iemand tandsteen vormt en de effectiviteit van de immuunrespons. Daarnaast spelen andere ziekten en levensstijl factoren een belangrijke rol bij het ontstaan en progressie van parodontitis. De belangrijkste zijn: diabetes, roken en stress (zie ook elders in dit boek, onder andere het hoofdstuk Parodontitis in relatie tot algemene gezondheid).

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Expression of ICAM‐1 and E‐selectin in gingival tissues of smokers and non‐smokers with periodontitis

Cited by 80 publications

References 47 publications

Subgingival Plaque in Periodontal Health Antagonizes at Toll-Like Receptor 4 and Inhibits E-Selectin Expression on Endothelial Cells

Subgingival Plaque in Periodontal Health Antagonizes at Toll-Like Receptor 4 and Inhibits E-Selectin Expression on Endothelial Cells

Smoking and periodontal tissues: a review

19 Modificerende factoren: diabetes, roken en stress

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