Oral nitric oxide during plaque deposition

Carossa, Stefano; Pera, Paolo; Doglio, P.; Lombardo, Simone; Colagrande, Paola; Brussino, Luisa; Rolla, Giovanni; Bucca, Caterina

doi:10.1046/j.1365-2362.2001.00902.x

Cited by 58 publications

(61 citation statements)

References 28 publications

(32 reference statements)

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“…In contrast, one report has described a reduction of salivary NO levels in individuals with adult periodontitis and with aggressive periodontitis (29). This report is in disagreement with the vast majority of the literature that describes increased levels of NO in periodontal disease (5,(30)(31)(32).…”

Section: Discussionmentioning

confidence: 74%

Nitric oxide levels in saliva increase with severity of chronic periodontitis

et al. 2007

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The aims of this study were to compare nitric oxide (NO) levels in stimulated whole saliva from individuals with and without generalized chronic periodontitis (GCP), and to evaluate correlations between these levels with a clinical diagnostic parameter. According to specific criteria, 30 individuals were divided into three groups: one comprising individuals without periodontitis (GC), a second comprising individuals with moderate GCP (GM), and a third comprising individuals with advanced GCP (GA). Samples were collected and NO levels measured. NO in the GCP group (GM: 7.78 µM; GA: 15.79 µM) was higher than in the GC group (5.86 µM). NO levels in the GA group were significantly higher (P < 0.0001) than in the GC group, and could also differentiate (P < 0.0001) the moderate and advanced forms of the disease.

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Section: Discussionmentioning

confidence: 74%

Nitric oxide levels in saliva increase with severity of chronic periodontitis

et al. 2007

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“…They to secrete arginase to inhibit NO production in gastric mucosa [77]. In the oral cavity, NO production normally occurs during plaque deposition but in patients affected by smoking, where NO levels are reduced, higher bacterial counts are observed [78]. …”

mentioning

confidence: 99%

Nitric Oxide: A Key Mediator of Biofilm Dispersal with Applications in Infectious Diseases

Barraud¹,

Kelso²,

Rice

et al. 2014

CPD

215

196

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Studies of the biofilm life cycle can identify novel targets and strategies for improving biofilm control measures. Of particular interest are dispersal events, where a subpopulation of cells is released from the biofilm community to search out and colonize new surfaces. Recently, the simple gas and ubiquitous biological signaling molecule nitric oxide (NO) was identified as a key mediator of biofilm dispersal conserved across microbial species. Here, we review the role and mechanisms of NO mediating dispersal in bacterial biofilms, and its potential for novel therapeutics. In contrast to previous attempts using high dose NO aimed at killing pathogens, the use of low, non-toxic NO signals (picomolar to nanomolar range) to disperse biofilms represents an innovative and highly favourable approach to improve infectious disease treatments. Further, several NO-based technologies have been developed that offer a versatile range of solutions to control biofilms, including: (i) NO-generating compounds with short or long half-lives and safe or inert residues, (ii) novel compounds for the targeted delivery of NO to infectious biofilms during systemic treatments, and (iii) novel NO-releasing materials and surface coatings for the prevention and dispersal of biofilms. Overall the use of low levels of NO exploiting its signaling properties to induce dispersal represents an unprecedented and promising strategy for the control of biofilms in clinical and industrial contexts. AbstractStudies of the biofilm life cycle can identify novel targets and strategies for improving biofilm control measures. Of particular interest are dispersal events, where a subpopulation of cells is released from the biofilm community to search out and colonize new surfaces. Recently, the simple gas and ubiquitous biological signaling molecule nitric oxide (NO) was identified as a key mediator of biofilm dispersal conserved across microbial species. Here, we review the role and mechanisms of NO mediating dispersal in bacterial biofilms, and its potential for novel therapeutics. In contrast to previous attempts using high dose NO aimed at killing pathogens, the use of low, non-toxic NO signals (picomolar to nanomolar range) to disperse biofilms represents an innovative and highly favourable approach to improve infectious disease treatments. Further, several NO-based technologies have been developed that offer a versatile range of solutions to control biofilms, including: (i) NO-generating compounds with short or long half-lives and safe or inert residues, (ii) novel compounds for the targeted delivery of NO to infectious biofilms during systemic treatments, and (iii) novel NO-releasing materials and surface coatings for the prevention and dispersal of biofilms. Overall the use of low levels of NO exploiting its signaling properties to induce dispersal represents an unprecedented and promising strategy for the control of biofilms in clinical and industrial contexts. 3 Increased antimicrobial tolerance in biofilms is the basis for chronic infecti...

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“…This endogen nitrosation is higher significantly in patient with bad oral hygiene [27]. If areca nut is combined with tobacco, then chewed by people with bad oral hygiene, there will be very high accumulation of nitrosamines product [28]. This process usually occurs continuously for long term because the seeds have addictive property.…”

Section: Discussionmentioning

confidence: 99%

Potential Antioxidant and Cytotoxic Activities of Areca Nut (Areca Catechu Linn.) Extract in Human Oral Squamous Cell Carcinoma and Keratinocyte Cells

Sari

Subita

Auerkari

2017

Asian J Pharm Clin Res

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Objectives: Areca (betel, Areca catechu) nuts have been reported to show high contents of phenolic and flavonoid compounds with associated antioxidant activity. This study was undertaken to assess the anticancer potential of areca nut extract on human squamous carcinoma (HSC)-3, HSC-2, and human keratinocyte (HaCat) cancer cell lines, and to elucidate the mechanism of its action. Methods:In this study, the areca nut extract was prepared in 96% ethanol and analyzed for the total phenolic and flavonoid content, 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay, and 5-(3-carboxymethoxyphenyl)-2-(4,5-dimenthylthiazoly)-3-(4-sulfophenyl)tetrazolium inner salt assay. Results:The indicated total phenolic content of the areca nut extract was 80.3 mg tannic acid equivalent/g and total flavonoid content 238.5 mg catechin equivalent/g. The extract showed good scavenging activity against DPPH radical (efficient concentration 15.95±0.84 μg/ml). The extract showed higher toxicity on HSC-3 than HSC-2 cells, IC 50 was 164.06 μg/ml in HSC-3 versus 629.50 μg/ml in HSC-2. The extract had no cytotoxic effect on HaCat cells. Conclusions:The antioxidant activity of the areca nut extract might be associated with the presence of high content of phenolic and flavonoid compounds. The extract showed selective cytotoxicity against HSC-3 and HSC-2 cells but not on HaCat cells. Instead, the extract induced high rate of proliferation in HaCat cells.

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Oral nitric oxide during plaque deposition

Abstract: Oral NO production increases during de novo deposition of dental plaque. NO might be an early host defence mechanism against bacterial proliferation in the plaque. Such a mechanism is inhibited by cigarette smoking.

Cited by 58 publications

References 28 publications

Nitric oxide levels in saliva increase with severity of chronic periodontitis

Nitric oxide levels in saliva increase with severity of chronic periodontitis

Nitric Oxide: A Key Mediator of Biofilm Dispersal with Applications in Infectious Diseases

Potential Antioxidant and Cytotoxic Activities of Areca Nut (Areca Catechu Linn.) Extract in Human Oral Squamous Cell Carcinoma and Keratinocyte Cells

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