Tobacco‐induced suppression of the vascular response to dental plaque

Buduneli, Nurcan; Scott, David A.

doi:10.1111/omi.12228

Cited by 28 publications

(33 citation statements)

References 151 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There is some evidence of tobacco‐induced suppressed angiogenesis, where a reduced number of gingival vessels or vessels of smaller caliber have been found in smokers relative to non‐smokers . Thermally induced nerve damage in the oral cavity of smokers could potentially affect the microvascular response of the gingiva . Additionally, tobacco smoking alters the dental plaque composition .…”

Section: Discussionmentioning

confidence: 99%

“…6,[40][41][42] Thermally induced nerve damage in the oral cavity of smokers 43,44 could potentially affect the microvascular response of the gingiva. 2 Additionally, tobacco smoking alters the dental plaque composition. 45 Findings from a large study of the human oral microbiome in US adults indicate that smoking promotes an anaerobic oral environment and a bacterial community with a reduced capability of degrading toxic components of cigarette smoke.…”

Section: F I G U R Ementioning

confidence: 99%

“…Smoking increases susceptibility to periodontitis and is associated with higher levels of periodontal destruction, 1 but also reduces the inflammatory response to dental plaque in the gingiva. 2 Gingival inflammation is considered a key risk factor for the development and progression of periodontitis. 3,4 Therefore, it is important to investigate the extent to which smoking affects the gingival bleeding response to dental plaque.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

Holde

Jönsson

Oscarson

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

Background and objective The aim of this study was to investigate the influence of smoking on the site‐specific association between bleeding on gingival probing and supragingival plaque and to assess whether this differs in different regions of the dentition. Methods Data from a representative sample of 1911 adults (20‐79 years old) in Northern Norway were analyzed. Periodontal examinations consisted of full‐mouth recordings of periodontal probing depth (PD), bleeding on probing (BOP), and presence of supragingival plaque. Smoking status and background characteristics were self‐reported by questionnaire. The association between plaque and BOP was assessed in several three‐level (subject, tooth, and site) random intercept logistic regression models adjusted for PD, smoking status, socioeconomic factors, and body mass index. In a further model, it was assessed whether the association between supragingival plaque and BOP differed in different parts of the dentition. Results For plaque‐free sites, bleeding tendency was lower in smokers, the odds ratio (OR) was 0.773 with a 95% confidence interval of 0.678‐0.881 as compared to non‐smokers (OR: 1; ref., P < .001). The odds of BOP at plaque‐covered sites in non‐smokers were increased twofold (OR: 2.117; 2.059‐2.177). Albeit bleeding tendency was slightly increased in plaque‐covered sites in smokers, it was considerably lower as compared to plaque‐covered sites in non‐smokers (OR: 1.459; 1.282‐1.662, P < .001). Smoking ≥ 20 pack‐years further attenuated the association. In smokers, the odds of BOP were reduced in all parts of the dentition, lower and upper anterior and posterior teeth (χfalse(4false)2= 32.043, P < .001). When restricting the data to younger adults (20‐34 year old), smoking had only a slight effect on the association between plaque and BOP. For plaque‐free and plaque‐covered sites, differences in ORs were not statistically noticeable (P = .221 and P = .235, respectively). Conclusions Smoking considerably attenuates the site‐specific association between plaque and BOP with a dose‐dependent effect. The effect of smoking did not differ across tooth types.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: F I G U R Ementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

Holde

Jönsson

Oscarson

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…Interestingly, gingival bleeding—an important clinical indicator for the presence of periodontal diseases—is suppressed in smokers. As we have recently reviewed, this discrepancy can be attributed to suppressed gingival angiogenesis in response to plaque . In a previous study, we were also able to show that P gingivalis becomes a less potent inducer of pro‐inflammatory responses from mononuclear cells upon exposure to cigarette smoke extract (CSE).…”

Section: Introductionmentioning

confidence: 87%

“…As we have recently reviewed, this discrepancy can be attributed to suppressed gingival angiogenesis in response to plaque. 18 In a previous study, we were also able to show that P gingivalis becomes a less potent inducer of pro-inflammatory responses from mononuclear cells upon exposure to cigarette smoke extract (CSE). This decrease in inflammatory potential could be due to differential regulation of several genes in CSE-treated bacteria; for example, genes involved in the biosynthesis of the inflammatory capsule were downregulated.…”

Section: Introductionmentioning

confidence: 94%

Cigarette smoke reduces short chain fatty acid production by a Porphyromonas gingivalis clinical isolate

Zeller

Malovichko

Hurst

et al. 2019

J of Periodontal Research

Self Cite

View full text Add to dashboard Cite

Objectives We hypothesized that short chain fatty acid (SCFA) production by oral pathogens is suppressed by exposure to cigarette smoke extract (CSE). Background Tobacco smoking is a major risk factor for plaque‐induced periodontal diseases. Despite increased disease susceptibility, overt oral inflammation is suppressed in smokers, presenting a diagnostic conundrum. Bacterial‐derived SCFAs can penetrate into oral tissues where they influence multiple components of immune and healing responses. Indeed, the SCFA burden has been correlated with the inflammatory condition of the gingiva. However, the influence of cigarette consumption on SCFA production is unknown. Methods GC/MS was employed to monitor the production of several SCFAs (propionic acid, isobutyric acid, butyric acid, and isovaleric acid) by representative anaerobic oral pathogens (Filifactor alocis 35896, Fusobacterium nucleatum 25586, Porphyromonas gingivalis 33277) that were exposed, or not, to a physiologically relevant dose of CSE (2000 ng/ml nicotine equivalents) generated from 3R4F reference cigarettes. Results The growth of all three bacterial species was unaffected by CSE. The capacity to produce SCFAs by these bacteria was highly varied. F alocis produced the highest concentration of a specific SCFA (butyrate); P gingivalis provided the most robust overall SCFA signal, while F alocis and F nucleatum did not release detectable levels of isobutyrate or isovalerate. As P gingivalis 33277 was the broadest SCFA producer, three low‐passage clinical isolates (10208C, 5607, and 10512) were also examined. Compared to unconditioned microbes, reduced SCFA release was apparent in CSE‐exposed low‐passage clinical isolates of P gingivalis which reached significance for one of the three isolates (propionic, isobutyric, butyric, and isovaleric acids, all P < 0.05). Conclusions There is high disparity in the SCFA profiles of variant chronic periodontitis‐associated bacteria, while CSE exposure reduces SCFA production by a specific clinical strain of P gingivalis. If the latter phenomenon occurs in vivo, a reduced SCFA burden may help explain the reduced vascular response to dental plaque in tobacco smokers.

show abstract

Whole transcriptome analysis of smoker palatal mucosa identifies multiple downregulated innate immunity genes

Wang

Anderson

Tatakis

2020

Journal of Periodontology

View full text Add to dashboard Cite

BackgroundSmoking has significant negative impact on periodontal health and treatment outcomes. The molecular effects of smoking on oral immune homeostasis have not been fully elucidated. The present study aimed to provide a comprehensive assessment of smoking‐associated gene expression changes in healthy palatal mucosa and to identify potentially implicated immunologic pathways.MethodsPalatal biopsies, in the form of connective tissue grafts, were obtained from periodontally healthy smokers and non‐smokers. Smoking status was biochemically verified (exhaled air CO and serum cotinine). Tissue samples were processed for next generation sequencing, quantitative real‐time polymerase chain reaction (qPCR), and immunohistochemistry. Gene set enrichment/pathway analysis and correlation analysis between gene expression and serum cotinine levels were also performed.ResultsAnalysis of palatal tissues from 12 non‐smokers and 10 smokers identified 830 significantly (P <0.05) differentially expressed genes (DEGs), 249 with fold change (FC) >2. Most increased in expression (≥5‐FC) were CYP1A1, CYP1B1, and USP17L9P; most decreased (≥6‐FC) were IL36A, DEFB4A, DEFB4B, SPRR2F, CCL20, KLK6, and ADH4. 203 DEGs (FC >2) were significantly correlated with serum cotinine levels. Significant enrichment pathways for cotinine‐associated genes include antimicrobial humoral response, regulation of humoral response and various metabolic processes. qPCR and immunohistochemistry confirmed gene and protein expression of selected DEGs.ConclusionsSmoking has a significant effect on the transcriptome of normal human palatal mucosa and seems to target genes important for innate immune defenses, which may prove to be one of the key mechanisms by which tobacco smoking leads to increased periodontitis susceptibility.

show abstract

Tobacco‐induced suppression of the vascular response to dental plaque

Cited by 28 publications

References 151 publications

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

Cigarette smoke reduces short chain fatty acid production by a Porphyromonas gingivalis clinical isolate

Whole transcriptome analysis of smoker palatal mucosa identifies multiple downregulated innate immunity genes

Contact Info

Product

Resources

About