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

Journal article
Authors G. E. Holde
Birgitta Jönsson
N. Oscarson
H. P. Muller
Published in Journal of Periodontal Research
Volume 55
Issue 2
Pages 277-286
ISSN 0022-3484
Publication year 2020
Published at Institute of Odontology, Section 2
Pages 277-286
Language en
Keywords dental plaque, gingival bleeding on probing, multilevel analysis, smoking, cigarette-smoking, blood-flow, clinical expression, heavy smokers, risk, inflammation, association, prevalence, modulation, severity, Dentistry, Oral Surgery & Medicine
Subject categories Periodontology


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 (chi(4)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.

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