Effect of cigarette smoking on subgingival bacteria in healthy subjects and patients with chronic periodontitis

Abstract

BackgroundCigarette smoking is known to increase the risk of periodontal destruction and developing chronic periodontitis (CP). It is also reported to affect the subgingival bacterial profile among CP patients. However, studies on the effect of smoking on the bacterial profile among healthy subjects are still limited. Therefore, the aim of this study was to investigate the impact of smoking on the subgingival bacterial profile in both healthy adults and CP patients.MethodsSubgingival plaque samples were collected from CP patients (30 nonsmokers and 9 smokers) and healthy subjects (37 non-smokers and 18 smokers). Genomic DNA was extracted and 25 bacterial species were detected using PCR of 16S rRNA. Comparing smokers to non-smokers from each group was conducted using chi2 and binary logistic regression analysis.ResultsAfter correcting for confounding factors, the odds of having Slackia exigua, Selenomonas sputigena and Campylobacter rectus was higher among healthy smokers (ORadj = 10.1, 6.62 and 5.62 respectively). While for CP group, the highest odds were observed for Treponema amylovorum, Treponema medium, Slackia exigua and Treponema vincentii (ORadj = 20.7, 7.97, 6.37 and 5.37 respectively) and the increase in Treponema amylovorum was statistically significant (p = 0.05).ConclusionSmoking affects the subgingival bacterial profile in healthy individuals and is responsible for the depletion of beneficial bacteria and the increase in periodontopathogenic bacteria. In the CP patient group, our study suggests that subgingival bacteria (particularly Treponema species) make a more substantial contribution in the etiology of CP among non-smokers. Further studies using a larger sample set and more sensitive and quantitative techniques (such as real -time PCR) are needed to enhance our understanding of the exact effect of smoking on subgingival biofilm.Electronic supplementary materialThe online version of this article (doi:10.1186/s12903-017-0359-4) contains supplementary material, which is available to authorized users.

Soft tissue status and crestal bone loss around conventionally‐loaded dental implants placed in cigarette‐ and waterpipe (narghile) smokers: 8‐years' follow‐up results

“…Studies [1][2][3][4] have shown that tobacco-smoking is a prospect of periodontal and peri-implant diseases, such as periodontitis and periimplantitis, respectively. Furthermore, outcomes of oral surgical interventions are undermined in tobacco smoking users compared to nonsmokers.…”

Effect of smoking on the DNA methylation pattern of the SOCS1 promoter in epithelial cells from the saliva of patients with chronic periodontitis

“…Among the environmental factors involved in periodontitis, oral epithelial injury caused by the overgrowth of commensal microorganisms (dysbiosis) is considered the initiator of periodontal destruction, while smoking modulates disease progression . Indeed, smoking is a major risk factor and has been shown to stimulate periodontal destruction and increase the risk of periodontitis in young adults . Based on epidemiological studies, smokers have more severe chronic periodontitis (CP) than non‐smokers and the relationship is dose‐dependent, both in terms of the number of cigarettes smoked per day and the number of years of smoking .…”

“…Indeed, smoking is a major risk factor and has been shown to stimulate periodontal destruction and increase the risk of periodontitis in young adults . Based on epidemiological studies, smokers have more severe chronic periodontitis (CP) than non‐smokers and the relationship is dose‐dependent, both in terms of the number of cigarettes smoked per day and the number of years of smoking . ‒ …”

“…3,4 Indeed, smoking is a major risk factor and has been shown to stimulate periodontal destruction and increase the risk of periodontitis in young adults. 5 Based on epidemiological studies, smokers have more severe chronic periodontitis (CP) than non-smokers and the relationship is dose-dependent, both in terms of the number of cigarettes smoked per day and the number of years of smoking. [5][6][7] As an inflammatory disease, periodontitis is known to alter the immune response, a complex process involving several factors with roles in the regulating of gene expression, including the cytokine network, gene polymorphisms, and epigenetic modulation.…”

“…5 Based on epidemiological studies, smokers have more severe chronic periodontitis (CP) than non-smokers and the relationship is dose-dependent, both in terms of the number of cigarettes smoked per day and the number of years of smoking. [5][6][7] As an inflammatory disease, periodontitis is known to alter the immune response, a complex process involving several factors with roles in the regulating of gene expression, including the cytokine network, gene polymorphisms, and epigenetic modulation. 8 Epigenetic modulation involves changes in gene expression without changes in the DNA sequence.…”