Microbiological and biochemical findings in relation with clinical periodontal status in active smokers, non-smokers and passive smokers

Abstract

INTRODUCTIONCigarette users are more susceptible than non-smokers to periodontitis, a bacterial-induced, inflammation-driven, destructive disease of the supporting tissues of the teeth. We hypothesized that clinical periodontal findings and microbiological and/or inflammatory marker levels would be intermediate in those exposed to environmental tobacco smoke compared to active smokers and non-smokers.METHODSSixty individuals were recruited from a University periodontal clinic and assigned as non-smokers, active smokers or passive-smokers according to their self reports. Clinical periodontal measurements, comprising plaque index, probing depth (PD), clinical attachment level (CAL) and bleeding on probing, were recorded at six sites per tooth. Cotinine levels were determined in whole saliva samples by EIA. Treponema denticola and Porphyromonas gingivalis infection was determined by PCR, while matrix metalloproteinase-8 (MMP-8) and interleukin-8 (IL-8) concentrations were determined by ELISA.RESULTSStudy groups were subsequently reassigned in accordance with the cotinine data. The smoker group exhibited higher mean PD and CAL values compared to the non-smoker group (p<0.05). Passive-smokers exhibited PD and CAL values smaller than those of the active smokers and greater than those of the non-smokers, but the differences were not statistically significant. PD and CAL values correlated with cotinine concentrations (p<0.05). P. gingivalis infection was noted in most subjects, irrespective of smoking status. T. denticola infection was noted in 4/23 (17.4%) smokers, 0/16 (0%) environmentally-exposed recruits and 2/21 (9.5%) non-smokers. Salivary MMP-8 and IL-8 levels were lower in smokers compared to both non-smokers and passive-smokers but the differences were not significant (all p>0.05).CONCLUSIONSThe present clinical periodontal findings provide further support for a negative, dose-related effect of tobacco exposure on periodontal health. The tendency for a more prevalent detection of T. denticola and for a suppressed inflammatory response observed in the smokers may partly explain the increased susceptibility to periodontal tissue destruction, but needs to be verified in larger scale studies.

The impact of smoking different tobacco types on the subgingival microbiome and periodontal health: a pilot study

“…Smoking increases the prevalence and severity of periodontal destruction by altering the host immune response, making the oral cavity more vulnerable to propagation of pathogenic bacterial species 10 . Several studies have linked smoking to dysbiosis of the oral microbiota, increasing the risk of periodontal disease [11][12][13] .…”

Periodontitis combined with smoking increases risk of the ulcerative colitis: A national cohort study

“…Cigarette smoking affects microbial diversity and composition resulting in decreases in Proteobacteria and Bacteroidetes and increases in Firmicutes [ 46 ]. A Treponema denticola infection is frequently detected in current smokers with periodontal disease[ 47 ]. Further research is needed to determine the combined effects of cigarette smoking and periodontitis on the pathogenesis of elderly onset UC, in terms of oral dysbiosis.…”

Environmental factors and periodontal microbiome

“…55 Smoking cessation in patients with periodontitis is beneficial for promoting a health-compatible subgingival microbial community. 58 Together with the clinical outcomes, the beneficial effects of smoking cessation on microbiologic parameters clearly warrant smoking cessation counseling along with periodontal treatment. 59 In a recent study, the influence of cigarette consumption on short chain fatty acid production by anaerobic oral pathogens was investigated.…”