Impact of supragingival therapy on subgingival microbial profile in smokers versus non-smokers with severe chronic periodontitis

Abstract

BackgroundThe aim of this study was to assess subgingival microbiological changes in smokers versus non-smokers presenting severe chronic periodontitis after supragingival periodontal therapy (ST).MethodsNon-smokers (n=10) and smokers (n=10) presenting at least nine teeth with probing pocket depth (PPD) (≥5 mm), bleeding on probing (BoP), and no history of periodontal treatment in the last 6 months were selected. Clinical parameters assessed were plaque index (PI), BoP, PPD, relative gingival margin position (rGMP) and relative clinical attachment level (rCAL). Subgingival biofilm was collected before and 21 days after ST. DNA was extracted and the 16S rRNA gene was amplified with the universal primer pair, 27F and 1492R. Amplified genes were cloned, sequenced, and identified by comparison with known 16S rRNA sequences. Statistical analysis was performed by Student's t and Chi-Square tests (α=5%).ResultsClinically, ST promoted a significant reduction in PI and PPD, and gain of rCAL for both groups, with no significant intergroup difference. Microbiologically, at baseline, data analysis demonstrated that smokers harbored a higher proportion of Porphyromonas endodontalis, Bacteroidetes sp., Fusobacterium sp. and Tannerella forsythia and a lower number of cultivated phylotypes (p<0.05). Furthermore, non-smokers featured significant reductions in key phylotypes associated with periodontitis, whereas smokers presented more modest changes.ConclusionWithin the limits of the present study, ST promoted comparable clinical improvements in smokers and non-smokers with severe chronic periodontitis. However, in smokers, ST only slightly affected the subgingival biofilm biodiversity, as compared with non-smokers.

Smoking decreases structural and functional resilience in the subgingival ecosystem

“…In addition, the lowest correlations were observed between the marginal and subgingival OTUs during Resolution 2. It has previously been demonstrated that subgingival colonization is significantly affected by the composition of marginal plaque (Gomes et al 2008, Meulman et al 2012. Thus, the present investigation indicates that with each episode of disease, the interactions between these two geographically connected habitats decreases.…”

“…, Meulman et al. ). Thus, the present investigation indicates that with each episode of disease, the interactions between these two geographically connected habitats decreases.…”

Tobacco‐induced suppression of the vascular response to dental plaque

“…It has now been firmly established that smoking profoundly influences the composition of the subgingival biofilm; that the microbiome of smokers is more diverse, pathogen rich and commensal poor; that it is more difficult to eradicate key pathogens from smokers, compared with nonsmokers; and that smokers are more susceptible to the re‐establishment of a pathogenic subgingival biofilm than are nonsmokers . The elegant study by Joshi et al.…”

“…It has now been firmly established that smoking profoundly influences the composition of the subgingival biofilm; 93-102 that the microbiome of smokers is more diverse, pathogen rich and commensal poor; 94,95,[97][98][99][100] that it is more difficult to eradicate key pathogens from smokers, compared with nonsmokers; 93,103 and that smokers are more susceptible to the re-establishment of a pathogenic subgingival biofilm than are nonsmokers. 93 The elegant study by Joshi et al showed that smokers exhibit early colonization by, and more abundant infection with, pathogens relative to nonsmokers, as established in an experimental gingivitis setting.…”

Systemic antibiotics in the treatment of periodontitis

“…Smokers are a group of individuals who might particularly benefit from systemic antibiotics because they respond less favorably to mechanical periodontal treatment (69,81,94,104,140). Apparently, it is more difficult to reduce periodontal pathogens and to foster the growth of host-compatible species in smokers than in nonsmokers (28,57,129,130), most probably because of their impaired immune system and inflammatory response (98,148,156,173).…”