Subgingival bacterial recolonization after scaling and root planing in smokers with chronic periodontitis M Feres,* MAC Bernal,* F Matarazzo,† M Faveri,* PM Duarte,* LC Figueiredo* *Department of Periodontology, Dental Research Division, Guarulhos University, Guarulhos, S~ ao Paulo, Brazil. †Department of Periodontology, State University of Maring a, Maring a, Paran a, Brazil. ABSTRACT Background: The aim of this study was to compare subgingival bacterial recolonization patterns after scaling and root planing in current smokers and non-smokers. Methods: 15 smokers and 15 non-smokers with chronic periodontitis received scaling and root planing in six visits lasting one hour each, over a period of 21 days. Clinical monitoring was performed at baseline and 180 days, and microbiological monitoring was performed at baseline, immediately after scaling and root planing (Day 0) and at 42, 63 and 180 days post-therapy. Subgingival plaque samples were analysed by checkerboard DNA–DNA hybridiza- tion. Results: An improvement in clinical condition was observed for smokers and non-smokers; however, non-smokers showed a greater reduction in mean clinical attachment level in intermediate sites in comparison with smokers (p < 0.05). At Day 0, there was a significant reduction in the mean counts of the three pathogens from the red complex, Eubacterium nodatum and Parvimonas micra only in non-smokers (p < 0.05). There was a significant increase in the proportion of host-compatible species in non-smokers and smokers from baseline to 180 days post- therapy (p < 0.05). However, a significant decrease in the pathogenic species was observed only in non-smokers. Conclusions: Smokers were more susceptible to the re-establishment of a pathogenic subgingival biofilm than non- smokers. Keywords: Chronic periodontitis, dental scaling, microbiology, smoking. Abbreviations and acronyms: BOP = bleeding on probing; CAL = clinical attachment level; MB = marginal bleeding; PCR = polymerase chain reaction; PD = probing depth; PI = plaque accumulation; SRP = scaling and root planing; SUP = suppuration. (Accepted for publication 20 September 2014.) INTRODUCTION There is a body of evidence suggesting that the onset, progression and severity of periodontal tissue destruc- tion may be modulated by some environmental and systemic factor modifiers, such as diabetes mellitus and smoking. There is consistent agreement about the existence of a strong positive correlation between cig- arette smoking, deeper periodontal pockets and increased alveolar bone loss, clinical attachment and teeth. 1 In contrast, conflicting results have been pub- lished about the influence of smoking on subgingival biofilm and periodontal tissue breakdown. While some investigations 2–8 have found little or no differ- ence in the composition of the subgingival biofilm between smokers and non-smokers, others have found that cigarette smoking is associated with a higher prevalence and/or levels of pathogenic species. 9–12 Several studies have shown that smoking is related to an unfavourable clinical response to both non- surgical and surgical periodontal therapy. 13,14 In regards to the microbiological data, some investiga- tions have suggested that smokers harbour higher lev- els of periodontal pathogens than non-smokers after scaling and root planing (SRP), 4,7,15,16 whereas others have demonstrated no influence of smoking on the microbiological outcomes of treatment. 8,17 The hypothesis that smoking could contribute to a lower reduction and faster re-establishment of subgingival pathogenic biofilm after periodontal therapy may explain the frequently observed negative clinical response of smokers. 17 Therefore, the aim of the pres- ent study was to compare the patterns of subgingival bacterial recolonization in moderate to deep sites right after, and up to 6 months post-SRP in current smok- ers and non-smokers with chronic periodontitis. © 2015 Australian Dental Association 1 Australian Dental Journal 2015; 60: 1–8 doi: 10.1111/adj.12225 Australian Dental Journal The official journal of the Australian Dental Association