Outcomes of Periodontal Therapy in Smokers and Non-smokers with Chronic Periodontitis
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Chronic periodontitis is a prevalent inflammatory disorder initiated by dental microbial plaque. Smoking is considered a major risk factor for chronic periodontitis and smokers are known to exhibit impaired treatment outcomes.
The overall aim of this work was to study clinical outcomes of active and supportive periodontal therapy in smokers and non-smokers with chronic periodontitis at patient, tooth, and site level. Moreover, to compare the periopathogenic microflora and inflammatory and bone remodeling markers in gingival crevicular fluid in smokers and non-smokers following therapy.
Eighty patients, 40 smokers and 40 non-smokers, with moderate to severe chronic periodontitis were included in this prospective cohort study and treated nonsurgically and surgically, and then followed-up in a supportive periodontal therapy program for 12 months. Smoking status was validated measuring serum cotinine levels at pre-treatment and 12 months following supportive periodontal therapy. Clinical measurements included full mouth recordings of clinical attachment level, probing depth, bleeding on probing, and plaque index at pre-treatment and following active and supportive periodontal therapy. At the same timepoints, subgingival plaque samples of 20 subgingival periopathogenic bacterial species were analysed using checkerboard DNA–DNA hybridization. From a subsample including 25 smokers and 25 nonsmokers, 27 inflammatory and two bone gingival crevicular fluid markers were analysed using bead-based multiplex assays. In all multilevel analyses probing depth ≥5 mm with bleeding on probing was used as the primary outcome variable.
In smokers and non-smokers all patient level clinical parameters improved following non-surgical and surgical periodontal therapy. Only non-smokers showed a significant reduction in red complex species. At site-level, impaired outcome was observed in smokers and particularly at dental plaque positive sites (Study I).
Following 12 months of supportive therapy bleeding on probing, dental plaque positive sites, and probing depths increased slightly for both groups. Nevertheless, a negative effect of smoking was observed, in particular at maxillary single-rooted teeth. At patient level, the multilevel analysis showed a suppressed variation in treatment outcome following supportive periodontal therapy in smokers (Study II).
Smokers demonstrated suppressed gingival crevicular fluid levels of several inflammatory markers and only non-smokers responded to periodontal therapy by altered marker profiles. An overall negative association was revealed between smoking and subgroups of markers at sites presenting ≥105 red complex periodontal microbial species (Study III).
In summary, smokers demonstrated unfavourable site-specific treatment outcomes compared with non-smokers, especially at plaque positive sites and at maxillary single-rooted teeth. Further, there seemed to be an immunosuppressive effect of smoking regulating the local inflammatory and bone remodeling response following periodontal therapy. Collectively, the results indicate a site-specific tissue response in smokers superimposed on the patient-specific systemic effect of smoking.