The Impact of Cigarette Smoking on Periodontal Therapy

Periodontitis patients, 40 cigarette smokers and 40 non-smokers (defined by cotinine measures in serum), were recruited to this double arm prospective cohort study. Data were collected 3 months following non-surgical and surgical periodontal treatment, and following 12 months with supportive periodontal therapy. Data collected were clinical attachment level, probing depth, bleeding on probing,oral bacteria, serum, blood (PAXgeneBlood), and gingival crevicular fluid.

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 markers in gingival crevicular fluid and in blood 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 non-surgically 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. Blood samples (PAXgeneBlood), serum, gingval crevicular fluid were also collected at the three timepoints.

Non-surgical periodontal therapy: motivation and instruction in oral hygiene, debridement using handinstrumentation (Hu-Firedy,Chicago, IL, USA;and American Eagle Instruments,Missoula, MT,USA).

Periodontal surgery: periodontal flap and gingivectomy with postoperative rinse with 0.2% chlorhexidine gluconate (Corsodyl, GlaxoSmithKline, London, UK).

Corrected for clustering within patients, teeth, and sites over time, was the unit of the analysis and PD ≥5 mm with BoP was the outcome (dependent variable) dichotomized as present (1) or absent (0).

Subgingival plaque samples of 20 subgingival periopathogenic bacterial species were analysed using checkerboard DNA-DNA hybridization.

Concentrations of gingival crevicular fluid biomarkers measured in pg/mLwere analysed using multiplex and singleplex micro-bed immunoassays.

Concentration of inflammatory serum markers measured in pg/ɥL determined using multiplex kit Bio-Plex Human ProTM Assay.

Inflammatory gene (RNA) expression levels is estimated by counting the reads that map to genes or exones using the the RPKM (Reads per Kilobases per Million reads) methods.

Inclusion Criteria: healthy subjects age 35-75 years diagnosed with chronic periodontitis at least four non-adjacent teeth with proximal sites with a PD ≥6 mm and clinical attachment loss ≥5 mm with BoP and no radiographic signs of apical pathology. either smokers (>10 cigarettes per day for at least 5 years) or non-smokers (never smoked or not within the last 5 years). Exclusion Criteria: subjects who presented with any current medical condition or used medications known to affect periodontal healing incorrectly reported smoking status use of antibiotics within 6 months of the study received subgingival scaling within 6 months of the study

Bunaes DF, Lie SA, Enersen M, Aastrom AN, Mustafa K, Leknes KN. Site-specific treatment outcome in smokers following non-surgical and surgical periodontal therapy. J Clin Periodontol. 2015 Oct;42(10):933-42. doi: 10.1111/jcpe.12462. Epub 2015 Oct 28.

Bunaes DF, Mustafa M, Mohamed HG, Lie SA, Leknes KN. The effect of smoking on inflammatory and bone remodeling markers in gingival crevicular fluid and subgingival microbiota following periodontal therapy. J Periodontal Res. 2017 Aug;52(4):713-724. doi: 10.1111/jre.12438. Epub 2017 Mar 17.