The Impact of Cigarette Smoking on Periodontal Therapy

Not Applicable

Completed

• Conditions: Periodontitis; Cigarette Smoking

• Registration Number: NCT05120206
• Lead Sponsor: University of Bergen

Brief Summary

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.

Detailed Description

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.

Study Timeline

• Study Start: 2012-04-01
• Primary Completion: 2015-03-01
• Study Completion: 2015-03-01
• Study First Submitted: 2021-10-05
• Status Verified: 2021-11
• Study First Submitted QC: 2021-11-02
• Last Update Submitted: 2021-11-02
• Study First Posted: 2021-11-15
• Last Update Posted: 2021-11-15

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 80

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).

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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

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Study & Design

• Study Type: INTERVENTIONAL
• Study Design: PARALLEL

Primary Outcome Measures

Name	Time	Method
PD ≥5 mm with BoP	24 months	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).

Secondary Outcome Measures

Name	Time	Method
Bleeding at site level	24 months	Bleeding on probing (yes or no)
Inflammatory gingival crevicular fluid markers (proteins)	24 months	Concentrations of gingival crevicular fluid biomarkers measured in pg/mLwere analysed using multiplex and singleplex micro-bed immunoassays.
Clinical periodontal attachmentloss	24 months	Clinical attachment loss in mm
Amount of periopathogenic bacteria	24 months	Subgingival plaque samples of 20 subgingival periopathogenic bacterial species were analysed using checkerboard DNA-DNA hybridization.
Teeth present	24 months	Number of teeth
Periodontal pocket depth	24 months	Probing depth in mm
Bleeding at patient level	24 months	Bleeding index in percentage (%)
Plaque at patient level	24 months	Plaque index in percentage (%)
Serum proteins	24 months	Concentration of inflammatory serum markers measured in pg/ɥL determined using multiplex kit Bio-Plex Human ProTM Assay.
Gene expression in blood	24 months	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.