Cigarette Smoking, Periodontitis
Conditions
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.
Interventions
PROCEDURENon-surgical periodontal therapy: motivation and instruction in oral hygiene, debridement using handinstrumentation (Hu-Firedy,Chicago, IL, USA;and American Eagle Instruments,Missoula, MT,USA).
Non-surgical and surgical periodontal therapy in cigarette smokers and non-smokers
Sponsors
University of Bergen
Study design
Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
NONE
Intervention model description
Prospective cohort study
Eligibility
Sex/Gender
ALL
Age
35 Years to 75 Years
Healthy volunteers
Yes
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
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| 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
| Measure | Time frame | Description |
|---|---|---|
| Clinical periodontal attachmentloss | 24 months | Clinical attachment loss in mm |
| Periodontal pocket depth | 24 months | Probing depth in mm |
| Bleeding at site level | 24 months | Bleeding on probing (yes or no) |
| Bleeding at patient level | 24 months | Bleeding index in percentage (%) |
| Teeth present | 24 months | Number of teeth |
| Amount of periopathogenic bacteria | 24 months | Subgingival plaque samples of 20 subgingival periopathogenic bacterial species were analysed using checkerboard DNA-DNA hybridization. |
| 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. |
| 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. |
| Plaque at patient level | 24 months | Plaque index in percentage (%) |
Outcome results
None listed