OBJECTIVE: To assess clinical and microbiological changes during experimental gingivitis in cigarette smokers and non-smokers. MATERIAL AND METHODS: Eleven current smokers (>/=5 years) and 11 (never-) non-smokers periodontally healthy or with gingivitis (PPD</=4 mm) were included. According to the original model (Löe et al. 1965), an experimental 3-week plaque accumulation period resulting in experimental gingivitis and a subsequent 2-week period of optimal plaque control were performed. Subgingival plaque samples were collected at days 0, 21 and 35 from one site per quadrant, pooled and analysed using checkerboard DNA-DNA hybridization. RESULTS: Smokers {mean age: 24.7+/-2.2 [standard deviation (SD)] years, range 21-28 years} had a mean lifetime cigarette exposure of 6.4+/-2.8 (SD) pack-years, while non-smokers presented with a mean age of 23.1+/-2.2 (SD) years (range 21-29 years). Between days 0, 21 and 35, no statistically significant differences in mean Plaque and mean Gingival Index scores were observed between smokers and non-smokers. In both smokers and non-smokers, mean total DNA probe counts did not significantly differ nor increase between days 0 and 21. Also, between days 21 and 35 they did not significantly differ nor decrease. This was also true for the various proportions of bacterial complexes. CONCLUSION: Both current smokers and (never-) non-smokers reacted to experimental plaque accumulation with gingival inflammation. Periodontal and microbiological parameters assessed in current cigarette smokers did not significantly differ from those in non-smokers during an identical period of experimental plaque accumulation. Hence, the early host response to the bacterial challenge appears to be of similar magnitude and timing in both groups.
OBJECTIVE: To assess clinical and microbiological changes during experimental gingivitis in cigarette smokers and non-smokers. MATERIAL AND METHODS: Eleven current smokers (>/=5 years) and 11 (never-) non-smokers periodontally healthy or with gingivitis (PPD</=4 mm) were included. According to the original model (Löe et al. 1965), an experimental 3-week plaque accumulation period resulting in experimental gingivitis and a subsequent 2-week period of optimal plaque control were performed. Subgingival plaque samples were collected at days 0, 21 and 35 from one site per quadrant, pooled and analysed using checkerboard DNA-DNA hybridization. RESULTS: Smokers {mean age: 24.7+/-2.2 [standard deviation (SD)] years, range 21-28 years} had a mean lifetime cigarette exposure of 6.4+/-2.8 (SD) pack-years, while non-smokers presented with a mean age of 23.1+/-2.2 (SD) years (range 21-29 years). Between days 0, 21 and 35, no statistically significant differences in mean Plaque and mean Gingival Index scores were observed between smokers and non-smokers. In both smokers and non-smokers, mean total DNA probe counts did not significantly differ nor increase between days 0 and 21. Also, between days 21 and 35 they did not significantly differ nor decrease. This was also true for the various proportions of bacterial complexes. CONCLUSION: Both current smokers and (never-) non-smokers reacted to experimental plaque accumulation with gingival inflammation. Periodontal and microbiological parameters assessed in current cigarette smokers did not significantly differ from those in non-smokers during an identical period of experimental plaque accumulation. Hence, the early host response to the bacterial challenge appears to be of similar magnitude and timing in both groups.
Authors: F R Teles; R P Teles; N G Uzel; X Q Song; G Torresyap; S S Socransky; A D Haffajee Journal: J Periodontal Res Date: 2011-09-05 Impact factor: 4.419
Authors: Anastasios M Gkatzonis; Spyridon I Vassilopoulos; Ioannis K Karoussis; Archontia Kaminari; Phoebus N Madianos; Ioannis A Vrotsos Journal: Clin Oral Investig Date: 2018-02-02 Impact factor: 3.573
Authors: Tatiana Meulman; Renato C V Casarin; Daiane C Peruzzo; Ana Paula Giorgetti; André Barbagallo; Márcio Z Casati; Enilson A Sallum; Reginaldo B Gonçalves; Francisco H Nociti Journal: J Oral Microbiol Date: 2012-01-05 Impact factor: 5.474