OBJECTIVE: To longitudinally examine patterns in supragingival and subgingival bacterial acquisition and colonization as well as host response in health and gingivitis in current and never smokers.
MATERIALS AND METHODS: 15 current and 15 non-smokers over 18 years of age with no history of systemic disease, current or planned pregnancy, recent or prophylactic antibiotic use were recruited. Following baseline evaluation and prophylaxis, stents were fabricated to protect 3 adjacent teeth in 2 quadrants during brushing. Clinical data, gingival crevicular fluid, supragingival and subgingival plaque samples were collected at day 0, 1, 2, 4, 7, 14 and 21. At each visit the patient was scaled, polished and flossed to ensure uninterrupted plaque formation for the next visit. 16S cloning and sequencing was utilized for bacterial identification and enumeration. A multiplexed bead-based assay was utilized to identify levels of 27 immune mediators in the crevicular fluid. Within-subject and between-subject comparisons were made using Wilcoxon signed rank and Kruskal-Wallis tests respectively.
RESULTS: Both current and never smokers developed gingivitis over the 21 days of plaque accumulation. No significant difference was noted in plaque index
(Rustogi), or gingival index (Loe & Silness) at any time point. A Shannon-Weiner diversity index revealed increased diversity in never smokers with no significant alterations in current smoker diversity in both supragingival and subgingival biofilms as the onset of gingivitis occurred. Current smokers had potentially pathogenic bacteria present (Fusobacterium), even in health. A Bray-Curtis similarity index revealed a significant shift in subgingival bacteria at day 14 of plaque accumulation in the similarity of the never smoker biofilm to health. No such shift was seen subgingivally in current smokers. An inflammation score was obtained and it revealed that current smokers exist in a hyper-inflamed state when compared to never smokers.
CONCLUSIONS: Smoking alters both the profile of the bacterial biofilm present in health as well as the host-response to the bacterial insult that results in gingivitis.