AIMS: Dysbiotic microbial communities underlie the aetiology of several oral diseases, especially in smokers. The ability of an ecosystem to rebound from the dysbiotic state and re-establish a health-compatible community, a characteristic known as resilience, plays an important role in susceptibility to future disease. The present investigation was undertaken to examine the effects of smoking on colonization dynamics and resilience in marginal and subgingival biofilms. MATERIALS AND METHODS: Marginal and subgingival plaque and gingival crevicular fluid samples were collected from 25 current and 25 never smokers with pre-existing gingivitis at baseline, following resolution, after 1, 2 4, 7, 14 and 21 days of undisturbed plaque formation and following resolution. 16S cloning and sequencing was used for bacterial identification and multiplexed bead-based flow cytometry was used to quantify the levels of 27 immune mediators. RESULTS: Smokers demonstrated an early pathogenic colonization that led to sustained pathogen enrichment with periodontal and respiratory pathogens, eliciting a florid immune response. Smokers also demonstrated greater abundance of pathogenic species, poor compositional correlation between marginal and subgingival ecosystems, and significantly greater pro-inflammatory responses following resolution of the second episode of disease. CONCLUSIONS: The ability of the subgingival microbiome to "reset" itself following episodes of disease is decreased in smokers, thereby lowering the resilience of the ecosystem and decreasing its resistance to future disease.
AIMS: Dysbiotic microbial communities underlie the aetiology of several oral diseases, especially in smokers. The ability of an ecosystem to rebound from the dysbiotic state and re-establish a health-compatible community, a characteristic known as resilience, plays an important role in susceptibility to future disease. The present investigation was undertaken to examine the effects of smoking on colonization dynamics and resilience in marginal and subgingival biofilms. MATERIALS AND METHODS: Marginal and subgingival plaque and gingival crevicular fluid samples were collected from 25 current and 25 never smokers with pre-existing gingivitis at baseline, following resolution, after 1, 2 4, 7, 14 and 21 days of undisturbed plaque formation and following resolution. 16S cloning and sequencing was used for bacterial identification and multiplexed bead-based flow cytometry was used to quantify the levels of 27 immune mediators. RESULTS: Smokers demonstrated an early pathogenic colonization that led to sustained pathogen enrichment with periodontal and respiratory pathogens, eliciting a florid immune response. Smokers also demonstrated greater abundance of pathogenic species, poor compositional correlation between marginal and subgingival ecosystems, and significantly greater pro-inflammatory responses following resolution of the second episode of disease. CONCLUSIONS: The ability of the subgingival microbiome to "reset" itself following episodes of disease is decreased in smokers, thereby lowering the resilience of the ecosystem and decreasing its resistance to future disease.
Authors: Francesco Beghini; Audrey Renson; Christine P Zolnik; Ludwig Geistlinger; Mykhaylo Usyk; Thomas U Moody; Lorna Thorpe; Jennifer B Dowd; Robert Burk; Nicola Segata; Heidi E Jones; Levi Waldron Journal: Ann Epidemiol Date: 2019-03-28 Impact factor: 3.797
Authors: Egija Zaura; Bernd W Brandt; Andrei Prodan; Maarten Joost Teixeira de Mattos; Sultan Imangaliyev; Jolanda Kool; Mark J Buijs; Ferry Lpw Jagers; Nienke L Hennequin-Hoenderdos; Dagmar E Slot; Elena A Nicu; Maxim D Lagerweij; Marleen M Janus; Marcela M Fernandez-Gutierrez; Evgeni Levin; Bastiaan P Krom; Henk S Brand; Enno Ci Veerman; Michiel Kleerebezem; Bruno G Loos; G A van der Weijden; Wim Crielaard; Bart Jf Keijser Journal: ISME J Date: 2017-01-10 Impact factor: 10.302