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. 2020 Jan 29;11:66. doi: 10.3389/fmicb.2020.00066

TABLE 3.

Clinical studies in relation to the effects of smoking on subgingival microflora (published between 2010 and 2019).

References Periodontal condition involved Laboratory techniques Microorganisms targeted Main results (smokers vs. non-smokers)
Heikkinen et al., 2012 / PCR Aa, Pg, Tf, Pi, Pn, Td Higher prevalence of Pi, Tf, and Td in female smokers.
Kubota et al., 2011 CP PCR Aa, Pg, Pi, Tf, Fn/Fp, Td, Cr Higher prevalence of Cr and lower prevalence of Aa in smokers.
Guglielmetti et al., 2014 CP Quantitative PCR Aa, Pg, Tf, Td Greater amounts of Pg, Aa, and Tf in smokers; a significant association between smoking and the presence of Aa.
Karasneh et al., 2017 Healthy, CP PCR 25 species No difference between smokers and non-smokers in healthy status; higher Ta in smokers with periodontitis.
Lanza et al., 2016 CP, AP High pure PCR Pg, Tf, Td, Pi, Aa No difference.
Bizzarro et al., 2013 Moderate to severe CP Culture Aa, Pg, Pi, Tf, Pm, Fn, Cr No difference.
Quantitative PCR Aa, Pg, Pi, Tf, Pm, Fn, Td No difference.
16S sequencing Community Higher abundance of Fusobacterium, Prevotella, and Selenomonas in smokers; one cluster was identified by PCoA composed mainly of smokers (80%) with lower taxonomic diversity.
Mason et al., 2015 Healthy 16S sequencing Community Microbial profiles of smokers and non-smokers were different at all taxonomic levels; a highly diverse, pathogen-rich, commensal-poor, and anaerobic microbiome in smokers.
Kumar et al., 2011 Healthy 16S sequencing Community A highly diverse and relatively unstable initial colonization of subgingival biofilms in smokers, with more periodontal pathogens of Fusobacterium, Cardiobacterium, Synergistes and Selenomonas.
Yu et al., 2017 Healthy 16S sequencing Community Microbial diversity and composition were not significantly different by smoking status.
Joshi et al., 2014 Gingivitis, healthy 16S sequencing Community An early pathogenic colonization that led to sustained pathogen enrichment with periodontal pathogens in the biofilm, and lower resilience of the ecosystem in smokers.
Shchipkova et al., 2010 Moderate to severe CP 16S sequencing Community Greater abundance of Parvimonas, Fusobacterium, Campylobacter, Bacteroides, and Treponema and lower levels of Veillonella, Neisseria, and Streptococcus in smokers.
Moon et al., 2015 Moderate CP 16S sequencing Community Higher abundance of Fusobacterium, Fretibacterium, Streptococcus, Veillonella, Corynebacterium, and Filifactor, and greater bacterial diversity in smokers.
Camelo-Castillo et al., 2015 CP 16S sequencing Community Higher prevalence of Granulicatella and lower bacterial diversity in smokers.

Studies related to smoking cessation and periodontal treatment are not included in this table (discussed in separate parts). Literature search was performed from the year 2000, but no 16S sequencing related study was found between 2000 and 2009. Besides, no additionally valuable information could be extracted from these reports apart from the main results listed in this table. Therefore, only papers published between 2010 and 2019 were summarized in this table. CP, chronic periodontitis; AP, aggressive periodontitis; PCR, polymerase chain reaction; PCoA, principal coordinate analysis. Aa, Aggregatibacter actinomycetemcomitans; Pg, Porphyromonas gingivalis; Tf, Tannerella forsythia; Pi, Prevotella intermedia; Pn, Prevotella nigrescens; Td, Treponema denticola; Fn/Fp, Fusobacterium nucleatum/periodonticum; Cr, Campylobacter rectus; Ta, Treponema amylovorum.