ArticleJournal of clinical periodontology2023
Tobacco smoke exacerbates Filifactor alocis pathogenicity.
Article in Journal of clinical periodontology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- The associations of human genetic variations with airway microbiome, environmental exposures, and respiratory health.mSystems · 2026Article
- The oral - X axis: from periodontal dysbiosis to systemic disease.Frontiers in immunology · 2026Review
- Oral Microbiota Linking Humoral Response, Periodontitis and Atherosclerosis.Journal of clinical periodontology · 2025Article
- Article
- Tobacco-enhanced biofilm formation by Porphyromonas gingivalis and other oral microbes.Molecular oral microbiology · 2024Review
- The association of composite dietary antioxidant index with periodontitis in NHANES 2009-2014.Frontiers in immunology · 2024Article
- Enhancement of innate immunity in gingival epithelial cells by vitamin D and HDAC inhibitors.Frontiers in oral health · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimFilifactor alocis has recently emerged as a periodontal pathobiont that appears to thrive in the oral cavity of smokers. We hypothesized that identification of smoke-responsive F. alocis genes would provide insight into adaptive strategies and that cigarette smoke would enhance F. alocis pathogenesis in vivo. MATERIALS AND
methodsF. alocis was grown in vitro and cigarette smoke extract-responsive genes determined by RNAseq. Mice were exposed, or not, to mainstream 1R6F research cigarette smoke and infected with F. alocis, or not, in an acute ligature model of periodontitis. Key clinical, infectious, and immune data were collected.
resultsIn culture, F. alocis growth was unaffected by smoke conditioning and only a small number of genes were specifically regulated by smoke exposure. Reduced murine mass, differences in F. alocis-cognizant antibody production, and altered immune profiles as well as altered alveolar bone loss were all attributable to smoke exposure and/or F. alocis infection in vivo.
conclusionsF. alocis is well-adapted to tobacco-rich conditions and its pathogenesis is enhanced by tobacco smoke exposure. A smoke-exposed ligature model of periodontitis shows promise as a tool with which to further unravel mechanisms underlying tobacco-enhanced, bacteria-induced disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.