Date on Master's Thesis/Doctoral Dissertation


Document Type

Master's Thesis

Degree Name



Oral Biology

Degree Program

Oral Biology, MS

Committee Chair

Scott, David

Committee Co-Chair (if applicable)

Lamont, Richard

Committee Member

Lamont, Richard

Committee Member

Potempa, Jan

Author's Keywords

Smoking; gene expression; Porphyromonas gingivalis; Filifactor alocis; Treponema denticola; RNA- Sequencing


Smoking is an established risk factor for periodontitis. Prior studies have shown that cigarette smoke extract (CSE) can induce profound phenotypic changes in Porphyromonas gingivalis and alters the virulence of this important periodontal pathogen. We hypothesized that CSE might also alter gene expression in established periodontal pathogens, Porphyromonas gingivalis and Treponema denticola, as well as in the emerging pathogen, Filifactor alocis. Oral bacteria were grown in CSE-conditioned medium (1000 ng/ml nicotine equivalents) or in unconditioned control medium. Total RNA was extracted and CSE-regulated genes were identified by comparison of the mRNA profiles of CSE with control cultures using RNA-Seq analysis. Approximately, 30% of genes in the P. gingivalis genome and 5% of genes in the F. alocis genome were found to be differentially expressed when exposed to cigarette smoke. Several genes responsible for DNA replication and repair, transfer (tra) genes, ABC transporter genes and several metabolic genes were found to be differentially expressed in both F. alocis and P. gingivalis. Validation of RNA-Seq differentially expressed genes was done by qPCR analysis for selected genes and similar results were found. More in depth study of these genes could provide some of the first insights into how cigarette smoke changes the P. gingivalis and F. alocis phenotype in a manner likely to promote their colonization and infection.