Tobacco smoking is the leading environmental cause of chronic periodontitis and other bacterial- induced periodontal diseases. Some components of dental plaque are highly resistant to the plethora of toxic insults contained in cigarette smoke. One such species is the emergent oral pathogen, Filifactor alocis. F. alocis has been consistently associated with periodontal diseases epidemiologically; thrives in tobacco-rich environments, both in vitro and in vivo; and is one of the most transcriptionally active bacterial species found in the disease-associated microbiome. We will identify (RNAseq), validate (qPCR) and classify (KEGG, DAVID, etc) those genes that are significantly regulated by cigarette smoke exposure in three strains of F. alocis. We will then assess in vivo relevance in a germ-free F. alocis infection smoke exposure model. We shall generate some of the first information to explain how this emergent periodontopathogen may survive and persist in the oral cavity of smokers. The smoke exposure chamber will also facilitate the development of a reproducible model of tobacco-induced and/or ?exacerbated bacteria-associated periodontitis. This will represent a much needed tool to the field.
Filifactor alocis is a Gram positive, anaerobic and assacharolytic microbe that has recently emerged as a key etiological agent of periodontal diseases. Cigarette use is a risk factor for gum diseases, while F. alocis is particularly well adapted to tobacco-rich environments and is one of the most genetically active bacteria in dental plaque. We will identify, confirm and classify those F. alocis genes that are activated or repressed during cigarette smoke exposure in vitro and in vivo. Therefore, we will begin to understand how F. alocis survives and thrives in the oral cavity of smokers. The in vivo arm will employ a murine smoke exposure chamber which will facilitate the development of a much needed animal model of tobacco-induced periodontitis.
