Tobacco smoking has long been recognized as a risk factor for cancer and periodontal disease (PD). Both of these diseases are documented to be associated with changes in oral microbes. A second similarity between these diseases is an etiological association with inflammation. In the case of cancers such as oropharynx (OPC) or oral squamous cell carcinoma (OSCC) a host inflammatory activity occurs in response to hundreds of mutagens, toxins, and carcinogen mucosal DNA damaging agents. In the case of periodontal disease host inflammatory response occurs in response to microbe related proteins, lipids, and carbohydrates antigens. Our study suggests a tobacco product habit can alter healthy commensal microbe organization biofilm enhance survival of microbes that are not normally present in human oral biofilm and increasing cancer risk.. This altered microbe population can themselves release of mutagens, toxins and carcinogens. One group of carcinogens specified in this project is poly-cyclic aromatic hydrocarbons (PAH) as constituents of tobacco smoke these chemicals are recognized as type I carcinogens by the World Health Organization. Moreover, tobacco leaf products have been identified with a similar set of microbes that are capable of survival from tobacco smoke and additionally metabolize/degrade PAH, which occurs in nature during petroleum spills.
This study will briefly discuss PAH and their presence in the environment and tobacco products, as well as review the literature for microbes recognized to be linked to human diseases such as OSCC and PD and an association with tobacco product use. This thesis therefore provides novel information for risk for DNA damage to oral mucosa and oral carcinogenesis mediated by microbes.