This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The oral cavity provides a biotope for many bacterial species, which may be considered commensal, opportunistic or pathogenic. The host defense systems are important for monitoring the composition of the bacterial microbiota and preventing disease initiation and progression. Innate and adaptive immune mechanisms serve to prevent inappropriate responses to commensal microbes, regulate opportunistic species, and sequester pathogens. Dysregulation of these responses can lead to chronic inflammatory conditions in the oral cavity, i.e., gingivitis and periodontitis. Understanding the molecular signaling mechanisms that maintain homeostasis in the oral cavity is key to understanding the pathology of diseases in response to oral bacteria. Host cells respond to microorganisms through pattern recognition receptors (PRRs) such as Toll-like Receptors (TLRs), which recognize broad classes of pathogen associated molecular patterns (PAMPs) including lipopolysaccharide (LPS), lipopeptides and microbial nucleic acids. Inflammatory bowel diseases (Crohn's and Ulcerative colitis) are chronic conditions that reflect an altered communication between resident gut flora and both the innate and acquired immune arms. The initiating factor is unknown, but lately a primary epithelial defect has been favored. A significant number of patients with inflammatory bowel diseases develop oral lesions but the incidence of periodontitis has not been adequately established. Patients with IBD (inflammatory bowel diseases) represent a heterogeneous group, more so when expression of individual genes within the gut mucosa is analyzed. We have recently identified unique subgroups of patients with Crohn's disease based on expression of biomarkers for innate immunity in the colonic mucosa. Additionally we have uncovered strong associations with a fat derived anti-inflammatory adipokine, adiponectin. The current proposal investigates the association between periodontitis and Crohn's disease and the relevance of disease specific biomarkers for this oral chronic inflammatory condition, using a GENERAL HYPOTHESIS that patients with IBD have a greater risk for periodontitis due to an underlying defect in innate immune responses at mucosal surfaces.