Dental plaque develops as a complex biofilm on the tooth surface and is a direct precursor of periodontal diseases, one of the most common bacterial infections in developed countries. The molecular and cellular events that cause the transformation of commensal plaque into a pathogenic entity are only partially understood and involve colonization by pathogenic organisms such as Porphyromonas gingivalis which them impinge upon the structural integrity of the periodontal tissues and disrupt the host immune response. Recently, there have been two major conceptual breakthroughs in our perception of the pathogenic process. The first is that bacteria in biofilm such as plaque are phenotypically distinct from their planktonic counterparts and these phenotypic changes have important implications for virulence. Secondly, epithelial cells that line mucosal surfaces are no longer simply regarded as a mechanical barrier, but instead function as sensors for microbial infection., generating and transmitting signals among bacteria and host immune cells. The goals of this project are to investigate the molecular cross-talk between biofilm mode P. gingivalis and gingival epithelial cells. Thus, the production of immune mediators and effector molecules of tissue destruction by gingival epithelial cells, and the signal transduction pathways that participate in these responses, following contact with biofilm-P. gingivalis in the context of a biofilm will be identified. The long term goal of the project is thus to identify bacterial and gingival epithelial cell molecules or signaling pathways that could sere as targets for novel therapeutic agents to prevent or reduce the severity of periodontal diseases. As children rarely develop periodontal disease, the preventive intervention with these new technologies in at risk children could significantly improve adult periodontal health.
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