Periodontitis develops due to subgingival infection with specific microbial pathogen from dental plaque. The bacteria can activate immunoinflammatory mechanisms within the local periodontal tissues that lead to destruction of collagen and alveolar bone. Human gingiva contains Langerhans and connective tissue dendritic cells. Signals from periodontal pathogen can induce dendritic cells to maturation,rapidly increasing surface expression of MHC class II, costimulatory molecules, and secrete proinflammatory cytokines to regulate adaptive T cell immune response. Studies on cytokines have led to controversy about different T cell subsets associated with the progression of periodontitis. Seymour proposed that susceptibility to periodontal disease progression involve a predominantly Th2 response while Ebersole speculated that Th2 cells providing protective function. It is possible that a given pathogen may produce different maturation signals by activating DCs induce a given type of immune response. In this study, we observed the profiles and amounts of cytokine production of DCs stimulated with P. gingivalis and T. forsythensis compared with E. coli, to see whether the periodontal pathogens may induce different response of dendritic cells in the innate immunity.