Human periodontal diseases (i.e. gingivitis, periodontitis) result from heterogeneous etiologies including complex biofilm in the subgingival microenvironment, social and behavior modulations and genetic or epigenetic traits of the host, each of which is influenced and/or modulated by the host's immune and inflammatory responses. Recent advances in the field suggest that the periodontitis-associated immune mechanism is a double-edged sword, with one edge fighting the invading pathogens and the other triggering tissue damage in the host. Thus in this books various different tissue interaction with immune system cells and their responses in periodontal disease has been discussed.