The interactions are dynamic, since both the microbial Survivin structure of the dental biofilm and the experience of host immune responses will vary in the same individual with time. This concept was developed in parallel to the developments on the understanding of the immune response, and analysis on periodontal disease has been focusing components of host microbial relationships to know the disease process, in addition to for the development of novel therapeutic approaches. Our research group has been investigating the position of p38 MAPK signaling pathway on number microbial communications during periodontal disease. This review intends to go over the significance of the p38 MAPK pathway and the potential to govern this pathway for therapeutic applications in vivo. Ever since the initial description of Toll like receptors in the middle late 90s, the field of innate immunity has been greatly stimulated and the implications of these potent FAAH inhibitor receptors on the regulation of host response has been intensively studied. Essentially, the functions of TLRs in inflammation and immune response have been expanded, so it’s now known why these receptors not only understand various microbial associated molecular patterns to stimulate innate immune response, nevertheless they can also bind to endogenous molecules derived from damaged tissue and have a task in inflammation and adaptive immune response. The TLR family currently consists of more than 13 people, each capable of realizing different PAMPs. These receptors are expressed by immune cells such as neutrophils, macrophages and dendritic cells in addition to by low immune resident cells, such as periodontal fibroblasts and gingival epithelial cells. In periodontal areas, expression of TLR2 and TLR4 has been positively correlated with inflammation, as well as in intestinal inflammation. On another hand, reduced Cellular differentiation expression of TLR mRNA in the oral mucosa of periodontitis patients has been noted, nevertheless concomitantly with increased infiltration of the mucosa with TLRpositive inflammatory cells. This has been regarded by the writers as a possible result of the extended and repeated concern of this tissue with PAMPs and a test of the host to reestablish tissue homeostasis, as within an immune tolerance mechanism. TLRs are single move transmembrane proteins with an N terminal offering leucine prosperous repeats that are accountable for the recognition of their ligands and with a C terminal cytoplasmic domain that is much like the cytoplasmic region of the interleukin 1 receptor. Nucleotide natural compound library oligomerization domain proteins are cytosolic proteins that also have leucine wealthy repeats and were originally called intracellular TLRs that recognize PAMPs related to bacteria invading the cytosol, nevertheless these proteins have also been proven to regulate different signaling pathways, including p38 MAPK and NF?B.