IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits

Figure 1

Representation of the biological mechanisms of the cytokines and MMP-9 in the immunopathogenesis of CP. (a) The initial trigger for the immune response is the recognition of components of periodontopathogens, as LPS, by TLRs (Toll-like receptor). This recognition generates an intracellular signaling cascade leading to increased secretion of proinflammatory cytokines, MMPs, and recruitment of osteoclasts by macrophages. (b) This innate immune mechanism of defense may not be sufficient to eliminate the pathogen and with this the adaptive immune response is activated. APCs (antigen-presenting cells) internalize and process bacterial antigens, which bind to MHC II and is transported to the cell surface to be recognized by specific T cell. The Th1 immune response is the main response activated. IL-18 is expressed by macrophages, osteoblasts, fibroblasts, and Kupffer cells, being the main cytokine inducing IFN-γ. This cytokine acts synergistically with IL-12 in NK cells to induce IFN-γ production and activation of macrophages and dendritic cells that direct the Th1 response. TNF-α, IL-1β, and proinflammatory cytokines, such as IL-12 and IL-18, orchestrate enzyme-producing events such as MMP-9 and recruitment of osteoclasts, macrophages, and NK cells, causing greater inflammation and destruction of periodontal tissues.

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