The Physiopathological Role of IL-33: New Highlights in Bone Biology and a Proposed Role in Periodontal Disease

Figure 2

Possible role of IL-33 in periodontal disease. The destruction (necrosis) of the epithelial cells and gum releases IL-33 and acts as a chemoattractant and cytokine. The influx of mast cells, Th1 cells, and monocytes to the inflammation site, in the presence of IL-33, activates mast cell degranulation and production of proinflammatory cytokines, inducing osteoclastogenesis. Almost, IL-33 induces neutrophil influx, production of activator of nuclear factor kappa-B ligand (RANKL), and decrease of osteoprotegerin (OPG) production by osteoblast, favoring osteoclastogenesis by increasing osteoclastogenic factors as spleen tyrosine kinase (SYK), nuclear factor of activated T cells (Nfatc1), and tartrate-resistant acid phosphatase (TRAP).