Crosstalk of Gingival Fibroblasts and Macrophages in Inflammatory Cytokine Cascade: Potential Mechanisms of Periodontitis

Periodontitis is a bacterial infectious disease, and many inflammatory cytokines regulate the pathophysiology through the crosstalk of tissue cells and immune cells [1,2]. Cytokine balance regulated by immune responses has an important role in the stability or progression of inflammation. Many researchers have shown the effects of inflammatory cytokines such as Interleukin (IL)-1 and IL-6 on periodontal cells, e.g. fibroblasts, epithelial cells and macrophages [3,4]. In periodontal inflamed tissues, IL-1 and IL-6 may be responsible to the tissue destruction by increasing matrixmetalloproteinases (MMPs) [5]. The evidence for the role of MMPs in periodontal destruction has been reported, and it is now recognized that an imbalance between activated MMPs and their endogenous inhibitors, i.e. tissue inhibitors of MMPs (TIMPs) leads to pathologic breakdown of the extracellular matrix seen in periodontitis, resulting in tooth loss [6]. Therefore, the imbalance induced by inflammatory cytokines should be important to understand the potential mechanism of periodontitis.