Immunohistochemistry study on expression of Tumor Necrosis Factor Like Weak Inducer of Apoptosis (TWEAK) and its receptor FN14 in normal and periodontitis tissues.

Abstract

Chapter 1: Periodontitis is a chronic inflammatory disease wherein microbial factors induce complex inflammatory and immune responses in a susceptible host. In periodontitis host-derived enzymes, cytokines and other proinflammatory mediators play an integral role in the destruction of tooth supporting structures and alveolar bone. TWEAK (TNF-like weak inducer of apoptosis), one of the members of the TNF superfamily, has recently been identified as an important inflammatory mediator. Fn14 (fibroblast growth factor-inducible 14) protein/TWEAKR has been identified as the cell surface receptor for TWEAK. TWEAK/Fn14 signaling results in multiple biologic effects including induction of inflammatory cytokines, modulating immune response angiogenesis and stimulation of apoptosis. TWEAK has also been shown to promote osteoclastic differentiation of cells from the monocyte/macrophage lineage. Expression of TWEAK and its receptor Fn14 is elevated in tissues and cells cultured from a number of chronic inflammatory diseases, such as rheumatoid arthritis, atherosclerosis, inflammatory skin, kidney and airway diseases. This review considers the biology of TWEAK and its receptor Fn14 in periodontitis.

Chapter 2: Periodontitis is a chronic inflammatory disease wherein microbial factors induce complex inflammatory and immune responses in a susceptible host. In periodontitis host derived enzymes, cytokines and other proinflammatory mediators play an integral role in the destruction of tooth supporting structures and alveolar bone. TWEAK (TNF-like weak inducer of apoptosis) is one of the newest members of the TNF superfamily to be identified. Fibroblast growth factor-inducible 14 (Fn14) protein/TWEAKR has been identified as the cell surface receptor for TWEAK. TWEAK/Fn14 signaling results in multiple biologic effects including induction of inflammatory cytokines, modulating immune response angiogenesis and stimulation of apoptosis. Recently, TWEAK has also been shown to promote osteoclastic differentiation of cells from the monocyte/macrophage lineage. Expression of TWEAK and its receptor Fn14, is elevated in tissues and cells cultured from a number of chronic inflammatory diseases such as rheumatoid arthritis, atherosclerosis, inflammatory skin, kidney and airway diseases. Accordingly, we hypothesised that the expression of TWEAK and Fn14/TWEAKR will be increased in tissue samples from periodontitis patients.