IL-17A inhibits osteoclast differentiation of RANKL-stimulated RAW264.7 cells by suppressing JNK phosphorylation and c-Fos expression

Abstract

Periodontitis is an infection-driven chronic inflammatory disease characterized by periodontal pocket formation and alveolar bone resorption. It is one of the most common chronic inflammatory diseases in aged populations and affects almost 90% of the population. A balance between bone resorption by osteoclasts and bone formation by osteoblasts determines the level of bone mass. Inflammation-mediated bone loss is a major feature of various bone diseases, including chronic periodontitis, rheumatoid arthritis, and osteoarthritis, and is caused by an imbalance in bone remodeling that favors resorption. This imbalance is caused by increased cytokines and mediators in the inflamed tissue. Inflammatory cytokines produced by immunoregulatory cells regulate the immune responses to periodontal bacteria and play a protective and/or destructive role in disease progression. However, the mechanisms of periodontal bone resorption remain to be established. Bone remodeling is a physiological process that involves bone formation and resorption. The two major cell types responsible for bone formation and resorption are osteoblasts and osteoclasts. Bone homeostasis results from tightly regulated activities of boneforming osteoblasts and bone-resorbing osteoclasts. Therefore, the balance between these two cell types is important for maintaining bone mass, and the disruption of this relationship leads to bone disorders such as osteoporosis, rheumatoid arthritis, and periodontal disorders. Usually, these pathological diseases are characterized by over formation and/or activation of osteoclasts. Osteoclasts are multinucleated giant cells formed by the fusion of monocyte/macrophage precursors, which are derived from hemaIL-17A inhibits osteoclast differentiation of RANKL-stimulated RAW264.7 cells by suppressing JNK phosphorylation and c-Fos expression