Coordinated effect of IL-17A and IL-27 on osteoclast differentiation of RANKL-stimulated RAW264.7 cells

Orthodontic treatment is done to obtain optimal occlusion through tooth movement. The treatment may take several years, and stress may occur during this time. Orthodontic tooth movement is associated with both mechanical and psychological stresses that may be associated with pain or discomfort. Measures that reduce the time of orthodontic treatment and accelerate the alveolar bone response would be welcomed by the patient. Tooth movement requires a bone remodeling that consists of bone resorption on the compressed side and bone formation on the tensile side of the tooth. Osteoclasts play a key role in modulating bone mass. During orthodontic tooth movement, alveolar bone resorption at the area of compression occurs through osteoclastic activity. Since osteoclast differentiation/activation is engaged in orthodontic tooth movement at the pressure side, the investigation of osteoclasts is crucial for orthodontics. However, the mechanism of osteoclast differentiation/activation in orthodontic tooth movement remains unknown. It is well known that two essential cytokines are required for osteoclastogenesis : macrophage colonystimulating factor (M-CSF) and receptor for activation of nuclear factor-κB (NF-κB) ligand (RANKL). M-CSF induces the proliferation of osteoclast precursor cells and sustains their survival. RANKL induces osteolast differentiation from osteoclast precursors and stimulates their bone resorption activity. RANKL was detected in osteoblasts and periodontal ligament cells during experimental tooth movement. RANKL plays a key role in osteoclast differentiation and activation. Coordinated effect of IL-17A and IL-27 on osteoclast differentiation of RANKL-stimulated RAW264.7 cells