Mechanical loading exerts important effects on the skeleton by controlling bone mass and strength. Osteoclasts are required for bone resorption and remodeling. Two cytokines are required for osteoclast formation: macrophage colony-stimulating factor and receptor activator of nuclear factor kappa-B ligand (RANKL). Tumor necrosis factor-a (TNF-α?) has also been recognized as an important factor for osteoclastogenesis. It has previously been reported that interleukin (IL)-12 and IL-18, and interferon gamma (IFN-γ?), which are type 1T helper cell (Th1) cytokines, inhibited RANKL- and TNF-α?-mediated osteoclastogenesis. It also been reported that TNF-α? plays an important role in mechanical loading-induced osteoclastogenesis and bone resorption. Orthodontic tooth movement is a good model for exploring the mechanism underlying mechanical loading-induced bone changes. Orthodontic tooth movement in a mouse model was established, and we investigated whether Th1 cytokines such as IL-12 and IFN-γ? inhibit osteoclastogenesis and bone resorption upon mechanical loading. The number of tartrate-resistant acid phosphatase (TRAP)-positive cells increased at the pressure side of the first molar. Conversely, the amount of tooth movement and the number of TRAP-positive cells at the pressure side in IL-12- and IFN-γ?-injected mice was less than that of non-injected mice. The results suggested that IL-12 and IFN-γ? might have an inhibitory effect on mechanical loading-induced osteoclastogenesis. In this review, we describe and discuss the effect of Th1 cytokines on mechanical loading-induced osteoclastogenesis and bone resorption.
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