The Role of Th1 Cytokines on Mechanical Loading-Induced Osteoclastogenesis and Bone Resorption

Abstract

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-α (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 loadinginduced 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 tartrateresistant 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 loadinginduced osteoclastogenesis and bone resorption.

Correlation between the non-use of cooking oil fume extractors and bone mineral density in population aged 45 years and older in China: a cross-sectional study

“…Subsequently, some inflammatory factors may increase receptor activators of nuclear factor k B expression in osteoclast precursors and macrophage colony-stimulating factor expression in stromal cells. Eventually, an imbalance of osteoblasts and osteoclasts leads to bone loss (18,35) (Figure 2).…”

Oral epithelial-derived mediators suppress RANKL expression in human mandibular-derived bone cells

“…Several factors, including 1α,25(OH) 2 D 3 , parathyroid hormone, and PGE 2 , stimulated RANKL upregulation and increased pit-forming activity when osteoblasts and osteoclasts from mouse bone marrow were cocultured (102). IFN-γ is commonly found in Th-1 type response associating with stable periodontal disease ( 73), but absent in progressive periodontitis, we therefore investigate whether IFN-γ is the cytokine responsible for the observed reduction in RANKL expression and its role in modulating bone homeostasis.…”