Abstract
A previous study showed that BMP-2 (bone morphogenetic protein-2) and wear debris can separately support osteoclast formation induced by the receptor activator of NF-κB ligand (RANKL). However, the effect of BMP-2 on wear debris-induced osteoclast formation is unclear. In this study, we show that neither titanium particles nor BMP-2 can induce osteoclast formation in RAW 264.7 mouse leukemic monocyte macrophage cells but that BMP-2 synergizes with titanium particles to enhance osteoclast formation in the presence of RANKL, and that at a low concentration, BMP-2 has an optimal effect to stimulate the size and number of multinuclear osteoclasts, expression of osteoclast genes, and resorption area. Our data also clarify that the effects caused by the increase in BMP-2 on phosphorylated SMAD levels such as c-Fos expression increased throughout the early stages of osteoclastogenesis. BMP-2 and titanium particles stimulate the expression of p-JNK, p-P38, p-IkB, and P50 compared with the titanium group. These data suggested that BMP-2 may be a crucial factor in titanium particle-mediated osteoclast formation.
Highlights
The biological response to wear particles at the boneimplant interface is considered the main cause of aseptic loosening and osteolysis [1,2] by increasing osteoclastogenesis and bone resorption [3,4]
A previous study showed that bone morphogenetic protein-2 (BMP-2) and wear debris can separately support osteoclast formation induced by the receptor activator of NF-kB ligand (RANKL)
To evaluate the effects of the titanium particles on the RANKL-mediated osteoclast differentiation of RAW 264.7 cells, we cultured the cells in the presence of suboptimal levels of 30 ng/mL RANKL and titanium particles
Summary
The biological response to wear particles at the boneimplant interface is considered the main cause of aseptic loosening and osteolysis [1,2] by increasing osteoclastogenesis and bone resorption [3,4]. A recent study showed that bone morphogenetic protein-2 (BMP-2), a member of the superfamily of transforming growth factor beta (TGF-b) ligands, could affect osteoclastogenesis [7,8]. It seems to have a double effect on osteoclast formation. In the absence of osteoblasts, BMP-2 appears to directly increase osteoclast formation and survival [11,12,13]
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