Abstract
Purposesto study the effect of titanium particles on MLO-Y4 and the effects of osteocytes alterations on osteoblasts.Methodscultured MLO-Y4 osteocytes were exposed to different concentrations of titanium (Ti) particles, cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay, apoptosis of MLO-Y4 cells was evaluated by flow cytometry, Real-time PCR quantification of mRNA expression of SOST, at the same time with Western Blot detection sclerosteosis protein expression levels.MC3T3-E1 cells culture with MLO-Y4 cells exposed to different concentrations of titanium (Ti) particles in vitro, in order to detection of osteoblast osteogenetic activity.ResultsOur results showed that Ti particles inhibited cell viability of MLO-Y4 osteocytes in a dose-dependent manner. Incubation with Ti particles caused apoptosis of MLO-Y4cells.Treatment with Ti particles significantly increased expression of the osteocytic marker SOST/sclerostin. Furthermore, treatment of MLO-Y4 cells with Ti particles produced a dose-dependent decrease in ALP activity and decreased mineralization of MC3T3-E1 cells through direct cell-cell contact.ConclusionsTitanium particles damage osteocytes and inhibit osteoblast differentiation.
Highlights
With the rapid increase in the number of joint replacements, the problem of aseptic loosening of the prosthesis is becoming more serious [22]
Ti wear particles inhibited cell viability of MLO-Y4 osteocytes in a dose- and time-dependent manner After MLO-Y4 cells were treated with various concentrations of Ti particles for 24 h, 48 h, and 72 h, cell viability was measured by Cell Counting Kit-8 (CCK-8) assay
These results clearly indicate that Ti particles can reduce cell viability and cause osteocyte death
Summary
With the rapid increase in the number of joint replacements, the problem of aseptic loosening of the prosthesis is becoming more serious [22]. Wear particles generated from prosthetic implant materials can activate a wide variety of cell types surrounding the prosthesis, including fibroblasts, monocytes, macrophages, and osteoclasts [7, 15, 33], which release IL-1, IL-6, TNF-α, and other pro-inflammatory cytokines. These pro-inflammatory mediators further stimulate osteoclast differentiation and maturation, leading to bone resorption [2, 18, 34].
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