Abstract
The aim of this study is to evaluate the biological safety of tantalum (Ta) particles and to further explore the effects of Ta particles on human monocyte toxicity and inflammatory cytokine expression. Human monocyte leukemia (THP-1) cells were cultured with Ta and hydroxyapatite (HA) particles. Cell counting kit-8 method was used to evaluate the cytotoxicity of Ta and HA particles. The apoptosis effects were evaluated by flow cytometry, and the protein expression levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were evaluated by ELISA. The protein levels of inflammation-related signaling pathways including nuclear factor-kappa B (NF-κB) and extracellular regulated kinase (ERK) were detected by western blotting. The cytotoxicity test showed that the toxicity level of Ta in vitro was grade l, which is within the clinically acceptable range. Compared with the HA control, Ta had no significant effect on THP-1 cell apoptosis, IL-6, and TNF-α release. The phosphorylated levels of NF-κB and ERK at 3 h in the Ta group were lower than those in the HA and control groups (P < 0.001 both). These results reveal Ta particles behave good biosafety properties and provide some new insights for the future clinical use of Ta.
Highlights
Dental implantation is one of the most effective means of repairing dentition defects and loss [1] and has been widely used in dental clinics
The purpose of this study was to evaluate the biological safety of Ta particles and to further explore the effects of Ta particles on human monocyte toxicity, the gene expression levels of inflammatory cytokines, and secretion of NF-κB and extracellular regulated kinase (ERK) pathways to understand the application prospects of Ta materials as implant coatings
It can be seen that Ta particles were irregular in shape
Summary
Dental implantation is one of the most effective means of repairing dentition defects and loss [1] and has been widely used in dental clinics. Previous data have shown that some patients and implants have bone loss with different degrees, which means that there is a risk of implant failure [3, 4]. The most common causes of failure are infection and implant surface preparation [5]. Periimplant inflammation is an important cause of implant failure. Interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) are related to bone resorption at the implant and bone interface. As a classic mediator of inflammation, the nuclear factor-kappa B (NF-κB) pathway plays an important role in bone resorption [6,7,8,9]
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