Abstract

Osteoarthritis (OA) is the most common joint disease type and is accompanied by varying degrees of functional limitation. Both hyaluronic acid (HA) joint injections and pain relievers are efficient treatments for early-stage osteoarthritis. However, for the decomposition by hyaluronidase and free radicals in the knee joint, HA injection treatment has limited effect time. The cerium oxide nanoparticles (CeO2) is a long time free radical scavenger. CeO2 combined with HA expected, may extend the HA decomposition time and have a positive effect on osteoarthritis therapy. In this study, CeO2 was successfully synthesized using the hydrothermal method with a particle size of about 120 nm, which possessed excellent dispersibility in the culture medium. The in vitro OA model was established by cell treated with H2O2 for 30 min. Our study found that the inhibition of chondrocyte proliferation dose-dependently increased with H2O2 concentration but was significantly decreased by supplementation of cerium oxide nanoparticles. COL2a1 and ACAN gene expression in chondrocytes was significantly decreased after H2O2 treatment; however, the tendency was changed after cerium oxide nanoparticles treatment, which suggested that damaged chondrocytes were protected against oxidative stress. These findings suggest that cerium oxide nanoparticles are potential therapeutic applications in the early stage of OA.

Highlights

  • Osteoarthritis (OA), the most common form of arthritis, has long been considered a complex metabolic disease disorder which leads to focal damage to articular cartilage at the weight-bearing areas [1]

  • The transmission electron microscopy (TEM) images showed that the grain size of cerium oxide nanoparticle was around 10 nm, and the exposing surface was unstable, where three crystal planes could be found by the lattice spacing, namely

  • The results demonstrated that cartilage degeneration was significantly improved after CeO2 nanoparticles treatment and this tendency suggested that cerium oxide nanoparticles can protect damaged chondrocytes against oxidative stress

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Summary

Introduction

Osteoarthritis (OA), the most common form of arthritis, has long been considered a complex metabolic disease disorder which leads to focal damage to articular cartilage at the weight-bearing areas [1]. This slowly progressive, disabling joint disorder can significantly impair life quality (QOL). Increased pressure on the joint, which leads to the cartilage matrix’s fragility, was considered to be the primary pathological process. As a result of the progress in molecular biology in the 1990s, scientists discovered that many soluble mediators could increase the synthesis of matrix metalloproteinases by chondrocytes and led to the inflammatory process. Recent data have shown that OA is a much more complex metabolic syndrome induced by the inflammatory mediators released by cartilage, subchondral bone, and synovium [5].

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