Abstract

The effects of interleukin-10 (IL-10) and glucose on mRNA and protein expression of osteoprotegerin (OPG), and its ligand, receptor activator of nuclear factor-κB ligand (RANKL), were investigated in human periodontal ligament fibroblasts (HPDLFs). Primary HPDLFs were treated with different concentrations of IL-10 (0, 1, 10, 25, 50, and 100 ng/mL) or glucose (0, 5.5, 10, 20, 30, and 40 mmol/L). Changes in mRNA and protein expression were examined using the reverse-transcription polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. After IL-10 treatment, mRNA and protein levels of OPG were increased, while mRNA and protein levels of RANKL were decreased (P<0.05), both in a concentration-dependent manner. Glucose stimulation had the opposite concentration-dependent effect to that of IL-10 on OPG and RANKL expression. IL-10 upregulated OPG expression and downregulated RANKL expression, whereas high glucose upregulated RANKL and downregulated OPG in HDPLFs. Abnormal levels of IL-10 and glucose may contribute to the pathogenesis of periodontal disease.

Highlights

  • Osteoprotegerin (OPG) and its ligand, receptor activator of nuclear factor-kB ligand (RANKL), are critical factors in regulating the differentiation and maturation of osteoclasts, as well as bone resorption [1]

  • Human periodontal ligament fibroblasts (HPDLFs) are the primary cell type in the periodontal ligament and they contribute to the integrity of the periodontium

  • The aim of this study was to explore the influence of IL-10 and elevated glucose concentrations on the expression of OPG and RANKL in HPDLFs

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Summary

Introduction

Osteoprotegerin (OPG) and its ligand, receptor activator of nuclear factor-kB ligand (RANKL), are critical factors in regulating the differentiation and maturation of osteoclasts, as well as bone resorption [1]. The equilibrium between OPG and RANKL activity has an essential role in the homeostasis of bone metabolism. In the pathological process of periodontal disease, the OPG/RANKL equilibrium is disrupted, leading to increased bone resorption [2,3]. HPDLFs express both OPG and RANKL, affecting the formation of osteoclasts by modulating the OPG/RANKL equilibrium [4]. Multiple cytokines, which have different effects on the expression of OPG and RANKL, are involved in the pathogenesis of periodontal disease [5]. The regulatory effect of IL-10 on the expression of OPG and RANKL has not yet been defined

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