Abstract

The aim of this study was to evaluate osteoclastogenesis signaling in midpalatal suture after rapid maxillary expansion (RME) in rats. Thirty male Wistar rats were randomly assigned to two groups with 15 animals each: control (C) and RME group. RME was performed by inserting a 1.5-mm-thick circular metal ring between the maxillary incisors. The animals were euthanized at 3, 7 and 10 days after RME. qRT-PCR was used to evaluate expression of Tnfsf11 (RANKL), Tnfrsf11a (RANK) and Tnfrsf11b (OPG). Data were submitted to statistical analysis using two-way ANOVA followed by Tukey test (a=0.05). There was an upregulation of RANK and RANKL genes at 7 and 10 days and an upregulation of the OPG gene at 3 and 7 days of healing. Interestingly, an increased in expression of all genes was observed over time in both RME and C groups. The RANKL/OPG ratio showed an increased signaling favoring bone resorption on RME compared to C at 3 and 7 days. Signaling against bone resorption was observed, as well as an upregulation of OPG gene expression in RME group, compared to C group at 10 days. The results of this study concluded that the RANK, RANK-L and OPG system participates in bone remodeling after RME.

Highlights

  • Mechanical stimulation, such as orthodontic/orthopedic treatment, may start and promote bone remodeling [1]

  • There was an upregulation of Tnfrsf11a gene, which encodes Receptor activator of nuclear factor-kappa B (RANK) receptor, in Rapid maxillary expansion (RME) group compared to C group at 7 and 10 days of healing (p

  • Alveolar bone remodeling consists of an interaction of bone resorption by osteoclasts with bone formation by osteoblasts [12]

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Summary

Introduction

Mechanical stimulation, such as orthodontic/orthopedic treatment, may start and promote bone remodeling [1]. Rapid maxillary expansion (RME) is usually used in the treatment of maxillary skeletal constriction. This procedure opens the midpalatal suture, and new bone remodeling and formation occur between palatal bones. In order to achieve bone formation, as well as biological changes and remodeling activities following RME, a previous inflammatory process is required. Mechanical stress evokes biochemical responses and structural changes in several cell types in vivo and in vitro [3]. Osteoblasts and osteoclasts are the main cells responsible for the alveolar bone remodeling and the interaction between these two cell types has been investigated [4]

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