Abstract
Objectives Dipeptidyl peptidase-4 (DPP-4) inhibitors are used as a treatment for type 2 diabetes mellitus and have also recently been applied to enhance bone quality and density, and increase the expression of bone markers. This study aimed to investigate the effect of a DPP-4 inhibitor on orthodontic tooth movement (OTM) and related root resorption in a mouse model. Materials and Methods Mice were randomly divided into three groups: those undergoing OTM with the addition of a DPP-4 inhibitor (30 μg), those undergoing OTM and receiving phosphate-buffered saline (PBS), and those without force loading (control group). OTM was achieved by means of a nickel–titanium closed coil spring that moved the first molar in a mesial direction for 12 days. The distance of OTM was measured using silicone impression. Maxillae were removed for histological analysis or real-time PCR analysis. Results The distance of OTM and the number of osteoclasts were significantly decreased after administration of the DPP-4 inhibitor, which also significantly suppressed the number of odontoclasts and root resorption after OTM. Furthermore, the mRNA expression of tumour necrosis factor-α (TNF-α) and the receptor activator of nuclear factor kappa-B ligand (RANKL) were decreased in DPP-4 inhibitor-treated mice compared with those receiving PBS and control animals. Conclusion The DPP-4 inhibitor inhibited tooth movement and associated root resorption by blocking the formation of osteoclasts and odontoclasts, respectively. It also appeared to inhibit osteoclastogenesis and odontoclastogenesis by suppressing the expression of TNF-α and/or RANKL.
Highlights
Type 2 diabetes mellitus is a major public health issue, and the number of patients is increasing worldwide
A Dipeptidyl peptidase-4 (DPP-4) inhibitor had a protective effect against tumour necrosis factor (TNF)-α-induced chondrocyte senescence [7], while we previously showed that a DPP-4 inhibitor inhibited lipopolysaccharide (LPS)-induced osteoclast formation and bone resorption by decreasing LPSinduced tumour necrosis factor-α (TNF-α) expression in macrophages [8]
Our current analysis showed that receptor activator of nuclear factor kappa-B ligand (RANKL) and TNF-α mRNA expression in alveolar bone was inhibited in mice receiving the DPP-4 inhibitor compared with phosphate-buffered saline (PBS)-administered mice
Summary
Type 2 diabetes mellitus is a major public health issue, and the number of patients is increasing worldwide. Hidayat et al argued that it was no effects of DPP-4 inhibitors on the risk of fracture according to cumulative real-world evidence [5]. In animal experiments, it was exhibited positive effects on bone metabolism by enhancing bone quality and density, and the expression of bone markers [6]. A DPP-4 inhibitor had a protective effect against tumour necrosis factor (TNF)-α-induced chondrocyte senescence [7], while we previously showed that a DPP-4 inhibitor inhibited lipopolysaccharide (LPS)-induced osteoclast formation and bone resorption by decreasing LPSinduced TNF-α expression in macrophages [8]
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