Myricetin Prevents Alveolar Bone Loss in an Experimental Ovariectomized Mouse Model of Periodontitis.

Jialiang Huang,Bo Tian,Yufen Qian,Chuanlong Wu,Xiao Zhou,Nian Ma

doi:10.3390/ijms17030422

Jialiang Huang, Bo Tian + Show 4 more

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https://doi.org/10.3390/ijms17030422

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Abstract

Periodontitis is a common chronic inflammatory disease, which leads to alveolar bone resorption. Healthy and functional alveolar bone, which can support the teeth and enable their movement, is very important for orthodontic treatment. Myricetin inhibited osteoclastogenesis by suppressing the expression of some genes, signaling pathways, and cytokines. This study aimed to investigate the effects of myricetin on alveolar bone loss in an ovariectomized (OVX) mouse model of periodontitis as well as in vitro osteoclast formation and bone resorption. Twenty-four healthy eight-week-old C57BL/J6 female mice were assigned randomly to four groups: phosphate-buffered saline (PBS) control (sham) OVX + ligature + PBS (vehicle), and OVX + ligature + low or high (2 or 5 mg∙kg−1∙day−1, respectively) doses of myricetin. Myricetin or PBS was injected intraperitoneally (i.p.) every other day for 30 days. The maxillae were collected and subjected to further examination, including micro-computed tomography (micro-CT), hematoxylin and eosin (H&E) staining, and tartrate-resistant acid phosphatase (TRAP) staining; a resorption pit assay was also performed in vitro to evaluate the effects of myricetin on receptor activator of nuclear factor κ-B ligand (RANKL)-induced osteoclastogenesis. Myricetin, at both high and low doses, prevented alveolar bone resorption and increased alveolar crest height in the mouse model and inhibited osteoclast formation and bone resorption in vitro. However, myricetin was more effective at high dose than at low dose. Our study demonstrated that myricetin had a positive effect on alveolar bone resorption in an OVX mouse model of periodontitis and, therefore, may be a potential agent for the treatment of periodontitis and osteoporosis.

Highlights

Periodontitis is a common chronic inflammatory disease that destroys the supporting structures of the teeth by complex and multifactorial pathogenic processes, which lead to alveolar bone resorption [1,2]
We demonstrated that myricetin inhibited alveolar bone resorption in vivo, which suggests its potential usefulness in the treatment of patients with osteoporosis and periodontitis
We mainly examine the effects of myricetin on alveolar bone loss (ABL) in mouse model of periodontitis, and mechanism caused by the abnormal osteoclast formation and function

Summary

Introduction

Periodontitis is a common chronic inflammatory disease that destroys the supporting structures of the teeth by complex and multifactorial pathogenic processes, which lead to alveolar bone resorption [1,2]. Recent studies have reported that myricetin inhibits osteoclastogenesis and Ti particle-induced osteolysis, indicating it may be potentially useful in the treatment osteoclast-related osteolytic diseases [13,14]. A study in vitro shows the anti-destructive effects of myricetin on human gingival fibroblasts under inflammatory conditions, and the anti-osteoclastogenetic effects of myricetin on the related receptor activators, which suggest that myricetin may have therapeutic effects in periodontal diseases [15]; no studies have been conducted to prove this, and its effect on inhibiting alveolar bone loss are not well understood. We conjecture that myricetin could block ABL, and may have potentially therapeutic effects in the periodontitis and osteoporosis

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