Human osteoprotegerin inhibits osteoclasts and promotes hydroxyapatite to repair the mandibular defects in ovariectomized rats.

Feng LIAO; Shi-Bo LIU; Yao LIU; Hang-Hang LIU; Jian HU; Xian LIU

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Human osteoprotegerin inhibits osteoclasts and promotes hydroxyapatite to repair the mandibular defects in ovariectomized rats.

Author: Feng LIAO ¹ ; Shi-Bo LIU ² ; Yao LIU ² ; Hang-Hang LIU ² ; Jian HU ¹ ; Xian LIU ²
Author Information

1. The State Key Laboratory Breeding Base of Basic Science of Stomatology, Hubei Province & Key Laboratory of Oral Biomedicine Wuhan University, Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan 430072, China.
2. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Publication Type:Journal Article
Keywords: bone defect; bone regeneration; gene transfection; osteoporosis; osteoprotegerin
From: West China Journal of Stomatology 2018;36(4):367-371
CountryChina
Language:Chinese
Abstract:
OBJECTIVEThis study aims to investigate the effect of human osteoprotegerin (hOPG) gene-modified rat bone marrow mesenchymal stem cells (rBMSCs) combined with hydroxyapatite (HA) scaffolds on the repair of mandibular defects in ovariectomized rats.
METHODSrBMSCs were transfected with adenovirus carrying pDC316-hOPG-EGFP. The expression of hOPG and the inhibition of osteoclast function were detected by Western blot and bone-grinding experiment respectively. The model of mandibular bone defect in rats with osteoporosis was established; HA, untransfected rBMSCs-conjugated HA, and transfected rBMSCs-conjugated HA scaffolds were implanted into the mandibular bone defects. After six weeks, tartrateresistant acid phosphatase staining and hematoxylin-eosin staining were used to observe the number of osteoclasts and repair of bone defect.
RESULTSAdenovirus carrying hOPG gene in vitro were successfully transfected into rBMSCs. The hOPG with anti-osteoclast activity was expressed by hOPG-rBMSCs, and rBMSCs expressing hOPG combined with HA scaffolds promoted mandibular defect repair.
CONCLUSIONSrBMSCs transfected with hOPG gene inhibited the function of osteoclasts both in vitro and in vivo, and transfected rBMSCs combined with HA scaffolds promoted the repair of mandibular defects in rats with osteoporosis.