Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway

被引:41
作者
Dong, Ming [1 ]
Yu, Xinxin [1 ]
Chen, Wanfang [1 ]
Guo, Zhenzhen [1 ]
Sui, Linlin [1 ]
Xu, Yuefei [1 ]
Shang, Yuhong [2 ]
Niu, Weidong [3 ]
Kong, Ying [1 ]
机构
[1] Dalian Med Univ, Coll Basic Med Sci, Dalian 116044, Liaoning, Peoples R China
[2] Dalian Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol Renal Dis, Dalian, Peoples R China
[3] Dalian Med Univ, Dept Endodont & Periodont, Dalian 116044, Liaoning, Peoples R China
关键词
Osteopontin; Bone absorption; Periapical periodontitis; NF-kappa B; EPITHELIAL-CELLS; EXPRESSION; MODULATION; KINETICS; LESIONS; RANKL;
D O I
10.1159/000493219
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both bone destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-kappa B was used to pretreat the transfected cells. Results: OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-kappa B pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus. Conclusion: This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-kappa B pathway. (C) 2018 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:884 / 898
页数:15
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