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Mediators of Inflammation
Volume 2016 (2016), Article ID 6430407, 13 pages
Research Article

Disturbed Expression of EphB4, but Not EphrinB2, Inhibited Bone Regeneration in an In Vivo Inflammatory Microenvironment

1Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Shandong University, Jinan, Shandong, China
2Liaocheng People’s Hospital, Liaocheng, Shandong, China
3Jinan Stomatological Hospital, Jinan, Shandong, China
4Department of Periodontology, School of Dentistry, Shandong University, Jinan, Shandong, China
5Department of Oral & Maxillofacial Surgery, Qilu Hospital and Institute of Stomatology, Shandong University, Jinan, Shandong, China
6Department of Endodontology, School of Dentistry, Shandong University, Jinan, Shandong, China

Received 18 September 2016; Accepted 22 November 2016

Academic Editor: Mirella Giovarelli

Copyright © 2016 Li-Li Shen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The important role of ephrinB2-EphB4 signaling pathway in bone remodeling has been well established. However, it is still unclear whether this bidirectional signaling also has effects on the regenerative processes of bone defects created in an inflammatory microenvironment. In this study, an experimental animal model of bone defects treated with lentiviruses was prepared and an inflammatory microenvironment was established. Expression levels of bone marker genes were monitored in the newly formed bone tissue using quantitative reverse transcriptase polymerase chain reaction and western blot. Immunohistochemical (IHC) staining and histomorphometric analysis were also performed to evaluate bone healing processes. Compared with the pLenti6.3-ctrl group, the pLenti6.3-ephb4siRNA group exhibited lower expression levels of bone formation marker genes and a higher level of NFATc1 in the new bone tissue. In addition, the newly formed bone was thinner and the number of giant osteoclasts was higher in the pLenti6.3-ephb4siRNA group than that in the pLenti6.3-ctrl group. In contrast, there was no significant difference between the pLenti6.3-efnb2siRNA group and the pLenti6.3-ctrl group. In conclusion, EphB4 plays an irreplaceable role in bone regeneration in an inflammatory microenvironment, whereas the functional loss of ephrinB2 can be effectively compensated, most possibly by other ephrins with similar chemical structures.