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BioMed Research International
Volume 2017, Article ID 1404650, 10 pages
Research Article

Extracorporeal Shock Wave Rebuilt Subchondral Bone In Vivo and Activated Wnt5a/Ca2+ Signaling In Vitro

1Xiamen Chang Gung Hospital, Xiamen, Fujian, China
2Key Lab for Biomedical Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China
3The Fourth Military Medical University, Xi'an, Shaanxi, China
4General Hospital of Chinese People’s Army Police Force, Beijing, China

Correspondence should be addressed to Gengyan Xing; moc.361@8310531ygx

Received 2 April 2017; Revised 14 August 2017; Accepted 29 August 2017; Published 15 October 2017

Academic Editor: Yves Renaudineau

Copyright © 2017 Lai Yu 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.


Background. This study aimed to identify the optimal extracorporeal shock wave (ESW) intensity and to investigate its effect on subchondral bone rebuilt in vivo and Wnt5a/Ca2+ signaling in vitro using an osteoarthritis (OA) rat model and bone marrow mesenchymal stem cells (BMMSCs), respectively. Methods. OA rats treated with (OA + ESW group) or without (OA group) ESW (/group) were compared with healthy controls (control group, ). Gait patterns and subchondral trabecular bone changes were measured. Western blot and quantitative real-time polymerase chain reaction detected protein expression and gene transcription, respectively. Results. The gait disturbances of OA + ESW group were significantly improved compared with the OA group at 6th and 8th weeks. The micro-CT analysis indicated that the BMD, BSV/BV, BV/TV, Tr.S, and Tr.Th are significantly different between OA group and OA + ESW group. Expression of Wnt5a was increased rapidly after ESW treatment at 0.6 bar and peaked after 30 min. Conclusions. ESW were positive for bone remodeling in joint tibial condyle subchondral bone of OA rat. ESW prevented histological changes in OA and prevented gait disturbance associated with OA progression. Optimal intensity of ESW induced changes in BMMSCs via activation of the Wnt5a/Ca2+ signaling pathway.