Journal
JOURNAL OF ORTHOPAEDIC RESEARCH
Volume 35, Issue 4, Pages 812-819Publisher
WILEY
DOI: 10.1002/jor.23339
Keywords
trabecular bone; cortical bone; difference; Wnt/beta-caten; bone remodeling
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Funding
- Foundation of State Key Laboratory of Trauma, Burns and Combined Injury [SKLZZ201124]
- National Science Foundation of China [81271935]
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Trabecular bone and cortical bone have different bone remodeling levels, and the underlying mechanisms are not fully understood. In the present study, the expression of Wnt/beta-catenin signaling and its downstream molecules along with bone mass in trabecular and cortical bone were compared in wild-type mice, constitutive activation of beta-catenin (CA-beta-catenin) mice and beta-catenin deletion mice. It was found that the expression level of most of the examined genes such as Wnt3a, beta-catenin, osteocalcin and RANKL/OPG ratio were significantly higher in trabecular bone than in cortical bone in wild-type mice. CA-beta-catenin resulted in up-regulated expression of the above-mentioned genes except for RANKL/OPG ratio, which were down-regulated. Also, CA-beta-catenin led to increased number of osteoblasts, decreased number of osteoclasts and increased bone mass in both the trabecular bone and cortical bone compared with wild-type mice; however, the extent of changes was much greater in the trabecular bone than in the cortical bone. By contrast, null beta-catenin led to down-regulated expression of the above-mentioned genes except for RANKL/OPG ratio. Furthermore, beta-catenin deletion led to decreased number of osteoblasts, increased number of osteoclasts and decreased bone mass when compared with wild-type mice. Again, the extent of these changes was more significant in trabecular bone than cortical bone. Taken together, we found that the expression level of Wnt/beta-catenin signaling and bone remodeling-related molecules were different in cortical bone and trabecular bone, and the trabecular bone was more readily affected by changes in the Wnt/-catenin signaling pathway. (C) 2016 Orthopaedic Research Society.
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