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Spontaneous Healing Capacity of Calvarial Bone Defects in mdx Mice
Version of Record online: 23 JAN 2012
Copyright © 2012 Wiley Periodicals, Inc.
The Anatomical Record
Volume 295, Issue 4, pages 590–596, April 2012
How to Cite
Nakagaki, W. R. and Camilli, J. A. (2012), Spontaneous Healing Capacity of Calvarial Bone Defects in mdx Mice. Anat Rec, 295: 590–596. doi: 10.1002/ar.22412
- Issue online: 12 MAR 2012
- Version of Record online: 23 JAN 2012
- Manuscript Accepted: 20 DEC 2011
- Manuscript Received: 15 SEP 2011
- FAPESP. Grant Numbers: 2007/07638-0, 2008/57041-2
- CAPES/PROEX, Brazil.
- mdx mice;
- bone healing;
- calvarial defect
The mdx mouse is an experimental model widely used for the study of Duchenne muscular dystrophy, which is characterized by the lack of dystrophin and cycles of muscle degeneration/regeneration. Studies demonstrated elevated levels of growth factors and accelerated skin wound repair in these animals. We therefore raised the hypothesis that the bone repair process might also be altered in these animals. Thus, the objective of this study was to evaluate the spontaneous healing of calvarial defects in mdx mice by histomorphometric analysis. Animals (45 days old) were divided into mdx and control groups. A defect measuring 2 mm in diameter was produced surgically in the right parietal bone of each animal. The animals were sacrificed 15, 30, and 60 days after surgery, and the skulls were processed by routine histological procedures. No difference in the volume of new bone inside the defect was observed between the two groups at any of the three postoperative time points. There was also no difference between the different periods of healing when each group was analyzed separately. The lower quality of femoral and calvarial bone in mdx mice reported in previous studies and the similar bone regeneration rates seen in two groups suggest that the healing capacity of calvarial defects was more expressive in mdx mice than in control animals. An increase in the amount of osteogenic factors released by damaged myofibers may have favored osteogenesis during bone defect healing in mdx mice. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.