AI Article Synopsis
- The study investigated how ectopic bone forms in mice's muscles when treated with rhBMP2 and collagen type I.
- Researchers used mRNA in situ hybridization to compare gene expressions between normal bone formation and BMP2-induced bone growth.
- Findings indicated that key molecules regulating embryonic bone development are also present during ectopic bone formation, supporting the idea that both endochondral and intramembranous ossification occur simultaneously in this process.
Article Abstract
We examined the molecular progression of ectopic bone development upon application of recombinant human bone morphogenetic protein-2 (rhBMP2), using a commercial collagen type I carrier, in the hind quarter muscles of mice. We performed a gene expression study using mRNA in situ hybridisation to compare embryonic cartilage and bone formation with BMP2-induced ectopic bone formation. As bone growth can be induced postnatally or in adult animals, we examined the expression of molecules regulating embryonic bone development. We found that the mRNAs of the same molecules, such as Indian hedgehog (IHH), parathyroid hormone (PTH)/PTH-related peptide receptor (PPR) and BMPs, that regulate embryonic cartilage and bone development, are expressed during BMP-induced ectopic bone formation, suggesting parallels in the mechanisms controlling these processes. Our studies support by molecular means the previous findings in rats that BMP2-induced ectopic bone formation in mice undergoes bone development involving both modes, endochondral and intramembranous ossification, simultaneously at different sites of the implant.
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| http://dx.doi.org/10.1080/0897719021000069579 | DOI Listing |
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