Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.biomaterials.2009.09.078
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dc.titleNeo-vascularization and bone formation mediated by fetal mesenchymal stem cell tissue-engineered bone grafts in critical-size femoral defects
dc.contributor.authorZhang, Z.-Y.
dc.contributor.authorTeoh, S.-H.
dc.contributor.authorChong, M.S.K.
dc.contributor.authorLee, E.S.M.
dc.contributor.authorTan, L.-G.
dc.contributor.authorMattar, C.N.
dc.contributor.authorChoolani, M.
dc.contributor.authorChan, J.
dc.contributor.authorFisk, N.M.
dc.date.accessioned2011-09-15T08:43:46Z
dc.date.available2011-09-15T08:43:46Z
dc.date.issued2010
dc.identifier.citationZhang, Z.-Y., Teoh, S.-H., Chong, M.S.K., Lee, E.S.M., Tan, L.-G., Mattar, C.N., Choolani, M., Chan, J., Fisk, N.M. (2010). Neo-vascularization and bone formation mediated by fetal mesenchymal stem cell tissue-engineered bone grafts in critical-size femoral defects. Biomaterials 31 (4) : 608-620. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biomaterials.2009.09.078
dc.identifier.issn01429612
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/26110
dc.description.abstractTissue-engineered bone grafts (TEBG) require highly osteogenic cell sources for use in fracture repair applications. Compared to other sources of mesenchymal stem cells (MSC), human fetal MSC (hfMSC) have recently been shown to be more proliferative and osteogenic. We studied the functional performance of hfMSC-mediated TEBG in 7 mm rat femoral critical-sized bone defects (CSD). Dynamically-cultured and osteogenically-primed hfMSC seeded onto macroporous poly-e{open}-caprolactone tri-calcium phosphate scaffolds were transplanted into CSDs. After 12 weeks, hfMSC-mediated TEBG induced 2.1× more new bone formation (43.3 ± 10.5 vs. 21.0 ± 7.4 mm3, p < 0.05), with greater compact and woven bone, and a 9.8× increase in stiffness (3.9 ± 1.7 vs. 0.4 ± 0.3 mNm/degree, p < 0.05) compared to acellular scaffolds, such that only animals transplanted with TEBG underwent full fracture repair of the CSD. Although hfMSC survived for <4 weeks, by 4 weeks they were associated with a 3.9× larger vasculature network in the defect area (35.2 ± 11.1 vs. 6.5 ± 3.6 mm3 p < 0.05), suggesting an important role for hfMSC in the promotion of neo-vasculogenesis. We speculate that hfMSC-mediated healing of the CSD by stimulating neo-vascularization through as yet undetermined mechanisms. This proof-of-principle study demonstrates the utility of primitive MSC for bone regeneration, and may be of relevance to vascularization in other areas of regenerative medicine. © 2009 Elsevier Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.biomaterials.2009.09.078
dc.sourceScopus
dc.subjectBone tissue engineering
dc.subjectCritical size defect
dc.subjectFetal mesenchymal stem cells
dc.subjectPoly-caprolactone
dc.subjectRat femur
dc.typeArticle
dc.contributor.departmentOBSTETRICS & GYNAECOLOGY
dc.contributor.departmentMECHANICAL ENGINEERING
dc.description.doi10.1016/j.biomaterials.2009.09.078
dc.description.sourcetitleBiomaterials
dc.description.volume31
dc.description.issue4
dc.description.page608-620
dc.identifier.isiut000273167400004
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