Templated repair of long bone defects in rats with bioactive spiral-wrapped electrospun amphiphilic polymer/hydroxyapatite scaffolds.
Templated repair of long bone defects in rats with bioactive spiral-wrapped electrospun amphiphilic polymer/hydroxyapatite scaffolds.
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DOI：
10.1021/am508984y
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发表时间：
2015-03-04
影响因子：
9.5
通讯作者：
Song J
中科院分区：
文献类型：
--
作者：
Kutikov AB;Skelly JD;Ayers DC;Song J
Effective repair of critical-size long bone defects presents a significant clinical challenge. Electrospun scaffolds can be exploited to deliver protein therapeutics and progenitor cells, but their standalone application for long bone repair has not been explored. We have previously shown that electrospun composites of amphiphilic poly(D,L-lactic acid)-co-poly(ethylene glycol)-co-poly(D,L-lactic acid) (PELA) and hydroxyapatite (HA) guide the osteogenic differentiation of bone marrow stromal cells (MSCs), making these scaffolds uniquely suited for evaluating cell-based bone regeneration approaches. Here we examine whether the in vitro bioactivity of these electrospun scaffolds can be exploited for long bone defect repair, either through the participation of exogenous MSCs or through the activation of endogenous cells by a low dose of recombinant human bone morphogenetic protein-2 (rhBMP-2). In critical-size rat femoral segmental defects, spiral-wrapped electrospun HA-PELA with pre-seeded MSCs resulted in laminated endochondral ossification templated by the scaffold across the longitudinal span of the defect. Using GFP-labeling, we confirmed that the exogenous MSCs adhered to HA-PELA survived at least 7 days post-implantation, suggesting direct participation of these exogenous cells in templated bone formation. When loaded with 500-ng rhBMP-2, HA-PELA spirals led to more robust but less clearly templated bone formation than MSC-bearing scaffolds. Both treatment groups resulted in new bone bridging over the majority of the defect by 12 weeks. This study is the first demonstration of a stand-alone bioactive electrospun scaffold for templated bone formation in critical-size long bone defects.
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通讯作者：
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