Premium
Dual growth factor‐immobilized asymmetrically porous membrane for bone‐to‐tendon interface regeneration on rat patellar tendon avulsion model
Author(s) -
Kim JoongHyun,
Oh Se Heang,
Min Hyun Ki,
Lee Jin Ho
Publication year - 2018
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.36212
Subject(s) - materials science , biomedical engineering , regeneration (biology) , tendon , membrane , growth factor , microporous material , biophysics , anatomy , microbiology and biotechnology , chemistry , composite material , medicine , biology , biochemistry , receptor
Insufficient repair of the bone‐to‐tendon interface (BTI) with structural/compositional gradients has been a significant challenge in orthopedics. In this study, dual growth factor (platelet‐derived growth factor‐BB [PDGF‐BB] and bone morphogenetic protein‐2 [BMP‐2])‐immobilized polycaprolactone (PCL)/Pluronic F127 asymmetrically porous membrane was fabricated to estimate its feasibility as a potential strategy for effective regeneration of BTI injury. The growth factors immobilized (via heparin‐intermediated interactions) on the membrane were continuously released for up to ∼80% of the initial loading amount after 5 weeks without a significant initial burst. From the in vivo animal study using a rat patellar tendon avulsion model, it was observed that the PDGF‐BB/BMP‐2‐immobilized membrane accelerates the regeneration of the BTI injury, probably because of the continuous release of both growth factors (biological stimuli) and their complementary effect to create a multiphasic structure (bone, fibrocartilage, and tendon) like a native structure, as well as the role of the asymmetrically porous membrane as a physical barrier (nanopore side; prevention of fibrous tissue invasion into the defect site) and scaffold (micropore side; guidance for tissue regeneration). © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 115–125, 2018.