Long-term hydrolytic degradation study of polycaprolactone films and fibers grafted with poly(sodium styrene sulfonate): Mechanism study and cell response.

Published on Nov 17, 2020in Biointerphases2.043
· DOI :10.1116/6.0000429
Amélie Leroux4
Estimated H-index: 4
(ISPG: Institut Galilée),
Tuan Ngoc Nguyen1
Estimated H-index: 1
(ISPG: Institut Galilée)
+ 4 AuthorsVéronique Migonney25
Estimated H-index: 25
(ISPG: Institut Galilée)
Sources
Abstract
Polycaprolactone (PCL) is a widely used biodegradable polyester for tissue engineering applications when long-term degradation is preferred. In this article, we focused on the analysis of the hydrolytic degradation of virgin and bioactive poly(sodium styrene sulfonate) (pNaSS) functionalized PCL surfaces under simulated physiological conditions (phosphate buffer saline at 25 and 37 °C) for up to 120 weeks with the aim of applying bioactive PCL for ligament tissue engineering. Techniques used to characterize the bulk and surface degradation indicated that PCL was hydrolyzed by a bulk degradation mode with an accelerated degradation—three times increased rate constant—for pNaSS grafted PCL at 37 °C when compared to virgin PCL at 25 °C. The observed degradation mechanism is due to the pNaSS grafting process (oxidation and radical polymerization), which accelerated the degradation until 48 weeks, when a steady state is reached. The PCL surface was altered by pNaSS grafting, introducing hydrophilic sulfonate groups that increase the swelling and smoothing of the surface, which facilitated the degradation. After 48 weeks, pNaSS was largely removed from the surface, and the degradation of virgin and pNaSS grafted surfaces was similar. The cell response of primary fibroblast cells from sheep ligament was consistent with the surface analysis results: a better initial spreading of cells on pNaSS surfaces when compared to virgin surfaces and a tendency to become similar with degradation time. It is worthy to note that during the extended degradation process the surfaces were able to continue inducing better cell spreading and preserve their cell phenotype as shown by collagen gene expressions.
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