Effect of soft‐segment chemistry on polyurethane biostability during <i>in vitro</i> fatigue loading

Wiggins, Michael J.; MacEwan, Matt; Anderson, James M.; Hiltner, A.

doi:10.1002/jbm.a.20081

Cited by 81 publications

(62 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5). Although a previous study comparing the oxidation of polyether PUs to a commercial MDI-containing PCNU showed the latter to be more resistant to oxidation both chemically (less chain scission and crosslinking) and physically (less pitting), 35 the present study found that changes in surface structures did occur following treatment with 20% H 2 O 2 . Therefore, degradation must always be discussed in the context of specific PUs and not PUs in general.…”

Section: Discussioncontrasting

confidence: 76%

The interaction between hydrolytic and oxidative pathways in macrophage‐mediated polyurethane degradation

McBane

Santerre

Labow

2007

J Biomedical Materials Res

View full text Add to dashboard Cite

Although relatively resistant to oxidation, polycarbonate-based polyurethanes (PCNUs) are degraded by monocyte-derived macrophages (MDM) by a co-mediated mechanism involving both hydrolytic and oxidative pathways. Since a previous study showed that PCNU pretreatment with H(2)O(2) modulated degradation by esterases, human MDM were used to further elucidate this dual pathway mechanism of degradation for (14)C-radiolabeled PCNUs (synthesized with 1,6-hexane diisocyanate:polycarbonatediol: butanediol with different stoichiometry (HDI431 and HDI321) or another diisocyanate 4,4'-methylene bisphenyl diisocyanate (MDI321)). Scanning electron microscopy of PCNU slips pretreated with 20% H(2)O(2) showed that HDI431 had visible holes with more radiolabel release than from the other PCNUs. When MDM were seeded on H(2)O(2)-treated PCNUs, degradation of HDI321 and MDI321, but not HDI431 was decreased. Esterase activity was inhibited in MDM on all surfaces except MDI321, whereas inhibition of acid phosphatase occurred on all surfaces. The material surface itself, induced H(2)O(2) release from live MDM, with more H(2)O(2) elicited by phorbol myristate acetate treated MDM when cultured on HDI431 but not the other materials. H(2)O(2) pretreatment affected cell function by chemically altering the material surface and MDM-mediated degradation, known to be dependent on surface chemistry. The findings highlight that both oxidative and hydrolytic mechanisms need to be understood in order to tailor material chemistry to produce desired cell responses for in vivo applications.

show abstract

Section: Discussioncontrasting

confidence: 76%

The interaction between hydrolytic and oxidative pathways in macrophage‐mediated polyurethane degradation

McBane

Santerre

Labow

2007

J Biomedical Materials Res

View full text Add to dashboard Cite

show abstract

“…However, in this case, hard segment domains constitute about 40% by weight [24], which is close to the composition where the phases become cocontinuous [10,11]. As a consequence, breakup and yielding of hard domains starts at lower strains and results in a higher level of irreversible deformation.…”

Section: Deformation Modelmentioning

confidence: 92%

Relationship between nanoscale deformation processes and elastic behavior of polyurethane elastomers

Christenson

Anderson

Hiltner

et al. 2005

Polymer

Self Cite

138

124

View full text Add to dashboard Cite

“…Polyurethanes derived their thermoplastic elastomeric properties from this two-phase morphology. 4,24 Wiggins et al 25 reported that the tensile properties of the silicone-modified polyurethanes retained elasticity and modulus of the control polyurethanes.…”

mentioning

confidence: 98%

Biostability and macrophage‐mediated foreign body reaction of silicone‐modified polyurethanes

Christenson

Dadsetan

Anderson

et al. 2005

J Biomedical Materials Res

Self Cite

View full text Add to dashboard Cite

In this study, the effect of soft segment chemistry on the phase morphology and in vivo response of commercial-grade poly(ether urethane) (PEU), silicone-modified PEU (PEU-S), poly(carbonate urethane) (PCU), and silicone-modified PCU (PCU-S) elastomers were examined. Silicone-modified polyurethanes were developed to combine the biostability of silicone with the mechanical properties of PEUs. Results from the infrared spectroscopy confirmed the presence of silicone at the surface of the PEU-S and PCU-S films. Atomic force microscopy phase imaging indicated that the overall two-phase morphology of PEUs, necessary for its thermoplastic elastomeric properties, was not disrupted by the silicone modification. After material characterization, the in vivo foreign body response and biostability of the polyurethanes were studied using a subcutaneous cage implant protocol. The results from the cage implant study indicated that monocytes adhere, differentiate to macrophages which fuse to form foreign body giant cells on all of the polyurethanes. However, the silicone-modified surfaces promoted apoptosis of adherent macrophages at 4 days and high levels of macrophage fusion after 21 days. These results confirm that the surface of a biomaterial may influence the induction of apoptosis of adherent macrophages in vivo and are consistent with previous cell culture studies of these materials. This study validates the use of our standard cell culture protocol to predict in vivo behavior and further supports the hypothesis that interleukin-4 is the primary mediator of macrophage fusion and foreign body giant cell formation in vivo. The impact of these findings on the biostability of polyurethanes is the subject of current investigations. Attenuated total reflectance-Fourier transform infrared analysis of explanted specimens provided evidence of chain scission and crosslinking at the surface of all of the polyurethanes. The silicone modification did not fully inhibit the oxidative biodegradation of the polyether or polycarbonate soft segments; however, the rate of chain scission of PEU-S and PCU-S seemed to be slower than the control polyurethanes. To verify this finding and to quantify the rate of chain scission in order to predict long-term biostability, an in vitro environment that simulated the microenvironment at the adherent cell-material interface was used to accelerate the biodegradation of the polyurethanes. Polyurethane films were treated in vitro for up to 36 days in 20% hydrogen peroxide/0.1M cobalt chloride solution at 37 degrees Celsius. Characterization with attenuated total reflectance-Fourier transform infrared and scanning electron microscopy showed soft segment and hard segment degradation consistent with the chemical changes observed after long-term in vivo treatment. The biostability ranking of these four materials based on rate of chain scission and surface pitting was as follows: PEU < PEU-S PCU < PCU-S. The silicone modification increased the biostability of the PEU and PCU elastomers while maintaining the the...

show abstract

Effect of soft‐segment chemistry on polyurethane biostability during in vitro fatigue loading

Cited by 81 publications

References 22 publications

The interaction between hydrolytic and oxidative pathways in macrophage‐mediated polyurethane degradation

The interaction between hydrolytic and oxidative pathways in macrophage‐mediated polyurethane degradation

Relationship between nanoscale deformation processes and elastic behavior of polyurethane elastomers

Biostability and macrophage‐mediated foreign body reaction of silicone‐modified polyurethanes

Contact Info

Product

Resources

About