In vivo biostability of polysiloxane polyether polyurethanes: Resistance to metal ion oxidation

Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxida...

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Published inJournal of biomedical materials research. Part A Vol. 77A; no. 2; pp. 380 - 389
Main Authors Ward, Bob, Anderson, James, Ebert, Mike, McVenes, Rick, Stokes, Ken
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.05.2006
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Abstract Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20–35% polysiloxane (PS‐20 and PS‐35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS‐35 samples, PS‐20 significantly delayed MIO, while the polysiloxane‐free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS‐20. We could not directly evaluate oxidation in PS‐35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS‐20 decreased. That of microcracked PS‐35 decreased negligibly while that of undamaged PS‐35 increased slightly after 2‐year in vivo. The polysiloxane‐free control was profoundly degraded. PS‐20 has much improved MIO resistance, while that for PS‐35 is highly MIO resistant compared with its polysiloxane‐free control. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
AbstractList Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20–35% polysiloxane (PS‐20 and PS‐35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS‐35 samples, PS‐20 significantly delayed MIO, while the polysiloxane‐free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS‐20. We could not directly evaluate oxidation in PS‐35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS‐20 decreased. That of microcracked PS‐35 decreased negligibly while that of undamaged PS‐35 increased slightly after 2‐year in vivo . The polysiloxane‐free control was profoundly degraded. PS‐20 has much improved MIO resistance, while that for PS‐35 is highly MIO resistant compared with its polysiloxane‐free control. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20-35% polysiloxane (PS-20 and PS-35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS-35 samples, PS-20 significantly delayed MIO, while the polysiloxane-free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS-20. We could not directly evaluate oxidation in PS-35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS-20 decreased. That of microcracked PS-35 decreased negligibly while that of undamaged PS-35 increased slightly after 2-year in vivo. The polysiloxane-free control was profoundly degraded. PS-20 has much improved MIO resistance, while that for PS-35 is highly MIO resistant compared with its polysiloxane-free control.
Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20-35% polysiloxane (PS-20 and PS-35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS-35 samples, PS-20 significantly delayed MIO, while the polysiloxane-free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS-20. We could not directly evaluate oxidation in PS-35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS-20 decreased. That of microcracked PS-35 decreased negligibly while that of undamaged PS-35 increased slightly after 2-year in vivo. The polysiloxane-free control was profoundly degraded. PS-20 has much improved MIO resistance, while that for PS-35 is highly MIO resistant compared with its polysiloxane-free control.Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20-35% polysiloxane (PS-20 and PS-35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS-35 samples, PS-20 significantly delayed MIO, while the polysiloxane-free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS-20. We could not directly evaluate oxidation in PS-35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS-20 decreased. That of microcracked PS-35 decreased negligibly while that of undamaged PS-35 increased slightly after 2-year in vivo. The polysiloxane-free control was profoundly degraded. PS-20 has much improved MIO resistance, while that for PS-35 is highly MIO resistant compared with its polysiloxane-free control.
Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20–35% polysiloxane (PS‐20 and PS‐35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS‐35 samples, PS‐20 significantly delayed MIO, while the polysiloxane‐free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS‐20. We could not directly evaluate oxidation in PS‐35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS‐20 decreased. That of microcracked PS‐35 decreased negligibly while that of undamaged PS‐35 increased slightly after 2‐year in vivo. The polysiloxane‐free control was profoundly degraded. PS‐20 has much improved MIO resistance, while that for PS‐35 is highly MIO resistant compared with its polysiloxane‐free control. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Author Stokes, Ken
McVenes, Rick
Ebert, Mike
Anderson, James
Ward, Bob
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Snippet Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of...
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wiley
istex
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StartPage 380
SubjectTerms Animals
Biocompatible Materials - chemistry
Biocompatible Materials - metabolism
biostability
Cobalt - chemistry
Hydrogen Peroxide - chemistry
In Vitro Techniques
Ions - chemistry
Materials Testing
MIO
Molecular Weight
Oxidants - chemistry
Oxidation-Reduction
polyurethane
Polyurethanes - chemistry
Polyurethanes - metabolism
Prostheses and Implants
Rabbits
silicone modified polyurethane
Siloxanes - chemistry
Siloxanes - metabolism
Surface Properties
Tensile Strength
Title In vivo biostability of polysiloxane polyether polyurethanes: Resistance to metal ion oxidation
URI https://api.istex.fr/ark:/67375/WNG-S6DS3Q8M-F/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjbm.a.30553
https://www.ncbi.nlm.nih.gov/pubmed/16425243
https://www.proquest.com/docview/29565403
https://www.proquest.com/docview/67807150
Volume 77A
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