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In the last 5 years, a wide variety of surface modification strategies are explored to improve the integration of poly(etheretherketone) (PEEK) implants with bone. Since PEEK does not support bone on-growth, its surface properties need to be tailored to promote osteogenesis at the bone-implant interface. Surface modifications applied to achieve this response range from simple surface morphology changes to the deposition of osteoconductive coatings. Of the many methods, titanium and/or hydroxyapatite coatings, extrusion to create surface pores, and an accelerated neutral atom beam treatment have been approved by the U.S. Food and Drug Administration to improve the integration of PEEK spinal cages. The success of these surface modifications brings hope for the clinical translation of other techniques in the future, but there are several limitations that may be preventing other treatments from reaching the clinic. This review describes numerous strategies that have been applied to PEEK-based implants for improving their osseointegration and enhancing their antibacterial properties. The review concludes with a discussion about future directions for the field and provides suggestions for advancing clinical translation of surface-modified PEEK implants to improve the lives of patients in need of these implants.
This article was published in the following journal.
Name: Macromolecular bioscience
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An in vivo study examining the functional osseointegration of smooth, rough, and porous surface topographies presenting polyether-ether-ketone (PEEK) or titanium surface chemistry.
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Post-translational modification of proteins with POLY ADENOSINE DIPHOSPHATE RIBOSE.
A poly(A) binding protein that is involved in promoting the extension of the poly A tails of MRNA. The protein requires a minimum of ten ADENOSINE nucleotides in order for binding to mRNA. Once bound it works in conjunction with CLEAVAGE AND POLYADENYLATION SPECIFICITY FACTOR to stimulate the rate of poly A synthesis by POLY A POLYMERASE. Once poly-A tails reach around 250 nucleotides in length poly(A) binding protein II no longer stimulates POLYADENYLATION. Mutations within a GCG repeat region in the gene for poly(A) binding protein II have been shown to cause the disease MUSCULAR DYSTROPHY, OCULOPHARYNGEAL.
Diet modification and physical exercise to improve the ability to carry out daily tasks and perform physical activities.
A poly(ADP-ribose) polymerase that contains two ZINC FINGERS in its N-terminal DNA-binding region. It modifies NUCLEAR PROTEINS involved in chromatin architecture and BASE EXCISION REPAIR with POLY ADENOSINE DIPHOSPHATE RIBOSE.
A poly(A) binding protein that has a variety of functions such as mRNA stabilization and protection of RNA from nuclease activity. Although poly(A) binding protein I is considered a major cytoplasmic RNA-binding protein it is also found in the CELL NUCLEUS and may be involved in transport of mRNP particles.
Osteoporosis is a disease in which the bones become extremely porous, are subject to fracture, and heal slowly, occurring especially in women following menopause and often leading to curvature of the spine from vertebral collapse. Follow and track&n...