Protecting Orthopaedic Implants from Infection: Antimicrobial Peptide Mel4 Is Non-Toxic to Bone Cells and Reduces Bacterial Colonisation When Bound to Plasma Ion-Implanted 3D-Printed PAEK Polymers

Author:

Kruse Hedi Verena123ORCID,Chakraborty Sudip4,Chen Renxun4ORCID,Kumar Naresh4ORCID,Yasir Muhammad5,Lewin William T.136ORCID,Suchowerska Natalka2ORCID,Willcox Mark D. P.5ORCID,McKenzie David R.123

Affiliation:

1. Arto Hardy Family Biomedical Innovation Hub, Chris O’Brien Lifehouse, Missenden Road, Camperdown, Sydney, NSW 2050, Australia

2. School of Physics, The University of Sydney, Sydney, NSW 2006, Australia

3. Sarcoma and Surgical Research Centre, Chris O’Brien Lifehouse, Missenden Road, Camperdown, Sydney, NSW 2050, Australia

4. School of Chemistry, University of New South Wales, Sydney, NSW 2052, Australia

5. School of Optometry and Vision Science, University of New South Wales, Sydney, NSW 2052, Australia

6. School of Medical Sciences, The University of Sydney, Sydney, NSW 2006, Australia

Abstract

Even with the best infection control protocols in place, the risk of a hospital-acquired infection of the surface of an implanted device remains significant. A bacterial biofilm can form and has the potential to escape the host immune system and develop resistance to conventional antibiotics, ultimately causing the implant to fail, seriously impacting patient well-being. Here, we demonstrate a 4 log reduction in the infection rate by the common pathogen S. aureus of 3D-printed polyaryl ether ketone (PAEK) polymeric surfaces by covalently binding the antimicrobial peptide Mel4 to the surface using plasma immersion ion implantation (PIII) treatment. The surfaces with added texture created by 3D-printed processes such as fused deposition-modelled polyether ether ketone (PEEK) and selective laser-sintered polyether ketone (PEK) can be equally well protected as conventionally manufactured materials. Unbound Mel4 in solution at relevant concentrations is non-cytotoxic to osteoblastic cell line Saos-2. Mel4 in combination with PIII aids Saos-2 cells to attach to the surface, increasing the adhesion by 88% compared to untreated materials without Mel4. A reduction in mineralisation on the Mel4-containing surfaces relative to surfaces without peptide was found, attributed to the acellular portion of mineral deposition.

Funder

National Health and Medical research Council of Australia

Ian Potter Foundation

Arto Hardy Family

Australian Government

Publisher

MDPI AG

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