Albumin suppresses oxidation of TiNb alloy in the simulated inflammatory environment

Author:

Sotniczuk Agata12ORCID,Kalita Damian1,Chromiński Witold12,Matczuk Magdalena3,Pisarek Marcin4,Garbacz Halina2

Affiliation:

1. NOMATEN Centre of Excellence National Centre for Nuclear Research Otwock Poland

2. Faculty of Materials Science and Engineering Warsaw University of Technology Warsaw Poland

3. Chair of Analytical Chemistry, Faculty of Chemistry Warsaw University of Technology Warsaw Poland

4. Laboratory of Surface Analysis Institute of Physical Chemistry, Polish Academy of Sciences Warsaw Poland

Abstract

AbstractLiterature data has shown that reactive oxygen species (ROS), generated by immune cells during post‐operative inflammation, could induce corrosion of standard Ti‐based biomaterials. For Ti6Al4V alloy, this process can be further accelerated by the presence of albumin. However, this phenomenon remains unexplored for Ti β‐phase materials, such as TiNb alloys. These alloys are attractive due to their relatively low elastic modulus value. This study aims to address the question of how albumin influences the corrosion resistance of TiNb alloy under simulated inflammation. Electrochemical and ion release tests have revealed that albumin significantly enhances corrosion resistance over both short (2 and 24 h) and long (2 weeks) exposure periods. Furthermore, post‐immersion XPS and cross‐section TEM analysis have demonstrated that prolonged exposure to an albumin‐rich inflammatory solution results in the complete coverage of the TiNb surface by a protein layer. Moreover, TEM studies revealed that H2O2‐induced oxidation and further formation of a defective oxide film were suppressed in the solution enriched with albumin. Overall results indicate that contrary to Ti6Al4V, the addition of albumin to the PBS + H2O2 solution is not necessary to simulate the harsh inflammatory conditions as could possibly be found in the vicinity of a TiNb implant.

Funder

Narodowe Centrum Nauki

European Regional Development Fund

Publisher

Wiley

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