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Macrophage responses to 316L stainless steel and cobalt chromium alloys with different surface topographies
Author(s) -
Anderson Jordan A.,
Lamichhane Sujan,
Mani Gopinath
Publication year - 2016
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.35808
Subject(s) - materials science , macrophage , secretion , biomaterial , substrate (aquarium) , adhesion , cytokine , biophysics , metal , nitric oxide , alloy , composite material , metallurgy , immunology , nanotechnology , in vitro , biology , medicine , biochemistry , ecology
The surface topography of a biomaterial plays a vital role in determining macrophage interactions and influencing immune response. In this study, we investigated the effect of smooth and microrough topographies of commonly used metallic biomaterials such as 316 L stainless steel (SS) and cobalt‐chromium (CoCr) alloys on macrophage interactions. The macrophage adhesion was greater on CoCr compared to SS, irrespective of their topographies. The macrophage activation and the secretion of most pro‐inflammatory cytokines (TNF‐α, IL‐6, and IP‐10) were greater on microrough surfaces than on smooth surfaces by day‐1. However, by day‐2, the macrophage activation on smooth surfaces was also significantly increased up to the same level as observed on the microrough surfaces, with more amount of cytokines secreted. The secretion of anti‐inflammatory cytokine (IL‐10) was significantly increased from day‐1 to day‐2 on all the alloy surfaces with the effect most prominently observed on microrough surfaces. The production of nitric oxide by the macrophages did not show any major substrate‐dependent effect. The foreign body giant cells formed by macrophages were least observed on the microrough surfaces of CoCr. Thus, this study demonstrated that the nature of material (SS or CoCr) and their surface topographies (smooth or microrough) strongly influence the macrophage responses. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 2658–2672, 2016.