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Updated: Jul 17, 2025
Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
Interaction pathways of implant metal localized corrosion and macrophage inflammatory reactions
Meng Li1, Jing Wu1, Wenbo Geng1
1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, PR China.
Insights
Localized corrosion of 316L stainless steel implants is worsened by macrophages. This interaction accelerates corrosion and inflammation, impacting implant performance and patient health.
Area of Science:
- Biomaterials Science
- Immunology
- Corrosion Engineering
Background:
- Macrophages are key immune cells involved in peri-implant inflammation.
- Metallic implants, like 316L stainless steel, can undergo localized corrosion.
- The interaction between corrosion products and immune cells is critical for implant success.
Purpose of the Study:
- To investigate the interaction pathways between localized corrosion of 316L stainless steel and macrophages.
- To understand how macrophage inflammatory responses affect implant corrosion.
- To elucidate the synergistic effects promoting corrosion and inflammation.
Main Methods:
- Electrochemical monitoring of 316L stainless steel under inflammatory conditions.
- Utilizing RAW264.7 macrophage cell line, induced to M1 pro-inflammatory phenotype with lipopolysaccharide (LPS).
- Assessing macrophage viability, morphology, and inflammatory marker expression (CD86, TNF-α, IL-6) in relation to corrosion.
Main Results:
- Macrophage presence decreased pitting corrosion resistance of 316L SS by disrupting adsorbed layers.
- Pro-inflammatory M1 macrophages further reduced pitting potential, with corrosion initiating near cells.
- Inflammatory conditions and corrosion accelerated ROS production, damaging surrounding macrophages.
- Corrosion pits induced region-dependent macrophage responses, with lower viability and altered morphology near pits.
- Corrosion stimulated macrophage expression of CD86, TNF-α, IL-6, and intracellular ROS.
- Uneven release of metallic ions (Fe²⁺, Cr³⁺, Ni²⁺) and surface potential stimulated inflammatory responses.
Conclusions:
- A synergistic feedback loop exists between 316L SS localized corrosion and macrophage inflammatory responses.
- This interaction accelerates both corrosion and inflammation, negatively impacting metallic implants.
- Direct evidence of corrosion-macrophage interaction provides insights into implant failure mechanisms.
Abstract:
Macrophages play a central role in immunological responses to metallic species associated with the localized corrosion of metallic implants, and mediating in peri-implant inflammations. Herein, the pathways of localized corrosion-macrophage interactions were systematically investigated on 316L stainless steel (SS) implant metals. Electrochemical monitoring under macrophage-mediated inflammatory conditions showed a decreased pitting corrosion resistance of 316L SSs in the presence of RAW264.7 cells as the cells would disrupt biomolecule adsorbed layer on the metal surface. The pitting potentials were furtherly decreased when the RAW264.7 cells were induced to the M1 pro-inflammatory phenotype by the addition of lipopolysaccharide (LPS), and pitting corrosion preferentially initiated at the peripheries of macrophages. The overproduction of aggressive ROS under inflammatory conditions would accelerate the localized corrosion of 316L SS around macrophages. Under pitting corrosion condition, the viability and pro-inflammatory polarization of RAW264.7 cells were region-dependent, lower viability and more remarkable morphology transformation of macrophages in the pitting corrosion region than the pitting-free region. The pitting corrosion of 316L SS induced high expression of CD86, TNF-α, IL-6 and high level of intracellular ROS in macrophages. Uneven release of metallic species (Fe2+, Cr3+, Ni2+, etc) and uneven distribution of surface overpotential stimulated macrophage inflammatory responses near the corrosion pits. A synergetic effect of localized corrosion and macrophages was revealed, which could furtherly promote localized corrosion of 316L SS and macrophage inflammatory reactions. Our results provided direct evidence of corrosion-macrophage interaction in metallic implants and disclosed the pathways of this mutual stimulation effect.
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