Fabricated titanium surfaces, smooth, rough, and rough-hydrophillic were characterized and implanted.
Fabricated titanium surfaces, smooth, rough, and rough-hydrophillic were characterized and implanted.

Researchers at Virginia Commonwealth University have identified how macrophages respond to surface roughness and hydrophilicity of titanium implants. Macrophages, activated innate immune cells, directly interact with the material’s surface and create a microenvironment that promotes an anti or pro inflammatory response. More specifically, their results demonstrate that a rough, hydrophilic implant can polarize the adaptive immune response to a pro-wound healing phenotype and promote stem cell recruitment and tissue regeneration.

In order to achieve successful implantation, biomaterials are normally assessed by their ability to integrate into biological tissue without causing an immune rejection response. Understanding the healing process is imperative to designing implants with long-term biocompatibility.

There are two stages of the wound healing response: pro-inflammatory and anti-inflammatory; these stages are distinguishable by the macrophage’s phenotype and subsequent recruitment of other factors to the implant. Pro-inflammatory macrophages, for example, chemoattract more immune cells to the site.

In this paper [Hotchkiss et al., Biomaterials(2018), 10.1016/j.biomaterials.2018.08.029]. the researchers fabricated three surfaces: smooth, rough and rough hydrophilic and characterized them by roughness, wettability, and surface chemistry. After implantation, they compared the surfaces’ influence on chemotaxis, macrophage phenotype, and stem cell recruitment/phenotype.

In vivo and in vitro models validated how local and systemic pro-inflammatory markers change in relation to each surface and over time. Those markers increase following hydrophilic, rough titanium implantation. Whereby, the macrophage phenotype M2 (pro-healing) recruits MSC (mesenchymal stem cells) and T-helper cells.  The results of the study suggest that this surface may trigger cells to resolve inflammation and support a faster clinical recovery of the implant site.