Implant Stiffness Leads to Foreign Body Reactions

A new study reveals that surgical implant stiffness is a major cause of foreign body reaction (FBR) inflammatory reactions.

Researchers at the University of Cambridge (United Kingdom) implanted composite foreign bodies—one side as soft as neural tissue and the other as stiff as muscle—into rats' brains to examine the impact of an implant's stiffness on the inflammatory process. The researchers found that both primary rat microglial cells and astrocytes responded to the increased contact stiffness by changes in morphology and upregulation of a multitude of inflammatory genes and proteins, with FBR significantly enhanced around the stiff portions of the implant.

The researchers found that the morphologically, the cells around the stiffer substrate were very flat, whereas those grown on the softer substrate looked much more like normal cells found in the brain. According to the researchers, the results suggest that adapting the surface stiffness of electrodes used as neural implants for the stimulation of nervous tissue could minimize adverse reactions and improve biocompatibility. The study was published early online on February 11, 2014, in Biomaterials.

“Brain tissue is as soft as cream cheese; it is one of the softest tissues in the body, and electrodes are orders of magnitude stiffer. The findings could have major implications for the design of implants used in the brain and other parts of the body,” said study coauthor Kristian Franze. “Our results suggest that in the short term, simply coating existing implants with materials that match the stiffness of the tissue they are being implanted into will help reduce foreign body reactions.”

Implant FBR in the brain can cause the implants to be encapsulated by reactive tissue, which in the CNS consists mainly of microglial cells and astrocytes, which are surrounded by extracellular matrix (ECM). The reactive process, which starts with the activation of glial cells, can damage local neurons, and the subsequent dendritic retraction and neuronal death may contribute to a gradual decline in the function of implanted electrodes.

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