Biomedical implants like breast implants, pacemakers, and orthopedic devices have revolutionized healthcare, yet a substantial number of these implants face rejection by the body and have to be removed. This rejection is primarily due to a little-understood immune process termed the foreign body response (FBR), where the body wraps the implant in scar tissue. While the exact causes of FBR remain largely unclear, it's generally thought to result from the implant's chemical composition. Existing solutions have involved using so-called biocompatible materials that the body tolerates better, although these materials don't completely eliminate FBR risk. Now, researchers have found that suppressing the production of an immune protein could reduce this risk.

In their effort to understand the cause behind the body rejecting biomedical implants, a team of researchers at the University of Arizona College of Medicine – Tucson (Tucson, AZ, USA) have identified a protein that seems to help drive this response. The research revealed that implants create stress points within the body, leading to an exaggerated immune response. As immune cells interact with the implant and nearby tissue, they activate due to increased mechanical stress. These activated immune cells recognize the implant as a foreign object and encase it in a fibrotic capsule. The more intense the immune response, the denser the capsule becomes. In some individuals, this capsule tightens around the implant, compromising its functionality and inducing discomfort. It's estimated that up to 30% of implants are removed because of FBR issues.

To investigate why some individuals develop thicker capsules than others, researchers analyzed capsule samples from 20 patients who had their breast implants removed. Among these, 10 had experienced severe reactions, and 10 had mild responses. The researchers found that a protein RAC2 was abundantly present in samples from patients with severe reactions. When activated by mechanical stress from the implants, immune cells trigger RAC2 and other proteins, which then call more immune cells to the scene, some of which can collaborate to fight off large foreign objects. To corroborate the role of RAC2 in FBR, researchers inhibited RAC2 expression in animal tests, resulting in a marked reduction of FBR levels—by up to three times. Since RAC2 is unique to immune cells, a drug that blocks it could potentially focus solely on immune cells without influencing other cells in the body. The research team is now actively working on developing a more targeted drug version fit for human application.

“Establishing a complete understanding of the molecular mechanisms driving the foreign body response presents the final frontier in developing truly bio-integrative medical devices,” said senior author Geoffrey Gurtner, MD, FACS. “We believe that local targeted therapy is better. Maybe there are ways to conjugate this drug onto an implant with some sort of coating to minimize systemic problems.” 

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