Fibrosis, the creation of dense scar tissue, often occurs around implanted medical devices, which inhibits the devices from performing their intended duties.
Researchers from Cambridge-based Massachusetts Institute of Technology and Boston Children's Hospital investigated the biology under fibrosis in an attempt to expand medical devices' lifespan, according to MIT News.
Nature Materials published the study.
Here are five observations:
1. Researchers shut down various parts of the immune system in mice, discovering that the fibrosis process requires the presence of macrophage cells. Without macrophages, scar tissue did not develop around the implanted devices.
2. The researchers found a signaling molecule, called CSF1, which pushes monocytes to differentiate into mature macrophages. Once this differentiation occurs, fibrosis starts.
3. The study demonstrated that blocking cell surface receptors for CSF1 could halt "implant-induced fibrosis from occurring," according to MIT News.
4. The researchers emphasized that blocking CSF1 did not impede other macrophage functions.
5. The study supported that blocking CSF1 receptors stopped fibrosis with alginate ceramic and polystyrene materials.