Fibrosis, an immune response that triggers fibroid encapsulation of the polymeric surface of an implant, is a leading cause of biomedical device and implant failure. Researchers at UCI have developed a new methodology for synthesizing polymers that, in addition to being inexpensive and simple to generate, uses unique structural features to discourage the immune response that leads to device failure.
The success of a biomedical implant hinges on its effective incorporation into host tissue. Successful integration occurs when the surrounding tissue, which has been damaged during the implantation process, is able to properly heal and fill with vessels (vascularize) at the tissue-device interface. Fibrosis, one of the leading causes of implant failure, occurs when an immune response triggers the adsorption of proteins at the interface, which leads to fibrotic encapsulation of the device. To minimize this immune response, many devices are coated with biocompatible polymers that reduce protein binding, however, these devices still eventually suffer from fibrosis.
Researchers at UCI have developed a novel method for synthesizing biocompatible polymers. These polymers utilize unique structural features that are generated by curved channels which penetrate through the depth of the biocompatible polymeric matrix, successfully preventing fibrotic encapsulation and encouraging device vascularization. Researchers are applying this technology to improve the lifetime of infusion sets to be over two weeks. Four week mouse studies have been completed resulting in minimal fibrosis. Studies in other mammals are underway.
Working prototype developed and tested in vivo (mouse studies). Studies on additional mammals in progress.