Fibroblastic activity is an innate function of the host response. In the presence of many percutaneous biomedical implants, this activity becomes uncontrollable, resulting in significant fibrous overgrowth at the soft tissue-implant interface [1]. The aberrant cell growth associated with pathological fibrosis can lead to extensive remodeling and excessive synthesis of extracellular matrix (ECM) components, preventing proper integration [2]. Furthermore, these areas of irregular fibrotic activity can also serve as sites for opportunistic infection [3]. In brief, interfacial fibrosis is often responsible for the ultimate failure and increased risk of infection of percutaneous biomedical implants.

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