Enhanced fibroblast activity at the implant-soft tissue interface is a key concern to the long-term success of many implanted biomaterials. Uncontrolled fibrosis has been shown to dramatically decrease the stability, function, and lifespan of biomedical implants. Fibrosis, defined as the overgrowth of various tissues about the implant, is caused by the excess synthesis of extracellular matrix components, primarily collagen, and often leads to walling off and hardening (calcification) of tissues at the biomaterial interface (1). Fibrosis is currently a major deterrent to stable bone anchored prostheses. These bone anchored mounting systems are designed to surgically attach a prosthesis mounting post directly into a patient’s bone. The attached post protrudes from the bone through the overlying soft tissue of the amputated limb providing an external connection point for the prosthetic. Although the bone anchoring system dramatically improves prosthetic limb mechanical stability, uncontrolled fibrosis at the soft tissue-mounting post interface is a significant problem (2). The fibrosis caused from aberrant cellular growth leads to the formation of irregular skin folds that prevent proper sealing to the bone anchoring post and also serves as a site for opportunistic infection and failure of the prosthetic system.

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