ABSTRACT
There has been a call to reexamine many of our current approaches to controlling biological interactions at surfaces [1,2]. Instead of preparing a surface, having proteins adsorb onto such surfaces, and examining the consequence, the new paradigm requires that we try to mimic what nature does all the time-i.e., design surfaces that will elicit precisely the biological reactions we want and no more. It is not easy to engineer surfaces that will elicit only specific reactions from the biological milieu they are in contact with. A truly biocompatible material is one that will be integrated with the host or one which allows only those pathways that will allow wound healing [1,2]. An obvious conclusion from such requirements is that engineered surfaces must inhibit all forms of nonspecific interactions, including the rejection of proteins that will not be involved in the wound-healing process.
