A common component of the foreign-body response to implanted materials is t
he presence of adherent macrophages that fuse to form foreign-body giant ce
lls (FBGCs). These multinucleated cells have been shown to concentrate the
phagocytic and degradative properties of macrophages at the implant surface
and are responsible for the damage and failure of the implant. Therefore,
the modulation of the presence or actions of macrophages and FBGCs at the m
aterial-tissue interface is an extensive area of recent investigations. A p
ossible mechanism to achieve this is through the induction of the apoptosis
of adherent macrophages, which results in no inflammatory consequence. We
hypothesize that the induction of the apoptosis of biomaterial adherent cel
ls can be influenced by the chemistry of the surface of adhesion. Herein, w
e demonstrate that Surfaces displaying hydrophilic and anionic chemistries
induce apoytosis of adherent macrophages at a higher magnitude than hydroph
obic or cationic surfaces. Additionally, the level of apoptosis for a given
surface is inversely related to that surface's ability to promote the fusi
on of macrophages into FBGCs. This suggests that macrophages fuse into FBGC
s to escape apoptosis. (C) 2001 John Wiley & Sons, Inc.