Tissue responses to implanted materials - Biomaterials and Devices for the Circulatory System - page 3

contains a description of the molecular and cellular pathways involved in
these processes.

1.2 Infl ammatory response

Infl ammation is the initial, non-specifi c response of vascularised tissue to a
variety of injuries. It represents the attempt of the body to eliminate the
injuring agent. Our knowledge of the complicated network of molecules
that interconnects different infl ammatory pathways during cardiac surgery
started to expand at a later time following advances in basic sciences. The
infl ammatory response may be local or systemic. Although infl ammation
aims to exercise a healing effect against injury, the immune system may
erroneously attack body tissues at a larger scale than necessary. The infl am-
mation process comprises primarily activation of serum molecular cascades
and responses of endothelium and leucocytes. It may be triggered by stimuli
such as infection, immune reaction, physical injury or foreign bodies (Rock
and Kono, 2008). Figure 1.1 illustrates mediators participating in acute
infl ammatory response.
Implantable materials are perceived as foreign bodies and elicit infl am-
matory response through injury to local tissues, which prompts the host to
repair the damage. The immediate injury results in activation of endothe-
lial cells and increased interaction with activated neutrophils. This process
results in damage of endothelial integrity, increased endothelial permea-
bility and tissue oedema. There is also activation of the coagulation
cascade and components of the immune system. The products of these
responses collectively form a provisional matrix consisting of fi brin, acti-
vated platelets, infl ammatory cells and endothelial cells. The provisional
matrix acts as a site for cell adhesion and provides activating and inhibit-
ing substances to facilitate proliferation within the lesion. The process is
well established and clearly illustrated in coronary stent insertion where
the immediate injury is to vascular endothelium caused by stent strut pen-
etration (Edelman and Rogers, 1998). The infl ammatory response is a part
of normal healing. However, abnormal proliferation of cells and formation
of an extracellular matrix may result in intimal hyperplasia (Farb et al. ,
2004), which can cause signifi cant stenosis and subsequent morbidity. A
similar process is recognised at anastomotic sites in vascular bypass grafts
(Glagov et al. , 1991). One realises the importance of this fact as signifi cant
efforts have been made to design and produce anastomotic devices facili-
tating construction of coronary graft anastomoses (Falk et al. , 2005;
Gummert et al. , 2007).
The infl ammatory response consists of an acute and a chronic phase and
is mediated by a vast array of chemicals released from the injured tissue,
plasma and cells. These include vasoactive agents, plasma proteases (kinins,

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