Biomedical Engineering Reference
In-Depth Information
Chapter 8
Bacterial Interactions with
Polyaryletheretherketone
Edward T.J. Rochford, David J. Jaekel, Noreen J. Hickok, R. Geoff Richards, T. Fintan Moriarty,
and Alexandra H.C. Poulsson
8.1 Introduction
polymer compared with other biomaterials are not
available.
Regardless of function, location, or biomaterial
used, infection is one of the most serious compli-
cations arising from the use of implanted medical
devices. Every surgical procedure has an inherent
risk for bacterial contamination with surgical site
contaminants originating from the patient's own
skin, the surgical theater or even the outside envi-
ronment. The reason why some patients become
infected and others do not is unfortunately less than
clear. In the majority of cases, host defenses and
prophylactic antibiotic administration effectively
clear any contaminating bacteria. However, in
a certain percentage of cases, the contaminating
bacteria manage to evade these defenses and
successfully survive and multiply in the vicinity of
the implant. When considering elective orthopedic
procedures such as joint replacements and spinal
surgery, the average infection rate remains rela-
tively low, around 5% [1 e 3] . However, for
nonelective, trauma cases involving open wounds,
infections occur in as many as 21% of cases [4] .
Infection is also a significant risk with spinal
fusions (up to 6.7%) where the resulting bone
destruction causes destabilization of the implant and
ultimately the entire spinal segment [5] . All cases of
infection arise from the complex interplay between
the virulence of the contaminating bacteria, the
immune defense mechanisms of the host, and
importantly in the context of the present topic, the
implanted biomaterial itself. Despite the use of
polyaryletheretherketone (PEEK) in medicine for
many years, published clinical infection rates of this
8.1.1 Adhesion: The First Step
Towards Infection
The first step in the development of biomaterial-
associated infection is often considered to be bacte-
rial adhesion to the implant surface. In a worst-case
scenario, an adherent bacterium may multiply and
spread on the surface of the biomaterial, eventually
forming a multilayered community of bacteria
embedded in a self-produced matrix of extracellular
polymeric substance, i.e., a biofilm [6,7] . Following
adhesion, bacteria switch phenotype from a plank-
tonic to a sessile growth form. Part of the alteration in
phenotype involves the upregulation of biofilm-
formation genes [6,8,9] . Biofilm-forming bacteria
begin to produce an encapsulating thick extracellular
polymeric matrix, which both protects the bacteria
against the host immune system and provides an
adhesion site for further bacterial attachment [6,10] .
Inside this matrix, bacteria divide and eventually
form a three-dimensional community ( Fig. 8.1 ) [11] ,
with increased resistance to antibiotic treatments
[12] , which can seed further infections [13] . There-
fore, when an implanted biomaterial becomes colo-
nized with a biofilm, the only remedy is often
removal of the infected material along with the
surrounding tissue (debridement) followed by an
extended course of antibiotic therapy. The occur-
rence of biomaterial-associated infection therefore
increases treatment cost, treatment time, and patient
morbidity [14] . The associated costs of both medical
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