Biomedical Engineering Reference
In-Depth Information
adhesion by producing surfaces with extremes of
wettability have been shown to be successful. For
example, the grafting of polyethylene glycol to poly-
urethane surfaces to increase wettability has been
shown to dramatically decrease E. coli and S. epi-
dermidis adhesion
[100]
. Additionally, surface thio-
cyanation has also been used to decrease wettability,
leading to a 90% reduction in bacterial adhesion
attributed to the altered surface chemistry and not
cytotoxicity
[101]
. However, the relationship between
surface wettability and bacterial adhesion is not
always clear due to the broad variation of bacterial
adhesins and the complexity of physicochemical
interactions in different media. For example, Cunliffe
et al.
[102]
grafted a range of functionalities to glass
and found that bacterial adhesion was species and not
surface hydrophobicity dependent.
Aside from wettability, other physicochemical
forces also play important roles in bacterial adhesion,
as already discussed in Section
8.2
. For this reason,
highly charged surfaces have been investigated as
a means to control bacterial adhesion. In general,
bacteria possess a negatively charged surface
[37]
;
therefore, a negatively charged surface would be
expected to reduce adhesion due to electrostatic
repulsion, while a positively charged surface should
improve adhesion
[103]
. Experimentally, the effect of
surface charge on bacterial adhesion has produced
mixed results
[35,39,98,104]
and may be difficult to
control in physiological fluids, where the effect of
surface charge can be neutralized by ions.
Studies of bacterial adhesion to the specific
surface chemistry of PEEK are somewhat scarce in
the literature. Barton et al.
[105]
compared the
adhesion of S. epidermidis, P. aeruginosa, and E. coli
to PEEK, polyorthoester, polysulfone, polyethylene,
and poly-
L
-lactic acid in both saline and bacterial
growth media solutions. Although the study did not
fully explore the role of topography, bacterial adhe-
sion to PEEK was similar to the other polymers in the
presence of bacterial growth media. Additionally, in
saline, P. aeruginosa adhesion to PEEK was signifi-
cantly lower than to polyethylene and polysulfone.
Although the study by Barton et al. was limited to
comparing single strains of each species to surfaces
in the absence of blood plasma proteins, it concludes
that the surface chemistry of PEEK does not
encourage
present
[106]
. This results in PEEK having a low
surface energy, making it a relatively hydrophobic
material
[107
e
109]
. This low surface energy leads to
the limited osseointegration of PEEK in vivo
[110]
.
To overcome this, the surface treatment of PEEK by
oxygen plasma treatment (Chapter 10) can be applied
to decrease hydrophobicity and thereby enhance
eukaryotic cell adhesion. Oxygen plasma treatment
of PEEK results in an increase in polar functional
groups that leads to an increase in surface wettability.
However, as with any surface modification, the
change in surface chemistry caused by this treatment
could affect bacterial adhesion. The plasma treatment
protocol used by Poulsson et al.
[23]
causes a
decrease in contact angle from 83.4
to 60.0
and
59.0
after 900 and 1800 s of plasma exposure, res-
pectively. We have therefore also evaluated bacterial
adhesion to the novel surface chemistry produced by
plasma treatment of orthopedic grade injection-
molded PEEK in our laboratory. The topography
aspect of this treatment was also previously discussed
in Section
8.3.1
. In phosphate-buffered saline (PBS),
the change in surface chemistry caused by the plasma
treatment resulted in no difference in bacterial
adhesion density for the four strains of S. aureus and
one strain of S. epidermidis tested. The change in
surface chemistry caused by the plasma treatment
was not great enough to elicit a major change in
direct bacterial adhesion in the absence of a condi-
tioning film. This result was then separately
confirmed using plasma-treated PEEK films in
a parallel plate flow chamber. To further explore the
effect of the treatment, the adhesion of two strains of
S. aureus to oxygen plasma-treated injection-molded
orthopedic grade PEEK preconditioned for an hour
with human blood plasma was investigated. The
adhesion of both these strains increased on the 900-
and 1800-s plasma-treated surfaces compared with
untreated PEEK. Additionally, S. aureus caused the
clotting of blood plasma on the treated PEEK
surfaces, thereby providing further attachment sites
for bacteria and amplifying the difference between
adhesion density on untreated and treated surfaces.
Further investigation revealed that the quantity of
adsorbed protein on the material surfaces was similar
after the conditioning period. Therefore, the bacteria
must have reacted to a change in the type or
conformation of adsorbed proteins and not the
amount. It is this change in protein adsorption to the
modified surfaces that improves eukaryotic cell
adhesion and is likely to improve de novo bone
bacterial
adhesion
any more
than
polyethylene.
In theory, the pristine model surface of unmodified
PEEK would have limited polar functional groups
