Biomedical Engineering Reference
In-Depth Information
sample had been in vivo for 6 months. There was no gross tissue reaction aside from the
thin capsule that had formed around the implant. Specifically, there was no purulence
or other evidence of inflammation, and surrounding tissues appeared intact. However,
in vivo fragmentation seems to occur more readily on ta-C riched in three-fold bonding
(more graphitic). There has been one report in the literature of damage to diamond-like
carbon films [139] and another of increased inflammation reported in an in vivo study
of diamond-like nanocomposite-coated stents [140]. Another report suggested that a-C
films can have porosity, depending on the deposition conditions [141] that may have made
them more susceptible to fragmentation. Those reports, along with the results presented
by LaVan et al. [138] strongly suggest that amorphous carbon films with a higher four-fold
bonding character (more diamond-like) are more resistant to in vivo fragmentation, and
those films with more three-fold character (more graphitic) may be susceptible to in vivo
fragmentation.
The tissue responses on ta-C particles were evaluated at 4-day, 8-week, and 6-month
intervals. After 6 months of implantation, the group with 30
μ
m particles showed a foreign
body giant cell reaction with mild fibrosis associated with the particles. In the 10 and 3
μ
m
particle sizes, there was a foreign body giant cell reaction with fibrosis ranging from none
to minimal. There was no evidence of acute inflammation, granulation tissue formation,
or myocyte damage or histologic changes within the nerves, even when the particles were
adjacent to these structures.
AntibacterialBehavior
Besides the ability of the implant surface to allow adhesion and proliferation of protec-
tive host cells, it is also desirable to develop implant coatings that are repellent to bacteria
to minimize the colonization of the implant surface with circulating planktonic bacte-
ria. Bacterial adhesion and colonization are followed by production of bacterial extracel-
lular polymeric matrix and the development of a biofilm that protects bacteria against
host defense, such as leukocytes, immunoglobulins, and complement as well as against
antibiotics. These are often the major reasons for implant-related infections and failure.
Staphylococci
cause the majority of the nosocomial implant-related infections initiated by
adhesion of planktonic bacteria to the implant surface.
The antibacterial behavior on polyethylene terephthalate (PET) coated with a thin layer
of hydrogenated amorphous carbon (a-C:H) was investigated [142]. The capacities of
Staphylococcus aureus
and
Staphylococcus epidermidis
to adhere onto PET are quantitatively
determined by plate counting and gamma-ray counting of
125
I radiolabeled bacteria in
vitro. The results indicate that the adhesion of the two kinds of bacteria to PET is sup-
pressed by a-C:H. From Figure 2.39, the adhesion efficiency of
S. epidermidis
on the coated
surface is only about 14% of that of the untreated PET surface, and that of
S. aureus
is
about 35% of that of the virgin surface. The electrokinetic potentials of the bacterial cells
and substrates are determined by zeta potential measurement. All the substrates and the
bacterial strain have negative zeta potentials. This means that bacterial adhesion is not
mediated by electrostatic interactions. The surface energy components of the various sub-
strates and bacteria are calculated later to obtain the interfacial free energies of adhesion
of
S. aureus
and
S. epidermidis
onto various substrates. It is found that bacterial adhesion is
energetically unfavorable on the a-C:H deposited on PET.
