Biomedical Engineering Reference
In-Depth Information
reactions [
4
], resulting in oxygen radicals and hydrogen peroxide as intermediate
products as indicated in (
4.5
-
4.8
).
Cathodic Reaction
Hydrogen development (pH < 4):
+
−
+→↑+
2H O
2e
H
2H O.
(4.3)
3
2
2
Oxygen reduction (pH > 4):
−
−
O2HO e
+
+
→
4OH,
(4.4)
2
2
−
•
−
O
+
H O
+
e
→ +
HO
OH ,
(4.5)
2
2
2
•
•
HO
+
H O
→ +
H O
OH,
(4.5a)
2
2
2
2
•
−
−
OH
+→
e
OH ,
(4.6)
−
•
−
HO
+→
e
OH OH ,
+
(4.7)
22
•
−
−
OH
+→
e
OH .
(4.8)
Formation of ROS and H
2
O
2
on the metal implant surface during cathodic half-
reaction of corrosion may have detrimental effects on surrounding tissues and con-
tribute to the complex processes eventually leading to aseptic loosening.
Formation of metal oxide at the interface with the environment is another impor-
tant result of anodic half-reaction. This usually terminates the metal corrosion pro-
cess. Oxide formation is especially important for Ti and Ti-based alloys. The
titanium oxide layer (mainly consisting of TiO
2
) is known to be relatively stable,
and this is believed to be the reason for inactivity of Ti-based materials and their
well-documented biocompatibility. Experimental thickening of TiO
2
layer was
shown to lead to a decreased release of Ti ions [
46
]. However, disruption of the TiO
2
layer immediately renews the corrosion process, resulting in further metal ion
release and ROS formation. Such TiO
2
layer disruption happens when the implant
is exposed to friction with other implant parts or surrounding tissues, especially
with bone tissue. Metal debris induces abrasive wear, causing further TiO
2
layer
breakdown on the implant surface, thus amplifying the corrosion process [
50
] .
Although TiO
2
is considered to be relatively inactive, ROS and H
2
O
2
formed in high
quantities by activated inflammatory cells can modify the TiO
2
layer, since H
2
O
2
in
a phosphate-buffered solution leads to pronounced thickening of the TiO
2
layer [
60
] .
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