Figure . Wear-debris induced
osteolysis. Wear debris releasing from implants initiates inflammatory
response. Various cells such as neutrophils, macrophages and fibroblasts
will be activated and recruited and release inflammatory cytokines.
Osteoclast progenitor cells will be initiated to differentiate into
osteoclasts. Osteoclasts are activated and responsible for osteocytic
osteolysis.
Current research on improving wear resistance of metallic alloys also
focuses on super-lubricous coating that mimics natural cartilage
function. PVPA is a hydrophilic polymer with a high density of phosphate
groups on the polymer backbone. Phosphate groups have a strong affinity
to metallic surfaces such as aluminum and
titanium[52]. PVPA was once deposited on Ti6Al4V
surface by the evaporation-induced self-assembly method to construct a
cartilage-like super-lubricous surface[53]. The
friction coefficient in the interface between PVPA-modified Ti6Al4V and
PTFE ball in the ball-on-disc machine showed a significant reduction in
friction coefficient (~70%) than unmodified implants.
The coefficient was approximately 0.006 under a contact pressure of 44.2
MPa (initial pressure), which suggests its superlubricity. Such low
friction coefficient can even maintain over a long period (over 8 h).
The wear particles in the interface were superlow owing to the coating
stability and most importantly, the fluid-like manner of the PVPA
coating that allows fast exchange of the water molecules.