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.