Chemokine proteins continued

Implant loosening invariably leads to clinical failure for a variety of reasons, which includes peri-prosthetic fracture of the implant or the bone adjacent to the implant. Numerous failure mechanisms limit the long-term success of endo-prosthetic implants including aseptic osteolysis, aseptic loosening, infection and implant instability (Holt et al., 2007). The key molecules of the host response at the protein level are chemokines, cytokines, nitric oxide metabolites and metallo-proteinases (Gallo et al., 2014). Aseptic osteolysis and subsequent implant failure occur because of a chronic inflammatory response to implant-derived wear particles. Despite many advances related to materials selection, and operation tool and techniques, aseptic osteolysis continues to limit implant longevity. 

In the foUowing, we wiU describe assays to assess several outcomes of chemokine receptor signaling, starting with G protein activation, secondary messenger production, and P-arrestin recruitment, continuing with further downstream signaUng (e.g., ERK phosphorylation), and finaUy assessing the chemotactic response. 

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