Thursday, June 21, 2012
Figure 1. Processes that lead to debris particle-induced
osteolysis. As joint
implants wear, debris triggers processes that lead to inflammation and osteolysis.
Together, these processes cause the implant to loosen and fail.
are the primary target of debris particles from an implant. These cells take up
debris via phagocytosis and secrete cytokines and chemokines in response [a]. One of these secreted cytokines, macrophage
colony-stimulating factor 1 (CSF1; M-CSF),
factor 1 receptor (CSF1R;
on osteoclast precursors [b].
M-CSF is present with another factor, receptor
activator of NF-kB ligand (RANKL;
osteoclast precursors differentiate into bone-resorbing osteoclasts [c]. RANKL activates tumor necrosis
factor receptor superfamily member 11a (TNFRSF11A;
and is produced by other cells such as T lymphocytes.
addition to promoting osteoclast generation, the cytokines and chemokines
secreted by the macrophage also attract additional macrophages, osteoclast
precursors and other proinflammatory cells to the area [d].
reported in Mediero et al., adenosine A2A receptor
agonists can block the inflammation- and osteolysis-promoting effects of wear
debris particles and thus have the potential to prevent joint implant failure.