Consequently, the enhanced osteoclastic activity contributes to a porous endplate that allows for the ingrowth of blood vessels,34,66 and the activated immune cells exacerbate IDD even without infiltrating the disc.79 Strikingly, the conditioned medium from OPN-deficient EPCs could not induce angiogenesis or osteoclastogenesis in vitro but could attract the migration of macrophages through high levels of CCL2 and CCL5, suggesting that macrophages might serve as downstream predominant effectors. The gene discussed is CCL5; the disease is intervertebral disk degenerative disorder.