However, and consistent with our previous studies that ES-62 suppresses development of joint disease (articular score and joint pathology) in CIA, at least in part by impacting on osteoclastogenesis (reduced osteoclast progenitors [OCPs], cathepsin K expression in joints, ex vivo functional maturation [TRAP+ staining of multinucleated OCs and bone resorption]), we now show that the levels of BM OCPs, a monocyte subset, correlate with joint damage in CIA (Figure 4J) and that microbiome depletion prevents the CIA-induced increase (Figure 4K). Here, CTSK is linked to arthropathy.