Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength.

By Charles A. O’Brien, D. Jia, L. Plotkin, T. Bellido, Cara C. Powers, S. Stewart, S. Manolagas, R. Weinstein. Endocrinology, 2004

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Glucocorticoid-induced osteoporosis: pathophysiology and therapy (2007, background): “Glucocorticoids have pro-apoptotic effects on osteoblasts and osteocytes due to activation of caspase 3, a common downstream effector of several apoptotic signaling pathways [23, 24].”
From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “(37) from our group have generated transgenic mice in which osteoblasts and osteocytes are protected from the direct effects of glucocorticoids, by virtue of the fact that they overexpress 11 -HSD type 2, an enzyme that inactivates glucocorticoids.”
Buried alive: How osteoblasts become osteocytes (2006, background): “…matrix metalloproteases, and glucocorticoids) that have an impact on osteoblast apoptosis and/or activity (Babij et al 2003; Winkler et al., 2003; Eswarakumar et al., 2004; Karsdal et al., 2004; O’Brien et al., 2004) and thus indirectly on the decision process to become an osteocyte (or not).”