Glucocorticoid-induced osteoporosis is mediated primarily by activity of glucocorticoid receptors expressed in osteoblasts, osteocytes and osteoclasts. Bone matrix harbors numerous osteocyte lacunae containing osteocytes. Each osteocyte extends numerous dendrites into canaliculi where dendrite tips make contact with dendrites of nearby neighboring osteocytes and form gap junctions between osteocytes. Osteocytes near the bone surface also contact osteoblasts and osteoclasts through dendrites, thereby establishing communication within an entire bone. Curiously, osteocytes themselves have been shown to dissolve bone matrix under several conditions in a process known as osteocytic osteolysis. The estimated surface area of osteocyte lacunae and canaliculi is huge, and the lacuno-canalicular network is well connected to the blood circulation, suggesting that osteocytic osteolysis may function in pathogenesis and treatment of osteoporosis. Glucocorticoids decrease bone formation by osteoblasts and induce apoptosis in osteocytes. Moreover, glucocorticoids reportedly increase the size of osteocyte lacunae, and enhance perilacunar remodeling. In this review, we discuss whether and how osteocytic osteolysis contributes to glucocorticoid-induced osteoporosis using mouse models.
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