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Rachel A Davey, Michele V Clarke, Suzanne B Golub, Patricia K Russell, and Jeffrey D Zajac

homeostasis. Stimulating the resorption of bone, classically mediated by osteoclasts, releases calcium and phosphate into the blood, while inhibiting bone resorption allows calcium to be deposited within bone by osteoblasts. In addition, osteocytes, the cells

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Viji Vijayan and Sarika Gupta

regulated by a third cell type called ‘osteocytes’ that originate from mesenchymal stem cells through osteoblast lineage differentiation by a process called ‘osteocytogenesis’. Interestingly, only 10–20% of osteoblasts differentiate into osteocytes ( Aubin

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Masaki Nakano, Mika Ikegame, Junko Igarashi-Migitaka, Yusuke Maruyama, Nobuo Suzuki, and Atsuhiko Hattori

is composed of three types of component cells, osteoclasts, osteoblasts and osteocytes, and an intercellular matrix consisting of type I collagen and hydroxyapatite. Osteocytes are the predominant cell type in bone tissue, accounting for more than 90

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Jonathan H Gooi, Ling Yeong Chia, Nicole C Walsh, Morten A Karsdal, Julian M W Quinn, T John Martin, and Natalie A Sims

. 2010 ). In addition to any coupling-mediated actions, we found that sCT treatment also increased the expression of sclerostin ( Gooi et al . 2010 ), an inhibitor of bone formation that is secreted by osteocytes. This stimulation of sclerostin by sCT is

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William F Powell Jr, Kevin J Barry, Irena Tulum, Tatsuya Kobayashi, Stephen E Harris, F Richard Bringhurst, and Paola Divieti Pajevic

Introduction Osteocytes are the most abundant cells in bone, outnumbering osteoblasts by 10-fold and osteoclasts by 1000-fold ( Aguirre et al . 2006 ), and yet their function is still incompletely understood. Osteocytes act as

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M Alexandra Sorocéanu, Dengshun Miao, Xiu-Ying Bai, Hanyi Su, David Goltzman, and Andrew C Karaplis

-dose rosiglitazone on the murine skeleton. We show that rosiglitazone impacts negatively on bone remodeling by promoting osteoblast and osteocyte apoptosis. Impairment in bone formation ensues leading to decreased trabecular bone volume and BMD

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M M Conradie, H de Wet, D D R Kotze, J M Burrin, F S Hough, and P A Hulley

loss of osteoblast precursors ( Weinstein et al . 1998 , Zalavras et al . 2003 ), osteocytes ( Weinstein et al . 1998 ), articular ( Van Offel et al . 2002 ) and growth plate chondrocytes ( Silvestrini et al . 2000 , Mehls et al . 2001

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Therese Standal, Rachelle W Johnson, Narelle E McGregor, Ingrid J Poulton, Patricia W M Ho, T John Martin, and Natalie A Sims

, and matrix-embedded osteocytes. PTH acts directly at each stage of differentiation, as follows. PTH promotes pre-osteoblast differentiation ( Dobnig & Turner 1995 ), inhibits osteoblast apoptosis ( Jilka et al . 1999 ), and reactivates quiescent

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Ichiro Kaneko, Rimpi K Saini, Kristin P Griffin, G Kerr Whitfield, Mark R Haussler, and Peter W Jurutka

) near or remote to each target gene ( Haussler et al . 2013 ). Fibroblast growth factor 23 (FGF23) is an osteoblast/osteocyte-elaborated, phosphaturic hormone that feedback represses CYP27B1 and induces CYP24A1 to limit the levels of active 1,25D

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Terhi J Heino, Andrei S Chagin, and Lars Sävendahl

by the direct action of estrogens on classical ERs. ERα is expressed in osteoblasts and osteocytes in vitro and in vivo ( Eriksen et al . 1988 , Komm et al . 1988 , Braidman et al . 1995 , Kusec et al . 1998 , Zaman et al . 2006 ). Mature