Increased cortical bone mass by treatment with ONO-5334, a cathepsin K inhibitor, is associated with high bone strength compared to alendronate in ovariectomized monkeys

Bone ◽  
2012 ◽  
Vol 50 ◽  
pp. S157
Author(s):  
H. Mori⁎ ◽  
Y. Ochi ◽  
H. Yamada ◽  
Y. Nakanishi ◽  
S. Nishikawa ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Bone Strength ◽  
Cathepsin K ◽  
Cathepsin K Inhibitor ◽  
High Bone ◽  
Cortical Bone Mass

ONO-5334, a cathepsin K inhibitor, improves bone strength by preferentially increasing cortical bone mass in ovariectomized rats

2013 ◽  
Vol 32 (6) ◽  
pp. 645-652 ◽  
Author(s):  
Yasuo Ochi ◽  
Hiroyuki Yamada ◽  
Hiroshi Mori ◽  
Naoki Kawada ◽  
Ryoji Kayasuga ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Bone Strength ◽  
Cathepsin K ◽  
Ovariectomized Rats ◽  
Cathepsin K Inhibitor ◽  
Cortical Bone Mass

Effects of long-term sedentary behaviour on the cortical bone mass and distribution during growth: The HAPPY bone study

2017 ◽  
Author(s):  
Rachel L Duckham ◽  
Timo Rantalainen ◽  
Christine Rodda ◽  
Anna Timperio ◽  
Nicola Hawley ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Sedentary Behaviour ◽  
Cortical Bone Mass

scholarly journals Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
Wild Type ◽  
Mineral Density ◽  
Cortical Bone Mass ◽  
Intermittent Pth

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.

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