scholarly journals A New Synthetic Steroid, Osaterone Acetate (TZP-4238), Increases Cortical Bone Mass and Strength by Enhancing Bone Formation in Ovariectomized Rats

1997 ◽  
Vol 12 (4) ◽  
pp. 590-597 ◽  
Author(s):  
Hiroaki Fuse ◽  
Seiji Fukumoto ◽  
Hideyuki Sone ◽  
Yoshiko Miyata ◽  
Tomoyuki Saito ◽  
...  
Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  

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.


2005 ◽  
Vol 20 (10) ◽  
pp. 1742-1755 ◽  
Author(s):  
Hua Zhu Ke ◽  
Hong Qi ◽  
D Todd Crawford ◽  
Hollis A Simmons ◽  
Gang Xu ◽  
...  

2018 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Mohammad Hossein Shahrezaee ◽  
Mostafa Shahrezaee ◽  
Ahmad Oryan ◽  
Seyed Akbar Kamali ◽  
Saeed Sajadi ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wida Razawy ◽  
Celso H. Alves ◽  
Marijke Koedam ◽  
Patrick S. Asmawidjaja ◽  
Adriana M. C. Mus ◽  
...  

AbstractThe IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R−/− mice have similar bone mass as age matched littermate control mice. In contrast, 12-week-old IL-23R−/− mice have significantly lower trabecular and cortical bone mass, shorter femurs and more fragile bones. At the age of 26 weeks, there were no differences in trabecular bone mass and femur length, but most of cortical bone mass parameters remain significantly lower in IL-23R−/− mice. In vitro osteoclast differentiation and resorption capacity of 7- and 12-week-old IL-23R−/− mice are similar to WT. However, serum levels of the bone formation marker, PINP, are significantly lower in 12-week-old IL-23R−/− mice, but similar to WT at 7 and 26 weeks. Interestingly, Il23r gene expression was not detected in in vitro cultured osteoblasts, suggesting an indirect effect of IL-23R. In conclusion, IL-23R deficiency results in temporal and long-term changes in bone growth via regulation of bone formation.


2017 ◽  
Vol 8 ◽  
Author(s):  
Xuqiang Liu ◽  
Xinhua Qu ◽  
Tao Nie ◽  
Zanjing Zhai ◽  
Haowei Li ◽  
...  

2006 ◽  
Vol 55 (4) ◽  
pp. 357-367 ◽  
Author(s):  
Jun IWAMOTO ◽  
Azusa SEKI ◽  
Tsuyoshi TAKEDA ◽  
Yoshihiro SATO ◽  
Harumoto YAMADA ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Jun Iwamoto ◽  
Yoshihiro Sato ◽  
Hideo Matsumoto

The aim of the present study was to examine the influence of gastrectomy (GX) on cortical and cancellous bones in rats. Twenty male Sprague-Dawley rats were randomized into the two groups of 10 animals each: a sham operation (control) group and a GX group. Seven weeks after surgery, the bone mineral content and density (BMC and BMD, resp.) and the mechanical strength of the femur were determined, and bone histomorphometric analyses were performed on the tibia. GX induced decreases in the BMC, BMD, ultimate force, work to failure, and stiffness of the femoral distal metaphysis and the BMC, BMD, and ultimate force of the femoral diaphysis. GX induced a decrease in cancellous bone mass, characterized by an increased osteoid thickness, osteoid surface, osteoid volume, and bone formation. GX also induced a decrease in cortical bone mass, characterized by increased endocortical bone resorption. The GX induced reductions in the bone mass and strength parameters were greater in cancellous bone than in cortical bone. The present study showed that the response of bone formation, resorption, and osteoid parameters to GX and the degree of GX-induced osteopenia and the deterioration of bone strength appeared to differ between cortical and cancellous bones in rats.


Sign in / Sign up

Export Citation Format

Share Document