Long-term minodronic acid (ONO-5920/YM529) treatment suppresses increased bone turnover, plus prevents reduction in bone mass and bone strength in ovariectomized rats with established osteopenia

Bone ◽  
2008 ◽  
Vol 43 (5) ◽  
pp. 894-900 ◽  
Author(s):  
Makoto Tanaka ◽  
Hiroshi Mori ◽  
Ryoji Kayasuga ◽  
Yasuo Ochi ◽  
Naoki Kawada ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Turnover ◽  
Bone Strength ◽  
Ovariectomized Rats ◽  
Minodronic Acid

scholarly journals Long-Term Treatment of Lasofoxifene Preserves Bone Mass and Bone Strength and Does Not Adversely Affect the Uterus in Ovariectomized Rats

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 1996-2005 ◽  
Author(s):  
Hua Zhu Ke ◽  
George L. Foley ◽  
Hollis A. Simmons ◽  
Victor Shen ◽  
David D. Thompson
Keyword(s):  
Bone Mass ◽  
Bone Strength ◽  
Term Treatment ◽  
Ovariectomized Rats ◽  
Long Term Treatment

scholarly journals Erratum to Fluoride Treatment Increased Serum IGF-1 Bone Turnover, and Bone Mass, But Not Bone Strength, in Rabbits

1997 ◽  
Vol 61 (4) ◽  
pp. 349-349 ◽  
Author(s):  
C. H. Turner ◽  
L. P. Garetto ◽  
A. J. Dunipace ◽  
W. Zhang ◽  
M. E. Wilson ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Turnover ◽  
Bone Strength ◽  
Fluoride Treatment

Raloxifene preserves bone strength and bone mass in ovariectomized rats.

Endocrinology ◽  
1994 ◽  
Vol 135 (5) ◽  
pp. 2001-2005 ◽  
Author(s):  
C H Turner ◽  
M Sato ◽  
H U Bryant
Keyword(s):  
Bone Mass ◽  
Bone Strength ◽  
Ovariectomized Rats

Fluoride Treatment Increased Serum IGF-1, Bone Turnover, and Bone Mass, but Not Bone Strength, in Rabbits

1997 ◽  
Vol 61 (1) ◽  
pp. 77-83 ◽  
Author(s):  
C. H. Turner ◽  
L. P. Garetto ◽  
A. J. Dunipace ◽  
W. Zhang ◽  
M. E. Wilson ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Turnover ◽  
Bone Strength ◽  
Fluoride Treatment

Turner Syndrome and Osteoporosis: Mechanisms and Prognosis

PEDIATRICS ◽  
1998 ◽  
Vol 102 (Supplement_3) ◽  
pp. 481-485
Author(s):  
Karen Rubin
Keyword(s):  
Bone Mass ◽  
Bone Turnover ◽  
Turner Syndrome ◽  
Bone Defect ◽  
Peak Bone Mass ◽  
Estrogen Therapy ◽  
Late Adolescence ◽  
Dual Photon Absorptiometry ◽  
The Impact

Despite only limited reports of a greater number of fractures during childhood or adulthood, osteoporosis historically has been described as a feature in Turner syndrome, because of the frequent observation of radiographic osteopenia and the coarse trabecular pattern of the carpal bones on radiographs. The pathogenesis of the skeletal demineralization remains unclear, but the data support the concept of an intrinsic bone defect that is then exacerbated by a number of hormonal factors, including the growth-regulating hormones, the gonadal steroids, and possibly the calcium-regulating hormones. The advent of more refined methods, such as single- and dual-photon absorptiometry and dual energy x-ray absorptiometry, has led to improved insights into bone mineral density (BMD) status in Turner syndrome (TS). A major limitation of these projection methods is that they report areal and not true volumetric BMD, resulting in an underestimation of the true BMD in smaller subjects. In assessing BMD in TS, various methods have been used to eliminate the confounding effect of bone size. Some consistent patterns do emerge in persons with TS who are not treated with long-term growth hormone (GH) or estrogen therapy. A significant deficit in cortical bone commonly appears in childhood and usually is associated with a low bone-turnover state. Significant osteopenia at predominantly trabecular sites develops during mid- to late adolescence and persists into adulthood, when it is associated with increased bone turnover. Preliminary BMD data on patients after long-term GH therapy show an absence of osteopenia. With respect to the impact of long-term estrogen therapy, the BMD deficit in adults with TS who have been treated adequately with estrogen, but who have not been treated with GH, is less than it is in those who have been insufficiently treated or not treated at all with estrogen. The available data indicate that long-term GH treatment during the prepubertal and early to midpubertal years optimizes BMD and improves the prognosis for adequate peak bone mass being achieved after a puberty that, most often, has been induced with exogenous estrogen. Long-term treatment with estrogen and progestin that is initiated during mid- to late adolescence and is continued throughout adulthood appears necessary for a normal peak bone mass to be achieved and the BMD to be preserved well beyond the time of peak bone mass. Additional measures to prevent osteoporosis must be used, such as ensuring adequate calcium intake and ample weight-bearing activities, focusing on preventing injuries and avoiding overtreatment with thyroid hormones. Long-term surveillance with measurement of BMD and of bone turnover in a large TS population into their later adult years is necessary before it can be concluded that the osteopenia observed in TS is a nonprogressive asymptomatic bone defect of no clinical consequences.

scholarly journals Altered bone mass, geometry and mechanical properties during the development and progression of type 2 diabetes in the Zucker diabetic fatty rat

2008 ◽  
Vol 199 (3) ◽  
pp. 379-388 ◽  
Author(s):  
Rhonda D Prisby ◽  
Joshua M Swift ◽  
Susan A Bloomfield ◽  
Harry A Hogan ◽  
Michael D Delp
Keyword(s):  
Mechanical Properties ◽  
Type 2 Diabetes ◽  
Bone Mass ◽  
Bone Strength ◽  
Skeletal Tissue ◽  
Glucose Levels ◽  
Zucker Diabetic Fatty Rats ◽  
Short And Long Term

Osteopenia and an enhanced risk of fracture often accompany type 1 diabetes. However, the association between type 2 diabetes and bone mass has been ambiguous with reports of enhanced, reduced, or similar bone mineral densities (BMDs) when compared with healthy individuals. Recently, studies have also associated type 2 diabetes with increased fracture risk even in the presence of higher BMDs. To determine the temporal relationship between type 2 diabetes and bone remodeling structural and mechanical properties at various bone sites were analyzed during pre-diabetes (7 weeks), short-term (13 weeks), and long-term (20 weeks) type 2 diabetes. BMDs and bone strength were measured in the femora and tibiae of Zucker diabetic fatty rats, a model of human type 2 diabetes. Increased BMDs (9–10%) were observed in the distal femora, proximal tibiae, and tibial mid- shafts in the pre-diabetic condition that corresponded with higher plasma insulin levels. During short- and long-term type 2 diabetes, various parameters of bone strength and BMDs were lower (9–26%) in the femoral neck, distal femora, proximal tibiae, and femoral and tibial mid-shafts. Correspondingly, blood glucose levels increased by 125% and 153% during short- and long-term diabetes respectively. These data indicate that alterations in BMDs and bone mechanical properties are closely associated with the onset of hyperinsulinemia and hyperglycemia, which may have direct adverse effects on skeletal tissue. Consequently, disparities in the human literature regarding the effects of type 2 diabetes on skeletal properties may be associated with the bone sites studied and the severity or duration of the disease in the patient population studied.

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