scholarly journals Relationship Between Pretreatment Rate of Bone Loss and Bone Density Response to Once-Yearly ZOL: HORIZON-PFT Extension Study

2015 ◽  
Vol 30 (3) ◽  
pp. 570-574 ◽  
Author(s):  
Richard Eastell ◽  
Steven Boonen ◽  
Felicia Cosman ◽  
Ian R Reid ◽  
Lisa Palermo ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Extension Study ◽  
Density Response ◽  
Rate Of Bone Loss

Vitamin D receptor polymorphism does not predict bone density or rate of bone loss in perimenopausal danish women

1996 ◽  
Vol 6 (S1) ◽  
pp. 146-146 ◽  
Author(s):  
B. Abrahamsen ◽  
J. Gram ◽  
F. Lund Henriksen ◽  
T. S. Hansen ◽  
M. Hørder ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Density ◽  
Bone Loss ◽  
Vitamin D Receptor ◽  
Vitamin D Receptor Polymorphism ◽  
Rate Of Bone Loss ◽  
Receptor Polymorphism

Osteoporosis and fragility fracture

2018 ◽  
Author(s):  
Kassim Javaid
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Mass ◽  
Fragility Fracture ◽  
Peak Bone Mass ◽  
Early Adulthood ◽  
Multifactorial Disease ◽  
The Uk ◽  
Rate Of Bone Loss

Osteoporosis is defined as a systemic bone disease with reduction in both bone density and microarchitectural integrity, resulting in an increase in fragility fracture risk. It is a multifactorial disease which, through effects on bone formation and resorption, reduces the peak bone mass achieved during early adulthood and increases the rate of bone loss in later adulthood. Osteoporosis is clinically silent until a fragility fracture occurs. There are 3 million patients with osteoporosis in the UK, with over 200 000 fractures per year and 80 000 hip fractures. This chapter addresses the causes, clinical features, diagnosis, and management of osteoporosis.

scholarly journals AT1 and AT2 Receptor Knockout Changed Osteonectin and Bone Density in Mice in Periodontal Inflammation Experimental Model

2021 ◽  
Vol 22 (10) ◽  
pp. 5217
Author(s):  
Maria Laura de Souza Lima ◽  
Caroline Addison Carvalho Xavier de Medeiros ◽  
Gerlane Coelho Bernardo Guerra ◽  
Robson Santos ◽  
Michael Bader ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Experimental Model ◽  
At2 Receptor ◽  
Micro Ct ◽  
Rt Pcr ◽  
Osteoblast Cells ◽  
Periodontal Inflammation ◽  
Bone Trabeculae

Background: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Methods: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). Conclusion: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.

scholarly journals Dietary Salt Accelerates Orthodontic Tooth Movement by Increased Osteoclast Activity

2021 ◽  
Vol 22 (2) ◽  
pp. 596
Author(s):  
Agnes Schröder ◽  
Joshua Gubernator ◽  
Alexandra Leikam ◽  
Ute Nazet ◽  
Fabian Cieplik ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Dietary Salt ◽  
Osteoclast Activity ◽  
Salt Uptake ◽  
Periodontal Bone Loss ◽  
The Impact

Dietary salt uptake and inflammation promote sodium accumulation in tissues, thereby modulating cells like macrophages and fibroblasts. Previous studies showed salt effects on periodontal ligament fibroblasts and on bone metabolism by expression of nuclear factor of activated T-cells-5 (NFAT-5). Here, we investigated the impact of salt and NFAT-5 on osteoclast activity and orthodontic tooth movement (OTM). After treatment of osteoclasts without (NS) or with additional salt (HS), we analyzed gene expression and the release of tartrate-resistant acid phosphatase and calcium phosphate resorption. We kept wild-type mice and mice lacking NFAT-5 in myeloid cells either on a low, normal or high salt diet and inserted an elastic band between the first and second molar to induce OTM. We analyzed the expression of genes involved in bone metabolism, periodontal bone loss, OTM and bone density. Osteoclast activity was increased upon HS treatment. HS promoted periodontal bone loss and OTM and was associated with reduced bone density. Deletion of NFAT-5 led to increased osteoclast activity with NS, whereas we detected impaired OTM in mice. Dietary salt uptake seems to accelerate OTM and induce periodontal bone loss due to reduced bone density, which may be attributed to enhanced osteoclast activity. NFAT-5 influences this reaction to HS, as we detected impaired OTM and osteoclast activity upon deletion.

Prevention of post-menopausal bone loss with transdermal estrogen: analysis of individual bone density changes

1996 ◽  
Vol 6 (S1) ◽  
pp. 227-227
Author(s):  
R. Bakshi ◽  
D. Serrurier ◽  
A-M. Vigneron ◽  
T. Darragon ◽  
M. Audran
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Transdermal Estrogen ◽  
Post Menopausal

Rate of Bone Loss Is Associated with Mortality in Older Women: A Prospective Study

2000 ◽  
Vol 15 (10) ◽  
pp. 1974-1980 ◽  
Author(s):  
Deborah M. Kado ◽  
Warren S. Browner ◽  
Terri Blackwell ◽  
Robert Gore ◽  
Steven R. Cummings
Keyword(s):  
Bone Loss ◽  
Prospective Study ◽  
Older Women ◽  
A Prospective Study ◽  
Rate Of Bone Loss

scholarly journals Skeletal Health After Continuation, Withdrawal, or Delay of Alendronate in Men With Prostate Cancer Undergoing Androgen-Deprivation Therapy

2008 ◽  
Vol 26 (27) ◽  
pp. 4426-4434 ◽  
Author(s):  
Susan L. Greenspan ◽  
Joel B. Nelson ◽  
Donald L. Trump ◽  
Julie M. Wagner ◽  
Megan E. Miller ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Density ◽  
Bone Loss ◽  
Bone Turnover ◽  
Androgen Deprivation Therapy ◽  
Bisphosphonate Therapy ◽  
Androgen Deprivation ◽  
Mineral Density ◽  
Skeletal Health ◽  
Oral Bisphosphonate

Purpose Androgen-deprivation therapy (ADT) for prostate cancer is associated with bone loss and osteoporotic fractures. Our objective was to examine changes in bone density and turnover with sustained, discontinued, or delayed oral bisphosphonate therapy in men receiving ADT. Patients and Methods A total of 112 men with nonmetastatic prostate cancer receiving ADT were randomly assigned to alendronate 70 mg once weekly or placebo in a double-blind, partial-crossover trial with a second random assignment at year 2 for those who initially received active therapy. Outcomes included bone mineral density and bone turnover markers. Results Men initially randomly assigned to alendronate and randomly reassigned at year 2 to continue had additional bone density gains at the spine (mean, 2.3% ± 0.7) and hip (mean, 1.3% ± 0.5%; both P < .01); those randomly assigned to placebo in year 2 maintained density at the spine and hip but lost (mean, −1.9% ± 0.6%; P < .01) at the forearm. Patients randomly assigned to begin alendronate in year 2 experienced improvements in bone mass at the spine and hip, but experienced less of an increase compared with those who initiated alendronate at baseline. Men receiving alendronate for 2 years experienced a mean 6.7% (± 1.2%) increase at the spine and a 3.2% (± 1.5%) at the hip (both P < .05). Bone turnover remained suppressed. Conclusion Among men with nonmetastatic prostate cancer receiving ADT, once-weekly alendronate improves bone density and decreases turnover. A second year of alendronate provides additional skeletal benefit, whereas discontinuation results in bone loss and increased bone turnover. Delay in bisphosphonate therapy appears detrimental to bone health.

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