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

2008 ◽  
Vol 87 (4) ◽  
pp. 323-327 ◽  
Author(s):  
R.M. Brennan-Calanan ◽  
R.J. Genco ◽  
G.E. Wilding ◽  
K.M. Hovey ◽  
M. Trevisan ◽  
...  

Studies have suggested that oral bone loss is independently influenced by local and systemic factors, including osteoporosis. This cross-sectional study of 1256 post-menopausal women, recruited from the Buffalo center of the Women’s Health Initiative Observational Study, evaluated the influence of oral infection and age on the associations between osteoporosis and oral bone loss. Systemic bone density was measured by dual-energy x-ray absorptiometry. Alveolar crestal height was measured from standardized dental radiographs. Oral infection was assessed from subgingival plaque samples. Total forearm density [β (SE) = −0.931 (0.447), p = 0.038] and presence of Tannerella forsythensis [β (SE) = 0.125 (0.051), p = 0.015] were independently associated with mean alveolar height among women aged < 70 years after confounder adjustment. Women aged 70+ years had worse oral bone loss, in general, but neither bone density nor oral infection was significantly associated with mean alveolar height in this age group. Systemic bone density and oral infection independently influenced oral bone loss in post-menopausal women aged < 70 years.





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 ◽  
...  

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.



2021 ◽  
Vol 22 (2) ◽  
pp. 596
Author(s):  
Agnes Schröder ◽  
Joshua Gubernator ◽  
Alexandra Leikam ◽  
Ute Nazet ◽  
Fabian Cieplik ◽  
...  

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.



2001 ◽  
Vol 4 (2) ◽  
pp. 263-269 ◽  
Author(s):  
Gordon Turner-Walker ◽  
Unni Syversen ◽  
Simon Mays

The application of medical scanning technologies to archaeological skeletons provides novel insights into the history and potential causes of osteoporosis. The present study investigated bone mineral density (BMD) in medieval skeletons from England and Norway. Comparisons between the two adult populations found no statistically significant differences. This compares with a modern fracture incidence for the femoral neck in women from Norway that is almost three times that in the UK. The pattern of age-related bone loss in medieval men was similar to that seen in men today. In contrast, the pattern in medieval women differed from that of modern young women. On average, medieval women experienced a decrease in BMD at the femoral neck of approximately 23 per cent between the ages of 22 and 35. These losses were partially recovered by age 45, after which BMD values show a decline consistent with post-menopausal bone loss in modern western women. A possible explanation of the rapid decline in BMD in young medieval women is bone loss in connection with pregnancy and lactation in circumstances of insufficient nutrition.



2012 ◽  
Vol 20 (5) ◽  
pp. 559-564 ◽  
Author(s):  
Alison Gartland ◽  
Kristen K Skarratt ◽  
Lynne J Hocking ◽  
Claire Parsons ◽  
Leanne Stokes ◽  
...  


1992 ◽  
Vol 11 (4) ◽  
pp. 492-497 ◽  
Author(s):  
J. M. Pouilles ◽  
F. Tremollieres ◽  
C. Ribot


2018 ◽  
Vol 103 (1) ◽  
pp. 5-15
Author(s):  
Maggie M. Minett ◽  
Lee Weidauer ◽  
Howard E. Wey ◽  
Teresa L. Binkley ◽  
Tianna M. Beare ◽  
...  


2006 ◽  
Vol 17 (8) ◽  
pp. 1165-1173 ◽  
Author(s):  
R. Abraham ◽  
J. Walton ◽  
L. Russell ◽  
R. Wolman ◽  
B. Wardley-Smith ◽  
...  


2008 ◽  
Vol 26 (27) ◽  
pp. 4426-4434 ◽  
Author(s):  
Susan L. Greenspan ◽  
Joel B. Nelson ◽  
Donald L. Trump ◽  
Julie M. Wagner ◽  
Megan E. Miller ◽  
...  

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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