Age-Related Bone Mineral Density, Bone Loss Rate, Prevalence of Osteoporosis, and Reference Database of Women at Multiple Centers in China

2007 ◽  
Vol 10 (3) ◽  
pp. 276-284 ◽  
Author(s):  
Xiao-Guang Cheng ◽  
Ding-Zhuo Yang ◽  
Qi Zhou ◽  
Tie-Jun Zhuo ◽  
Hua-Chou Zhang ◽  
...  
2017 ◽  
Vol 10 (1) ◽  
Author(s):  
Mitsunori Shioji ◽  
Takehisa Yamamoto ◽  
Takeshi Ibata ◽  
Takayuki Tsuda ◽  
Kazushige Adachi ◽  
...  

1999 ◽  
Vol 84 (9) ◽  
pp. 3058-3063 ◽  
Author(s):  
E. Dennison ◽  
P. Hindmarsh ◽  
C. Fall ◽  
S. Kellingray ◽  
D. Barker ◽  
...  

Exogenous glucocorticoids are known to increase the risk of osteoporosis. However, the contribution made by endogenous circulating cortisol concentrations to adult skeletal status remains unknown. We examined this issue in a sample of 34 healthy men, aged 61–72 yr. Venous blood samples were obtained under standard conditions every 20 min over a 24-h period. Measurements were made of serum cortisol and cortisol-binding globulin. Bone mineral density was measured at the lumbar spine and proximal femur using dual energy x-ray absorptiometry. Measurements were made at baseline and 4 yr later. There was a weak negative association between integrated cortisol concentration and lumbar spine bone density (r = −0.37; P < 0.05); similar relationships (P < 0.05) existed at three of five proximal femoral sites. There were also statistically significant positive associations between the trough cortisol concentration and bone loss rate at the lumbar spine (r = 0.38; P < 0.05), femoral neck (r = 0.47; P < 0.001), and the trochanteric region (r = 0.41; P = 0.02) over the 4-yr follow-up period. The cross-sectional relationships between cortisol concentration and bone density were removed by adjustment for body mass index, but the influence on bone loss rate remained significant after adjusting for adiposity, cigarette smoking, alcohol consumption, dietary calcium intake, physical activity, and serum testosterone and estradiol levels. These observations suggest that the endogenous cortisol profile of healthy elderly men is a determinant of their bone mineral density and their rate of involutional bone loss.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 680-681
Author(s):  
Carlos Isales ◽  
Ke-Hong Ding ◽  
Wendy Bollag ◽  
Meghan McGee-Lawrence ◽  
William Hill ◽  
...  

Abstract Aging is associated with accumulation of various tryptophan degradation products that may having either bone anabolic or catabolic effects. In epidemiologic studies, elevated levels of 3-hydroxyanthranilic acid (3-HAA) are associated with a higher bone mineral density (BMD). We have previously shown that the C57BL/6 mouse loses bone mass with age. Thus, we hypothesized that administering 3-HAA via a daily intraperitoneal (IP) injection would result in preserved or increased BMD. In an IACUC-approved protocol, we injected 26-month-old C57BL/6 mice with either a low dose (0.5 mg) or high dose (5 mg) of 3-HAA IP five days a week for eight weeks. At the end of this time mice were sacrificed and body composition and bone mineral density measured by DigiMus. BMD was significantly lower in the high dose 3-HAA group: 0.0570 + 0.004 vs 0.0473 + 0.006 vs 0.0432 + 0.0075 gm/cm2, (means+SD, Control vs 0.5 mg 3HAA vs 5 mg 3HAA, p=0.004, 0 vs 5.0 mg, n=6-9/group). 3-HAA had no significant impact on body composition (lean body mass: 86.7 + 1.7% vs 86.2 + 2.7% vs 86.1 + 2.0%, Control vs 0.5 mg vs 5.0 mg 3-HAA, p=ns; and fat mass 12.6 + 2.0% vs 13.8 + 2.7% vs 13.9 + 2.0% vs 0.2%, Control vs 0.5 vs 5 mg 3-HAA, p=ns). Thus, 3-HAA did not prevent bone loss in older mice but instead significantly worsened bone loss. 3-HAA is known to have both pro- and anti- oxidant effects depending on the environment. These data would suggest that at the higher concentrations 3-HAA is acting predominantly as a pro-oxidant molecule accelerating age-related bone loss.


2009 ◽  
Vol 400 (1-2) ◽  
pp. 8-13 ◽  
Author(s):  
Zhang-Rong Xu ◽  
Ai-Hong Wang ◽  
Xian-Ping Wu ◽  
Hong Zhang ◽  
Zhi-Feng Sheng ◽  
...  

1999 ◽  
Vol 187 (2) ◽  
pp. 141-147 ◽  
Author(s):  
Tsutomu Kamei ◽  
Kiyoshi Aoyagi ◽  
Tadashi Matsumoto ◽  
Yutaka Ishida ◽  
Kentaro Iwata ◽  
...  

2020 ◽  
Author(s):  
Lungwani Muungo

Although it is well established that estrogen deficiencycauses osteoporosis among the postmenopausalwomen, the involvement of estrogen receptor (ER) in itspathogenesis still remains uncertain. In the presentstudy, we have generated rats harboring a dominantnegative ERa, which inhibits the actions of not only ERabut also recently identified ERb. Contrary to our expectation,the bone mineral density (BMD) of the resultingtransgenic female rats was maintained at the same levelwith that of the wild-type littermates when sham-operated.In addition, ovariectomy-induced bone loss wasobserved almost equally in both groups. Strikingly, however,the BMD of the transgenic female rats, after ovariectomized,remained decreased even if 17b-estradiol(E2) was administrated, whereas, in contrast, the decreaseof littermate BMD was completely prevented byE2. Moreover, bone histomorphometrical analysis ofovariectomized transgenic rats revealed that the higherrates of bone turnover still remained after treatmentwith E2. These results demonstrate that the preventionfrom the ovariectomy-induced bone loss by estrogen ismediated by ER pathways and that the maintenanceof BMD before ovariectomy might be compensatedby other mechanisms distinct from ERa and ERbpathways.


2019 ◽  
Vol 19 (3) ◽  
pp. 259-273 ◽  
Author(s):  
Neelam Kaushal ◽  
Divya Vohora ◽  
Rajinder K Jalali ◽  
Sujeet Jha

Background And Objective:Osteoporosis is a common bone disorder that increases susceptibility to fragility bone fractures. The clinical and public health repercussions of osteoporosis are huge due to the morbidity, mortality, and cost of medical care linked with fragility fractures. Clinical assessment of osteoporotic risk factors can help to identify candidates at an early stage that will benefit from medical intervention and potentially lowering the morbidity and mortality seen with fractures and complications. Given this, research is ongoing to evaluate the association of osteoporosis with some novel or less well-studied risk factors/bio-markers such as uric acid (UA).Discussion:Uric acid’s antioxidant activity has been proposed to be one of the factors responsible for increasing longevity and lowering rates of age-related cancers during primate evolution, the level of which increased markedly due to loss of uricase enzyme activity (mutational silencing). Accumulated evidence shows that oxidative stress is the fundamental mechanism of age-related bone loss and acts via enhancing osteoclastic activity and increasing bone resorption. Antioxidant substances such as ascorbic acid scavenge free radicals are positively related to bone health. Thus, it is hypothesized that uric acid holds bone-protective potential owing to its potent antioxidative property. Several correlation studies have been conducted globally to investigate the relationship between serum uric acid with bone mineral density and osteoporosis. Few pre-clinical studies have tried to investigate the interaction between uric acid and bone mineral density and reported important role played via Runt-related transcription factor 2 (RUNX2)/core-binding factor subunit alpha-1 (CBF-alpha-1), Wingless-related integration site (Wnt)-3a/β-catenin signaling pathway and 11β Hydroxysteroid Dehydrogenase type 1.Conclusion:In this review, the authors provided a comprehensive summary of the literature related to association studies reported in humans as well work done until date to understand the potential cellular and molecular mechanisms that interplay between uric acid and bone metabolism.


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