Vertebral fractures are the hallmark of osteoporosis. They are the most common osteoporotic fracture, with prevalence estimates of 35% to 50% among women older than 50 years. Women with vertebral fractures experience decreased survival and an increased risk of future vertebral, hip, and other nonspinal fractures. It was previously shown that, over an average follow-up of 3.7 years, low bone mineral density (BMD) is associated with an increased risk of vertebral fracture, and that a prevalent vertebral fracture is associated with a 5-fold increased risk of sustaining a new vertebral fracture. The aim of this study [1] was to examine the absolute risk of incident vertebral fractures by spine and hip BMD and prevalent vertebral fracture status over 15 years of follow-up in a population-based cohort of community-dwelling older women.
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Clinical data evidence the strong correlation between fracture risk and serum thyroid-stimulating hormone (TSH). Recent evidence that TSH receptor polymorphisms are associated with low bone mass, and evidence that bone loss occurs in patients with subclinical hyperthyroidism with normal and low TSH levels all support a role for low TSH in the pathogenesis of hyperthyroid osteoporosis, hitherto attributed solely to high circulating levels of thyroid hormones. In mice, TSH receptor deficiency induces a high-turnover osteoporosis, with elevated bone formation and resorption. In cell cultures continually exposed to TSH, both osteoblastic bone formation and osteoclastic bone resorption were suppressed. Recent studies on both mice and human subjects provide compelling evidence that thyroid hormones and TSH have the opposite effects on the skeleton.
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CD200: a new modulator of bone mass which promotes osteoclast fusion and differentiation
14/04/2009 in Cell BiologyMultinucleate osteoclasts originate from the fusion of macrophages, and play a major role in the resorption of bone. Osteoclasts are essential for bone development and remodelling, and increases in the number and/or activity of osteoclasts lead to diseases associated with generalized bone loss, such as osteoporosis, and others associated with localized bone loss, such as rheumatoid arthritis and periodontal disease. Because fusion is a key step in the differentiation of osteoclasts, a detailed understanding of the molecular mechanism of macrophage fusion should help develop strategies to prevent bone loss.
Expression of an estrogen receptor agonist in differentiating osteoblast cultures
07/04/2009 in Clinical dataThe skeleton is a well-recognized target for sex steroids. Bone fragility is notable when sex steroid levels fall in women after menopause, in elderly males, or after sex organ ablation. In such cases, bone loss follows a release from native constraints on bone resorption that largely result from changes in growth regulators expressed by osteoblasts and from opposing effects on osteoblast and osteoclast activation and apoptosis, leading to an overall increase in bone remodeling. Importantly, imbalances in bone remodeling are restored by sex hormone replacement therapy. Osteoblasts respond in direct and indirect ways to estrogens, and express the estrogen receptor.
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