Disease relevance of Osteoporosis, Postmenopausal

• Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis [1].
• CONTEXT: Risedronate, a potent bisphosphonate, has been shown to be effective in the treatment of Paget disease of bone and other metabolic bone diseases but, to our knowledge, it has not been evaluated in the treatment of established postmenopausal osteoporosis [2].
• Interleukin-6 (IL-6) is a differentiation and growth factor for a variety of cell types and its excessive production plays a major role in the pathogenesis of multiple myeloma and post-menopausal osteoporosis [3].
• PURPOSE: To determine the effectiveness and safety of the bisphosphonate risedronate in preventing bone loss in young women with breast cancer and early menopause induced by chemotherapy who are at major risk for the development of postmenopausal osteoporosis [4].
• To define the potential role of subclinical vitamin D deficiency in postmenopausal bone loss, we analyzed the levels of circulating 25-hydroxyvitamin D (25OHD) in 539 midwestern caucasian women screened for osteoporosis [5].

High impact information on Osteoporosis, Postmenopausal

• CONCLUSIONS: Treatment of postmenopausal osteoporosis with parathyroid hormone (1-34) decreases the risk of vertebral and nonvertebral fractures; increases vertebral, femoral, and total-body bone mineral density; and is well tolerated [6].
• Alendronate in postmenopausal osteoporosis [7].
• Treatment of postmenopausal osteoporosis with calcitriol or calcium [8].
• Our preliminary data suggest that calcium supplementation in the dosage we used is not as effective as estrogen therapy for the prevention of early postmenopausal bone loss [9].
• In order to establish whether the favorable effect of estrogen therapy on postmenopausal bone loss was dose related, we measured sequential changes in the cortical diameters of the metacarpals by radiographic morphometry in 120 normal postmenopausal women who were being treated with ethinyl estradiol in doses ranging from 5 to 50 micrograms daily [10].

Chemical compound and disease context of Osteoporosis, Postmenopausal

• Contributions of aging and estrogen deficiency to postmenopausal bone loss [11].
• These results provide grounds for optimism about the efficacy of combinations of available agents with sodium fluoride for fracture in postmenopausal osteoporosis [12].
• CONCLUSIONS: These data suggest that risedronate therapy is effective and well tolerated in the treatment of women with established postmenopausal osteoporosis [2].
• CONTEXT: Data on the efficacy and safety of ipriflavone for prevention of postmenopausal bone loss are conflicting [13].
• Skeletal uptake of diphosphonate. Method for prediction of post-menopausal osteoporosis [14].

Biological context of Osteoporosis, Postmenopausal

• We studied the effects of oral alendronate, an aminobisphosphonate, on bone mineral density and the incidence of fractures and height loss in 994 women with postmenopausal osteoporosis [15].
• Serum bone Gla-protein: a specific marker for bone formation in postmenopausal osteoporosis [16].
• However, compared with wt littermates female ArKO animals showed a bone remodeling picture consistent with increased bone turnover, much like early postmenopausal osteoporosis in humans [17].
• However, discordant studies have been published and it is still not clear whether VDR genotypes influence bone mass accretion and/or postmenopausal bone loss [18].
• Analysis of gene expression in human bone biopsies by polymerase chain reaction: evidence for enhanced cytokine expression in postmenopausal osteoporosis [19].

Anatomical context of Osteoporosis, Postmenopausal

• Understanding the cellular and biochemical mechanisms responsible for increased depth of osteoclast resorption when estrogen is withdrawn may allow the development of new strategies for preventing postmenopausal bone loss [20].
• To elucidate the role of PTH in postmenopausal bone loss, we studied 33 postmenopausal patients who received total thyroidectomy due to thyroid carcinoma [21].
• Although QBS values were higher in the lumbar region in 39 women with postmenopausal osteoporosis (4.59 +/- 1.45) and in 27 women with HPT (4.30 +/- 1.52), as compared with the normal group (4.28 +/- 1.61), the difference was not statistically significant [22].
• If direct changes in the IL-6 system in bone tissue are involved in postmenopausal bone loss, these changes appear to be below the detection limit of our assay system [23].
• Extraglandular aromatase expression in adipose tissue and skin (via increasing circulating levels of estradiol) and bone (via increasing local estrogen concentrations) is of paramount importance in slowing the rate of postmenopausal bone loss [24].

Gene context of Osteoporosis, Postmenopausal

• Mutation in a gene for type I procollagen (COL1A2) in a woman with postmenopausal osteoporosis: evidence for phenotypic and genotypic overlap with mild osteogenesis imperfecta [25].
• It has been suggested that one of the mechanisms by which estrogen protects against postmenopausal osteoporosis is by modulating the production of cytokines, such as interleukin-1 (IL-1), tumor necrosis factors (TNF), and interleukin-6 (IL-6), in the bone microenvironment [19].
• These results suggest that variation of IRAK1 may be an important determinant of postmenopausal osteoporosis, in part through the mechanism of accelerated postmenopausal bone loss [26].
• Human parathyroid hormone has been approved for the treatment of post-menopausal osteoporosis [27].
• The data also suggest that in normal women a progressive increase in the secretion of IL-1ra contributes to restore a normal IL-1/IL-1ra ratio after the menopause, a phenomenon which, in turn, may play a role in limiting postmenopausal bone loss [28].

Analytical, diagnostic and therapeutic context of Osteoporosis, Postmenopausal

• Using PAF receptor-deficient mice, we evaluated the role of PAF in the development of bone resorption following ovariectomy, a model of postmenopausal osteoporosis [29].
• To quantify the degree to which estrogen replacement therapy prevents postmenopausal osteoporosis, a retrospective study was done comparing the occurrence of fractures in 245 long-term estrogen users and 245 case-matched controls, followed for an average of 17.6 years [30].
• Cyclical clodronate is effective in preventing postmenopausal bone loss: a comparative study with transcutaneous hormone replacement therapy [31].
• Tibolone acts in this animal model for postmenopausal bone loss as an estrogen agonist on bone [32].
• Three monthly intravenous injections of ibandronate in the treatment of postmenopausal osteoporosis [33].

References