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020			_a 1907673288
020			_a9781907673283
040			_cDLC
082			_a616.723 RIZ
100			_aRene Rizzoli _940129
222			_aactivity alendronate Ammann assessment associated bisphosphonates bone density bone formation bone loss Bone Miner Res bone mineral density Bone Quality bone remodeling bone resorption bone strength bone tissue bone turnover calcitonin calcium clinical compared with placebo cortical thickness decreased denosumab Diagnosis of Postmenopausal EnglJ Epidemiology and Diagnosis femoral neck fracture in women fracture risk fractures Figure Genant hip fracture ibandronate incidence increased bone intake Kanis lumbar spine markers menopause microarchitecture mineral density BMD nonvertebral fractures osteoclasts osteocytes Osteoporos Int osteoporotic fractures ovariectomized parathyroid hormone Pathophysiology of Postmenopausal patients placebo Postmenopausal Osteoporosis Postmenopausal Osteoporosis Effect postmenopausal women Prevention and Treatment protein Quality and Strength radiograph raloxifene RANKL rats Reproduced with permission risedronate risk factors risk of fracture risk of hip risk of vertebral Rizzoli skeletal strontium ranelate T-score total hip trabecular bone Treatment of Postmenopausal trial vertebral fractures vitamin women with osteoporosis
245			_aAtlas of Postmenopausal Osteoporosis
250			_a3rd edition, illustrated, revised
260			_aLondon _bSpringer Science & Business Media _c2011
300			_a118 pages
511			_aContents: Chapter 1 Pathophysiology of postmenopausal osteoporosis Chapter 2 Epidemiology and diagnosis ofpostmenopausal osteoporosis Chapter 3 Bone quality and strength Chapter 4 Prevention and treatment of postmenopausalosteoporosis Chapter 5 Conclusion Index
520			_aRené Rizzoli Menopause is the time in a woman’s life when reproductive capacity ends. Ovaries decrease their activity and the production of sex hormones ceases. This period may be associated with a large variety of symptoms affecting the cardiovascular and urogenital systems, as well as skin, hair and bone. Bone capital is accumulated by the end of the second decade and remains more or less constant up to the time of menopause. Sex hormone deficiency leads to accelerated bone turnover, a negative balance and microarchitectural deterioration, which compromises bone strength, thereby increasing bone fragility and, thus, fracture risk. By the age of 80, it is estimated that 50% of trab- ular bone will have been lost. Natural menopause occurs between the ages of 45 and 54 years all over the world. This age does not appear to have changed significantly over the centuries. In contrast, since the middle of the 19th century, life expectancy, particularly in women, has increased considerably, with most women living to the age of 80 years or more in many regions of the world. This means that at the age of 50 years, a woman will live for more than 30 years without bone protection by sex hormones. This r- resents more than one-third of a woman’s life. At the age of 50 years, the lifetime risk to experience a fracture is about 50% (ie, one out of two women will have a fracture during this period).
600			_xMedical / Rheumatology _926925
600			_xMedical / Orthopedics _926926
600			_xMedical / Gynecology & Obstetrics _926832
600			_xMedical / Clinical Medicine _926816
600			_xMedical › Rheumatology _932171
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