Titlebook: Atlas of Osteoporosis; Eric S. Orwoll (Professor of Medicine, Program Dir Book 2003Latest edition Springer Science+Business Media New York

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Genetics of Osteoporosis,rength, which results in fractures from relatively minor trauma. Although osteoporotic fractures are most commonly observed among the elderly, the pathogenesis of osteoporosis starts early in life and involves the interaction of multiple factors [1, 2]. Genetic epidemiologic studies provide descript

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Laboratory Assessment of Skeletal Status,s Paget’s disease of bone. The changes in bone turnover in osteoporosis are small; thus, markers that are not specific to bone were not very useful in investigating this disease. However, assays have recently been introduced that are more specific for bone. In this chapter, we consider the evidence

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Bone Densitometry in Osteoporosis Care,ring bone density were developed several decades ago. The transition of these technologies from the research setting to the patient care arena began as the relationships between bone density and fracture risk were defined and when a definition of postmenopausal osteoporosis, based on bone density va

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Osteoporosis in Men,porosis in men has only recently occurred, and tew data exist concerning its character and etiology. Epidemiologic data indicate that one in four 50-year-old white men will experience an osteoporotic fracture during his remaining lifetime. Thus, osteoporosis in men represents a serious public health

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Osteoporosis Associated with Systemic Illness and Medications,e estrogen deficiency after menopause and advanced age. Ten secondary causes of osteoporosis have been categorized by organ system or systemic disease. Each of these secondary causes is associated with a negative calcium balance or defects in bone formation or resorption at the bone remodeling unit.

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Glucocorticoid-induced Osteoporosis,oplastic, and immunosuppressive properties of glucocorticoids have been useful for treating many diseases. Patients exposed to long-term glucocorticoid therapy have distinct clinical features associated with the suppression of the hypothalamic-pituitary-adrenal axis [1]. Glucocorticoid-induced osteo