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Q: A somewhat frial 76-year-old female visits, her physician's office for an annual checkup. Her social history shows she smokes a pack of cigarettes a day and she is a heavy coffee drinker. She has
had several fractured bones in the last fiv year that required medical attention. During initial examination measurements show that the patient has lost approximately an inch of height over the past year. She has also lost several pounds but states she still wears the same size clothes. Describe the bone changes in this condition on a macro and cellular level?
A: The underlying mechanism in all cases of osteoporosis is an imbalance between bone resorption and bone formation. [ In normal bone, there is constant matrix remodeling of bone; up to 10% of all bone mass may be undergoing remodeling at any point in time. The process takes place in bone multicellular units (BMUs) as first described by Frost in 1963.[43] Bone is resorbed by osteoclast cells (which
derive from the bone marrow), after which new bone is deposited by osteoblast cells.[9] The three main mechanisms by which osteoporosis develops are an inadequate peak bone mass (the skeleton develops insufficient mass and strength during growth), excessive bone resorption, and inadequate formation of new bone during remodeling. An interplay of these three mechanisms underlies the development of fragile bone tissue.[9] Hormonal factors strongly determine the rate of bone resorption; lack of estrogen (e.g. as a result of menopause) increases bone resorption as well as decreasing the deposition of new bone that normally takes place in weight-bearing bones. The amount of estrogen needed to suppress this process is lower than that normally needed to stimulate the uterus and breast gland. The a-form of the estrogen receptor appears to be the most important in regulating bone turnover.[9] In addition to estrogen, calcium metabolism plays a significant role in bone turnover, and deficiency of calcium and vitamin D leads to impaired bone deposition; in addition, the parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH), which increases bone resorption to ensure sufficient calcium in the blood. The role of calcitonin, a hormone generated by the thyroid that increases bone deposition, is less clear and probably not as significant as that of PTH.[9] Osteoblasts, several displaying a prominent Golgi apparatus, actively synthesizing osteoid containing two osteocytes. The activation of osteoclasts is regulated by various molecular signals, of which RANKL (receptor activator for nuclear factor ?B ligand) is one of best studied. ]
Expert answered|emem0910|Points 189|
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Asked 5/10/2012 11:04:13 PM
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