Osteoporosis is a skeletal disease in which bones lose mineral density, making them fragile and more prone to fracture. Peak bone mass is reached by the age of 40, and thereafter is a steady decrease in bone mass of about 0, point, 5-1, percent per year for both men and women. Age-related changes in parathyroid hormone and calcitonin, as well as the production of active vitamin D by the kidneys, contribute to this slow decline in bone mass.
The rate of bone loss increases to 2-3, percent for postmenopausal women and continues for approximately 8-10 years after menopause before reverting back to the previous rate. Thus, postmenopausal women are at a significantly increased risk of suffering from osteoporosis and pathologic fractures. The increased rate of bone loss is partly attributed to a deficiency in estrogen, though the exact mechanism remains unknown.
Dietary calcium supplements, vitamin D, and exercise can all be prescribed to help slow bone loss. Bisphosphonates and estrogen receptor modulators are other options for postmenopausal women suffering from osteoporosis. Patients with severe osteoporosis and an intolerance of bisphosphonates may be candidates for parathyroid hormone therapy. Calcitonin therapy is less preferred because of its relatively modest effect on bone mineral density and fracture prevention.
What is the end effect of calcitonin?
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