Abstract

As our population ages and becomes more sedentary, osteoporosis and its complications encompass greater numbers of people. Osteoporosis begins as osteopenia, which is a reduction of bone mass (i.e., reduction in the quantity of matter comprising bone) without the presence of a fracture. This reduction in bone mass is considered a universal phenomenon of aging. However, osteopenia often progresses to osteoporosis, a condition in which bone mass and strength are severely compromised. Because early symptoms of osteopenia and osteoporosis are negligible, they can progress undetected until a fracture occurs. Osteoporosis is commonly related to a reduction in estrogen that occurs in postmenopausal women. Estrogen deficiency is thought to be detrimental to bone physiology for 2 reasons. First, the efficiency of calcium absorption by the body is diminished. Second, the resorption of bone by osteoclasts is facilitated. In addition to estrogen deficiency, other risk factors for osteoporosis include a lack of physical activity, cigarette smoking, calcium and vitamin D deficiencies, and excessive consumption of caffeine, protein, and alcohol. During childhood and adolescence, bone formation is greater than bone resorption. From adolescence to approximately 30 years of age, the deposition and resorption of bone are essentially equal. Subsequently, bone mass is maximum in both sexes at approximately 30 years of age. However, beyond approximately 30 years of age, bone mineral density begins to decrease, with both men and women losing approximately 0.3% of their skeletal bone calcium per year. As women progress through menopause, their loss of skeletal bone calcium increases to approximately 3% per year. This loss of skeletal bone calcium increases the risk for fracture; for this reason, estrogen replacement therapy and calcium/vitamin D supplementation are prescribed to decrease the risk of fracture by preventing bone mineral density loss after menopause. Textauszug