Theoretical overview: bone development, peak bone mass, bone loss, and fracture risk

Article Abstract:

Osteoporosis (a condition of reduced bone density) is common in postmenopausal women. The factors that determine the extent of osteoporosis and the resulting risk of bone fracture include peak bone mass achieved during adolescence, the ability to maintain peak bone mass prior to menopause, and the rate of bone mass loss after menopause. Females achieve maximal bone mass in the spine and femur by age 15, while bone mass in males continues to increase between ages 15 and 18. There are several different factors that contribute to peak bone mass, including genetic, nutritional, exercise, and environmental factors. One study reported that the daughters of mothers who had bone fractures due to osteoporosis tended to have less bone mass in their lower spines than the daughters of mothers who did not have osteoporosis. Dietary calcium has been the most widely studied nutritional factor in relation to bone density. Inadequate calcium intake and retention can reduce the ability to attain peak bone mass and increase the risk of osteoporosis later in life. Amenorrhea (lack of menstrual bleeding) is common in young female athletes. Studies have reported that these females often have reduced bone mass in the spine. Spinal bone mass may improve after normal menses are restored, but calcium and estrogen supplements cannot restore previously lost bone mass. Other studies have reported that environmental factors, such as smoking and drinking alcohol, may have detrimental effects on peak bone mass. Based on the results of previous studies it seems reasonable to assume that deficient peak bone mass density in adolescent girls may contribute to osteoporosis later in life. However, conclusive scientific data to support this theory are limited. If this theory is true, ways to identify adolescents at risk will need to be developed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Fractures

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Bone mineral density in postmenopausal women treated with L-thyroxine

Article Abstract:

Bone mineral density was assessed in 19 women aged 50 to 75 years, who were past the stage of menopause and were receiving treatment with l-thyroxine. The relationships among changes in bone mineral density, thyroid hormone treatment, and levels of the thyroid hormone calcitonin (important in bone metabolism) were also examined. The results were compared with those obtained in 19 women without thyroid disease. Women treated with l-thyroxine had lower bone density in the lumbar (lower) spine and portions of the thigh bone as compared with untreated women. The calcitonin response, or release of calcitonin following administration of calcium into the circulation, was lower in l-thyroxine-treated women than untreated women. Although thyroxine levels were normal in 16 of 19 treated women, thyroid stimulating hormone levels were low in 13 of 19 women; this suggests that hormone treatment produced greater than physiological levels of l-thyroxine. The group of treated women was then divided into two subgroups: those with and those without a history of hyperthyroidism. Seven of 19 patients had a history of hyperthyroidism, or increased activity of the thyroid gland, and they had reduced bone mineral density in the hip. The remaining 12 patients did not have a significant loss of bone density when considered separately from the seven who had hyperthyroidism. The findings suggest that long-term l-thyroxine treatment is associated with a decrease in bone mineral density in the spine and hip. Subclinical hyperthyroidism, a decreased calcitonin response, and a history of hyperthyroidism may be factors that contribute to the decrease in bone density. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Diseases, Postmenopausal women, Thyroxine

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Effect of calcium on skeletal development, bone loss, and risk of fractures

Article Abstract:

Bone fractures are related to the fragility of the bone and skeletal stress. In turn, bone fragility is related to reduced bone mass, accumulated fatigue damage, and disconnections within the inner bone matrix. Several different factors contribute to reduced bone mass. These factors include a low dietary intake of calcium, sex hormone deficiencies, genetic factors (e.g. small skeletal structure), and lack of physical activity. The amount of calcium in the body may be low because dietary intake is low or because of a lack of absorption of calcium or an increase in the excretion of calcium in the urine. Although calcium is required for normal bone development and maintaining bone mass, it cannot substitute for other essential factors such as estrogen or exercise. Studies have shown that increasing the dietary intake of calcium can slow the loss of bone mass that occurs with aging and it will prevent bone loss associated with calcium deficiency. Calcium has been reported to protect against bone loss in women prior to menopause and in late postmenopause. The results of several studies indicate that a significant number of all osteoporotic bone fractures are related to calcium. More than half of all American women receive less than 500 milligrams of calcium per day. Doses of calcium equal to 1,500 milligrams per day are safe and natural, and are recommended for normal bone growth during adolescence. The same dose is recommended for women who are estrogen-deficient, and 1,000 milligrams per day is recommended for women with normal estrogen levels. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Calcium (Nutrient), Calcium, Dietary

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