The foundation of bone health is established by the age of thirty. The peak bone mass acquired in early adulthood serves as a bone reservoir for later life activities. The greater the peak bone mass, the greater the amount of bone loss (due to aging, menopause, etc.) that the body can tolerate without clinical signs of osteoporosis. Peak bone mass accounts for at least half of the change in bone mass in older adults, with subsequent gradual loss of the remaining bone mass. Bone mineral salts are acquired at a rate similar to linear bone growth, with a faster rate of increase in infancy, a slower rate of increase in childhood, and acquisition primarily during adolescence. Approximately 50% of peak bone mass is acquired during adolescence, which makes this a critical period for achieving ideal bone health. However, due to differences in growth patterns, peak bone mineral acquisition lags behind peak height growth rate (PHV) by 8 months. This is a period of increased fracture incidence and the number of fractures has been on the rise for the past three decades. Peak bone mass is largely predetermined by genetic factors. Family and twin studies have shown that 60%?80% of the variation in peak bone mass between individuals is due to genetics. Scholars have also observed differences in bone mass between races. Although some of the differences are clearly due to artifacts of densitometry techniques, it has been demonstrated that healthy blacks at puberty have higher bone density than non-blacks. Although genes including vitamin D and estrogen receptors are thought to be associated with osteoporosis, genes causing osteoporosis or associated genes have not been identified. There may be a link between genes associated with pubertal timing and bone mass acquisition. Lifestyle factors also have a considerable impact on bone mass acquisition and can cause a 20% to 40% difference in bone mass in young adults. Maximum bone mineral gain can only occur when nutrition, physical activity and hormone production are all adequate. Body weight, especially the non-fat component, is strongly associated with BMD in healthy youth. The positive correlation between weight and BMD may reflect common genetic determinants, overall nutritional status, or the effects of mechanical loading on bone. As shown in calcium supplementation experiments, calcium intake affects the rate of bone acquisition. The children’s calcium supplementation group had more bone mineral acquisition than the control group. A recent meta-analysis of calcium supplementation experiments in children? analysis, which had a representative focus on looking at habitual intakes above 700 mg/d in white populations, concluded that the above intakes were small given the positive effects of calcium supplementation on bone mass. The report has been criticized for using bone mineral density rather than bone mineral content as an indicator of observation. The recommended calcium intake was determined based on the amount of calcium intake needed to obtain maximum calcium stores. Differences in calcium stores as a function of intake by race and sex are not associated with differences in the amount of calcium required to obtain optimal calcium stores. Weight-bearing physical activity can stimulate a 5% to 17% increase in bone mineral and can alter bone geometry. Exercise can only increase bone acquisition and bone strength if calcium intake is adequate. And the results depend on the stage of maturation of the body at the beginning of the sport. Normal endocrine function is necessary for ideal bone mineral acquisition. The high correlation between pubertal bone mass and puberty far exceeds the correlation with actual age, reflecting the critical role of sex steroid hormones in bone mass gain. Sex steroid hormone deficiency or resistance can lead to a decrease in peak bone mass. Growth hormone deficiency, hyperthyroidism and glucocorticoid overload are also associated with low bone mass in children and adults. The annual cost of osteoporosis exceeds $20 billion in the United States and $30 billion worldwide. To stem the rising cost of treatment, an effective intervention designed to increase peak bone mass and reduce subsequent bone loss is needed. Adolescent bone health programs include maintaining proper body weight, adequate calcium intake and regular physical activity. Unfortunately, the gap between the recommended and actual calcium intake of Americans continues to widen. More than 90 percent of girls and 50 percent of boys actually consume less than the ideal amount of calcium during adolescence. In addition, exercise among young people in the United States is declining each year, with only half of adolescents (ages 12-21) engaging in regular, vigorous physical activity and 25% reporting no vigorous physical activity. Girls are less physically active than boys and black girls are less physically active than white girls. Bone health is an urgent concern for early bone loss associated with various chronic diseases in adolescence. Anorexia nervosa, exercise-related amenorrhea, cystic fibrosis, braking disorders, and systemic glucocorticoid therapy are all diseases that can jeopardize bone gain, or how much bone is lost, or accelerate bone mineral loss. In patients with severe skeletal fragility, fractures can occur with little or no trauma, a condition known as osteoporosis. It remains uncertain whether timely diagnosis and treatment of bone loss in childhood can be reversed. Efforts to identify ways to fully utilize peak bone mass must continue and be widely publicized, and prevention of osteoporosis should begin in childhood.