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The dramatic bone growth during puberty encompasses three distinct but integrated processes: accelerated linear growth, bone maturation, and rapid acquisition of bone mass. Compelling evidence indicates that the estrogen-primed enhancement of the axis of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in both sexes is the main mediator of the accelerated linear growth and increase in bone dimensions during early puberty and midpuberty. The surge in estrogen at menarche in girls and in late puberty in boys inhibits growth, closes the epiphyses, and increases true volumetric bone mineral density (vBMD). Knowledge of estrogen’s central role in these aspects of bone growth has important therapeutic implications for the management of pubertal disorders.The potential impact of calcium intake and exercise on bone mass accrual during puberty is generally supported. Genetic polymorphisms in genes thought to influence bone mass might ultimately be used in combination with known hormonal and environmental risk factors and clinical parameters to identify adolescents at risk for osteoporosis for early intervention.