Peak bone mass (PBM) is an important determinant of osteoporotic fracture risk later in life. Bone mineral mass accumulation from infancy to postpuberty is a complex process implicating interactions of genetic, endocrine, mechanical, and nutritional factors. PBM is attained in the axial skeleton and in the proximal femur by the end of the second decade of life. The increase in mass and strength is essentially due to an increment in bone size, with volumetric bone mineral density (BMD) changing very little during growth. In adult women, an increase of PBM by 10%, that is, by approximately 1 standard deviation (SD), could decrease the risk of fragility fracture by 50% or be equivalent to retarding menopause by 14 years. Bone mineral mass during growth follows a trajectory. The main influencing factor is genetics. Increasing calcium intake or mechanical loading can shift upward the age-bone mass trajectory, while chronic diseases and their treatment can shift it downward. Prepuberty appears to be an opportune time for obtaining a substantial benefit of increasing physical activity with appropriate intakes of calcium and proteins.