Skeletal growth and changes in body composition during growth present important variations; body mass index and lean body mass related to age show important gender differences. The process of ossification is developed in two different ways, endochondral and intramembraneous. The former is characterised by the formation of bone from growth cartilage. Intramembraneous ossification is characterised by the formation of bone from a mesenchymal structure, as occurs with the flat bones of the skull. During childhood and adolescence and up to the acquisition of adult stature, two phenomenons are produced simultaneously: the synthesis of new bone from growth cartilage due to the process of endochondral ossification, and modeling-remodeling of previously synthesized bone. Bone growth and mineralisation of its extracellular matrix are simultaneous phenomenons, the final result being the acquisition and maintenance of body bone mass. A positive calcium balance is necessary during adolescence in order to achieve the maximum peak of bone mass and even with the termination of longitudinal growth of bone, the process of mineralisation can last a further 4 years. Childhood and adolescence are the period of life in which the peak of bone mass must be achieved, and if during this time this does not happen there will be a greater risk for the later development of osteoporosis. Regulation of bone mass is a polygenic process and during recent years studies have been centred on the receptor genes of vitamin D and estrogens. A maximum calcium retention during adolescence may influence the achievement of a high peak of bone mass but at a certain level of calcium intake the calcium retention reaches a plateau. The expression of grams of hydroxyapatite per square centimetre has been used clinically, or expressed in volume as g/cm3. From birth until 3 years, the increase represents approximately 30% of the total increase, from 3 years until the beginning of pubertal development the increase is 20%. During pubertal development there is an increase of 30-40% and from the end of growth until the age of 21 years there is an increase of 15-20%. Both prepubertal boys and girls show a progressive increase of leptin levels during the years prior to the onset of puberty and until Tanner's stage 11 and higher levels are observed in girls in this period, possibly in relation to their earlier onset of puberty. This increase of leptin in girls during pubertal development suggests that leptin may be a link between adipose tissue and puberty.