The fetal skeleton at term contains about 21 g of calcium, the adult skeleton about 1000 g. Many studies evaluated the factors controlling calcium accumulation in the skeleton during growth and development. Maximal accumulation occurs during puberty. Ninety percent of adult bone mass is accumulated by age 18 years, while the remaining 10% will be added in the subsequent skeletal consolidation phase. It is important to know that bone mass acquisition has different characteristics in cortical and trabecular bone. Trabecular bone density is strongly influenced by the hormonal and metabolic factors associated with sexual development during adolescence. On average, spine bone mass (mostly trabecular bone) increases by 13% during puberty, in both sexes. Beyond their direct action, sex hormones act also indirectly, through the modifications that they induce on protein and calcium metabolism, and through the sequence of events triggered by the higher production of GH and IGF-1. Consolidation of cortical bone is slower. So, the "peak of bone mass" is reached at the end of the second decade in the axial skeleton, while in the appendicular skeleton it is reached much later, somewhere between age 30 and 35 years (10).
Puberty is a complex maturational process involving genetic, environmental, endocrine, and nutritional factors, and has a profound impact on bone mass accrual (11). Longitudinal studies have demonstrated that bone mass accrual is extremely rapid during adolescence, and that about 25% of the peak bone mass is accumulated during the two years of peak height gain. Sabatier et al. (12) have followed with dual energy X-ray absorptiometry (DXA) a large group of healthy females, showing that the four perimenarcheal years, beginning with the first pubertal clinical signs, are essential for bone acquisition. A recent study has confirmed that the age of the onset of menstruation is a predictor of BMD in the lumbar spine (13).
Specific Determinants of Bone Density in Adolescents
Many factors influence bone mass accrual during growth and development: heredity, nutrition, mechanical forces (physical activity and body weight), endocrine factors, and presence of other risk factors. The influence of all these factors on bone mass as well as their interrelationships are very complex and only some key points can be presented here.
Heredity: Genetic factors are considered the most important determinants of the variability of bone mass gain during pubertal maturation. Several genes are involved in bone modeling and remodeling, and influence bone mass determining also its peak value. The polymorphisms of more than 20 candidate genes have been studied (14).
Physical activity: The response of bone to mechanical strain is greater during the growing age than in adult life. Several studies demonstrated that intense physical exercise is associated with an increase in bone mass acquisition at weight-bearing skeletal sites during childhood and especially during adolescence (15). Some studies have observed a positive association also between bone mass and mild physical activity, even if some other studies reported controversial data (16,17). In young girls excessive physical activity, such as that of adolescents female athletes, may lead to hypogo-nadism with amenorrhea, and a secondary low bone mass.
Nutrition: Increasing dietary calcium intake during childhood and adolescence is associated with a greater bone mass gain and a higher peak of bone mass. The skeleton seems to be more responsive to an increase in calcium intake before the onset of pubertal maturation (18). Benefits are more marked in the appendicular than the axial skeleton. Among other nutrients, protein intake is especially important (19). During the period of growth, inadequate energy and protein intake can affect bone development. Low protein intake also reduces the production of IGF-1. During adolescence, a relative deficiency in IGF-1 may result not only in a reduction of bone longitudinal growth but also of cross-sectional growth. Young people affected by anorexia nervosa or other forms of eating disorders are at high risk of osteoporosis, also because they may have severe calcium, protein or energy (caloric) deficits.
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