Before puberty, the skeletal system develops predominantly without the influence of sex hormones, with bone growth controlled by genetic predisposition responsible for 60-80% of bone mass and fracture resistance (“bone fracture resistance”), the calcium–vitamin D system, and physical stress. The situation changes with the onset of puberty. During puberty, the skeletal system becomes sex hormone dependent, so from this point on, without sex hormones, bones cannot develop optimally. In other words, the possible “maximum built-up bone mass” (“peak bone mass”) cannot then be achieved without sex hormones. Furthermore, sexual differentiation of the skeleton occurs after puberty, with testosterone being the main controlling hormones in males and 17-β-estradiol in females. On the other hand, 17-β-estradiol in males and the androgens in females also have important regulatory functions, the significance of which has not yet been fully elucidated. In individuals with pubertas tarda (delayed, incomplete, or complete absence of pubertal development in boys older than 16 or girls older than 15.), “peak bone mass” is decreased. An equally important factor for the normal development of the skeleton is body weight, so that anorexia nervosa (anorexia), for example, results in a reduced “peak bone mass” that does not return to normal even after successful treatment and achievement of a normal weight. Inadequately treated anorexics suffer from severe osteoporosis with fractures (broken bones) in 10% of cases. Sex hormones can only regulate bone metabolism to a limited extent without sufficient mechanical stress on the bones. Thus, balanced physical activity is also a basic requirement for healthy bone growth, whereas sporting excesses can lead to suppression of endogenous sex steroids and thus to a reduction in bone density and even stress fractures. Bone density also decreases in the presence of calcium insufficiency, especially when calcium intake is less than 300 mg/d. Calcium requirements are controlled by the rate of synthesis of the bone matrix. Reduced supply of calcium results in reduced mineralization and thus reduced bone formation while the rate of bone remodeling remains the same or increases. Children with insufficient calcium intake also remain smaller, since calcium also promotes the longitudinal growth of long bones. The German Nutrition Society (DGE) therefore recommends a calcium intake of at least 1,000 mg/d for all adults, pregnant and nursing women. Children (13-15 years) and adolescents (15-19 years) should intake 1,200 mg/d. Calcium absorption from the intestine as well as bone mineralization are vitamin D-dependent, so that prolonged vitamin D deficiency leads to short stature, reduced “peak bone mass” and osteomalacia or rickets. Adequate vitamin D production can be achieved by sunlight, but in northern countries the required exposure times are usually not reached during the winter months, so that osteoporosis can also result. Furthermore, culturally determined clothing can cover the skin to such an extent that even here – even with adequate exposure to sunlight – not enough vitamin D can be produced. Up to the age of 35, the build-up processes predominate and bone mass constantly increases. An increase in bone mass and bone density and a strengthening microarchitecture can be observed, with the maximum bone mass – “peak bone mass” – being reached around the age of 35. Thereafter, bone undergoes degradation processes and bone mass normally decreases by up to 1.0% per year, which can progress much faster in women compared to men as a result of physiological hormonal changes – menopause. The physiological changes of age have an impact on the bone formation phase as well as on the bone resorption phase, as well as on factors and metabolic changes that can favor the development of osteoporosis, so that, for example, the possible measure of the greatest bone density is not reached or that increased bone resorption takes place. Under physiological conditions, there are about 2 million active microunits in the skeleton, which make the bones a dynamic structure.Ideally, a bone is in a state of homeostasis (equilibrium) due to a balanced relationship between the build-up and breakdown processes of osteoblasts (bone-building cells) and osteoclasts (bone-degrading cells). The build-up and breakdown processes, which take place in physiological cycles, last about four months. A shift in this equilibrium in favor of osteoclasts, i.e. in favor of bone resorption, ultimately leads to osteoporosis. There are two main types of bone tissue: cortical or compact bone and cancellous or trabecular bone. Most bones are composed of the outer cortical (“cortex”) surface with two layers: a periosteal (“around the bone”) and a cortical-endosteal (“pertaining to the inner periosteum (endost)”) surface, and an inner trabecular (“belly-shaped”) bone and medullary cavity. The cancellous (“spongy”) bone contains trabecular plates and pegs that are interconnected and oriented predominantly along the load lines of the bone. Furthermore, a bone consists of an organic matrix, a mineral phase and the bone cells. The matrix is predominantly composed of collagen fibers, and this makes up approximately 90% of the skeletal weight of an adult. The predominant collagen formed by osteoblasts in the matrix is type I – mainly tropocollagen – and forms the collagen fibrils via cross-links to other collagen macromolecules. Important other proteins in the matrix include proteoglycans, glycoproteins, osteocalcin, and osteonectin. The mineral phase consists of calcium, phosphate and carbonate, which together form hydroxyapatite crystals – elongated hexagonal crystals – and align according to the orientation of the collagen fibrils. Furthermore, sodium, magnesium and fluoride are present within the mineral phase. The metabolic activity of bone takes place mainly on its surface. All bone surfaces have three major cell types: Osteoblasts, Osteoclasts and Osteocytes (mature bone cells). Osteoblasts synthesize collagen and other bone proteins and help mineralize the matrix. After mineralization, some osteoblasts remain in the surface as “dormant” or “dormante” osteoblasts. Osteocytes are former osteoblasts that were “trapped” within the matrix during the formation of bone and have developed longer cell “dendrites” or projections and act as mechanoreceptors of bone to register stresses on the bone. Osteoclasts are multinucleated cells that can degrade bone tissue with the help of acids and enzymes and occupy a key position in bone remodeling. The renewal of existing bone always begins with the help of osteoclasts, which first break down the bone tissue, creating “gaps” in the bone tissue that are filled back to the original level in healthy individuals. This “filling up” is no longer completely successful in osteoporosis. On the one hand, osteoporosis can be caused locally by osteoclast activity (breakdown) outweighing osteoblast activity (buildup), which is called “high-turnover osteoporosis.” On the other hand, osteoporosis may be due to decreased osteoblast attachment with concomitant normal osteoclast activity, which is called “low-turnover osteoporosis.” These disorders may be due to endocrine factors, calcium balance disorders, decreased mechanical stress, or genetic factors.