There are many hormones involved in the metabolic processes of bone, such as parathyroid hormone, calcitonin, sex hormones, adrenocorticotropic hormone, thyroxine, and growth hormone. The first two of these have the greatest role. Parathyroid hormone (PTH) is secreted by the parathyroid glands, and its main role is to raise blood calcium and lower blood phosphorus, maintain normal plasma calcium levels by increasing calcium reabsorption by the renal tubules, reducing phosphorus reabsorption, and promoting bone reconstruction processes. The secretion of parathyroid hormone is influenced by blood calcium, calcitonin and vitamin D. In particular, the blood calcium concentration, which decreases within a certain range, increases parathyroid hormone, showing a negative feedback change. In contrast, calcitonin can directly stimulate parathyroid hormone secretion only when it exceeds physiological levels, and l,25(OH)2D3 concentration must be increased to a certain level before parathyroid hormone secretion can be reduced. The effect of parathyroid hormone on bone is mainly manifested by the promotion of bone resorption. Its combined effect on various cells of bone is manifested by increasing the cytoplasmic calcium concentration by causing extracellular calcium to enter the cytoplasm and mitochondrial calcium to be released. The increased plasma calcium concentration in mesenchymal cells accelerates their conversion to osteoclasts, increasing the number of the latter. Increased calcium concentration in the osteoclast plasma produces large amounts of citric and lactic acids, which lower the pH of the bone matrix and cause bone salt dissolution. At the same time, lysosomes are stimulated to release hydrolases to dissolve the bone matrix. Increased intracytoplasmic calcium concentration in osteoblasts is manifested by impaired organic matter synthesis, while increased intracytoplasmic calcium concentration in osteocytes is manifested by highly differentiated organelles and increased osteoclastic osteolysis. However, when parathyroid hormone is continuously secreted, it can cause a certain degree of increased bone formation. Calcitonin is secreted by the parafollicular C cells of the thyroid gland and this process is influenced by a number of factors, the more clearly defined being blood calcium concentration and parathyroid hormone levels. Calcitonin secretion increases when blood calcium is increased to lower it and maintain its normal level. In contrast, parathyroid hormone is considered to be the only antagonist of calcitonin, but has a synergistic effect in reducing phosphorus reabsorption by the renal tubules. As for the effects of thyroxine, insulin, glucagon, gastrin and magnesium on calcitonin, there are still many questions to be investigated. The effect of calcitonin on bone is mainly direct inhibition of bone resorption. It inhibits the activity of osteoclasts and reduces their number, while also promoting the osteogenic process, resulting in a decrease in osteocalcin release and the uptake of blood calcium into newly formed bone, thus reducing blood calcium. In addition, estrogen indirectly inhibits osteoclast activity through calcitonin and acts directly on osteoblasts to promote bone formation, androgens and growth hormone promote bone growth and development, thyroxine promotes the process of bone resorption, and adrenal glucocorticoids reduce the number of osteoblasts and inhibit collagen formation, and reduce intestinal calcium absorption and increase renal calcium excretion through their effect on vitamin D. Development plays a regulatory role. There are several hormones involved in regulation and they have different effects. The main hormones that are closely related to human height are growth hormone, thyroid hormone, gonadal hormone, insulin, etc. Growth basically depends on the synergistic action of the endocrine glands and is accomplished under the mutual regulation of the endocrine glands and the skeletal system. Growth hormone, thyroid hormone, insulin and corticosteroids have important effects on growth; parathyroid hormone, vitamin D and calcitonin can affect bone development and ossification; gonadotropins and sex hormones are related to skeletal maturation and growth rate at puberty. Growth hormone is secreted by the pituitary gland and is a peptide hormone consisting of 191 amino acids, which produces growth hormone mediators through its effect on the liver. Growth hormone mediators are a group of peptides that directly stimulate the growth of bones. Growth hormone is secreted intermittently, while the concentration of growth hormone mediators is relatively constant. Each person’s pituitary gland contains about 4-8 mg of growth hormone. Normal adult plasma contains very little growth hormone, 3-5 mcg per milliliter of plasma, but it is very useful. One of the most significant physiological effects is to promote bone growth. The growth of body height depends on the continuous growth of long bones such as upper limb bones and lower limb bones. There are many chondrocytes in the epiphyseal plate. Under the action and stimulation of growth hormone, chondrocytes continue to divide, proliferate, secrete collagen matrix, and then calcify into bone. Thus, the long bones continue to grow at both ends, and the body grows taller. People who secrete more growth hormone grow faster, while too much growth hormone can cause gigantism or acromegaly, and not enough growth hormone can cause dwarfism. Growth hormone still has physiological effects after several years of storage under frozen conditions. Since 1958, foreign countries have used growth hormone extracted from the human pituitary gland to treat pituitary dwarfism, and the effect of promoting its growth is certain. The general growth rate after treatment is about three times that before treatment, and the length can reach 1 cm per month during the first two years of treatment, after which the treatment is less effective. The earlier the age of initiation of this treatment, the better the final results, and the more years of continuous treatment. Since human growth hormone secretion levels tend to rise during the night, human growth hormone injections are generally most effective when given one hour before bedtime. However, it is difficult to extract growth hormone from the human pituitary gland, and with the continuous development of biogenetic engineering technology, synthetic human growth hormone was introduced in 1979. This is obtained from the protein synthesized by E. coli through genetic engineering, and can completely replace the growth hormone extracted from the human pituitary gland. However, it is worth mentioning that imported products are expensive, which makes it prohibitive according to our current living standard. Thyroid hormone can act directly on bone cells to stimulate bone remodeling activities and accelerate bone resorption and osteogenesis at the same time. The effect on bone, cartilage and skeletal plate is to promote their maturation. This is manifested by the appearance of ossification centers in the cartilage of the epiphysis and its eventual fusion with the backbone. It is clinically proven that in children with hypothyroidism, cartilage ossification and dental growth are both impaired, and radiographs show a significant delay in the appearance of ossification centers in the long bones compared to normal children, with bone age significantly behind the actual age. The development of the face and the main long bones of the body is impaired, resulting in an infantile ratio between the upper and lower body, characterized by a shorter lower body than the upper body. This resting state is more prominent in hypothyroidism (cretinism, cretinism), and is more pronounced the earlier the onset of the disease, and is most severe in congenital cases. Sex hormones, especially androgens, are secreted in large amounts during puberty to promote sudden skeletal growth, resulting in rapid height growth. In males, the testes mature during puberty and secrete large amounts of androgens; androgens from the adrenal cortex are also involved. In females, the growth spurt during puberty mainly depends on androgens secreted by the adrenal cortex, while the ovaries can also secrete a small amount of androgens. Androgens begin to stimulate growth during puberty, but it is also the hormone that finally ends the growth process. It induces the healing of the epiphyseal plate, which stops growth. Insulin also plays a role in growth. The principle is that insulin has a stimulating effect on protein synthesis. Growth is affected in children with diabetes, indicating that a lack of insulin affects the normal growth process. However, in physiological situations, growth hormone is the hormone that plays a dominant role and insulin is auxiliary to growth.