Osteoporosis refers to a decrease in the amount of bone tissue per unit. With reference to the World Health Organization (WHO) diagnostic criteria, osteoporosis is defined as a bone density value equal to or less than 2.5 standard deviations from the peak bone density of a healthy adult of the same sex and race, based on dual-energy X-ray absorptiometry; osteoporosis is a social health problem, and low bone density is a major factor in osteoporotic fractures. Bone density reaches its peak between the ages of 20 and 30, when most women are pregnant and lactating, the two periods of greatest change in the hormonal environment of women of childbearing age. In this fluctuating hormonal environment, calcium transport and redistribution from mother to fetus and infant occurs. Bone mineral depletion from these reproductive activities may affect premenopausal bone mass accumulation and perimenopausal bone loss. With the development of medical science, pregnancy and lactation bone calcium metabolism are receiving increasing attention. The status of recent studies related to osteoporosis is reviewed as follows. 1, the regulation of calcium metabolism in pregnant women during pregnancy, especially in late pregnancy due to the rapid development of the fetal skeleton, calcium absorption from the mother gradually increases, thus prompting the mother to produce a series of changes to regulate calcium metabolism, the intestinal absorption of calcium increases, the increase in circulating 1 ,25 -(OH) 2 Vitamin D, promoting the maternal intestinal absorption of calcium significantly increased. The pathways of calcium distribution after absorption during pregnancy mainly include: (1) regulation of bone calcium homeostasis: elevated serum calcitonin helps to protect maternal bones from excessive calcium absorption. Early studies have shown that serum parathyroid hormone (PTH) is elevated during pregnancy, but recent longitudinal studies have shown that serum intact PTH concentrations are not elevated during pregnancy and are reduced or not significantly altered compared to non-pregnant periods. (2) Mediation of calcium between the mother and fetus: studies have shown that fetal growth and development requires a large amount of calcium to be supplied by the mother, and if the maternal calcium supply is insufficient, the calcium deficiency in the body, coupled with vitamin D deficiency, blood calcium levels are bound to decrease secondary to hyperthyroidism, mobilization of bone calcium, resulting in increased bone resorption to meet fetal needs and maintain the physiological level of maternal blood calcium; in addition, the pregnant woman herself has a reduced osteogenic role in ensure the normal level of blood calcium. Elevated serum PTHrP levels may be related to embryonic differentiation, maintenance of maternal-fetal calcium transfer, promotion of fetal bone development, initiation of labor and lactation, but its origin is unclear. Fetal hypocalcemia is associated with maternal hypocalcemia, low PTH, low 1 ,25-(OH) 2 Vita2min D and high calcitonin concentration. Maternal hypoparathyroidism can cause a stress response in the fetal parathyroid glands leading to neonatal hypercalcemia. Maternal hyperparathyroidism may cause elevated fetal plasma parathyroid hormone, resulting in increased fetal bone resorption. In recent years, studies have shown that the decrease in maternal serum albumin and calcium-binding protein during pregnancy decreased total serum calcium, while the concentration of physiologically active serum ionized calcium did not change significantly. This reflects the adaptive changes of the mother. (3) The increase in urinary calcium excretion reflects the increase in calcium absorption and the increase in glomerular filtration rate after the expansion of blood volume during pregnancy. (2) Maternal calcium metabolism during lactation The intestinal calcium absorption is lower during lactation than during pregnancy, and the urinary calcium excretion is significantly lower than during both pregnancy and non-pregnancy. (1) Maintenance and regulation of bone calcium homeostasis: a large amount of data show that the loss of calcium sources during lactation is greater than the increase in bone resorption. The rate of bone mineral loss during the first 6 months of lactation exceeds 7% and is even higher than after menopause, and this bone loss can even lead to rare fractures. The release of bone calcium into the blood during lactation is not necessarily regulated exclusively by calcium-regulating hormones, and serum concentrations of PTH and 1,25-(OH) 2 Vitamin D are not different from those during non-pregnancy. Low estrogen and high PTHrP concentrations and lactogen may play a role in increasing bone resorption[1 ]. (2) Regulation of calcium in lactation: recent studies in animal models have shown that an increase in certain cytokines can lead to an increase in osteoclast activity. For example, increased IL-6 production can be induced under low estrogen conditions, resulting in increased osteoclast activity and decreased osteoblast activity, and increased bone resorption induced by lower estrogen, ensuring that the concentration of calcium in maternal milk is sufficient to meet the calcium requirements of infants and children in the absence of dietary calcium. Bone loss during lactation is different from postmenopausal bone loss in that bone loss during lactation is transient. After lactation ceases, with the return of menstruation, increased intestinal calcium absorption, and decreased urinary calcium excretion, the lost bone mass can be recovered within one year after delivery, even if another pregnancy occurs during this period. Studies have shown that calcium supplementation during lactation has no effect on milk calcium concentration and bone mineral, but only an increase in urinary calcium excretion is seen. (3) Urinary calcium reabsorption does play a major role in meeting calcium needs during lactation. 3. The effect of vitamin D during pregnancy and lactation on the development of the fetal and infant skeletal systems Studies on vitamin D levels in mothers during pregnancy and lactation have received much attention in recent years, and some studies have pointed out [1 ] that vitamin D may affect the growth and development of the functional fetal skeletal system as well as other systems, and this effect may last until the growth and development of the newborn and later, and for vitamin D supplementation during pregnancy and lactation The benefits and adverse effects of vitamin D supplementation during pregnancy and lactation on pregnant women and fetuses and newborns have not been reported. In a study [1 ], vitamin D levels were measured late in a group of pregnant women, 78% (466) of whom had vitamin D levels measured at birth, 74% of whom had blood vitamin D concentrations measured again at 9 months of age, and 30% (178) of whom had blood vitamin D concentrations measured again at 9 years of age, showing that maternal blood vitamin D concentrations greater than 75 nmol/L did not affect The results showed that maternal vitamin D concentrations greater than 75 nmol/L did not affect neonatal birth weight, neurological and cardiovascular development. Another study [2] showed that maternal vitamin D deficiency increases the risk of low birth weight babies and neonates with vitamin deficiency, and increases the incidence of preeclampsia in pregnant women. 4. The effect of pregnancy on bone mass The bone calcium reserve in humans starts from the embryonic period and is usually completed by the age of 30 years, and usually after the age of 25 years, the bone density of mature women has reached its peak, so the effect of pregnancy on bone mass is not obvious. However, in young women who have not reached peak BMD, pregnancy can affect BMD due to simultaneous maternal and infant growth and development. Sowers (1992) showed that women who became pregnant before the age of 20 had significantly lower tibial BMD during perimenopause than women who became pregnant at maturity, corresponding to a bone loss of more than 5 years after menopause. A recent foreign study enrolling more than 600 women showed that delaying pregnancy until the maximum bone mass is restored seems to have a protective effect on the bone. Bone calcium will be lost by 8% to 10% at the end of pregnancy and delivery, which will reduce maternal bone calcium. The secretion of adrenocorticotropic hormone increases during pregnancy, which hinders the absorption of calcium; in late pregnancy, the fetal head presses on the closed nerve after pelvic compression, and mechanical compression leads to local neurotrophic disorders, such as hip bone, which is prone to osteoporosis; during pregnancy, women have less vitamin D production due to outdoor exercise and reduced sunlight exposure, which leads to insufficient bone formation; during pregnancy, women often have biochemical and endocrine changes, which leads to abnormal bone metabolism. Pregnancy-related osteoporosis may be associated with vitamin D deficiency, low-calcium diet and elevated PTH concentrations, prolonged lack of appropriate outdoor activity during pregnancy, use of corticosteroids, sedative drugs and contraction-inhibiting fetal medications, and some uncertain pathological factors [3], pregnancy itself is not a risk factor for low bone mass or fracture. Therefore, according to the characteristics of maternal bone calcium metabolism during pregnancy, it is recommended that calcium and vitamins should be supplemented from the beginning of pregnancy, and in fact, the majority of pregnant women do not suffer from osteoporosis-induced fractures during pregnancy, which is related to their own internal In fact, the vast majority of pregnant women do not experience osteoporosis-induced fractures during pregnancy, which is related to various regulatory and compensatory mechanisms of bone calcium metabolism in their own bodies. The relationship between the number of births and bone mass is difficult to determine. Theoretically, the increased demand for calcium during pregnancy decreases bone mass. On the other hand, the increase in estrogen levels and weight gain during the second trimester are conducive to an increase in bone mass. Biberogluk (1993) showed that bone mass was negatively associated with the number of births, especially for pregnancies greater than four, but some studies failed to find this relationship and differences in BMD between multiple and uncomplicated pregnancies. Recent studies have shown no relationship between the number of births and the occurrence of future osteoporotic fractures, and that the number of births is not a predictive risk factor for future fractures. Several studies in recent years have shown that women with multiple pregnancies have less bone loss than women who have not had a previous pregnancy. 5. The effect of breastfeeding on bone mass Over the years, studies of bone mass and breastfeeding have yielded inconsistent results. The mobilization of calcium from bone is greater during lactation than during pregnancy, the extent of which depends on the amount of milk and the duration of lactation. Some cross-sectional studies have shown that breastfeeding is positively associated with bone mineral density and does not increase the risk of fracture. Breastfeeding for 3 months was not significantly associated with bone loss, with 2% of the lost bone mineral in the femoral stem or spine fully recovered by 6 months postpartum, and long-term breastfeeding did not decrease bone mineral nor bone mass in the lumbar spine or flexures. Recent studies have shown that the number of pregnancies and duration of breastfeeding have no effect on bone mineral density, and in recent years Dr. Peter F. Schnatz found that the incidence of osteoporosis was significantly lower in breastfeeding women (8%) than in non-breastfeeding women (19%), and in the group of breastfeeding women, the age at first pregnancy.