Osteoporosis is defined as a decrease in the amount of bone tissue per unit. Referring to the diagnostic criteria of the World Health Organization (WHO), based on dual-energy X-ray absorptiometry: osteoporosis is defined as a bone mineral density value equal to or lower than 2 or 5 standard deviations below the peak bone mineral value of healthy adults of the same sex and race; osteoporosis is a social health problem, and low bone mineral density is one of the main factors of osteoporotic fracture. Bone density reaches its peak between the ages of 20 and 30, when most women are pregnant and breastfeeding, the two periods of greatest change in the hormonal environment of women of childbearing age. In this fluctuating hormonal environment, calcium is transported and redistributed from the mother to the fetus and infant. The bone mineral depletion associated with these reproductive activities may affect both premenopausal bone mass accumulation and perimenopausal bone loss. With the development of medicine, pregnancy and breastfeeding bone calcium metabolism have been increasingly scrutinized. The research status of pregnancy and lactation in relation to osteoporosis in recent years is summarized as follows. 1. Regulation of calcium metabolism in pregnant women during pregnancy During pregnancy, especially in late pregnancy, due to the rapid development of fetal bones, the absorption of calcium from the mother’s body gradually increases, thus prompting the mother’s body to produce a series of changes in order to regulate calcium metabolism, the intestinal absorption of calcium increases, and the increase in circulation, which promotes the mother’s intestinal absorption of calcium increases significantly. The main pathways of calcium distribution after absorption during pregnancy include: (1) Regulation of bone calcium homeostasis: Elevated serum calcitonin elevation favors the protection of maternal bone against excessive calcium absorption. Early studies have shown that serum parathyroid hormone (PTH) is elevated during pregnancy; more recent longitudinal studies have shown that serum intact PTH concentrations are not elevated during pregnancy and are reduced or not significantly altered compared with non-pregnancy. (2) Mediation of calcium between the mother and the fetus: Studies have shown that fetal growth and development requires a large amount of calcium supply by the mother, if the mother’s calcium supply is insufficient, the lack of calcium in the body, coupled with the lack of vitamin D, the level of blood calcium is bound to be lowered, secondary to hyperthyroidism, mobilization of osteocalcin, so that bone resorption is increased in order to satisfy the fetal needs and to maintain physiological levels of maternal blood calcium; in addition, the pregnant woman herself osteogenesis is lowered, to Ensure the normal level of blood calcium. Elevated serum PTHrP levels may be related to embryonic differentiation, maintenance of maternal interfetal calcium transfer, promotion of fetal bone development, initiation of labor and lactation, but its source is not clear. Fetal hypocalcemia is associated with maternal hypocalcemia and high calcitonin concentrations. Maternal hypoparathyroidism can lead to neonatal hypercalcemia as a result of a stress response in the fetal parathyroid glands. Maternal hyperparathyroidism may cause fetal plasma parathyroid hormone to rise, resulting in increased fetal bone resorption. In recent years, studies have shown that the decrease in maternal serum albumin and the decrease in calcium-binding proteins during pregnancy result in a decrease in total serum calcium, while the concentration of physiologically active serum ionized calcium does not change significantly. This reflects the adaptive changes in the mother. (3) Increased urinary calcium excretion: reflecting the increase in calcium absorption and the increase in glomerular filtration rate after the expansion of blood volume during pregnancy. Calcium metabolism in lactating mothers: intestinal calcium absorption during lactation is lower than that during pregnancy, and urinary calcium excretion is significantly lower than that during pregnancy and non-pregnancy. (1) Maintenance and regulation of bone calcium homeostasis: A large number of data show that the loss of calcium sources during lactation is greater than the increase in bone resorption. Bone mineral loss exceeds 7% during 6 months of lactation, and the rate of bone loss is higher than that of postmenopause, and this bone loss can even lead to rare fractures. The release of bone calcium into the bloodstream during lactation is not necessarily fully regulated by calcimimetic hormones, and serum concentrations of PTH are not different from those during non-pregnancy. Low estrogen high PTHrP concentration and lactogen may play a role in increasing bone resorption [1]. (2) Calcium regulation in lactation: Recent animal model studies have shown that an increase in certain cytokines can increase osteoclast activity. For example, in the case of low estrogen can be induced to increase the production of IL-6, so that osteoclast activity increases osteoblast activity decreases osteoclast activity, estrogen lowering induced bone resorption increases, to ensure that the maternal in the case of dietary calcium shortage of calcium concentration in breast milk in order to meet the infant’s need for calcium. Unlike postmenopausal bone loss, bone loss during lactation is transient. After the cessation of breastfeeding, with the return of menstruation, increased intestinal calcium absorption, and decreased urinary calcium excretion, bone loss can be restored within one year postpartum, even if another pregnancy occurs during this period. Studies have shown that calcium supplementation during lactation has no effect on breast milk calcium concentration and bone mineral, but only increased urinary calcium excretion. 3, pregnancy and lactation vitamin D on the development of the fetal and infant skeletal system The study on the level of vitamin D in the maternal body during pregnancy and lactation has attracted much attention in recent years, and some studies have pointed out that [1] vitamin D may affect the growth and development of the functional fetal skeletal system as well as other systems, and that this effect may continue to the neonate and later growth and development, for the supplementation of vitamin D in pregnancy and lactation. There are no reports on the benefits or adverse effects of vitamin D supplementation during pregnancy and lactation on pregnant women and fetuses and newborns. In a [1] study, vitamin D levels were measured in a group of pregnant women at a late stage, 78% (466) of the newborns had their vitamin D levels measured at birth, 74% of the newborns had their blood vitamin D concentrations measured again at 9 months of age, and 30% (178) of the newborns had their blood vitamin D concentrations measured again at the age of 9 years, which showed that maternal blood vitamin D concentrations of more than 75 nmol/L did not affect the birth weight, neurological status of the newborns. The results showed that maternal vitamin D concentrations greater than 75 nmol/L did not affect neonatal birth weight, neurologic and cardiovascular development. Another study[2] showed that maternal vitamin D deficiency will increase the risk of delivering low birth weight babies and neonates with vitamin deficiency disease, and increase the incidence of preeclampsia in pregnant women. The above studies make it necessary to monitor maternal vitamin D at the beginning of pregnancy, and to supplement and regulate the vitamin D level according to the need. 4, the effect of pregnancy on bone mass Bone calcium reserves from the embryonic period has begun, generally to 30 years of age before the completion of the bone calcium reserves, usually 25 years of age after the mature women’s bone density has reached its peak, the effect of pregnancy on bone mass is not obvious. However, in younger women who have not reached peak BMD, pregnancy-related osteoporosis may be associated with vitamin D deficiency, low-calcium diets and elevated PTH concentrations, prolonged lack of appropriate outdoor activity during pregnancy, the use of corticosteroids, sedative medications, and contraction-suppressing birth control medications, as well as a number of indeterminate etiologic factors [3], and pregnancy per se is not a risk factor for low BMD or fracture. Several studies in recent years have shown that women with multiple pregnancies have less bone loss than those without previous pregnancies. 5, The effect of breastfeeding on bone mass The results of studies of bone mass and breastfeeding over the years have been inconsistent. Calcium mobilization from bone is greater during lactation than during pregnancy, and the extent 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, without an increased risk of fracture [6]. Lactation for 3 months was not significantly associated with bone loss, and 2% of the bone mineral lost from the femur shaft or spine was fully recovered by 6 months postpartum. In conclusion, the effects of hormonal and supply/demand changes induced by pregnancy and lactation on bone metabolism are inevitable, and the role of vitamin D in maternal bone health during pregnancy and lactation is certain by increasing calcium supplementation during pregnancy and lactation, as well as monitoring vitamin D levels during pregnancy and adjusting vitamin D as appropriate. Pregnancy itself is not a risk factor for osteoporosis, and the results of studies on the immediate and long-term effects of pregnancy and lactation on bone metabolism are still inconsistent. There is still a lack of multicenter, large-scale, randomized, controlled clinical trials on the effects of pregnancy and lactation on osteoporosis, so it is necessary to provide sufficient evidence to guide mothers and infants to adjust their bone homeostasis during pregnancy and lactation. We need to further investigate the effects of pregnancy and lactation on bone metabolism in the near and long term to provide a favorable basis for regulating bone homeostasis during pregnancy and lactation, and to provide guidance for the immediate and long-term bone health of mother and child.