Introduction:
Calcium requirements rise during pregnancy and lactation stages due to a complicated set of hormonal changes. The alterations in the bone structure during pregnancy and lactation, both at the tissue and entire bone levels, mostly seem to resolve over time. The degree of the variations detected during lactation may be influenced by the amount and duration of breastfeeding and the resumption of normal menstruation. Research on the long-term effects of lactation and pregnancy indicates that bone density may benefit slightly at specific sites and that bone morphology may also be impacted.
What Is the Process of Bone Metabolism During Pregnancy?
Pregnancy and lactation cause significant changes in the body's calcium level. During the second and third trimesters of pregnancy, the fetus receives about two to three percent of the maternal calcium. The calcium that enters breast milk during lactation is 300 to 400 mg daily. This leads to the stimulation of numerous regulatory processes, including intestinal absorption, resorption of bone, and renal calcium reserve. The increased calcium requirement accelerates the reabsorption of intestinal calcium and bone turnover during pregnancy. The kidneys store calcium during lactation to support bone metabolism.
Pregnancy causes a three percent drop in bone mineral density despite the involvement of multiple counter-regulatory processes. Higher levels of circulating dihydroxyvitamin D, alterations in prolactin, estrogen, growth hormone, parathyroid hormone (PTH), dietary habits, body weight, or lifestyle factors counterbalance bone loss. Although the exact mechanism controlling calcium metabolism during lactation is unknown, PTH-related peptide (PTHrP) and the hypoestrogenic state are thought to play a major role. PTHrP is secreted from the tissues of the mother and the fetus during pregnancy. It preserves the maternal skeleton, inhibits PTH, raises dihydroxyvitamin D3, and regulates placental calcium transport.
On top of that, ovarian activity decreases throughout pregnancy and the lactation period. Elevated estrogen levels during lactation could correct the bone growth and resorption discrepancy. There is a significant correlation between postpartum bone mineral density (BMD) and serum estradiol, and bone loss results from estrogen shortage during postpartum amenorrhea; yet, the role of estrogen remains unclear. In the meantime, it has been suggested that the resumption of menses is a key regulator of bone metabolism during lactation and pregnancy. Low estrogen and high calcium demand during lactation and pregnancy promote bone metabolism.
How Does Pregnancy Impact Maternal Bone?
The endocrine and accompanying metabolic alterations that transpire throughout gestation and breastfeeding impact the skeleton's microstructural and whole-bone composition. Results from human iliac crest bone biopsies indicate increased bone resorption in the early stages of pregnancy (8 to 10 weeks), but at term, resorption normalizes, and signs of enhanced bone production are seen. Early pregnancy bone loss due to trabecular thinning and decreased trabecular connectivity appears to be compensated by developing new trabeculae in the later stages of pregnancy.
It has been demonstrated that during pregnancy, bone mineral density (BMD), as measured by clinical dual-energy X-ray absorptiometry (DXA), can drop by up to 5% in the lumbar spine and by many smaller percentages in the hip. Other skeletal sites provide more variable results. Research has not revealed any alteration in the distal radius cortical BMD or the lumbar spine trabecular BMD after pregnancy nor in the cortical, trabecular, or entire BMD at the radius or tibia. When comparing pregnant women to non-pregnant women, the authors discovered that trabecular microarchitecture degenerated and that there were signs of periosteal and endocortical growth in women aged 30 to 45.
How Does Lactation Impact Maternal Bone?
Lactation is linked to reductions in bone mass, especially in areas rich in trabecular bone like the hip and spine. These bone loss rates are significant; after three months of feeding, a 4% decrease in lumbar spine bone mineral density was found. In contrast, formula-feeding mothers and non-pregnant, non-lactating women see fewer or no alterations. The bone loss during lactation varies greatly; 38% of women lose more than 5% of their spine's BMD. The volume of breast milk production is positively correlated with the magnitude of bone loss. Additionally, rates of microstructural change in the bone increased with the length of breastfeeding and were higher during exclusive feeding as opposed to intermittent feeding.
Together, these findings indicate an elevated rate of bone loss due to the increased calcium requirement brought on by exclusive breastfeeding or by increasing the amount or length of feedings. While calcium supplementation has been demonstrated to have minor or temporary effects on bone loss during pregnancy and lactation, most studies indicate that vitamin D and calcium levels are either unrelated to bone turnover markers or weakly associated with them.
There seems to be complete healing and bone mass growth after breastfeeding. Evidence shows that the trabecular-rich spine heals more quickly than other areas. Additionally, better bone healing during and after lactation was linked to the return of normal menses and the use of progestin-only contraceptives.
How Does Pregnancy Promote Fracture Healing?
Pregnancy speeds up fracture healing due to quicker bone bridging of the fracture callus and a shorter time before the bony union. This seems unrelated to the gestational age at which the fracture happened.
A number of pregnancy-associated growth factors, including placental growth factor and pregnancy-associated plasma protein-A, have been shown in experimental tests to have a beneficial effect on fracture healing, which may account for accelerated bone regeneration. Better bone regeneration may be explained by elevated estrogen levels since estrogen administration has been demonstrated to hasten fracture repair.
Conclusion:
The endocrine-mediated mechanisms of mineral, calcium, mineral, and bone metabolism are altered during reproduction. This is constant for human and other mammal pregnancies since the developing fetal skeleton requires certain building blocks. Additionally, physical alterations that arise in pregnant or nursing women, such as bearing too much weight in the lumbar spine, result in physiological and pathophysiological alterations that are still being studied. It also seems that fracture healing improves during pregnancy; this may be because estrogen promotes bone regeneration.
