There are two processes by which fetuses form bone. One depends upon the presence of a cartilage model, while the other does not. Ossification, or replacement of the cartilage model with bone, isn't completed at the time of birth. This allows some flexibility in the skeleton of a newborn, which helps prevent skeletal trauma during birth. There are a number of maternal factors that can affect development of fetal bone, including maternal vitamin and mineral status, which refers to whether the mother has adequate quantities of vitamins and minerals in her system.
Bone Development
The two processes by which fetal bone forms are called endochondral ossification and intramembranous ossification. The former involves the formation of bony matrix out of an ossification -- bone-forming -- site located near the center of a bone shaft. Endochondral ossification occurs in the long bones of the body, such as the bones of the arms and legs. Around the time a baby is born, the majority of a long bone's shaft has ossified, or become bony. Secondary ossification sites have formed near the ends of each bone, and the ends generally ossify within months. A plate of cartilage, however, remains between the shaft and ossified bone ends; this allows the bone to grow, and it remains cartilage until you reach your mid-20s.
Intramembranous ossification takes place in irregularly shaped, flat bones such as those that form the skull and the bones of the pelvis. Bone spicules, or small bits of bone, form and connect to one another. Over time, a spongy network of bone forms, with denser material closer to the bone surface; this process begins before birth, but continues afterward.
Movement
One of the factors that influences bone development in fetuses is their ability to move around in the uterus. This may help to stimulate bone modeling -- formation of new bone -- and may also affect bone remodeling, which is a process that continues throughout life and involves the destruction and reformation of bone in response to stress. A 1988 study by Dr. Jose Rodriguez and colleagues in "Calcified Tissue International" found that fetuses that could not move normally in utero showed signs of osteopenia, a precursor to osteoporosis. The bones of these babies also fractured easily and showed mechanical defects. This suggests that fetal movement conditions bone just as it conditions muscle.
Maternal Nutrient Status
Because fetuses depend completely upon nutrients they receive through the placenta to fuel growth, a nutrient-deficient mother can result in physiological problems in the fetus. Calcium is one of the major minerals in bone; it's part of the insoluble salt that makes bones hard. Insufficient calcium can result in weakened or insufficiently mineralized bones. In a 1999 article published by Dr. Koo and colleagues in "Obstetrics and Gynecology," researchers noted that maternal calcium status had the ability to impact fetal bone mineralization, leading to the recommendation that women receive calcium supplements starting in the second trimester, which corresponds to the beginning of ossification.
Similarly, maternal vitamin D status can affect fetal bone development. Insufficient vitamin D in a child can lead to rickets, which results in weakened, soft bones, because vitamin D helps the body take up calcium from the digestive tract. Similarly, insufficient vitamin D in a pregnant mother can lead to formation of fetal bones that resemble those of a child with rickets, reports Dr. P. Mahon and colleagues in a 2009 article in the "Journal of Bone and Mineral Research." The researchers recommend checking maternal vitamin D status early in pregnancy, and supplementing where necessary.
Hormones
While sufficient maternal calcium and vitamin D help provide the raw materials a fetus needs to build bone, fetal hormones also play a role. Parathyroid hormone helps to trigger bone formation; its role in the body is to decrease blood calcium levels by, among other things, stimulating bone cells called osteoblasts, which lay down new bone salts. If fetal levels of parathyroid hormone are low, bones will have reduced ossification, explains Dr. D. Miao and colleagues in a 2002 article in the "Journal of Clinical Investigation." While this particular study was conducted on mice, results can be reasonably extrapolated to humans because of the similar function of parathyroid hormone in the two species. The study indicates that parathyroid hormone doesn't just induce existing bone to remodel and become more dense, but also helps induce osteoblasts to form bone.
References
- "Calcified Tissue International"; Effects of Immobilization on Fetal Bone Development; Jose Rodriguez et al; 1988
- "Obstetrics and Gynecology"; Maternal Calcium Supplementation and Fetal Bone Mineralization; W. Koo et al; 1999
- "Journal of Bone and Mineral Research"; Low Maternal Vitamin D Status and Fetal Bone Development: Cohort Study; P. Mahon et al; 2009
- "Journal of Clinical Investigation"; Parathyroid Hormone is Essential for Normal Fetal Bone Formation"; D. Miao et al; 2002
