Bone Modeling in Childhood and Adolescence
Bone growth begins in childhood in boys and girls. The bone growth spurt in both genders begins earlier is commonly appreciated as shown in the chart below of 500 normal predominately white children and adolescents between the ages of 4 and 20 years. In both genders, rapid bone mineral accumulation in the spine seen in the graph is clearly evident by age 7 and the pace continues unabated through puberty and beyond. The graph depicts bone density of the lumbar spine measured by DXA bone densitometry and is typical of what is seen in the whole body or other regions of interest. What DXA is measuring is the bone mineral content divided by the area of the bone and the value, bone mineral density (BMD) is plotted on the graph vs. the children’s age. As these normal children age, their bones accumulate calcium mineral and become denser as a result.
It is quite apparent from this data that the time to provide our children with the various essential environmental nurturing inputs needed for them to realize the skeletal genetic potential begins in early childhood. While every child needs a total health package, for optimal bone health these include vitamin D, protein, calcium, magnesium, and exercise.
During childhood and adolescence bone mineral is added to the skeleton through the process known as bone modeling. During modeling specialized bone cells, the osteoclasts remove bone from the skeleton and other specialized bone cells osteoblasts replace it. The principal characteristic of modeling is considerably more bone is added to the skeleton than removed. This results in a net gain of bone with each modeling cycle.
Modeling is bone’s method for shaping the skeleton into its adult form. In girls rapid addition of bone ceases in the late teens but continues in boys well into the 20s. This prolongation in bone modeling seen in boy’s results in their depositing about 10% more calcium mineral in their skeleton. This phenomenon is seen in all humans. The point where calcium mineral deposition reaches its greatest extent is known as the peak bone mass (PBM). The PBM occurs in the spine before the hip. It is an asynchronous event occurring at different times for different bones in the body but about the same time for paired bones like the right and left humerus.
Studies show that calcium nutrition in particular and by extension vitamin D3, in my opinion is critical to obtaining optimal PBM. It is incumbent upon the parent to ensure that her child eat calcium rich foods and provide them with 1000 IU of supplemental vitamin D3 every day beginning as soon as they begin eating. A breast fed infant needs no external nutrients but once his or her nutrition comes by way of the garden or grocery then yes, begin the vitamin D3. In little babies, <50 lbs, 1000 IU every other day is fine. Vitamin D3 is a fat-soluble vitamin usually sold in sesame or soy oil filled capsule. Simply puncture the capsule and squeeze the benign tasting vitamin D3 oil into the baby’s food and give it to them. Pick something they like so they eat it all up. When their weigh increases to above 50 lbs, increase the dose to 1,000 IU daily. All dairy products are calcium rich. There is a list of high calcium non-dairy foods provided in the Prevention section of the website for your use. Many of these foods can be processed into baby food in a food processor or purchased already processed.
The long-term value for a whole host of reasons to habituate your child to a healthy calcium and magnesium rich diet from the get go is enormous. The risk of common chronic diseases are lower because the risk for obesity is lower and obesity is the common pathway to all acquired chronic human disease that plague modern people.
Genetics, calcium, vitamin D, exercise, protein, sex steroid hormone levels, and calorie nutrition are important determinates of PBM. For a child to achieve their genetically predetermined peak bone mass these modifiable imputes should be optimized. On reason for a child not reaching their potential PBM is developing a serious illness, being poorly nourished or being treated with a drug that damages bone development during childhood like glucocorticoids. Studies have shown that exercise and a calcium rich diet during childhood and adolescence improve DXA bone density. Those who achieve the optimal genetically predetermined PBM during growth and development begin bone remodeling and therefore the inevitable loss of bone from a higher level than would be the case if their PBM was sub-optimal at the peak. The lower the peak, the less time it takes to reach osteoporosis.