The growth in width of a long bone is due primarily to subperiosteal formation of new bone, a process referred to as modeling, which begins before birth and continues even into the ninth and tenth decades. In all population samples studied, subperiosteal formation of new bone is greater in males than in females. The growth in width of long bones is particularly accelerated in the first 2 years of life. For example, by age 2, the diameter of the medullary canal at the mid-diaphysis of the femur is nearly equal to the diameter of the entire mid-diaphysis at birth. Thus, the rate of cortical modeling approaches 50% per year in the first 2 years of life. The growth in width of long bones continues at a slower rate in childhood and then increases rapidly during the adolescent growth spurt. During this period of rapid longitudinal as well as latitudinal growth, as much as 300 mg of elemental calcium is incorporated into bone apatite every day.

Most traditional views of bone development imply that all growth ceases after skeletal maturity, near the beginning of the third decade. However, results of cross-sectional studies on large samples of the adult population and longitudinal studies on individuals indicate that subperiosteal bone apposition continues throughout adulthood and into old age. The greatest increase in bone width occurs in the femur, but the general process is observed in the entire skeleton, in bones as diverse as the skull, ribs, and vertebrae. Also, subperiosteal bone formation occurs in both men and women and in all population samples studied. Although the total subperiosteal area is greater in men than in women, the percentage of gain is greater in women.

In conjunction with the age-specific subperiosteal bone apposition that continues throughout life, a complex age-related activity, characterized by alternating phases of resorption and apposition in a process referred to as remodeling, occurs at the endosteal surface. Whereas subperiosteal activity determines the width of the bone, endosteal activity determines the width of the medullary canal. The combination of the relative activities at the two surfaces over a period of time determines the thickness of the cortex, and remodeling within the individual osteons of the cortex determines intracortical porosity.

During the first few years of life, a great deal of modeling and remodeling activities takes place at both the subperiosteal and the endosteal surface of cortical bone, tremendously increasing the width of both the bone and the medullary canal. Then, for the next several years, subperiosteal bone formation continues at a slower rate, accompanied by a large decrease in endosteal resorption and a short period of endosteal apposition. These processes enlarge the diameter of the bone and reduce the width of the medullary canal. Then, from about age 6 until the middle teenage years, endosteal bone resorption resumes, with resultant enlargement of the medullary canal.

The greatest natural uncoupling of bone activity in favor of bone formation occurs during adolescence. (For a more complete discussion of coupling, see Plates 2-30 and 2-31.) The growth in bone length by endochondral bone formation at the growth plates is accompanied by a corresponding burst of subperiosteal bone formation at mid-diaphysis; once again, endosteal activity is reversed, with a new wave of endosteal bone apposition taking place. These processes increase the length and width of the bone, increase the thickness of the cortex, and decrease the width of the medullary canal. The apposition of bone at the endosteal surface begins earlier in females and continues until nearly age 40 in both sexes. After age 40, the activity at the endosteal surface again reverses, with endosteal bone resorption persisting for the remainder of life. Subperiosteal bone formation continues for the rest of life as well, at a slow but steady rate.