The process of bone growth is influenced by two main and complementary factors: first, the regulation of longitudinal growth by the metaphyseal cartilage, and second, the shaping of bone by the periosteum. These two factors are synchronized in their action, in that the new bone created at the metaphyseal cartilage is molded into its predestined shape by periosteal osteoclastic and osteoblastic activity. This synchronized action was designated by Hunter “modeling of the bone.” The new bone is formed with a waist-like “constriction” above the metaphysis and not as a direct continuation of the old bone. The “double contour” seen in roentgenograms of the long bones of infants in the first months of life, regarded by Glaser as the “effect of crests of bone,” is in my opinion to be attributed to periosteal activity, in the sense of normal modeling. This modeling process, which conserves the tubular form at the metaphysis, can be observed by superimposing roentgenograms of a limb of an infant obtained at different ages. Thus we can follow the modeling of the newly created bone within the limits of the old metaphysis, in the form of a waist-like “constriction” (Fig. 1A). When this normal process of modeling is disturbed, the bone continues its growth in a straight line and is broadened in a club-like form at the metaphysis, losing the tubular shape of normal bone (Fig. 1B). This failure in modeling manifested as “underconstriction,” or under-tubulation, is present in several diseases of bone in which the normal coordination of cartilaginous growth and periosteal bone shaping is interrupted. The club-like metaphyseal swelling of Gaucher's disease and Cooley's anemia, for example, is well known. This metaphyseal broadening is caused not by augmented intramedullary pressure, as was once thought—and expressed by the word “swelling”—but, rather, I believe, by a failure in the normal function of the periosteum. Bone transformation, being a slow and gradual process, does not lend itself easily to exact radiological observation. We were able, however, in a child of nine with Cooley's anemia of several years duration, to observe the presence of new bone formation, apparent as thin calcified paraosseal deposits near the femoral metaphysis (Fig. 2A) while at the same time the breakdown of bone was demonstrable in the form of cortical defects at the distal end of the tibia (Fig. 2B). The abnormal modeling of bone in Cooley's anemia is presented graphically in a diagram comparing the roentgenograms over a period of six months. In this way the metaphyseal broadening caused by the absence of the normal rate of constriction can be demonstrated (Fig. 3). Disturbance of normal calcification of the metaphyseal cartilage in rickets also causes a metaphyseal broadening which may be due to “under-tubulation” or to “underconstriction.”