Although the adult orthopaedic literature is replete with papers addressing the effects of fractures and consequent treatment on bone density and the potential effect of low bone density in terms of refracture, little has been written about fractures in children and their effect on bone density. This paucity of literature certainly is not related to a lack of recognition that refractures occur in the pediatric population; indeed, refracture following pediatric forearm fractures has long been recognized as a serious and common complication1,2. Nor is the paucity of literature related to a lack of recognition that osteopenia occurs following fractures and subsequent immobilization3. Rather, the tools to begin to quantitatively understand these changes are only now beginning to be applied to the pediatric population. This paper by Ceroni et al. and a recent paper by Fung et al.4 represent the beginnings of a real effort to understand the changes that occur in pediatric bones as a result of immobilization following fracture.
Ceroni et al. examined a prospective group of adolescents followed during cast treatment for a distal tibial fracture. The injured limbs were compared with both the normal limb in the injured group as well as with a control group of healthy adolescents. The authors concluded that the bone mineral density of the injured limb was not significantly different from that of the controls and thus the original fracture was unlikely to be related to osteopenia. Furthermore, the authors observed a substantial decrease in bone mineral density and bone mineral content at multiple sites throughout the affected limb at the time of cast removal, which may have contributed to later refracture. It is of note that, although multiple measurements of bone density were obtained at the time of cast removal, no specific measurements were performed at the fracture site itself.
In their recent study, Fung et al.4 examined the bone mineral density of the distal part of the radius in children following distal radial fracture. They compared the bone mineral density at the fracture site in the distal part of the involved radius with that in the distal part of the uninvolved radius without measuring bone mineral density at distant sites. They noted an increase in bone mineral density at the fracture site during cast immobilization with a continued increase in bone mineral density up to twenty-four weeks postinjury and then a return to levels comparable with those in the distal part of the uninvolved radius at fifty-two weeks.
Clearly, a complete understanding of the changes in bone mineral density and the mechanisms involved following fractures eludes us at this time. Questions remain as to whether there are differences between the upper and lower extremities; what mechanisms control bone density; and whether these mechanisms are mediated by the presence of a fracture, immobilization, decreased weight-bearing, or some combination of these factors. In addition, both of these studies addressed only relatively simple fractures treated with cast immobilization. We do not know whether operatively treated fractures respond similarly or the exact biological mechanisms by which this change in bone mineral density is controlled. Practically, understanding these changes in a more quantitative way could allow for a reduction in refractures in these children as well as improved rehabilitation with more rapid return to activities. A fuller understanding of the biological mechanisms could potentially shed light on a number of different problems associated with the development of osteopenia after fractures and with prolonged bed rest as well as osteoporosis later in adulthood.