Paediatric musculoskeletal radiologyMetabolic bone disease
Bone loss in children can be due to osteoporosis, rickets, which is the pediatric form of osteomalacia, and hyperparathyroidism.
Simple observation of the density of plain radiographs is a very inaccurate method of quantitating bone loss in children. The apparent density of bone on radiographs is very dependent upon technical factors such as film screen characteristics, KV used, fog from scatter, and part thickness. A useful method of evaluating bone loss in children is measurement of cortical thickness of bones. In the neonate the humerus can be measured and compared to normal standards. In the hand the cortical measures of the second metacarpal are also useful. Osteoporosis in children occurs as in adults with resorption at the endosteal surface. There is usually no bone loss on the outside of the bone. When the outside diameter of the bone is small this is a manifestation of lack of growth which suggests the disease process causing it is of long standing. Dual energy x-ray absorptionmetry (DXA) shows some promise as a tool for measuring bone
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Figure 67.
a and b Rickets. There is irregularity of the metaphyses particularly in the distal femur radius and ulna with widening of the growth plates. This is a characteristic appearance of rickets. The evidence of rickets is proportional to the growth rate at the bone ends. Thus, it is greater in the distal femur than in the proximal tibia.
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mass in children.
Many pediatric conditions are associated with osteoporosis including juvenile rheumatoid arthritis, Crohn disease, other chronic diseases, and nutritional problems. In the neonate with severe pulmonary problems there may be extremely severe osteoporosis. The bones may be so thin that they fracture during usual handling (Fig. 66).
Rickets
Rickets has a very characteristic radiographic appearance which is seen only when the growth plates are open. After closure of the growth plates the disease is called osteomalacia. In rickets, there is widening of the growth plates with irregularity and fraying of their metaphyseal boarders (Fig. 67). There is often cupping of the anterior rib ends. The bones may have a very washed out appearance with very thin, fuzzy cortex (Fig. 68). Intracortical striations may be seen. Most forms of rickets have a very similar appearance except for vitamin D resistant rickets (hypophosphotemic rickets) where in older children there are thick, short, bowed bones (Fig. 69). The changes in rickets are most severe where
 a | Figure 68. Severe Rickets
a) At ten-months of age note the marked separation between the distal femur and proximal tibia with marked irregularity and fuzziness of the metaphysis. Overall mineralization is very poor.
b) Six months later after therapy the epiphyses have appeared and now there is some sclerosis of the distal metaphysis. The space between the ossified metaphyses of the femur and tibia has decreased due to their increased ossification with healing. |
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bone growth is the greatest. Therefore, the knees, ankles, and wrist are the best sites for evaluating possible rickets and monitoring therapy. The changes also are most marked when growth is rapid. Thus, in some chronic rickets, such as vitamin D resistant rickets, they may appear to increase in adolescence. In some forms of rickets there may be associated secondary hyperparathyroidism. This is particularly common in vitamin D dependent rickets, a familial condition due to lack of the second hydroxylation of vitamin D in the kidney. It is never seen in vitamin D resistant rickets. The bones affected by rickets may be bowed and fractured. During healing of rickets the zone of provisional
calcification often calcifies first and there may be lucent bands in the metaphyses. Periosteal elevation may also be seen during the healing process Fig. 68 b).
 | Figure 69.
Vitamin D resistant rickets (hypophosphatemic rickets). There is shortening and bowing of the bones which appear somewhat thickened. This appearance is not seen in other forms of rickets. The rachitic changes are not severe. |
There are many conditions that mimic rickets. These include copper deficiency in infancy, hypophosphatasia, hyperparathyroidism both primary and secondary, Shwachman syndrome, several forms of metaphyseal chondrodysplasia as well as other disorders. In many of these disorders the appearance of the metaphyses although similar to rickets, usually can be distinguished from it on radiographs.
Renal osteodystrophy
This may be difficult to separate radiologically from rickets unless the hyperparathyroidism is severe, which is uncommon in ordinary rickets. The best sign of hyperparathyroidism in older children as well as in adults is subperiosteal resorption along the radial side of the middle phalanges. It is best seen on radiographs obtained with high detail such as on mammography film. In infants and very young children resorption is often better seen in the medial part of the upper tibia, the medial proximal humerus, and medial femoral neck. Brown tumors may be seen and fractures are common. The ends of the ribs may be cupped. Diagnosis is possible on a chest radiograph by looking at the humeri, clavicles, and ribs. Slipped capital femoral epiphyses (Fig. 59) and similar changes in the shoulder joint may occur. The "slips" are really Salter I fractures and are usually symptomatic.
Andrew K. Poznanski