A Mechanism of the Production of Pseudofractures in Osteomalacia (Milkman's Syndrome)

Abstract
Osteomalacia is a metabolic disease of bone in which there is a deficient mineralization of the bony matrix. The amount of matrix present is normal or slightly increased. The defective deposition of calcium salts is due to the lowered concentration of calcium or phosphorus, or both, in the body fluids, as a result either of impaired absorption from the gastrointestinal tract or increased renal excretion. Because of their decreased mineral content, the bones are weakened, becoming soft and bending readily. Deformities of the extremities, pelvis, vertebrae, and skull may occur. As a result of the weakening of the bones, the osteoblasts are stimulated to lay down new bone matrix and elaborate alkaline phosphatase, which is usually present in abnormal concentration in the blood serum (1). In some cases of osteomalacia, multiple, almost symmetrical, radiolucent bands of diminished density, resembling fractures, occur in the cortex of the bone. These pseudofractures are seen most frequently in the axillary border of the scapula, the ribs, the pubic rami, the medial aspect of the neck of the femur, the iliac bones, and the radii and ulnae. They were first described by Milkman and have come to be known as “Milkman's syndrome” (7, 8). Milkman did not realize that the pseudofractures in his patient were due to osteomalacia, but a review of his case and of similar cases, by Albright (1), indicates that the classical syndrome of Milkman is invariably associated with a primary osteomalacia. In some instances pseudofractures are apparent on roentgenograms before there has been sufficient generalized demineralization of the skeleton to be determined by the ordinary roentgen examination. There have been many differences of opinion as to the actual mechanism of the production of pseudofractures in osteomalacia. Camp and McCullough (3), in an excellent review of the literature before 1941, concluded that pseudofractures were always associated with conditions that weaken the bones or that produce unusual strains to which the bones are not adapted. They believed that those bones which were subjected to the greatest mechanical stresses were the ones most frequently involved. According to these writers, pseudofractures occurred in many diseases other than osteomalacia, such as early and late osteogenesis imperfecta, fragilitas ossium, hyperparathyroidism, hyperthyroidism, Paget's disease, adrenal-pituitary bone dystrophy, severe chronic acidosis or hyperglycemia, congenital syphilis, osteomyelitis, osteopetrosis, states of overloading of bone, and certain blood dyscrasias. We disagree with Camp and McCullough and agree with Albright in his assertion that the radiolucent bands found in the diseases mentioned are not the same as those present in Milkman's syndrome. It is true that in these diseases there are occasionally shadows resembling the radiolucent bands found in Milkman's syndrome, but they differ in the following respects: they usually are not bilaterally symmetrical; there are no definite sites of predilection; they heal rapidly without therapeutic measures to increase the body stores of calcium and phosphorus; and they usually are present in areas of localized bone disease or as a result of trauma.
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