Hypothesis: fetal movement influences fetal and infant bone strength

Infants who present with multiple unexplained fractures in which there is no prior trauma, no radiographic evidence of metabolic bone disease, and no biochemical evidence of metabolic bone disease are almost always diagnosed as victims of child abuse, even though parents and caregivers deny wrongdoing. Such a diagnosis has far reaching implications for the infant and family. This article describes the clinical features of 65 such infants with multiple unexplained fractures in which the parents and caregivers deny wrongdoing and in which child abuse was diagnosed. These infants have the phenotype of temporary brittle bone disease that was described by Paterson. A striking observation in these young infants is the pregnancy history of decreased fetal movement. A hypothesis is suggested as an alternative explanation for the mechanism of these fractures in these infants--namely temporary brittle bone disease from fetal immobilization. This hypothesis states that fetal bone loading through fetal movement is essential for the formation of bones of normal strength. This hypothesis is an application of Frost's mechanostat/bone-loading model of bone physiology to the prenatal period of bone formation. This hypothesis explains many of the other observations about temporary brittle bone disease including the early onset of the fractures in the first several months of life, the lack of bruising, the lack of other internal organ injury, and the low risk profile of many of the parents for committing child abuse.