Abstract
The etiology of Legg-Calvé-Perthes' disease (LCPD) is unknown. There are many insights however from epidemiologic/demographic information. A systematic medical literature review regarding LCPD was performed. The incidence ranges from 0.4/100,000 to 29.0/100,000 children <15 years of age. There is significant variability in incidence within racial groups and is frequently higher in lower socioeconomic classes. The typical age at presentation ranges from 4 to 8 years (average 6.5 years), except for children from the Indian subcontinent (average 9.5 years). There is a mild familial component. The children demonstrate impaired growth in height, skeletal age, and birth weight. This impaired growth coincides with an age appropriate reduced somatomedin A activity and decreased levels of IGF. LCPD can be associated with abnormalities in the coagulation cascade, including an increase in factor V Leiden mutation, low levels of protein C and/or S, and decreased antithrombin activity. There is decreased turnover in type I collagen and synthesis of type III collagen, as well as reduced levels of urinary glycosaminoglycans in the active phases of the disorder. Subtle abnormalities in the opposite hip and other minor/major congenital defects are reported. Children with LCPD are active and score abnormally in certain standardized psychological tests.
Highlights
Legg-Calve-Perthes’ disease (LCPD) is an idiopathic osteonecrosis of the proximal capital femoral epiphysis in children
The children demonstrate impaired growth in height, skeletal age, and birth weight. This impaired growth coincides with an age appropriate reduced somatomedin A activity and decreased levels of IGF
As with any pathologic process, LCPD goes through a course of disease denoted by the Waldenstrom stages, which are synovitic, avascular, fragmentation, reossification, and healed
Summary
Legg-Calve-Perthes’ disease (LCPD) is an idiopathic osteonecrosis of the proximal capital femoral epiphysis in children. The epiphysis undergoes collapse, resorption, reossification, and eventual healing. As with any pathologic process, LCPD goes through a course of disease denoted by the Waldenstrom stages, which are synovitic, avascular, fragmentation (collapse), reossification (healing), and healed (residual). The magnitude of epiphyseal involvement is determined by the Catterall class [1], Salter-Thompson group [2], and/or lateral pillar group [3]. The Catterall class is determined on both anteroposterior and frog-lateral radiographs during the stage of maximum fragmentation, the Salter-Thompson group is determined on the frog-lateral radiograph during the avascular/precollapse stage using the subchondral crescent fracture, and the lateral pillar classification is determined on the anteroposterior radiograph during early fragmentation
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