Background: Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in Legg-Calve-Perthes disease are due to repair. Little is known if bone material properties are altered following ischemic necrosis of the juvenile femoral head. Purpose of this study was to determine bone matrix mineralization density, an important determinant of bone quality and strength, in an experimental model of juvenile ischemic osteonecrosis.

Methods: Ten piglets were surgically induced with ischemic osteonecrosis and euthanized at 4- and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone Mineralization Density Distribution (BMDD) parameters were determined using quanitative backscattered electron imaging (qBEI) in the epiphyseal calcified cartilage, subchondral and central trabecular bone region. Histological assessment was also performed.

Results: In necrotic calcified epiphyseal cartilage matrix as well as subchondral bone matrix, a significant increase in the degree (CaMean, Ca Peak) as well as the homogeneity of mineralization (CaWidth reduction) and a significantly reduced amount of low mineralized matrix (CaLow) were observed at 4 and 8 weeks post ischemia induction. In the necrotic central trabecular region a significant increase in the degree and homogeneity of mineralization, as well as a decrease in the amount of low mineralized bone was found at 8 weeks post-ischemia induction, but not at 4-weeks, indicating that changes in necrotic trabecular bone occur more slowly. Changes in the necrotic calcified cartilage region were more dramatic than in necrotic bone.

Discussion: Our findings indicate that the mineralization process continues in the necrotic calcified cartilage and bone following femoral head infarction. This leads to an increased degree and homogeneity of mineralization in calcified cartilage and bone matrices and therefore altered material properties. These alterations in matrix mineralization status would lead to more brittle bone, prone to micro-fractures and may partly explain the weakening of structural properties of necrotic bone. Moreover, an increase in calcified cartilage and bone mineralization may also explain the increased radiodensity seen in the early stage of Perthes disease prior to repair and/or structural failure.