Objectives. An experimental piglet model induces avascular necrosis (AVN) and deformation of the femoral head but its secondary effects on the developing acetabulum have not been studied. The aim of this study was to assess the development of secondary acetabular deformation following femoral head ischemia. Methods. Intracapsular circumferential ligation at the base of the femoral neck and sectioning of the ligamentum teres were performed in three week old piglets. MRI was then used for qualitative and quantitative studies of the acetabula in operated and non-operated hips in eight piglets from 48 hours to eight weeks post-surgery. Specimen photographs and histological sections of the acetabula were done at the end of the study. . Results. The operated-side acetabula were wider, shallower and misshapen, with flattened labral edges. At eight weeks, increased acetabular cartilage thickness characterised the operated sides compared with non-operated sides (p < 0.001, ANOVA). The mean acetabular width on the operated side was increased (p = 0.015) while acetabular depth was decreased anteriorly (p = 0.007) and posteriorly (p = 0.44). The cartilage was thicker, with delayed acetabular bone formation, and showed increased vascularisation with fibrosis laterally and focal degenerative changes involving chondrocyte hypocellularity, chondrocyte cloning, peripheral pannus formation and surface fibrillation. . Conclusions. We demonstrate that femoral head AVN in the young growing piglet also induced, and was coupled with, secondary malformation in acetabular shape affecting both articular and adjacent pelvic cartilage structure, and acetabular bone. The femoral head model inducing AVN can also be applied to studies of acetabular maldevelopment, which is less well understood in terms of developing hip malformation. Cite this article: Bone Joint Res 2014;3:130–8

Introduction: Shortening of the affected limb has frequently been observed in children with Legg-Calvé-Perthes disease (LCPD). Many factors have been thought as the cause of this residual shortening after LCPD. There has been no clear answer regarding which is more responsible for the residual shortening between coxa plana and the disturbed physeal growth. To clarify the main cause of residual shortening, clinical and experimental studies were conducted. Materials and Methods: For clinical study, 40 LCPD children with definite shortening were evaluated. This included 20 children with active disease and 20 children at skeletal maturity. Teleoroentgenograms were obtained for all children. For the experimental study, LCPD simulation in 30 piglets was achieved by disrupting the blood supply to the capital femoral epiphysis. Results: In the clinical study, total shortening in the skeletal maturity group was 14.6 mm, which consisted of 3.2 mm (16%) shortening by decreased epiphyseal height and 11.5 mm (84%) shortening by physeal growth disturbance. Total shortening in the active disease group was 7.9 mm, which consisted of 6.4 mm (84%) decrease of epiphyseal height and 1.5 mm (16%) shortening by physeal growth disturbance. In the experimental study, overall shortening (13.6 mm) in the piglet model showed a predominance of disturbed physeal growth. The proportions were 3.2 mm (24%) by epiphyseal height decrease and 10.4 mm (76%) by physeal growth disturbance. Conclusion: Physeal growth disturbance was mostly responsible for the residual shortening following LCPD. However, in the stages of active disease, the shortening of the extremity was mainly caused by a decrease of epiphyseal height

Aims

We wanted to evaluate the effects of a bone anabolic agent (bone morphogenetic protein 2 (BMP-2)) on an anti-catabolic background (systemic or local zoledronate) on fixation of allografted revision implants.