Legg-Calvé-Perthes disease (LCPD) is a relatively common condition affecting around 4 in 100 000 children aged four to ten years. The extent of femoral head collapse and deformity following LCPD is the single most important factor contributing to long-term outcome.1,2 The severity of the residual deformity at skeletal maturity is most commonly described using the Stulberg classification.3 Treatment strategies during the active stage of LCPD frequently involve measures to minimise loads across the hip joint whilst maintaining movement, with the hope that this will prevent femoral head collapse and deformity. Treatment includes activity limitation, active/passive range of motion exercises and bracing, all complemented by appropriate analgesic medication. However, these strategies have not been proven to be effective in preventing femoral head collapse. In the long-term follow-up study by Larson et al,1 no difference was found between hip-related morbidity in patients that were treated with bracing, those treated with active range of motion strategies and those receiving no treatment. A recently published review also failed to demonstrate any benefit of bracing over no treatment.4 The failure of these treatment methods could possibly be ascribed to the fact that, even during slow walking, the forces acting across the hip joint far exceed body weight.5 Therefore, if, as it appears, we cannot prevent collapse of the ‘vulnerable/dead’ epiphysis, researchers will have to resort to exploring strategies that might strengthen the weakened epiphysis, rendering it more resistant to forces that lead to collapse and subsequent deformity.
This article summarises the recent advances and experimental strategies directed at preventing femoral head deformity in LCPD.
Pathophysiology of collapse and deformity
During the initial phase of LCPD as described by Waldenstrom,6 there is disruption of the blood flow to the femoral head with subsequent necrosis of the marrow space and deep layers of articular …