Biomechanical properties of bone and cartilage in growing femoral head following ischemic osteonecrosis.

Legg-Calve-Perthes disease (LCPD) is one of the most common causes of a permanent deformity of the femoral head among pediatric hip disorders. Mechanical loading of the osteonecrotic femoral head undergoing repair is thought play a significant role in the development of the femoral head deformity. This study measured the mechanical properties in uniaxial unconfined compression tests of epiphyseal bone and cartilage from immature femoral heads following surgical induction of osteonecrosis using an established piglet model. Both the modulus and yield strength of bone cores from the infarcted heads were significantly lower by 50%-60% than those of the contralateral normal control heads by 2 weeks after surgery and they remained this low for 8 weeks. No consistent difference in the bone mineral or collagen content per dry weight in the bone cores was observed. Cartilage modulus and yield strength were significantly lower at 2 weeks and remained low for 8 weeks. Cartilage collagen and glycosaminoglycan content per dry weight did not differ significantly between control and infarcted heads at any time point. However, the relative proportion of chondroitin 6-sulfate increased significantly over the 8-week postoperative period, which correlated with an increase in cartilage thickness. These results indicate that the deterioration of the mechanical properties of the epiphyseal bone and cartilage likely plays a significant role in the pathogenesis of the femoral head deformity in LCPD. (

Indentation properties of growing femoral head following ischemic necrosis.

Little is known about the mechanical properties of the growing femoral head as it develops deformity following ischemic injury. The purpose of this study was to determine the indentation stiffness of growing femoral head following ischemic injury and to correlate the changes in stiffness with radiographic and histopathologic changes in the femoral head as it develops deformity. Following the induction of ischemia in 24 piglets, indentation testing of whole femoral heads was performed at 2, 4, and 8 weeks, as well as on femoral heads from eight sham operated animals. At 2 weeks, a 52% reduction of indentation stiffness was observed in the infarcted femoral heads compared to the control heads (p=0.004). The bony epiphyses in infarcted femoral heads were smaller due to growth arrest but they were not deformed. Histologically, no evidence of repair was seen. At 4 and 8 weeks, the indentation stiffness in the infarcted femoral heads was reduced by 75% (p<0.000001) and 72% (p=0.001) respectively compared to the control heads. Variable degree of femoral head deformity and repair was observed at 4 weeks. Severe deformity with extensive revascularization and repair were observed at 8 weeks. Although epiphyseal cartilage was thickened on the infarcted femoral heads only a weak correlation was found between the increase in the cartilage thickness and the decrease in the indentation stiffness (R(2)=0.55). These results indicate that the indentation properties of growing femoral head were significantly affected by ischemic injury, prior to the presence of repair process and deformity. A further decrease in the indentation stiffness was concomitant with repair of the infarcted head. These findings suggest that a reduction in the mechanical properties of the infarcted femoral head include both a cartilage and a bony component, which cannot be differentiated at this point. The study validates early institution of treatments that are aimed at limiting the mechanical loading of the affected hip. The study also suggests that in order to minimize the mechanical compromise of the infarcted femoral head, early institution of treatments aimed at stimulating new bone formation and retarding osteoclastic bone resorption may be beneficial.