Effect of Curettage and DBM-CaSO4 Graft for the Treatment of Ischemic Necrosis of the Capital Femoral Epiphysis in Immature Pigs

Lee, Ki Seok; Kim, Sun Yong; Choi, In Ho

Abstract

PURPOSE
The purpose of this study was to determine the effect of curettage and DBM complex graft as a new treatment modality for LCP disease using piglet capital femoral epiphysis ischemic necrosis model.
MATERIALS AND METHODS
Five to six weeks old piglets were used for the experiment. Ischemic necrosis of the capital femoral epiphysis was surgically induced by cervical ligation on both sides. Three weeks following ischemic insult, the left hip joint was approached medially. About 15% of the necrotic capital femoral epiphysis was curetted through a window which was opened at medial cervical cortex, then, demineralized bone matrix complex was engrafted. The right femoral heads served as controls. Piglets were sacrificed three, six, nine, and twelve weeks following were harvested for histologic examination.
RESULTS
In control group, photomicrographs of specimens showed central necrosis and fibrovascular invasion in capital femoral necrosis at three weeks after ischemic insult. Six, nine, and twelve weeks following ischemic insult, fibrovascular invasion advanced without noticeable new bone formation and collapse of femoral head progressed. At twelve weeks, definite coxa plana developed. In curettage and DBM complex graft group, there was evident new bone formation observed in the site of DBM complex graft. At three weeks, new bone formation along with fibrovascular invasion was observed around the engrafted DBM complex mainly in the cervical metaphyseal area. At six and nine weeks, new bone formation progressed into the engrafted DBM complex in the cervical metaphysis and around the engrafted DBM complex in the capital femoral epiphysis. At twelve weeks, new bone along with new cartilage formation was observed in the capital femoral epiphysis.
CONCLUSION
In conclusion, curettage and DBM complex graft is thought to be an effective treatment modality that promote regeneration of ischemic necrosis of capital femoral epiphysis.