Extract
Hip impingement as a mechanism of hip pain and osteoarthritis continues to be an active area of investigation. Previously, theoretical analysis of slipped capital femoral epiphysis deformity demonstrated that with increasing proximal femoral deformity (i.e., increasing severity of the slipped capital femoral epiphysis), the proximal head-neck junction will start to impinge against the acetabulum with less hip flexion. Abraham et al.1 compared the cartilage degeneration pattern in sixteen hips with osteoarthritis due to slipped capital femoral epiphysis with that in eighty-four hips with primary osteoarthritis in a study of patients undergoing hip arthroplasty. The patients in the slipped capital femoral epiphysis group were collected over a ten-year period and were identified on the basis of a history of hip surgery in adolescence for a diagnosis consistent with slipped capital femoral epiphysis. The patients in the primary osteoarthritis group were identified from an arthroplasty practice after the exclusion of other causes of osteoarthritis such as hip dysplasia or trauma. The patients in the slipped capital femoral epiphysis group underwent arthroplasty at a mean age of forty-six years, which was eleven years younger than the mean age of the patients in the primary osteoarthritis group at the time of surgery. As expected, the patients in the slipped capital femoral epiphysis group had loss of the anterior head-neck offset, causing femoroacetabular impingement, whereas most of those in the primary osteoarthritis group had a preserved anterior head-neck offset. The cartilage degeneration patterns in these two groups were characteristically different. The patients in the slipped capital femoral epiphysis group had superior peripheral acetabular cartilage damage, consistent with the area of impingement, whereas those in the primary osteoarthritis group had more central acetabular cartilage damage and preservation of the superior peripheral cartilage. The patterns of cartilage loss suggested that the mechanism of cartilage damage in these two groups is different. The coincident location of the area of impingement with the loss of cartilage in the slipped capital femoral epiphysis group is highly suggestive that the abnormal mechanics in patients with slipped capital femoral epiphysis are responsible for the development of osteoarthritis in this group.