Femoroacetabular Impingement: A Newly Opened Window

The pathomechanisms of secondary osteoarthritis (OA) of the hip such as avascular necrosis (AVN), posttraumatic OA, infection, and hip dysplasia were widely known. However, until the introduction of the theory of femoroacetabular impingement (FAI) syndrome by Ganz et al (1) the exact pathogenesis for early onset idiopathic OA in hips without dysplasia was covered. They described the clinical, radiographic and intraoperative findings of this syndrome. From the advent of this topic a surge in the number of the published articles regarding the various aspects of FAI has appeared. This cleanly reveals its clinical importance. Today most physicians believe that untreated impingement or nonsurgical treatment leads to early OA, whereas the optimal surgical treatment would basically hamper or postpone the need for hip replacement. FAI initiates from abutment of the femoral head-neck junction with acetabular-labral complex due to the morphologic deformities of femoral head or acetabulum. Any developmental, posttraumatic or surgically induced deformity can alter the normal anatomic shape of the femoroacetabular unit and then this deformity elicits the impingement in the terminal range of hip motion. New evidences show that in young active patients, subtle morphologic deviations affecting the proximal femur and/or the acetabulum are the most common causes of FAI .