Femoroactabular Impingement (FAI)
An abnormal shape of the hip can lead to impingement of the labrum and the edge of the acetabulum (chondrolabral junction) between the femoral head and acetabular rim during hip movements, especially deep flexion and internal rotation. These abnormalities can be grouped as ‘femoroacetabular impingement’ (FAI). There are two main types of impingement. Firstly caused by an aspherical femoral head (cam impingement lesion) or prominent acetabular rim (pincer lesion) or a combination of the two (Figure 2 a-d).
Repetitive forceful impact of the femoral head neck junction at or against the acetabular rim causes damage, exposing the articular cartilage to abnormal shear stress resulting in chondral cleavage and delamination which over a period of time leads to progressive chondral loss and more advanced degeneration-osteoarthritis.
Cam lesion can be secondary to other pathologies in the hip like slipped capital femoral physis or perthes or idiopathic pistol grip deformity (Figure 3) leading to lack of anterior clearance and reduced femoral head-neck offset.
Pincer lesion can be secondary to deep sockets as in coxa profunda and protrusion acetabuli or acetabular retroversion (Figure 4) leading to acetabular overcoverage by the anterior acetabular wall.
The concept of FAI is relatively new and was first introduced when Ito et al. in 2001, working under the supervision of Professor Reinhold Ganz, published a dynamic MRI-based study looking at the morphology of the femoral head/neck junction. They hypothesised that asphericity of the femoral head, with decreased anterior offset, may cause impingement between the femur and acetabular margin, causing labral tears.
Subsequently, Ganz et al., 2003, reviewed over 600 non-dysplastic patients who had a surgical dislocation for the treatment of FAI, mapping the areas of cartilage damage or loss and expanded on the concept of FAI, proposing that the condition was a precursor of osteoarthritis (OA). Similarly, Tanzer et al., 2004, linked osseous abnormality caused by FAI with early OA.
They linked patients from three separate studies and found a common aetiology between patients requiring hip arthroscopy for labral tear, hip cheilectomy for FAI and hip replacement for idiopathic arthritis. They found that repetitive anterior FAI resulted in groin pain, labral tear and chondral damage, leading to arthritis. Pistol grip deformity caused impingement in 97% of patients in the arthroscopic labral tear study and 100% of cases in idiopathic arthritis. These studies concluded that FAI leads to osteoarthritis.
Hip shape abnormalities characteristic of FAI are common in the young adult population. The prevalence of hip shape abnormality is reported to be higher in asymptomatic athletes than in the general population, the reasons for this remain unclear. A recent systematic review identified 26 studies for inclusion, comprising 2,114 asymptomatic hips. The prevalence of an asymptomatic cam deformity was 37%; 54.8% in athletes versus 23.1% in the general population. The prevalence of asymptomatic hips with pincer deformity was 67%. Only 7 studies reported on labral injury, which was found on MRI without intra-articular contrast in 68.1% of hips.
It is not yet understood why some people develop symptoms (FAI syndrome) while others do not. The mechanism of development probably involves a combination of factors; with hip shape abnormality combining with the level and type of activity to provoke impingement. There may also be a genetic predisposition to shape abnormality and/or soft tissue damage in these patients. The natural history of FAI and long-term progression to OA remain topics of much debate and ongoing research. Although Ganz et al. and Tanzer et al. have proposed a link between arthritis of the hip and FAI, it is too soon to conclude whether surgery will delay the progression of osteoarthritis.