FAI (femoroacetabular impingement)

FAI is an incongruent ball-and-socket leading to repetitive impingement at terminal hip motion.  It is a recognized cause of hip pain and a risk factor for future arthritis [1-3].

Background. There is always natural variation to the shape of our bones and there is a wide spectrum that falls within "normal".  However, its becoming increasingly apparent that certain hip morphology can increase the risk of acute pain and future osteoarthritis.  The correlation between anatomy and symptoms, anatomy and osteoarthritis, is not clear in many cases due to confounding variables.  Yet a properly identified patient can avoid debilitating pain or the moderate probability of early hip arthritis by undergoing targeted procedures that re-reshape the hip joint.  

The abnormal shape can be femur-based, called Cam Impingement, and is due to an aspherical head (increased anterior-lateral contour) or reduced head-neck offset that causes the prominent part of the head to cause repetitive “outside-in” microtrauma, also know as an inclusion type injury, meaning that the asphericity enters the joint and damages the cartilage. Cam impingement is most common in young, athletic males, and may be associated with a subclinical SCFE that was missed in childhood [4-6].

The abnormal shape can be acetabulum-based, called Pincer Impingement, whereby an area of rim over-coverage causes repetitive trauma via direct impact of the rim against the femoral neck.  The pincer impingement may be caused by acetabular retroversion, general over-coverage, or protrusio.   This linear contact between the rim and head-neck junction causes anterior-superior labral separation and chondral damage of the acetabulum (similar to Cam impingement).  Chronic leverage of the head in the acetabulum creates chondral injury in the ‘contre-coup’ region of the posteroinferior acetabulum. Pincer deformities are more common in middle-aged women. The lesions created are also smaller than those from cam deformities, and, thus, more benign.

FAI can also be a combined Cam-Pincer deformity.

Importantly, the pathology of FAI is not only created by abnormal anatomy, but also by vigorous activity particularly at the extremes of motion.  Impingement occurs at terminal motion, and daily activity rarely pushes the hip to this limit.  Therefore, FAI is most commonly seen in athletes, even though subtle abnormalities of hip morphology may present commonly in the general population.

Association with Osteoarthritis (natural history). Solomom suggested that over 90% of hip OA can be to attributed to underlying etiology: mechanical, traumatic, inflammatory, or metabolic [7].  Ganz and others expanded on this theory by defining pathologic hip morphology (hip dysplasia and FAI) [8, 9].

Patients with FAI demonstrate peripheral cartilage degeneration in contrast to primary hip arthritis, which shows a central distribution. [10] [11]

It has been reported that 40% of people who develop OA have a pistol-grip deformity.  There are many studies that examine the hip morphology of patients under 60 yo with “idiopathic” osteoarthritis and identified high incidence of “abnormal” parameters [12].  Between 40 – 90% of patients under 60 yo with end-stage OA have significant FAI morphology.

There is an association [13] [14] [15] [16]. Particularly the association between an increasing alpha-angle in Cam impingement (over 60°) and more severe arthritis at time of arthroscopy [17] [18].  MRI studies also identified cartilage damage with CAM deformity despite normal x-ray [19] [20].

What is the association? The cause and effect of FAI is less clear. Some studies suggest a high incidence of Cam or Pincer morphology in non-OA patients [21], suggesting FAI may not be a direct cause in many cases, but rather result of selection bias. 

Some believe it is a normally occurring variant in active populations.  Reports of FAI athletic teams – ballet 90%, hockey 68% [22], 50% youth soccer [23], 48% track and field [24] show a high prevalence of “abnormal” hip morphology. The number that progress to clinically relevant OA will assuredly be less.  Abnormal morphology in the general population was seen in 15% of men, 7% of women [21] [25].  

Examining a rather homogenous population of 1,000 young males in the Swiss military, 24% incidence based on MRI of cam-type deformity, which increased to 60% if they presented with low hip internal rotation (<25°) [26].  There was correlation between these Cam deformities and risk for hip disease – 2.3x risk for cystic changes and 2.8x risk for labral tears [27].  While this demonstrates a risk for MR associated pathologic changes, it is not an association with arthrosis (joint disease seen on xray) or arthritis (clinically significant degenerative joint disease). This study was not likely to show degenerative changes in such a young population, as degeneration takes decades to occur, yet by showing signs of early hip damage, it hints at risk for future OA.  Nonetheless, there is no good quality study to demonstrate a direct correlation between FAI and OA.

There is controversy about the generally high incidence of FAI.  There is always person-to-person variation in bone morphology, and the more measurements made, the more chance that something will be “abnormal”.  The challenge with FAI is the large gray area of morphology that may be abnormal but is probably within “normal”, meaning not clinically significant variation.  Furthermore, the aforementioned study examining the Swiss military, demonstrated a 40% incidence of asymptomatic antero-lateral labral tears, suggesting that general wear occurs in an active population and may not be directly caused by FAI [27]

There are some studies that evaluate patients with hip pain and mild arthritis [28], or a sampling of the normal population, and identify FAI (particularly the alpha angle) as a risk factor for future THA [29].  The majority of pathologic hips demonstrated signs of arthrosis without an endpoint of end-stage DJD or THA, questioning whether FAI leads to clinically significant disease, requiring surgical intervention. Beyond the elevated alpha angles, it is less clear what additional risk factors are associated with progression to clinically significant OA.

History and Physical. Most patients are young, active individuals.  Patients present with groin pain and may report that it travels to their buttock or greater trochanter. It may initiate after minor trauma, but tends to be insidious in onset. The pain can be intermittent and exacerbated by excessive demand on the hip from athletic activities or even from prolonged walking or sitting. They often will have delay in diagnosis, mild-moderate, prolonged, and generalized groin symptoms.

On physical examination, patients may present with a limp.  They can have decreased ROM, particularly with internal rotation; the impingement test has been found to correlate with surgical findings of FAI. This maneuver is done with the patient supine, the hip is flexed to 90 degrees and then internally rotated. Passive adduction brings the femoral neck in contact with the acetabular rim and if it increases pain, this is suggestive of anterior impingement. Posterior impingement is tested with the provocative test. The patient is supine with the leg hanging free off the bed to create extension at the hip. The hip is then externally rotated. Pain in this position is positive for posteroinferior impingement.

Imaging. XRs of FAI can often be normal or only show subtle changes.  This is due to the location of the Cam deformity.  The most common location is at the 1 o'clock position, which cannot be seen on AP or lateral view of the femur.  The 2nd most common location is at the 2 o'clock position, which can be seen on a lateral X-ray, and 3rd most common is at the 12 o'clock position, which can be seen on AP x-ray.  Thus, while the x-ray can pick up some cases of offset, it misses the most common site of occurence.

A reduced offset at the femoral neck/head junction and changes to the acetabular rim from ossification of the labrum, as seen with a double line or os acetabuli, can be seen. Herniation pits are fibrocystic changes of the anterosuperior femoral neck visualized as round or oval radiolucencies with thin zones of sclerosis. These are signs of acquired degenerative changes.

Evaluation for coxa profunda or protrusio acetabuli is done on an AP pelvis as an AP hip can change the projection. The acetabular fossa is medial to the ilioischial line with coxa profunda, but the femoral head is still lateral. With protrusio, both the acetabular fossa and femoral head lay medial. 

MR arthrogram is also used for evaluation. Labral pathology can be identified both on degree and position. The labrum can be described as detached, with separation of the labral-bone interface; as showing an intrasubstance tear, where there is fluid or contrast extending into the labrum; or as denuded, where it is absent.  

The alpha angle can be measured on axial oblique views or using an axial reconstruction of the images.  The angle is between a line down the center of the femoral neck and a line to “Point A”.  Point A is the anterior point where the distance from the center of the head (HC) exceeds the radius of the femoral head. There is debate over the value of this measurement, where the sensitivity, specificity, positive and negative predictive values have been reports as 39.3%, 70.1%, 54.7%, and 53.5% [30]. In this study, the best test was actually the clinical impingement test. Furthermore, a wide neck, osteophytes, and posterior displacement of the head can all increase the alpha angle. The cutoff has been debated, between 50 and 55 degrees.

            -MEN alpha: Pathologic: > 83; Borderline: 69-82, normal < 68.

            -WOMEN: Pathologic > 57, borderline: 51-56, , normal < 5

Treatment. Nonoperative treatment includes activity modification by restriction of athletics and general demand on the hip.  Therapy to increase ROM and strength is often not helpful or counterproductive.

Surgical treatment aims to improve clearance for hip motion and alleviation of femoral abutments against the acetabular rim. Open treatment has mostly been done with the surgical hip dislocation, which requires a greater trochanter osteotomy and careful preservation of the blood supply to the femoral neck. However, it does allow for 360° inspection and treatment of the acetabulum and femoral head. To address the femoral head, an excision osteoplasty is normally done. There is often a clear demarcation between normal femoral articular cartilage and the area of the head subjected to FAI. The hyaline cartilage may show fraying and furrowing and areas of reddish or blue hue. The acetabulum rim is also usually treated with resection osteoplasty. In cases of retroversion causing FAI, the role for a reverse PAO has also been discussed. Patients are usually toe touch weight bearing for 8 weeks to allow for full healing.

More recently, arthroscopic management of these pathologies has increased in popularity. For arthroscopic resection of a cam lesion, complications do exist, including residual cam lesion, over-resection of the femoral neck, femoral neck fracture, AVN, and capsular adhesion. For the acetabulum, procedures entail accessing the joint capsule, identifying the impinging lesion, protecting uninjured labrum, resection of bony impingement, and reattachment of uninjured labrum to the bony rim.

Treatment is more successful in patients with less signs of arthritis. Patients with Tonnis grade 2 or 3 may have temporary relief in pain, but no long-term difference with conversion to THA.  Furthermore, patients with more retroversion have a decreased, albeit still clinical, improvement compared to those with normal or ante-version [31]. The role for a reverse PAO versus just arthroscopic procedures needs to be further delineated in this patient population.


1.         Sankar, W.N., et al., Femoroacetabular impingement: defining the condition and its role in the pathophysiology of osteoarthritis. J Am Acad Orthop Surg, 2013. 21 Suppl 1: p. S7-S15.

2.         Sankar, W.N., T.H. Matheney, and I. Zaltz, Femoroacetabular impingement: current concepts and controversies. Orthop Clin North Am, 2013. 44(4): p. 575-89.

3.         Sankar, W.N., et al., Staging of hip osteoarthritis for clinical trials on femoroacetabular impingement. J Am Acad Orthop Surg, 2013. 21 Suppl 1: p. S33-8.

4.         Bedi, A., et al., Assessment of range of motion and contact zones with commonly performed physical exam manoeuvers for femoroacetabular impingement (FAI): what do these tests mean? Hip Int, 2013. 23 Suppl 9: p. S27-34.

5.         Bedi, A., et al., Elevation in circulating biomarkers of cartilage damage and inflammation in athletes with femoroacetabular impingement. Am J Sports Med, 2013. 41(11): p. 2585-90.

6.         Bedi, A. and B.T. Kelly, Femoroacetabular impingement. J Bone Joint Surg Am, 2013. 95(1): p. 82-92.

7.         Solomon, L., Patterns of osteoarthritis of the hip. J Bone Joint Surg Br, 1976. 58(2): p. 176-83.

8.         Harris, W.H., Etiology of osteoarthritis of the hip. Clin Orthop Relat Res, 1986(213): p. 20-33.

9.         Ganz, R., et al., The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin Orthop Relat Res, 2008. 466(2): p. 264-72.

10.       Wagner, S., et al., Early osteoarthritic changes of human femoral head cartilage subsequent to femoro-acetabular impingement. Osteoarthritis Cartilage, 2003. 11(7): p. 508-18.

11.       Reiman, M.P., et al., Diagnostic accuracy of clinical tests for the diagnosis of hip femoroacetabular impingement/labral tear: a systematic review with meta-analysis. Br J Sports Med, 2015. 49(12): p. 811.

12.       Kowalczuk, M., et al., Does Femoroacetabular Impingement Contribute to the Development of Hip Osteoarthritis? A Systematic Review. Sports Med Arthrosc, 2015. 23(4): p. 174-9.

13.       Ganz, R., et al., Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res, 2003(417): p. 112-20.

14.       Clohisy, J.C., et al., Radiographic structural abnormalities associated with premature, natural hip-joint failure. J Bone Joint Surg Am, 2011. 93 Suppl 2: p. 3-9.

15.       Lung, R., et al., The prevalence of radiographic femoroacetabular impingement in younger individuals undergoing total hip replacement for osteoarthritis. Clin Rheumatol, 2012. 31(8): p. 1239-42.

16.       Ecker, T.M., et al., Pathomorphologic alterations predict presence or absence of hip osteoarthrosis. Clin Orthop Relat Res, 2007. 465: p. 46-52.

17.       Johnston, T.L., et al., Relationship between offset angle alpha and hip chondral injury in femoroacetabular impingement. Arthroscopy, 2008. 24(6): p. 669-75.

18.       Pollard, T.C., et al., The hereditary predisposition to hip osteoarthritis and its association with abnormal joint morphology. Osteoarthritis Cartilage, 2013. 21(2): p. 314-21.

19.       Zilkens, C., et al., Symptomatic femoroacetabular impingement: does the offset decrease correlate with cartilage damage? A pilot study. Clin Orthop Relat Res, 2013. 471(7): p. 2173-82.

20.       Kumar, D., et al., Association of cartilage defects, and other MRI findings with pain and function in individuals with mild-moderate radiographic hip osteoarthritis and controls. Osteoarthritis Cartilage, 2013. 21(11): p. 1685-92.

21.       Frank, J.M., et al., Prevalence of Femoroacetabular Impingement Imaging Findings in Asymptomatic Volunteers: A Systematic Review. Arthroscopy, 2015. 31(6): p. 1199-204.

22.       Brunner, R., et al., Prevalence and Functional Consequences of Femoroacetabular Impingement in Young Male Ice Hockey Players. Am J Sports Med, 2016. 44(1): p. 46-53.

23.       Johnson, A.C., M.A. Shaman, and T.G. Ryan, Femoroacetabular impingement in former high-level youth soccer players. Am J Sports Med, 2012. 40(6): p. 1342-6.

24.       Kapron, A.L., et al., In-vivo hip arthrokinematics during supine clinical exams: Application to the study of femoroacetabular impingement. J Biomech, 2015. 48(11): p. 2879-86.

25.       Jung, K.A., et al., The prevalence of cam-type femoroacetabular deformity in asymptomatic adults. J Bone Joint Surg Br, 2011. 93(10): p. 1303-7.

26.       Reichenbach, S., et al., Prevalence of cam-type deformity on hip magnetic resonance imaging in young males: a cross-sectional study. Arthritis Care Res (Hoboken), 2010. 62(9): p. 1319-27.

27.       Reichenbach, S., et al., Association between cam-type deformities and magnetic resonance imaging-detected structural hip damage: a cross-sectional study in young men. Arthritis Rheum, 2011. 63(12): p. 4023-30.

28.       Agricola, R. and H. Weinans, Femoroacetabular impingement: what is its link with osteoarthritis? Br J Sports Med, 2016. 50(16): p. 957-8.

29.       Nicholls, A.S., et al., The association between hip morphology parameters and nineteen-year risk of end-stage osteoarthritis of the hip: a nested case-control study. Arthritis Rheum, 2011. 63(11): p. 3392-400.

30.       Lohan, D.G., et al., Cam-type femoral-acetabular impingement: is the alpha angle the best MR arthrography has to offer? Skeletal Radiol, 2009. 38(9): p. 855-62.

31.       Fabricant, P.D., et al., The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am, 2015. 97(7): p. 537-43.