The definition of the clinical condition of FAI has recently been described in detail by Sankar et al. [19]. The Medical Subject Headings thesaurus of the United States National Library of Medicine defines FAI as a clinical entity in which a pathological mechanical process causes hip pain when morphological abnormalities of the femur and/or acetabulum, combined with vigorous hip motion (especially at the extremes), lead to repetitive collisions that damage the soft tissue structures within the joint itself. This definition contains five essential elements: (1) abnormal morphology of the femur and/or acetabulum; (2) abnormal contact between the two structures; (3) vigorous, supra-physiologic motion which underlies the latter; (4) repetitive motion resulting in the continuous insult; and (5) the presence of soft tissue damage. In order to diagnose an individual with FAI accurately, three criteria must be met: the patient must (1) be symptomatic in the affected hip, as well as exhibit (2) clinical and (3) radiological features consistent with FAI. Clearly, the spectrum of disease presentation must be weighed against the signs and symptoms of the individual patient when considering the diagnosis of FAI.

Femoroacetabular impingement is not a disease per se but rather a process by which the human hip can fail [20]. A variety of abnormalities of the bony acetabulum and/or femur, combined with terminal and/or rigorous hip motion, can lead to repetitive collisions that damage the soft tissue structures (labrum and/or cartilage) at the acetabular rim. More than one century ago, collisions between the femur and the acetabulum had been reported anecdotally [1–6]; these reports described intra-articular damage of the hip caused by a pathological relationship between the proximal femur and the acetabulum as sequelae of childhood disorders and femoral neck fracture. As these reports were merely single observations without conceptual follow-up, it was not until the introduction of a surgical technique for dislocating the hip that direct observations could be made of such pathomechanical process [7]. These observations and clinical follow-up lead to the development of the concept of FAI as a mechanical cause of hip OA. The concept of FAI, as pioneered by Ganz et al. [7], associates subtle, often unrecognized developmental alterations of the hip with the subsequent development of OA. This theory has been compared to previous work [1, 3, 5, 21] which has described secondary OA in the setting of grossly visible deformities (e.g., acetabular dysplasia, femoral pistol grip, and head tilt).

Based upon intraoperative inspection of patients suffering from hip pain, Ganz et al. [7] described two distinct types of intra-articular pathologies frequently found in these patients. The pathomechanical concept was called FAI based upon the mechanism of joint damage leading to a distinct pattern of chondral and labral lesions of the hip. Femoral-sided pathomorphologies were called cam-type FAI, and acetabular-sided alterations were termed pincer-type FAI . These two types of impingement can coexist, and a wide variation in the frequency may also exist across different ethnic and racial subgroups.

Another mechanical distinction within the diagnosis of FAI is inclusion injuries (cam-type FAI) and impaction injuries, which are due to pincer FAI but also may be caused by a decreased head-neck offset. As the terms cam- and pincer-type FAI are well established in the literature, this report will stay within the confines of this terminology. In a Swiss cohort described by Beck et al., 47 % (27 of 57 hips) with cam-type impingement had an associated acetabular deformity, and 63 % (34 of 54 hips) with pincer-type impingement had an abnormally shaped femoral head [22].

Cam-type impingement is caused by insufficient concavity of the femoral head-neck junction anterolaterally. Therefore, this region of the femoral head has an increased radius of curvature that cannot be accommodated by the tightly congruent acetabulum. As a consequence, the femoral head, with its abnormal morphology, repetitively collides with the rim of the acetabulum during supra-physiologic motions. These collisions lift up the labrum; rather than predominantly direct damage, a shearing of the adjacent articular cartilage may potentially disrupt the chondrolabral junction. This process can cause the labrum and articular cartilage to delaminate from the subchondral bone, which is seen most frequently at the anterosuperior aspect of the acetabular rim [23]. Intraoperative findings suggest that the predominant lesion due to cam FAI is delamination of the cartilage, while the labral tissue is relatively spared [23].

Pincer-type impingement is an acetabular-based deformity caused by over-coverage of the femoral head by the acetabulum. The over-coverage may be focal (cephalad retroversion or true acetabular retroversion) or global (acetabular protrusion), depending on the underlying pathoanatomy. The deformity leads to contact of the labrum against the femoral neck during hip motion [24]. The mechanical features of pincer-type FAI are different from those of cam-type FAI: the contact between the proximal femur and the acetabulum is linear, leading to failure of the labrum, but damage to the articular cartilage is initially limited to the acetabular rim [23]. Pincer-type impingement caused by focal over-coverage may be secondary to cephalad over-coverage or true acetabular retroversion, with only the posterior wall insufficiently covering the posterior femoral head. Both conditions present with similar clinical symptoms; however, true acetabular retroversion represents an entirely different mechanical problem of over-coverage anteriorly combined with under-coverage posteriorly e.g., in PFFD hips or posttraumatic dysplasia (Lit). In the case of acetabular protrusion, global over-coverage of the hip leads to impingement that occurs circumferentially around the rim.

Using the cam-/pincer-type classification, not all damage mechanisms are sufficiently covered, as they describe merely bony morphological abnormalities, such as the asphericity of the femoral head (cam type) or the focal/global over-coverage (pincer type). This schema does not include extracapsular alterations, such as varus or valgus femoral deformity or femoral torsion. Using inclusion-type or impaction-type joint damage places focus on the damage mechanism, and therefore, all impingement-causing deformities should be covered in theory. Of note, in the presence of combinations of deformities, it may be difficult to decide which condition (impaction or inclusion) predominates.

The prevalence of cam and pincer impingement has been found to be substantially higher in college football players compared to the reported prevalence in the general population [25]. This may suggest that the former group may have a higher propensity to develop symptomatic FAI related to higher body mass index (BMI) and activity level, leading to greater loads on the hip and with abnormal morphology contributing to the labral and articular cartilage damage. In one study, 39 % of asymptomatic professional and collegiate hockey players were found to have an abnormally high alpha angle [26]. Seventy-two percent of male and 50 % of female professional soccer players had at least one radiographic abnormality that could cause FAI [27]. Although these athletes were asymptomatic at the time of radiographic study, 50 % of men and 25 % of women reported a past groin or hip injury [27].

There is some evidence that increased stress on the proximal femoral physis around the time of closure is responsible for the cam deformity [28]. In a study of elite adolescent soccer players, 26 % had an alpha angle >60°, 13 % had a prominence at the head-neck junction, and 53 % had flattening; this was in comparison to rates of 17 %, 0 %, and 18 %, respectively, for these measures in nonathlete control patients [29]. Elite club basketball players who had played basketball year-round since age 8 were found to have greater mean alpha angles than controls, as well as higher mean alpha angles after physeal closure [30]. Clinical examination of these athletes revealed that 48 % had pain on impingement testing, and 19 % of the athletes reported hip or groin pain in the preceding 6 months [30]. In comparison, 1.3 % of the controls had a positive impingement test. In a case-control study of elite basketball players and age-matched nonathletes, Siebenrock et al. presented evidence for growth plate alterations, rather than simply reactive bone formation, contributing to cam-type deformity in the athletic subgroup [31].

In many cases of FAI, the underlying structural abnormality is secondary to residual deformity from the sequelae of childhood hip disorders, such as Legg-Calve-Perthes disease (LCPD), slipped capital femoral epiphysis (SCFE), and hip dysplasia. However, in most cases of FAI, there is no history of previous hip pathology, and the impingement etiology may be considered as primary FAI. The prevalence of radiographic signs of classic FAI (ranging between 10 % and 74 %) is high in the asymptomatic, or pain-free, population. Asphericities of the femoral head-neck (cam-type deformities) vary between the sexes, with males having three to five times the rates of those seen in females [33–36] and bilateral cam-type deformities being more prevalent in males [36]. Pincer-type deformities, such as acetabular over-coverage or increased acetabular depth, are observed in 10–15 % of Caucasian hips and, when present, were bilateral in 75–77 % of cases [34–37].

There are various theories to explain the development of the so-called primary FAI. However, the etiology of this condition is still open to speculation. The morphological abnormalities seen in primary cam-type impingement is similar to the deformity seen in SCFE and LCPD. Therefore, it has been suggested that these conditions may have occurred subclinically during development. Other propositions include abnormal bone extension from the epiphysis, abnormal patterns of ossification owing to congenital factors, low-grade infection, or autoimmune reactions [30, 31, 38]. High-intensity sports activity causing physeal stress surrounding adolescence has also been suggested as a risk factor for the development of cam-type deformity: observations have found FAI more frequently in athletes than in age-matched individuals not participating in high-level sports [30, 31, 38].

Genetic influences have also been implicated in the development of primary FAI [39]. Pollard et al. screened 96 siblings of 64 patients with primary FAI clinically and radiologically for the presence of cam and pincer lesions. They found that the siblings of patients with a cam deformity or a pincer deformity had a relative risk ratio of 2.8 and 2.0, respectively, of having the same deformity. It is unclear whether the genetic component determines the deformity at conception or if it predisposes to abnormal development or subclinical hip pathology before skeletal maturity.

Childhood diseases, in particular SCFE and LCPD, can cause secondary pincer- and cam-type FAI. The same is true for acetabular protrusion, which leads to global pincer FAI. Protrusion may be caused by metabolic or inflammatory disease, although for some no such definitive etiology can be found. In SCFE, FAI occurs between the prominent metaphysis and the acetabular rim, as confirmed by intraoperative findings during surgical hip dislocation from various reports [40, 41]. This has revealed that, even in mild stable slips, there is evidence of labral injury and chondromalacia in the anterosuperior quadrant of the acetabulum. These studies highlight the potential need to address proximal femoral deformity leading to cam and pincer FAI (impaction and inclusion) in SCFE, in order to prevent subsequent OA due to FAI. There exists, however, controversy surrounding the remodeling potential of residual SCFE deformity. Some authors believe that metaphyseal remodeling can be expected with time, resulting in minimal consequence of the deformity, and that FAI will not develop in most patients. The latter concept is supported by a long-term follow-up study by Boyer et al. [42].

Residual deformity in LCPD is a cause of hip pain in adolescents and young adults owing to the altered mechanics of the hip joint. The condition results in abnormal femoral head shape, growth disturbance of the proximal femoral physis, and acetabular dysplasia due to secondary remodeling processes. The symptoms may be related to hip joint instability, FAI, or a combination of both [43]. The cause of FAI in LCPD is the due to the aspherical femoral head [44, 45], acetabular retroversion [46, 47], or secondary to surgical procedures like innominate osteotomy [48]. These can lead to intra-articular impingement, but extra-articular impingement can also result from overgrowth of the greater trochanter or, less commonly, impingement of the lesser trochanter due to a shortened femoral neck [43].