Hoaglund and Steinbach (89) report racial differences in the prevalence of hip OA with Caucasians (3–6 %) having a higher prevalence than East Indians, Blacks, Hong Kong Chinese, and Native Americans (all <1 %). Other anatomic studies of the proximal femur have shown structural differences between Caucasian and Asian hips (90,92), specifically differences in femoral anteversion and head sphericity (90,91), with Caucasian hip joints indicating a “barrel-shaped” femoral head (90). There was also a tendency toward slightly larger femoral head diameters in caucasian females (mean, 4.3 cm) compared with Chinese females (mean, 4.0 cm) (90). Dudda et al. (92) compared radiographs of Chinese and Caucasian women without osteoarthritis and found that Caucasian women had a higher prevalence of femoral head asphericity, in addition to a higher prevalence of acetabular overcoverage. Studies in Japan have shown that most hip OA cases are due to developmental dysplasia of the hip [45, 46]. The prevalence of FAI was low 0.6 % and acetabular retroversion was more likely the cause of non-dysplastic hips [47, 48]. In contrast in Denmark Gosvig concluded high-risk OA due to deep socket and pistol grip deformity similar to that reported by Hoaglund [45, 49]. This evidence can in part explain the racial differences of hip shape and the development of OA.

Identifying sex-specific disease patterns is important to improving diagnostic and treatment algorithms. An accurate understanding of differences in FAI disease patterns between males and females may improve sex-dependent diagnostic criteria. Cam-type FAI previously has been described as a problem in young males, while pincer-type FAI has been noted as most common in middle-aged females (3,2).

The prevalence of cam-type deformity in asymptomatic volunteers is reportedly between 14 and 24 %, with males being more affected than females by a ratio of 3.8:1 (93,94). Females have a higher incidence of coxa profunda, positive crossover sign, and increased Sharpe angles (95) (Fig. 5.2). All are consistent with the findings showing a higher prevalence of deep acetabular socket in women but a higher prevalence of pistol grip deformity in men.

Studies have shown that females had significantly smaller alpha angles but increased anteversion compared with men with symptomatic FAI (97,98), reporting only 34 % (compared with 72 % of males) having a maximum alpha angle of >60°. Internal rotation in flexion was greater in females indicating that diagnostic criteria for males and females are different (96).

Pollard and colleagues evaluated the siblings of patients undergoing treatment for idiopathic FAI and compared them to a cohort of spouses of both the siblings and patients. Their study found that siblings of patients treated for a cam-type FAI have a relative risk of 2.8 of also having a cam-type deformity (99). This risk was highest (3.2; range, 1.9–5.4) in brothers of male patients and lowest (1.9; range, 0.8–4.9) in sisters of female patients (Table 5.1). The authors went on to state that deformities contributing to FAI are “determined at conception or that there is a genetic predisposition to abnormal development or subclinical hip disease before skeletal maturity” (99). Further, they add, “the high prevalence of cam deformity in the siblings in the absence of clinical features and OA suggests that the deformity is a primary, not secondary, phenomenon” (99). Their conclusion may not explain the low risk in sisters of female patients and that activity level in highly active families and sex differences may play a part. Some evidence exists that race, sex, and genetics may partly explain that FAI development is established prior to birth; it may also be due to cultural differences and how we live our daily lives impacts the development of our hip. Further studies looking at different ethnic groups living in the same culture may answer this question.

Initially following the establishment of FAI, some proposed the cam and pincer lesions were simply bony growths resulting or adapting from bony impingement perhaps as a protective mechanism from further damage. The likelihood of bony changes occurring beyond physeal closure is low as previously described; certainly calcification of the labrum and bony rim developments can result from Pincer impingement but they don’t grow beyond the boundary of the labrum. Unlike osteophytes, the cam lesions do not appear to have the potential for growth or recurrence following resection. In contrast evidence of recorticalization of the bone in the first 2 years following cam resection has been shown [37, 38]. Histological analysis of cartilage overlying the cam and pincer lesions reveals normal hyaline cartilage and hyaline cartilage is unable to form after skeletal maturation (Fig. 5.3). If cam lesions were a result of the impingement process, they would continue to enlarge with time and would consist of fibrocartilage as opposed to hyaline cartilage. There is no correlation with age and the degree of deformity or severity of alpha angles, loss of anterior offset, or other radiographic measurements [50]. The reactive changes that are seen with age and deformity are osteoarthritic changes and will be explored further when looking at the evidence of whether FAI leads to OA.

In contrast the physiological stresses that occur on the hip during childhood and the potential for remodeling are more likely. The level of sporting activity in childhood through running and climbing and perhaps more so in such sports requiring flexion and internal rotation has been linked to FAI. One study showed a higher prevalence of cam deformity in adolescents involved in high impact activity during skeletal maturation [51] (101). There have been multiple reports describing the relationship between vigorous sporting activity in young people and the prevalence of cam deformities of the proximal femur (100,101).

One theory to explain the higher prevalence of cam deformity in athletes is that vigorous sporting activity during development of the proximal femur may lead to abnormal or altered development of the capital femoral physis (102). Epiphyseal extension toward the femoral neck is 12–15 % greater throughout the entire cranial hemisphere in young elite basketball players versus age-matched controls. Although the control hips showed an increase in epiphyseal extension as they progressed through physeal closure, epiphyseal extension in basketball players was markedly increased before physeal closure (102). If morphological changes do occur due to stresses through sports, it is before skeletal maturation and would most likely occur during hormonal changes when the bone is prone to softening and remodeling through the growth plate. Carter et al. found that the location of the cam lesion associated with symptomatic FAI in skeletally immature patients occurs in close proximity to the level of the proximal femoral physis. With maturation, the origin of the cam lesion becomes further away from the physis, presumably as additional growth occurs after the inciting event. This suggests that the growth plate—or more specifically, repetitive microtrauma to it—may play a causal role in the pathogenesis of cam-type FAI [52]. Philippon et al. showed an association between age and alpha angle in the skeletally immature patient. The increase in alpha angle with age in this active population corroborates the theory of a developmental characteristic to cam-type FAI [53]. When the open femoral physis is submitted to high stresses in competitive sports as the adolescent grows, it may be prone to development of a cam deformity.

Slipped capital femoral epiphysis is one of the leading theories as to the cause of the cam lesion. The resultant head slips posteriorly and leads to loss of the anterior offset at the head-neck junction. Similarly a cam lesion is the loss of asphericity of the femoral head mainly anteriorly or anterolaterally on the femoral head-neck junction with loss of head-neck offset in this region.

SCFE typically occurs in teenagers before the growth physes fuse with symptomatic children with detectable slips requiring surgery. Severe slips fixed in situ have been a source of impingement with reports of femoral osteotomies being required to correct and alleviate such impingement. A higher prevalence of SCFE is seen in males more than females. The presentation of such children and their level of symptoms vary and it is recognized that many mild slips could and can go undetected.

Goodman previously described SCFE as a posterior angulated head-neck tilt, translation of the femoral head with loss of anterior offset between head and neck that can result in an asphericity as the head slips and moves posteriorly [6] (Fig. 5.4).

The radiographic measurements that assess head-neck tilt, anterior offset ratio (AOR), and alpha angle are described (Fig. 5.4). Abnormal alpha angles in these individuals indicate the loss of the head-neck junction or asphericity of the femoral head. Loss of AOR depicts the translation of the femoral head on the neck. Head-neck tilt describes the angle of the femoral head in relationship to the angle of the neck. The occurrence of abnormal values in all three of these measurements would reflect a femoral head position as depicted and explained by Goodman consistent with SCFE. In contrast an abnormal alpha angle and AOR but with normal head-neck tilt would depict a translated but not tilted femoral head—a shape or abnormality that may not be consistent with SCFE. The same radiographic appearances described by Goodman are found in cam lesions and were also more prevalent in the male population. The prevalence of abnormal radiographic measurements as defined for SCFE was found in up to 70 % of patients [50, 54]. These measurements and their severity showed no correlation with age indicating it was a static deformity that did not deteriorate with time [50, 54].

FAI is not detected until symptoms start and similar to SCFE could reflect the subtle nature of the disease process that preceded the onset of symptoms. The pathology goes undetected and it is for this reason it has been proposed that subclinical SCFE, not acute enough to come to medical attention, is a major contributor to the development of cam-type FAI. A study looking at asymptomatic children who underwent radiographs and CT scans performed for other reasons revealed no evidence of abnormal morphology of the hip indicative of cam deformity until approximately age 10–12 years [55]. Beaule in a MRI study assessment of asymptomatic pediatric patients pre- and post-physeal closure concluded cam deformity likely develops during physeal closure and is associated with increased activity levels [56]. The coincidental timing of these changes prior to physeal closure corresponds to the age that SCFE occurs and perhaps why most patients suffering the discomfort of FAI are seen in their late teens, 20s, and 30s. A counter argument against SCFE as a cause of FAI, are reports that patients with cam deformity do not show orientational growth plate disturbances found in SCFE [57, 58]. Failure of the beta angle to change with the increased alpha angle may refute the evidence for the capital physes slipping to be a causative factor in cam pathology [59]. Others propose that SCFE is a cause with the osteocartilaginous bump a result of an extended physis as a result of a SCFE or similar type injury.

Pincer-type impingement is seen when a deep socket provides functional overcoverage on a well-centered femoral head. Focal pincer lesions involve bony overhang of the anterosuperior acetabulum, often due to acetabular retroversion. Classic radiographic findings of a crossover sign, ischial spine sign, and sometimes a posterior wall sign (indicating posterior wall insufficiency) are detected on an anteroposterior (AP) pelvis projection. In contrast, a deep socket causes global pincer impingement, with relative global overcoverage of the femoral head. Generally accepted as a medialization of the acetabulum, there are various radiographic criteria that have been used to define acetabular protrusio. A center-edge angle (CEA) of Wiberg greater than 40° is considered diagnostic of protrusio (Fig. 5.5) (103,105,106). In contrast, coxa profunda is considered a less severe form of global pincer impingement with the medial acetabular wall overlapping or medial to the ilioischial line (104). Moreover, global pincer impingement (whether protrusio or profunda) has a prominent posterior wall lateral to the femoral head center (104). Any of these acetabular dysmorphisms may coexist with acetabular retroversion and/or cam morphology. In some cases, the softening of bone due to underlining hormonal or metabolic causes is thought to lead to this deformity. It is for those reasons patients can develop pincer impingement through time after skeletal maturity. Similarly acetabular overcoverage can be functional due to hyperlordosis at the lumbosacral junction leading to anterior pelvic tilt [60, 61]. If not functional, most likely genetic and must be assessed for posterior wall deficiency. Like DDH, this is most likely a developmental problem that may stem from intrauterine and the first years of life. All radiographic assessments must be done in at least two planes as subtleties of radiographic findings can be due to more than one abnormality or patient position. The complexity of these deformities that can coexist has led many to using 3 Dimensional CT reconstruction images to evaluate the painful hip.

Periacetabular osteotomies provide a temporary surgical solution for the treatment of symptomatic acetabular dysplasia and have shown good functional, clinical, and radiographical outcomes (139,141) and good preservation of the hip joint at 10 (136) and 20 years (143). However, several studies, which include retrospective reviews and case series, have described the occurrence of impingement symptomatology such as pain and range of motion restriction following periacetabular osteotomies (PAO) (136-143).

In conditions of hip dysplasia, there is a lack of femoral head-neck offset with a deformed, aspherical femoral head but this is usually compensated by decreased anterior acetabular coverage. However, after surgical correction is achieved with the osteotomy, an iatrogenic pincer-type impingement can be created, and with the asphericity of the femoral head, this can lead to combined-type impingement causing anterior impingement. This has been noted to be as high as 30–48 % postoperatively (136,139). Myers et al. in 1999 describe five cases of “secondary impingement syndrome” following periacetabular osteotomy (137). All their patients presented with groin pain and symptoms of anterior impingement and reduced range of motion in flexion, adduction, and internal rotation. MR arthrograms confirmed labral injury and chondral damage in the involved hips.

Preoperative asphericity of the femoral head is protected by under coverage of the acetabulum. Following reorientation, relative overcoverage produces anterior impingement (144).

Albers et al. describe the concept of “optimal acetabular orientation” which was introduced in order to maximize the final position of the acetabulum at reorientation in order to minimize the problem of overcorrection and retroversion (144). The authors use six radiographic parameters such as femoral coverage, anterior coverage, posterior coverage, lateral center edge angle, acetabular index, and extrusion index and consider reorientation optimal if at least 4/6 of these parameters are within an acceptable range. The same researchers performed a retrospective study to determine whether proper acetabular reorientation with periacetabular osteotomy and a spherical femoral head would improve hip 10-year survivorship or slow the progression of osteoarthritis. They reviewed 147 patients who underwent 165 periacetabular osteotomies and divided these patients into two groups: proper orientation and spherical femoral head vs. improper reorientation and aspherical head with a minimal follow-up of 10 years. They found that proper reorientation with a spherical femoral head increased survivorship and decreased the progression of osteoarthritis.

Ganz et al. were the first to describe FAI secondary to malunion and bony overgrowth following surgical fixation of proximal femur fractures (107). They postulated that malreduction and malunion following surgical reduction and fixation could lead to abnormal morphology of the femoral head-neck junction such as varus malunion, shortening, retroversion, and decreased femoral head-neck offset resulting in abnormal hip mechanics and impingement (108-111). Since their original description, this concept has been supported by several reports and case series (108,109,114).

Eighty-five percent of elderly patients (>85 years) who had undergone surgical fixation with multiple cancellous screws or sliding hip screw construct for femoral neck fractures had radiographic evidence of cam-type FAI (109), significantly higher than the 1–17 % reported in the asymptomatic general population (112,45). They also found that 86 % of Garden type III and IV fractures showed evidence of cam-type FAI while only 72 % of Garden I and II fractures. Whether the radiographic changes are the result of the surgical fixation and malunion or due to changes in the proximal femoral head-neck offset seen with aging is unclear (113) and previous reports have described a high incidence of cam impingement in patients over 50 years who were undergoing hip resurfacing arthroplasty [50] (114).

In contrast, another study compared hip fracture in patients under 50 years of age who were treated with reduction and internal fixation with population-based controls (135). Radiographic signs of impingement and degenerative arthritis were analyzed and the authors found that 75 % of hips treated with internal fixation had at least one sign indicative of impingement versus 17 % in the general population (112,45). These findings would seem to contradict previous reports that have suggested that femoral head-neck abnormalities are a consequence of advanced age (113) rather than fracture malunion. Furthermore, 22 hips (31 %) had radiographic evidence of degenerative arthritis at final follow-up as judged by their Tonnis score and again displaced subcapital B-3 fractures were most likely to display arthritic changes. Interestingly, 94 % of hips without any radiographic signs of impingement also did not have signs of arthritis at last follow-up (109).

Eijer et al. reported 9 patients with a mean age of 33 years who had sustained a femoral neck fracture and experienced subsequent pain, gait disruption, and decreased range of motion especially in flexion, adduction, and internal rotation with positive impingement test in the affected hip (108). Radiographs and intraoperative assessment showed insufficient fracture reduction and malunion in all patients. The authors stated that femoral head retroversion and varus malalignment lead to anterior and anterolateral impingement, respectively. Intraoperatively, anterior labral damage and acetabular cartilage lesions, similar to those seen with FAI, were seen in all patients with an abnormal femoral head-neck contour.

In contrast, some authors have suggested that the impingement and the radiographical changes seen postoperatively in patients with femoral neck fractures were the cause of the nonunion or malunion rather than the effect (115). Regardless, a proximal femur fracture and subsequent malreduction and/or malunion appear to increase the risk of developing radiographical and clinical signs of cam-type impingement. The cause and effect between these postoperative radiographical findings and the subsequent development of hip arthritis remain unclear. These findings however do support the importance of initial anatomic reduction in both the AP and axial planes and stable fixation when dealing with proximal femoral fractures (111,116). The results also highlight the importance of close monitoring and early postoperative detection when treating a patient who has suffered a similar type fracture with subsequent malunion. Surgical intervention may facilitate hip preservation, in this specific patient population, preventing possible FAI symptomatology and its sequelae.

FAI symptomatology and radiographic changes can also be caused by pathological lesions. Several case reports and series have been published describing classical FAI symptomatology resulting from both benign and malignant lesions in the proximal femur (117-122). The patients are typically young active adults who present with pain and progressive decrease in hip range of motion (117). The widened and dysplastic femoral head and neck create a mechanical block leading to abnormal contact between the proximal femur and acetabular rim, limiting the range of motion and leading to the typical FAI presentation of pain, positive impingement and FABER test, and decreased flexion, adduction, and internal rotation. The changes seen on the femoral side are often associated with acetabular labral tears and cysts with signs of progressive arthritic changes.