Early degenerative hip disease has often been noted in patients with abnormal acetabular morphology usually secondary to developmental dysplasia of the hip (DDH), and it has been hypothesized to be the consequence of abnormal edge loading on the anterosuperior acetabular cartilage from an eccentrically centered femoral head. However, the role femur morphology played in the development of degenerative hip disease was not as defined. In 1936, Smith-Petersen classically described a concept of impingement in which hip pain was theorized to be caused the femoral neck impinged against anterior acetabular margin [1]. Surgical correction, by way of impingement correction, was successful in his small case series. Decades later, Murray et al. described a tilt deformity of the proximal femur and its association with the development of osteoarthritis of the hip [2]. In 1986, Harris described his theory on how derangements in femoral anatomy development caused primary or “idiopathic osteoarthrosis of the hip” in the non-dysplastic hip [3]. Harris wrote that based on his numerous radiographic observations, the convex, “pistol grip” femoral deformity at the femoral head-neck junction following the sequelae of a recognized or undetected slipped capital femoral epiphysis (SCFE), Legg-Calve-Perthes disease, or the congenital epiphyseal dysplasia was a common pathway for development of the so-called “idiopathic” degenerative hip disease. Although Harris reported of the association of abnormal femoral head-neck deformity and osteoarthritis, he did not elaborate on the underlying mechanisms that such deformity can result in the development of primary degenerative hip disease.

In this early report, Harris also implied that the acetabular labrum may play an important role in the development of primary osteoarthritis. Harris described what he termed the “intra-acetabular” labrum. He viewed the labrum as an extra-articular structure, and any presence of labrum within the intra-articular space should be considered abnormal and represented an “internal derangement” of the hip, analogous to a torn glenoid labrum in the shoulder or meniscus in the knee [3, 4]. Such observations were early suggestions that acetabular labral pathology could play a part in the development of primary degenerative hip disease.

Subsequently to the assertions made by Harris, McCarthy et al. reported that chondral injury was noted in 73 % of 436 consecutive hip arthroscopies where labral fraying or tears were present, thus suggesting the role of labral pathology in the development of degenerative hip disease in a patient population. These findings were further supported in the authors’ cadaveric examination of 52 acetabula in the same report [5, 6]. Subsequently, basic science studies further demonstrated that the labrum was found to be a critical structure in hip joint preservation by maintaining a “fluid seal” that prevents the efflux of synovial fluid from the central compartment, thus maintaining hydrostatic pressure to lower contact stresses between the femoral and acetabular cartilage surfaces [7–9].

The interplay between the femoroacetabular anatomy, labral and chondral injury, and the development of degenerative hip disease in the non-dysplastic hip was best narrated in the work done by Ganz et al. and Lavigne et al. [11, 12]. In 2003, Ganz and colleagues outlined the biomechanical rationale on how the disease they coined “femoroacetabular impingement” can cause labral and articular cartilage degradation in the non-dysplastic hip [11]. The authors suggested that the mechanism of articular cartilage and labral damage and degradation in these hips was that of aberrant hip motion rather than isolated, abnormal eccentric axial loading of the anterosuperior acetabulum that was hypothesized to occur in hip dysplasia. The authors arrived at their hypothesis based on the observations seen of labral injury and cartilage wear patterns in over 600 surgical dislocations performed for patients with hip pain without dysplasia. The authors proposed three mechanisms of femoroacetabular impingement: (1) cam impingement, (2) pincer impingement, or (3) a combination of both. Cam impingement resulted from decreased clearance of the acetabulum from a convex, femoral head-neck junction, particularly during flexion. The “abutment,” as the authors described it, between the diminished femoral head-neck offset and acetabulum is thought to cause shear injury to the adjacent cartilage and labro-chondral junction, thus leaving the bulk of the labrum undisturbed. Pincer impingement was described to originate from the acetabular side, where general (coxa profunda) or regional acetabular retroversion may cause direct, crushing injury to the labrum with a normal femoral head-neck surface. The continuous labral injury could cause intra-labral substance degeneration or labral ossification. Moreover, the premature impact on the femoral head-neck junction could cause chondral injury to the posteroinferior acetabulum secondary to abnormal shear stresses from the excessive premature levering, which the authors termed the “contrecoup” lesion. Finally, there can be a combination of both, which we now know occurs most commonly in clinical practice. The authors found that pincer impingement was more commonly seen in middle-aged women, and cam impingement was more often observed in young, athletic male populations.