Hip impingement, formally known as femoroacetabular impingement (FAI), is a condition where the bones of the hip joint abnormally contact one another. The hip operates as a ball-and-socket joint, and FAI occurs when the non-spherical shape of either the ball, the femoral head, or the socket, the acetabulum, leads to friction during movement. This abnormal friction causes mechanical stress and pain, which can damage the joint over time. Understanding the causes of FAI requires examining both the precise mechanical action within the joint and the underlying anatomical reasons for the irregularly shaped bones.
Understanding the Mechanics of Hip Impingement
The healthy hip is designed to allow the femoral head to glide smoothly within the acetabulum, the hip socket, facilitating a wide range of motion. This seamless movement is protected by articular cartilage, which covers the bony surfaces, and the labrum, a ring of fibrocartilage that lines the rim of the socket. Impingement occurs when a bony abnormality causes premature contact between the femoral head or neck and the acetabular rim, particularly during deep hip flexion or internal rotation.
This collision generates mechanical stress, physically pinching the softer tissues caught between the bones. The hip labrum is a common victim of this abnormal contact, frequently becoming compressed, torn, or detached from the socket rim. Repeated mechanical impact also damages the articular cartilage, the joint’s primary shock absorber. Over time, this chronic collision and subsequent tissue damage can restrict movement and contribute to the development of hip osteoarthritis.
Specific Structural Deformities
The immediate cause of femoroacetabular impingement is a bony malformation on either the femur or the acetabulum, which dictates the type of FAI experienced. These irregularities fundamentally change the joint’s geometry, leading directly to the damaging collision.
Cam Impingement
Cam impingement involves an abnormality on the femoral head and neck junction, where the “ball” is not perfectly spherical but instead has an extra prominence or bump of bone. This non-round section creates a poor transition between the head and the neck. When the hip is flexed and rotated, this bony bump jams into the acetabulum rim, causing a shearing force that can peel the articular cartilage away from the bone.
Pincer Impingement
Pincer impingement is caused by an issue with the acetabulum, the hip socket, where the bony rim excessively covers the femoral head. This over-coverage can occur if the socket is too deep, a condition known as coxa profunda, or if the socket is angled backward, called acetabular retroversion. The deep or misaligned socket rim acts like a clamp, causing the femoral neck to abut against it sooner than normal during motion. The resulting force primarily compresses the labrum between the socket rim and the femoral neck, often leading to a crushing injury of the labral tissue.
Mixed Impingement
Mixed impingement is the most common presentation of FAI, involving a combination of both Cam and Pincer deformities. This means the individual has both a bony bump on the femoral head-neck junction and excessive over-coverage of the socket rim. The co-occurrence of these two malformations often results in more complex mechanical forces and a greater overall risk of damage to both the labrum and the articular cartilage.
Developmental and Contributing Factors
The structural defects responsible for FAI primarily originate during skeletal maturation in childhood and adolescence, rather than developing later in life. Genetic factors play a role, as the anatomical shapes that predispose individuals to impingement are often shared among family members. However, most FAI is considered an acquired, developmental condition influenced by various factors.
Issues with the growth plates, the areas of soft, growing tissue at the ends of long bones, are significant contributors to bony defects. Slipped Capital Femoral Epiphysis (SCFE) is a well-established cause of severe Cam deformity. Here, the growth plate of the femoral head weakens and the head slips backward off the neck. The healing process of SCFE results in an anterolateral prominence on the femur that directly causes the impingement.
Another major theory focuses on high-impact athletic activity during the years when the growth plates are still open. Repetitive, extreme ranges of motion, particularly deep hip flexion and internal rotation common in sports like soccer, hockey, and basketball, place stress on the vulnerable proximal femoral physis. This mechanical stress may stimulate extra bone formation around the femoral head-neck junction before the growth plates fully fuse. This bony prominence is an adaptive response to the high forces experienced, explaining why a high prevalence of Cam deformities is found in athletes who trained intensively during their adolescent growth spurt.