The most favorable mechanical environment for the hip is one that is free of both instability and impingement, creating a concentric articulation with optimum femoral head coverage by the acetabulum. Anatomic variations such as acetabular dysplasia with associated instability, and femoroacetabular impingement with abnormal constraint, will lead to abnormal joint mechanics, articular damage, and osteoarthritis. Surgical techniques such as periacetabular osteotomies, and femoral and acetabular osteoplasties enable correction of anatomic variations that cause mechanical damage to the hip joint, thereby potentially preventing or delaying development of osteoarthritis and subsequent need for joint replacement.
Key points
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The most favorable mechanical environment for the hip is one that is free of both instability and impingement, creating a concentric articulation with optimum femoral head coverage by the acetabulum.
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Anatomic variations such as acetabular dysplasia with associated instability, and femoroacetabular impingement with abnormal constraint, will lead to abnormal joint mechanics, articular damage, and osteoarthritis.
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Surgical techniques such as periacetabular osteotomies, and femoral and acetabular osteoplasties enable correction of anatomic variations that cause mechanical damage to the hip joint, thereby potentially preventing or delaying development of osteoarthritis and subsequent need for joint replacement.
Introduction
Osteoarthritis (OA) is thought to be caused by a combination of intrinsic vulnerabilities of the joint, such as anatomic shape and alignment, and modulatory factors, such as body weight, injury, and activity level. The current concept of the mechanical cause of hip OA is that anatomic variations create an unfavorable mechanical environment for the hip, leading to joint damage. OA is rarely considered purely idiopathic in this framework, and this observation is supported by previous studies. Aronson noted that 43% of his population of OA hips had developmental dysplasia of the hip (DDH), 22% had Perthes disease, 11% had slipped capital femoral epiphysis (SCFE), and only 12% were classified as idiopathic. Even earlier, Murray, Stulberg, and Harris recognized that prominence of the femoral head-neck junction, or the pistol grip deformity of the proximal femur, predisposed to OA.
Population-based studies on hip OA have shown some role for mild dysplasia as a significant risk factor. Work by Ganz and colleagues and others, showed that subtle anatomic abnormalities of the hip, such as acetabular retroversion, acetabular overcoverage, and decreased head-neck offset of the femoral head-neck junction, are clinically significant anatomic variants that may lead to pain, intra-articular damage, and eventual OA in the young adult population. The limiting factor in treatment outcome in many mechanically compromised hips is the amount of cartilage damage that has occurred before treatment. Therefore, it is critical to understand and recognize the signs and symptoms of these painful hips in a timely fashion.
A useful paradigm for thinking about the mechanical function of the hip, as it relates to the development of OA, is that the most favorable mechanical environment of the hip is one that is free of both instability and impingement. Long-lasting and pain-free function of the hip joint requires a concentric articulation with optimum femoral head coverage by the acetabulum ( Fig. 1 A). Hip dysplasia represents an anatomic deformity in which the basic pathologic mechanical abnormality is instability. Lack of femoral head coverage (see Fig. 1 B) in acetabular dysplasia can lead to hip instability and overloading of the articular cartilage, which can lead to joint damage.
In contrast, femoroacetabular impingement represents an anatomic deformity at the other end of the mechanical spectrum, in which the primary mechanical disorder is abnormal constraint to normal hip motion. Overcoverage of the femoral head by the acetabulum anteriorly in acetabular retroversion (see Fig. 1 C) or globally as in acetabular protrusio (see Fig. 1 D) can lead to pincer-type impingement between the prominent acetabular rim and the femoral head-neck junction. A static form of impingement is seen in conditions such as Perthes disease, in which the articular surfaces are incongruent. A dynamic form of impingement is seen in subtler cases of aspherical femoral heads or prominent femoral head-neck junctions, in which the incongruency may only occur in certain positions of the hip. The femoral CAM deformities can be subtle and only detected on lateral radiographs. Normal hips have a spherical femoral head on the anteroposterior ( Fig. 2 A) and lateral views (see Fig. 2 B). If the femoral head-neck junction is too broad or aspherical (see Fig. 2 C, D), this can lead to CAM-type impingement and pain. Therefore, all of these anatomic variations along this spectrum must be recognized to fully evaluate and treat the painful hip.
Introduction
Osteoarthritis (OA) is thought to be caused by a combination of intrinsic vulnerabilities of the joint, such as anatomic shape and alignment, and modulatory factors, such as body weight, injury, and activity level. The current concept of the mechanical cause of hip OA is that anatomic variations create an unfavorable mechanical environment for the hip, leading to joint damage. OA is rarely considered purely idiopathic in this framework, and this observation is supported by previous studies. Aronson noted that 43% of his population of OA hips had developmental dysplasia of the hip (DDH), 22% had Perthes disease, 11% had slipped capital femoral epiphysis (SCFE), and only 12% were classified as idiopathic. Even earlier, Murray, Stulberg, and Harris recognized that prominence of the femoral head-neck junction, or the pistol grip deformity of the proximal femur, predisposed to OA.
Population-based studies on hip OA have shown some role for mild dysplasia as a significant risk factor. Work by Ganz and colleagues and others, showed that subtle anatomic abnormalities of the hip, such as acetabular retroversion, acetabular overcoverage, and decreased head-neck offset of the femoral head-neck junction, are clinically significant anatomic variants that may lead to pain, intra-articular damage, and eventual OA in the young adult population. The limiting factor in treatment outcome in many mechanically compromised hips is the amount of cartilage damage that has occurred before treatment. Therefore, it is critical to understand and recognize the signs and symptoms of these painful hips in a timely fashion.
A useful paradigm for thinking about the mechanical function of the hip, as it relates to the development of OA, is that the most favorable mechanical environment of the hip is one that is free of both instability and impingement. Long-lasting and pain-free function of the hip joint requires a concentric articulation with optimum femoral head coverage by the acetabulum ( Fig. 1 A). Hip dysplasia represents an anatomic deformity in which the basic pathologic mechanical abnormality is instability. Lack of femoral head coverage (see Fig. 1 B) in acetabular dysplasia can lead to hip instability and overloading of the articular cartilage, which can lead to joint damage.
In contrast, femoroacetabular impingement represents an anatomic deformity at the other end of the mechanical spectrum, in which the primary mechanical disorder is abnormal constraint to normal hip motion. Overcoverage of the femoral head by the acetabulum anteriorly in acetabular retroversion (see Fig. 1 C) or globally as in acetabular protrusio (see Fig. 1 D) can lead to pincer-type impingement between the prominent acetabular rim and the femoral head-neck junction. A static form of impingement is seen in conditions such as Perthes disease, in which the articular surfaces are incongruent. A dynamic form of impingement is seen in subtler cases of aspherical femoral heads or prominent femoral head-neck junctions, in which the incongruency may only occur in certain positions of the hip. The femoral CAM deformities can be subtle and only detected on lateral radiographs. Normal hips have a spherical femoral head on the anteroposterior ( Fig. 2 A) and lateral views (see Fig. 2 B). If the femoral head-neck junction is too broad or aspherical (see Fig. 2 C, D), this can lead to CAM-type impingement and pain. Therefore, all of these anatomic variations along this spectrum must be recognized to fully evaluate and treat the painful hip.
Anatomic abnormalities: dysplasia and instability
Acetabular Dysplasia
Acetabular dysplasia is shallowness of the acetabulum and obliquity of the weight-bearing zone, leading to overloading of the acetabular cartilage, labral tears, and OA. It is often a component of DDH, which predominantly affects women. Patients with residual DDH as an adult may have been treated as an infant for either a dislocated or dysplastic hip with apparent success. However, many adults with symptomatic acetabular dysplasia have no history of clinical abnormality before adulthood.
Patients often present with anterior groin pain and sensations of instability during activities such as walking. Patients may also describe or demonstrate clicking or snapping of the hip with range of motion. Physical examination may show variable changes in range of motion. There may be a positive anterior impingement test with the hip in flexion and internal rotation, particularly if the labrum has been injured. Patients may also have a positive anterior apprehension test with the hip in extension and external rotation. There may be hip abductor weakness, an abductor lurch with ambulation, or a positive Trendelenburg sign.
Acetabular dysplasia can range from the most severe form, which can result in a subluxated or dislocated hip, to subtle variants that may go unrecognized for a long period of time. The lateral acetabular deficiency is the most commonly recognized abnormality in acetabular dysplasia and is measured as the lateral center-edge angle (LCEA) ( Fig. 3 A). However, anterior deficiency as quantified by the anterior center-edge angle of Lequesne (ACEA), seen on the false profile view (see Fig. 3 B), is also important to evaluate, because anterior deficiency is more severe than lateral deficiency in some hips.
Among the anatomic deformities of the hip that lead to OA, the natural history of acetabular dysplasia is the best understood. Wiberg postulated that an LCEA less than 20° is abnormal. Murphy and colleagues later showed that no hips with an LCEA less than 16° survived into the sixth decade of life without OA. Thus, symptomatic hips with an LCEA of less than 20° are generally considered for surgical intervention such as periacetabular osteotomy (PAO) to reorient the acetabulum and to provide more femoral head coverage.
Hip Instability and Borderline Dysplasia
A more recent focus of research has been the identification and treatment of hips that are not grossly dysplastic by traditional definitions but still behave in an unstable manner. Patients with hip instability may have underlying connective tissue disorders or generalized ligamentous laxity, and may describe a history of past events of subluxation or a sensation of instability during physical activities. Hips with an LCEA between 20° and 25° are considered borderline dysplastic, especially if patients are symptomatic. If instability or borderline dysplasia is suspected, assessing the anterior coverage with a radiographic false profile view is important to rule out undercoverage of the femoral head anteriorly and instability in that anatomic plane. Arthroscopic studies have shown that, in instances of instability, the pattern of labral damage is typically more anterior and medial.
The challenge in treating these patients is deciding whether a soft tissue procedure such as labral repair and capsular plication is sufficient, or whether the underlying structure of the acetabulum is sufficiently dysplastic that bony reorientation is necessary. Arthroscopic labral debridement, labral repair, and labral reconstructions, with either thermal or suture capsular plication to address hip instability, have been described with success in short-term follow-up studies, but further studies on the long-term effects of such procedures are necessary.
Anatomic abnormalities: femoroacetabular impingement
Femoroacetabular impingement is a condition in which there is mechanical conflict between the femoral head-neck junction and the acetabular rim, causing intra-articular damage to the labrum and articular cartilage. This condition can either be caused by acetabular morphology, such as a deep or retroverted acetabulum causing overcoverage of the femoral head, or caused by femoral morphology, such as prominence or convexity of the femoral head-neck junction.
Coxa Profunda and Acetabular Protrusio
Although insufficient acetabular coverage leads to instability and mechanical overloading at the acetabular rim, overcoverage may lead to a pincer-type impingement between the acetabular rim and the femoral head-neck junction. The acetabular overcoverage may be global and severe, as in acetabular protrusio (see Fig. 1 D), or milder, as in coxa profunda.
Acetabular protrusio may be caused by conditions such as rheumatoid arthritis or Marfan syndrome. However, most cases are idiopathic. The deep acetabulum leads to global limitation of hip motion and impingement of the femoral head-neck junction against the acetabular rim, resulting in labral degeneration/tear and pain. Patients may complain of anterior impingement as well as lateral and/or posterior impingement pain. It is generally considered that protrusio is present when the femoral head is medial to the ilioischial line. However, the upper limits of normal femoral head coverage as measured on radiographs and the natural history of protrusio and coxa profunda are not well understood.
For deep acetabulums, safe acetabuloplasty or rim trimming through a surgical dislocation approach or arthroscopic approach have both been described. Although surgical dislocation may provide more global access to the acetabular rim, labral repair and reconstruction have been described with both approaches.
Acetabular Retroversion
Unlike acetabular protrusio and coxa profunda, which are global increases in femoral head coverage, acetabular retroversion creates isolated anterior overcoverage and anterior pincer impingement between the acetabular rim and the femoral head-neck junction, especially problematic in positions of hip flexion. Up to 33% of hips with acetabular dysplasia may also have acetabular retroversion, which must be recognized and taken into account when performing pelvic osteotomies for acetabular dysplasia. In addition, acetabular retroversion is common in posttraumatic dysplasia, Down syndrome, SCFE, and proximal femoral focal deficiency. If mild, the anterior overcoverage may be addressed arthroscopically, but often the global malorientation of the acetabulum must be addressed with total acetabular reorientation, such as is achieved with a reverse PAO.
CAM/Inclusion Femoroacetabular Impingement and Pistol Grip Deformity
Deformities on the femoral side can also lead to abnormal hip joint mechanics. The most commonly recognized femoral abnormality is the retrotilted femoral head or pistol grip deformity initially described by Murray. This anatomic variant is thought to be a major cause of hip OA in men. Some of the pistol grip proximal femur is similar to that found in a mild SCFE and may be a developmental variant related to SCFE. In severe SCFE, the prominent femoral metaphysis may be sufficiently large to cause a pincer-type impingement that crushes the acetabular labrum. In milder SCFE, the prominent metaphysis is small enough to enter the acetabulum, which may cause a greater mechanical problem for the articular cartilage than a more prominent metaphysis that is too large to enter the acetabulum; the intra-articular extent of the prominent neck causes increased loading within the joint, causing cartilage delamination and OA. In addition to the pistol grip deformity, focal prominence in the head-neck junction may cause sufficient decrease in head-neck offset to cause a similar disorder. Siebenrock and colleagues showed that many CAM deformities are caused by an extension of the epiphysis onto the anterior femoral neck, which is distinct from an SCFE deformity. CAM morphology may be common in the community, with an incidence of around 30%.
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