Hip Dysplasia and Instability

Hip Dysplasia

Hip dysplasia encompasses a complex and variable group of deformities of the hip. Acetabular dysplasia is the most commonly recognized and treated component of hip dysplasia. Classic acetabular dysplasia results from insufficiency of the anterosuperior acetabulum. This results in overload of the anterosuperior acetabular rim, which Klaue et al. termed “acetabular rim syndrome.” In the nondysplastic hip, the acetabular labrum functions to seal the hip joint rather than absorb direct load. However, in the dysplastic hip, the labrum and acetabular rim are subjected to direct load, which contributes to the typical labrochondral pathology in these locations. The increased forces seen by the anterosuperior labrum may play a role in the development of labral hypertrophy, which is generally but not uniformly present. The hypertrophic labrum may provide increased hip stability in the setting of acetabular dysplasia but also appears susceptible to ultimate overload and tearing. The radiographic appearance of acetabular dysplasia is variable ( Fig. 81.1 ). Severe acetabular dysplasia, with associated hip dislocation or subluxation, is generally well recognized on plain radiographs, with a break in the Shenton line recognized as a simple radiographic marker of hip subluxation. Mild or borderline acetabular dysplasia requires a thorough assessment of hip morphology to avoid missing this diagnosis. The variability of acetabular version in the dysplastic hip and recognition of the variable patterns of deformity are increasingly noted. Nepple et al. defined three common patterns of acetabular deformity in hip dysplasia based on low-dose computed tomography (CT). Anterosuperior, global, and posterosuperior insufficiency of the acetabulum were all fairly common ( Fig. 81.2 ).

The femoral deformity in hip dysplasia is generally less severe and less commonly treated than the acetabular deformity, although in some cases femoral deformity may predominate. Increased femoral anteversion is commonly present in the dysplastic hip and places additional stress on the anterior hip stabilizers. Normal femoral anteversion is approximately 5 to 15 degrees. In the setting of hip dysplasia, hips with anteversion more than 20 degrees above normal are relatively common, with severe increases in femoral anteversion greater than 35 degrees being less common. Coxa valga may be present in some dysplastic hips, although plain radiographic assessment of the femoral neck-shaft angle in high with increased femoral anteversion may give the appearance of more severe coxa valga than is truly present. Wells et al. reported the variability of femoral morphology in the dysplastic hip.

The natural history of acetabular dysplasia has been fairly well defined, compared with other young adult hip disorders. However, this natural history is solely based on radiographic characterization of the lateral center edge angle. The role of other factors, including femoral version, sex, soft tissue laxity, and activity level, remains to be better defined. Wiberg described the lateral center edge angle in his 1939 study on hip dysplasia and suggested that a value less than 20 degrees was linked to osteoarthritis. He reported a cohort of 18 such patients who all developed osteoarthritis at 4- to 29-year follow-up. This threshold appears to capture the lowest 5% of acetabular coverage within a population. It is important to note that deformities of acetabular dysplasia occur less commonly than those of FAI morphology, which are generally 10% to 25%. Cooperman et al. subsequently demonstrated similar progression of osteoarthritis among a cohort of 20 hips. However, the rates of osteoarthritis development did not appear to correlate with the severity of dysplasia and are likely influenced by a number of other patient-specific factors. In another key study in 1986, Murphy et al. reported the outcomes of the contralateral hip of 286 patients undergoing total hip arthroplasty for hip dysplasia. All hips with an lateral center edge angle (LCEA) less than 16 degrees developed osteoarthritis by the age of 65. However, not all studies have been in agreement on the link between hip dysplasia and osteoarthritis. Jacobsen et al. followed 81 dysplastic hips over 10 years (compared with controls) and demonstrated no difference in joint space width in hips with dysplasia. Hips with mild dysplasia (LCEA 15 to 25 degrees) did not uniformly develop osteoarthritis during the 10-year period. Lane et al. performed perhaps the best level of evidence in a prospective cohort study. They demonstrated that LCEA less than 30 degrees was associated with a 3.3 times increased risk of osteoarthritis at 8-year follow-up. This supports the potential increased risk for structural instability and hip osteoarthritis in hip with borderline dysplasia (LCEA 20 to 25 degrees). Li et al. demonstrated the potential role of femoral anteversion in the dysplastic hip and found that hip osteoarthritis development was associated with increased femoral anteversion (osteoarthritis, mean femoral anteversion 18 degrees; compared with 15 degrees with no osteoarthritis). Combined acetabular and femoral anteversion appears to play a similar role. The authors recommended combined anteversion greater than 40 degrees or femoral anteversion greater than 20 degrees as risk factors for hip osteoarthritis. The natural history of dysplasia in males is less clear. Croft et al. found no association of hip dysplasia (LCEA <25 degrees) with osteoarthritis in a study of 1516 pelvic radiographs.