Hip dysplasia

In the normal hip, the acetabulum provides sufficient coverage of the femoral head to distribute joint reaction forces across a broad area of articular cartilage. The osseous architecture, acetabular labrum, capsule, and surrounding musculature collectively maintain femoral head containment and stability.

Hip dysplasia in the skeletally mature patient is a structural abnormality in which the acetabulum provides insufficient coverage or containment of the femoral head. The deficient acetabulum is commonly shallow and may have abnormalities of orientation as well as volume, resulting in a smaller effective weight-bearing surface and altered distribution of forces across the hip 1,2. As such, the acetabular labrum can assume a disproportionately important role in load support and stability in the dysplastic hip, and is frequently hypertrophied as an adaptive response to deficient bony coverage 3; however, chronic overload can ultimately result in labral degeneration, tearing, or detachment.

The central mechanical consequence is insufficient osseous stability. Unlike femoroacetabular impingement syndrome (FAIS), where excessive or abnormal contact is the dominant mechanism, dysplasia primarily produces excessive loading at the acetabular rim and, in some hips, abnormal femoral head translation or instability. This predisposes to secondary labral and chondral injury and ultimately increases the risk of premature osteoarthritis 1,4. The term borderline dysplasia can be used for hips with mild acetabular undercoverage. These hips can either behave predominantly as unstable dysplastic hips and others have relatively stable mechanics with concomitant impingement morphology 5.

The acetabular deficiency may be predominantly lateral, anterior, posterior, or more global, and abnormalities in acetabular orientation may coexist with deficient coverage 1. The resulting mechanical environment varies according to the location and severity of the deficiency.

Associated abnormalities may include altered femoral version, proximal femoral morphology, or concomitant cam morphology. These additional features can modify whether a particular hip behaves predominantly through instability, impingement, or a combination of both mechanisms 2,5.

The characteristic pathophysiologic sequence is: Acetabular undercoverage → reduced weight-bearing surface area and deficient osseous containment → increased rim loading ± abnormal femoral head translation → labral overload and cartilage stress → labral/chondral failure → progressive joint degeneration —-------

Hip dysplasia is particularly important to the hip arthroscopist because the intra-articular abnormalities encountered (most notably labral tears and chondral lesions) may be secondary consequences of an underlying osseous deficiency. Treating the damaged labrum or cartilage without recognizing deficient acetabular containment may leave the principal mechanical abnormality unchanged.

Selected patients with mild or borderline dysplasia may achieve favorable outcomes following arthroscopic treatment when the dominant pathology is appropriately identified; however, outcomes are less predictable when significant structural instability is present 5,6. In more substantial dysplasia, the fundamental abnormality is osseous rather than purely intra-articular, and isolated arthroscopy cannot restore deficient acetabular coverage.