Gluteus Minimus Indentation Is Associated With Acetabular Undercoverage and Increased Femoral Torsion in Patients With Nontraumatic Hip Pain.
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BACKGROUND: Although the hip is generally considered a stable joint, certain morphological configurations-such as acetabular dysplasia or abnormal femoral torsion-can predispose it to instability. Gluteus minimus indentation, a lateral femoral head morphologic finding, has been described in patients with cerebral palsy and severe dysplasia; however, whether it occurs in other instability-related hip morphologies and whether it has clinical relevance remains unclear. QUESTIONS/PURPOSES: (1) Did a higher percentage of patients with hip dysplasia (defined as a lateral center-edge angle [LCEA] < 22°) have gluteus minimus indentation than patients without dysplasia? (2) Was there an association between gluteus minimus indentation and acetabular or femoral radiological parameters? (3) Were there differences in three-dimensional (3D) cartilage and labral parameters between hips with and without gluteus minimus indentation? METHODS: Between November 2019 and December 2024, 761 hips (703 patients) underwent MR arthrography for nontraumatic hip pain at our institution and were included in this retrospective, single-center study. MR arthrography was ordered for patients whose hip pain had not improved after at least 3 months of conservative treatment and who were being considered for hip preservation surgery. We excluded 47% (357 of 761) of hips for previous hip surgery, trauma, avascular necrosis, advanced osteoarthritis, tumors, childhood conditions, or inadequate imaging, and a further 2% (12 of 761) to retain one hip per patient, leaving 392 hips for analysis. The included patients had a mean ± SD age of 32 ± 10 years, and 58% (229 of 392) of patients were females. In all, 18% (69 of 392) had dysplasia (LCEA < 22°) and 59% (231 of 392) had increased femoral torsion (> 25°). No patients had cerebral palsy. Gluteus minimus indentation and its topographic distribution, reported using a clockface system, were assessed on radial MR sequences. Radiographic parameters were measured on AP pelvis radiographs. Three-dimensional models of the acetabular cartilage and labrum were generated from an MRI sequence (magnetization-prepared 2 rapid gradient-echo) that produces high-contrast images in which cartilage and the labrum can be clearly distinguished. The models were created using a previously validated deep-learning algorithm trained to outline these structures. In the validation study, agreement with manual segmentation was excellent. RESULTS: Gluteus minimus indentation was present in 7% (29 of 392) of hips. A higher percentage of patients with hip dysplasia had gluteus minimus indentation than patients without dysplasia (22% [15 of 69] versus 4% [14 of 323]; p < 0.01). After controlling for acetabular version, retroversion index, caput-collum-diaphyseal angle, age, and sex, each 5° decrease in LCEA was associated with a 1.5 times higher odds of gluteus minimus indentation (95% confidence interval (CI) 1.2 to 1.9; p < 0.01), and each 5° increase in femoral torsion was associated with a 1.3 times higher odds (95% CI 1.1 to 1.6; p < 0.01) of gluteus minimus indentation. In dysplastic hips, defined as a LCEA < 22°, and hips with increased femoral torsion (> 25°), those with gluteus minimus indentation had a smaller relative cartilage surface area, a greater labral volume, and a greater labral contribution to the joint surface. These differences persisted after accounting for LCEA and for femoral torsion, respectively. CONCLUSION: Gluteus minimus indentation was most common in dysplastic hips, although it also occurred in hips with increased femoral torsion and normal coverage. Its association with a smaller cartilage surface area and greater labral contribution suggests that it may be a marker of instability that warrants closer evaluation. The frequency and clinical significance of gluteus minimus indentation in asymptomatic hips are unknown, and the presence of gluteus minimus indentation should not influence treatment until its relevance to prognosis, natural history, or treatment response is established. LEVEL OF EVIDENCE: Level IV, prognostic study.