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- Kyle M Moulton, Abdel-Rahman Aly, Sathish Rajasekaran, Michael Shepel, and Haron Obaid.
- Department of Medical Imaging, University of Saskatchewan, Saskatoon, SK, Canada, kyle.m.moulton@gmail.com.
- Skeletal Radiol. 2015 Jan 1; 44 (1): 47-54.
ObjectiveGluteal tendinopathy and greater trochanteric pain syndrome (GTPS) remain incompletely understood despite their pervasiveness in clinical practice. To date, no study has analyzed the morphometric characteristics of the hip on magnetic resonance imaging (MRI) that may predispose to gluteal tendinopathy. This study aimed to evaluate whether acetabular anteversion (AA), femoral neck anteversion (FNA), and femoral neck-shaft angle (FNSA) are associated with MRI features of gluteal tendinopathy.Materials And MethodsA total of 203 MRI examinations of the hip met our inclusion and exclusion criteria. A single blinded investigator measured AA, FNA, and FNSA according to validated MRI techniques. Two blinded subspecialty-trained musculoskeletal radiologists then independently evaluated the presence of gluteal tendinosis, trochanteric bursitis, and subgluteal bursitis. Statistical analysis was performed using a one-way analysis of variance (ANOVA; post-hoc Tukey's range test).ResultsAt MRI, 57 patients had gluteal tendinosis with or without bursitis, 26 had isolated trochanteric bursitis, and 11 had isolated subgluteal bursitis. AA was significantly (p = 0.01) increased in patients with MRI evidence of gluteal tendinosis with or without bursitis [mean: 18.4°, 95 % confidence interval (CI): 17.2°-19.6°] compared with normal controls (mean: 15.7°, 95 % CI: 14.7°-16.8°). Similarly, AA was significantly (p = 0.04) increased in patients with isolated trochanteric bursitis (mean: 18.8°, 95 % CI: 16.2°-21.6°). No association was found between FNA or FNSA and the presence of gluteal tendinopathy. Interobserver agreement for the presence and categorization of gluteal tendinopathy was very good (kappa = 0.859, 95 % CI: 0.815-0.903).ConclusionOur MRI study suggests that there is an association between increased AA and gluteal tendinopathy, which supports a growing body of evidence implicating abnormal biomechanics in the development of this condition.
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