Abstract

Most acetabular labral tears are caused by abnormal osseous morphology, such as cam and/or pincer morphology and dysplasia. There is a high prevalence of asymptomatic cam morphology, pincer morphology, dysplasia, and acetabular labral tears in the general population. The addition of subjective patient symptoms and objective physical examination findings to imaging (plain radiographs, magnetic resonance imaging, and computed tomography) may yield the diagnosis of femoroacetabular impingement syndrome. Most glenoid labral tears (e.g., Bankart lesion, posterior labral tear, or SLAP tear) are caused by either glenohumeral instability or a degenerative process. Similarly to the acetabular labrum, there is a high prevalence of asymptomatic glenoid labral tears in an asymptomatic population. Hip pathomorphology (e.g., cam impingement) can have a significant biomechanical impact both upstream and downstream on the kinetic chain (lumbosacral spine, periarticular hip musculature [athletic pubalgia, core muscle injury, sports hernia], knee [anterior cruciate ligament], and shoulder and elbow). Thus, it is tempting to believe that the hip issue may cause the shoulder issue or that an innate genetic (or acquired) abnormality may predispose both joints to labral injury. However, the wise clinician will not be lured into this trap—correlation does not equal causation. Biomechanical studies that evaluate stress transfer from the hip to the shoulder, in addition to clinical studies that prospectively follow these groups, will help to answer this highly relevant question.

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