Quantifying the Pathophysiology of Femoroacetabular Impingement Syndrome

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PROJECT SUMMARY By some estimates, femoroacetabular impingement syndrome (FAIS) accounts for 82% of hip osteoarthritis (OA) cases. FAIS patients present with a loss of sphericity of the femoral head, reduction in femoral-neck offset, and/or an excessively prominent acetabular wall. Patients report pain that is position- or motion-related. Often, cartilage is delaminated from bone and the labrum is torn. The theory of FAIS pathophysiology is that pathoanatomy causes pathomechanics. However, we lack a quantitative understanding of the disease. Studies that have examined hip anatomy and biomechanics in FAIS patients have yielded conflicting data, likely due to the application of inaccurate measurement techniques. There is also a high prevalence of FAI morphology among the asymptomatic population (i.e., positive controls), which has hindered progress to understand why FAI morphology causes damage. Herein, we improve our understanding of FAIS pathophysiology. We propose a cross-sectional design with three cohorts: FAIS patients, negative controls, and positive controls. Aim 1 will quantify the pathomorphology of FAIS. More specifically, we will visualize and compare 3D hip anatomy using statistical shape modeling. We hypothesize shape modeling will detect differences in the 3D shape of the pelvis and proximal femur between symptomatic and asymptomatic hips; we posit this difference will occur whether controls are analyzed together or as separate positive/negative groups. Completion of Aim 1 will improve our clinical understanding of this disease and inform the development of better radiographic imaging techniques to evaluate hip anatomy. Aim 2 will quantify the pathomechanics of FAIS. More specifically, we will quantify in-vivo hip kinematics using dual fluoroscopy and chondrolabral mechanics using patient-specific finite element models. We hypothesize hip kinematics are altered, load transfer to the labrum is increased, and cartilage shear stresses and strains at the osteochondral and chondrolabral junctions are elevated in FAIS patients. We theorize individuals in the positive control group cope with FAI morphology through alterations in hip joint motion, which serve to keep chondrolabral mechanics within the normative range (i.e. no difference in FE predictions between positive and negative controls). Aim 2 will improve our clinical understanding of FAIS by enabling us to ‘see’ the disease process during dynamic loading. Aim 2 data will also guide development of new treatment options through a better understanding of compensation mechanisms that occur across the three groups. Aim 3 will improve our understanding of the pathogenesis of OA in hips with FAIS by identifying relationships between anatomy, chondral mechanics, and cartilage ultrastructure. Here, quantitative magnetic resonance imaging will estimate proteoglycan content and collagen organization within hip cartilage. These data may also inform new methods to diagnose, stage, and monitor the disease.