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Abstract
This thesis presents an investigation into pathomechanisms of hip osteoarthritis (OA) associated with cam-type femoroacetabular impingement (FAI). OA involves degeneration of the articular cartilage layer and subchondral sclerosis, although the pathomechanism is not completely understood.
Subchondral sclerosis was investigated using three dimensional quantitative computed tomography. Bone density around the acetabulum and at the femoral head-neck junction was measured in subjects with cam-type deformities with and without symptoms, and compared to normal controls. Cartilage degeneration was assessed in osteochondral biopsies of patients undergoing surgical correction of FAI and compared to control specimens. The mechanical properties were determined by optimization of a finite element simulation combined with in vitro indentation stress relaxation data. The cartilage region was modelled as a fibril-reinforced poroelastic (FRPE) material to mimic the macromolecular and water content of the tissue. The effects of degenerative changes in bone and cartilage properties on cartilage stresses and pressure were investigated in an axisymmetric finite element model of the hip.
BMD was higher in subjects with cam deformities, regardless of symptomatic status, by up to 40%. The largest differences were seen in the antero-superior region of the acetabulum where impingement is expected to occur. On the femoral side, subchondral BMD was higher in the deformity compared to the peripheral bearing region of control subjects.
Cartilage from the cam deformity exhibited a non-fibrillar modulus approximately 80% lower than normal cartilage, and permeability was an order of magnitude higher. The non-fibrillar modulus and permeability were explained by the lower proteoglycan content.
Simulated cartilage degeneration resulted in increased cartilage consolidation in an axisymmetric model of the hi p. Lower stiffness of the components was offset by higher strains, resulting in cartilage stresses and fluid pressure similar to the healthy model. Increased subchondral stiffness resulted in higher non-fibrillar compressive stresses, fluid pressure and tangential fibril stress. Increased volumetric compressive strain was found due to cartilage degeneration as well as increased bone stiffness.
These results support the hypothesis that subchondral sclerosis plays an important early role in OA degeneration and may be a disease potentiator. OA treatments that target only cartilage may have minimal efficacy and should address sclerotic bone changes.
