Changes in cartilage-on-cartilage contact area and cartilage deformation were investigated and related with MR relaxation times during acute loading. Contact area and cartilage deformation in the medial compartment was larger than in the lateral compartment in both normal and OA subjects. The same trend was observed in MR relaxation times of cartilage (T1ρ and T2). After loading, larger increases in cartilage-on-cartilage contact area and cartilage deformation were observed in OA patients compared to normal subjects. In addition, when data were stratified based on relaxation times and compartments, increased contact area was observed in the medial compartment of subjects with high T1ρ values.
Higher contact area in subjects with OA is likely due to changes in mechanical and structural properties of damaged cartilage. Higher contact area in the medial compartment suggests a larger share of the load compared to the lateral compartment. The change to loading differed between groups, whereby normal subjects responded with a significantly larger increase in contact area in the medial compared to the lateral compartment, but the same relationship was not observed in OA subjects. The difference in contact area between OA patients and normal subjects was higher in lateral than the medial compartment, suggesting a change in load sharing pattern due to OA. Despite this difference, the overall magnitude and the absolute change in contact area in response to loading was greater in the medial compartment in both groups. Support for altered loading mechanics in subjects with OA comes from Astephen et al.,20
who reported that knee moment and angle data during self-selected gait were significantly different between healthy and OA subjects. They reported a higher adduction moment in OA subjects, consistent with the larger load sharing in the medial compartment observed in our study.
The increase in contact area in subjects with OA may indicate that the damaged collagen network allows migration of proteoglycans out of the ECM, thus losing an important source of compressive stiffness. Severe changes in mechanical properties were reported in OA cartilage.5,21
While recent studies reported contact mechanics using dual-orthogonal fluoroscopy and MR images, differences in methodology make a direct comparison to our study difficult.13
used simple interaction of 3D geometric models for measuring cartilage deformation and contact area, considering cartilage as a rigid body. But Neu et al.23
reported non-uniform cartilage deformations in a cadaver knee under unconfined compression testing. However, in our cross-sectional study, it cannot be determined if differences in contact areas are the cause of the disease process or a result of it.
Cartilage deformation in the medial compartment was higher than in the lateral compartment when all subjects were combined. These findings agree with previous studies that showed more medial compartment deformation.14,22,23
Consistent with our observations of contact area, deformation was higher in OA patients. These results taken together with the contact area findings suggest that structural degradation indeed affects the load bearing capacity of cartilage.13,14,22
These findings suggest that fibrillation of the collagen network lowers its ability to restrain PG swelling forces, leading to increased tissue permeability, and decreased compressive stiffness, all reflected in the larger deformation and contact areas in the OA subjects.
The same trend was observed in our low-T1ρ
groups, consistent with the clinical observation of an increased incidence of medial OA in the general population. Earlier studies suggested that exchange of protons between PG and the tissue water content could be an important relaxation mechanism contributing to T1ρ
This suggests that T1ρ
may be sensitive to changes of PG in the cartilage matrix during early OA. Furthermore, T1ρ
values seem to be less affected by the orientation of collagen that can affect T2
relaxation times are inversely correlated with PG content, while T2
relaxation times are related to cartilage collagen and water content.26
values in OA subjects indicate that cartilage degeneration results in alterations in the structure of the collagen network and an increase in water content. Change in T1ρ
relaxation times of the superficial cartilage layer in OA subjects was lower than in normal subjects. This change may be due to alteration of contents in the superficial layer than in the deep layer under loading. Histological studies showed that biochemical cartilage composition is heterogeneous; near the articular surface, the PG concentration is relatively low, and water content is high. Conversely, in the deeper region near the subchondral bone, PG concentration is relatively high, and water content is low. Our subjects with elevated relaxation times displayed greater contact area in the medial, but not in the lateral, compartment. To date, no studies have investigated the effects of acute loading using relaxation time stratification.
Limitations of the study must be considered when interpreting our findings. One limitation is that the alignment of the lower limb was not measured, which is an important element in analyzing biomechanics of the limb. Also, a small number of subjects may have prevented significance from being reached in some measures; large standard deviations were observed. However, consistent trends were observed within each subject. Since the quantified contact area and deformation are in “relative % change,” the results are still valid even if a subject had a big knee (initial larger contact area) or thicker cartilage (larger deformation). The joint integrity and muscle strength to hold the dead weight and joint balancing mechanism may also be responsible for the large standard deviations. For example, a relatively large translation of the contact point on the lateral tibial plateau consistently occurred within each subject. Also, the load application was performed at only one flexion angle. Li et al.13
showed that, beyond 30° of knee flexion, there was a minimal change and movement of the contact region. Todo et al.27
showed that flexion is accompanied by internal tibial rotation. Also, tall and large size subjects may not be able to flex the knee with the circular knee coil around it inside the magnetic bore beyond 20–30°. So, we decided to flex the knee 20° while imaging. Replication of this study using high-field open MRI would enable a larger flexion range and various standing postures under true physiological loading. Integration of high-field open MRI and quantitative MRI methods would give insight into the non-invasive evaluation and monitoring cartilage biomechanics.
In conclusion, we provide evidence of an association between the mechanical response of cartilage to physiological loading (cartilage-on-cartilage contact area and cartilage deformation) and MR relaxation (T1ρ and T2) in both OA patients and normal subjects. In clinical applications, these imaging biomarkers and response of cartilage to physiologic load may be used as metrics to measure progression and development of OA, but further large cohort studies are required with long-term follow up to evaluate their effectiveness.