Purpose:

To develop a method for depth-wise analysis of subchondral bone that considers the gradient of bone volume, density and organization between the articular surface and the marrow cavity.

Method: Since 30% of patients fail microfracture for contained chondral lesions, our hypothesis was that early subchondral sclerosis increases compaction of bone around microfracture holes, leading to failed cartilage repair. Human osteochondral segments from the knee joint were characterized macroscopically using the Outerbridge score, then imaged at 45 micron resolution using microCT. Regions of interest (ROI) were chosen under normal cartilage and abnormal cartilage (Outerbridge Score=1). Routine Bone mineral density (BMD) analysis was performed on each ROI using GE MicroView™ analysis software. Additional depth-wise analysis of BMD was done by exporting each ROI was a density map, and calculating the mean, standard deviation and rate of change of BMD by slice in the vertical (coronal) plane. Plots of normal and early OA data by depth were compared. Microfracture holes were made in normal and sclerotic subchondral bone, and depth-wise measurements of subchondral compaction around the holes were made were made.

Results: Bone under normal versus OA cartilage was very subtly different in microCT images, but ROI microCT analysis showed that the OA samples were more mineralized and contained more bone. Using the depth-wise analysis algorithm, automated detection and measurement of the subchondral bone plate and other discrete structures was possible. The depth-wise analysis confirmed that the osteoarthritic subchondral bone plate had a higher BMD and bone volume fraction, but also showed that the rate of change (gradient) in BMD was greater. Horizontally orientated trabeculae and other anomalies were found in OA bone that contributed a more variable BMD in trabecular bone at up to 5 mm from the articular surface. Bone with early sclerotic changes had significantly (p< .01) more bone volume fraction and BMD (p< .05) around microfracture holes in this ex vivo experiment.

Conclusion: An enhanced picture of subchondral bone plate and trabecular bone anomalies can be appreciated using a depth-wise approach to image analysis. Both sclerosis and osteopenia have been reported in OA and models of OA, but this analysis shows that variability and gradient of BMD change adjacent to the articular cartilage is a significant feature of OA. This is consistent with some theories of OA progression that implicate stress concentration between the cartilage and subchondral bone plate leading to cartilage degeneration. More importantly, bone sclerosis has a direct effect on the amount of compaction around microfracture holes, so improvements in microfracture technique are needed to avoid this.