High-resolution microCT analysis of sclerotic subchondral bone beneath bone-on-bone wear grooves in severe...

Osteoarthritis (OA) is associated with sclerosis, a thickening of the subchondral bone plate, yet little is known about bone adaptations around full-thickness cartilage defects in severe knee OA, particularly beneath bone-on-bone wear grooves. This high-resolution micro-computed tomography (microCT) study aimed to quantify subchondral bone microstructure relative to cartilage defect location, distance from the joint space, and groove depth. Ten tibial plateaus with full-thickness cartilage defects were microCT-scanned to determine defect location and size. Wear groove depth was estimated as the thickness from its deepest point to a surface interpolated from the defect edges. Two 5 × 5 mm specimens were sampled from three regions (defect, edge, and cartilage-covered areas) and two from the contralateral condyle, then scanned at higher resolution. Bone density profiles were analyzed as a function of distance from the joint space to identify cortical and trabecular regions of interest and and compute their respective bone density and microstructure. Cortical bone beneath defects was four times thicker under wear grooves than beneath cartilage. Bone density profiles significantly differed between the three specimen types at depths up to 5 mm. Below defects, cortical porosity was 85 % higher, and trabecular density 14 % higher, than in cartilage-covered specimens. Some trabecular spaces were filled with woven bone-like tissue, forming a new cortical layer. These changes were confined to the defect region and ceased abruptly at the defect edge. No correlation was found between bone microstructural indices and the estimated groove depth. Our findings suggest an ongoing migration of the cortical layer during formation of the groove from its original position into the underlying trabecular bone, a process we termed "trabecular corticalization." Under deeper wear grooves, the new cortical layer exhibited large pores connecting bone marrow to the joint space, suggesting physiological limits to corticalization. These results highlight specific bone adaptations beneath cartilage defects in severe OA and provide insights into the progression of subchondral bone changes under bone-on-bone contact areas.