Micro-computed tomographical and histopathological analyses of medial tibial plateaus from patients with subchondral insufficiency fracture or osteoarthritis of the knee

Background: Subchondral insufficiency fracture of the knee (SIFK) is a rare and rapidly progressing knee joint disease. The typical diagnostic finding of SIFK by magnetic resonance imaging (MRI) is a subchondral hypointense line around the bone marrow lesions (BMLs), which are also commonly observed in knee osteoarthritis (OA). Subchondral bone fracture and its repair reactions are implicated for SIFK. However, pathological changes of SIFK and BMLs and the mechanism by which SIFK is induced remain elusive. We aimed to examine characteristics of SIFK and OA by micro-computed tomography (micro-CT) and histology together with biomarker analysis. Methods: Nineteen patients with femoral or tibial SIFK (10 F-SIFK and 9 T-SIFK patients) and 24 knee OA patients, who were diagnosed by radiography and MRI and underwent unicompartmental knee arthroplasty, were enrolled for this study, and their medial tibial plateaus were examined by micro-CT and pathology. Serum and urine biomarkers were also analyzed. Results: All the T-SIFK patients showed BMLs with a subchondral hypointense line by MRI. Micro-CT analysis revealed that the T-SIFK lesion comprises multiple subchondral bone fragments covered with articular cartilage. Histologically, the lesion was composed of articular cartilage-covered subchondral bone fragments, debris of bone and bone marrow, fibrogranulation tissue, cartilage and woven bone. The medial tibial plateaus from OA patients frequently exhibited eburnation, which was commonly accompanied by microfracture. All the BMLs observed in T-SIFK and OA were associated with fat necrosis, which was characterized by disrupted fat cells and foamy macrophage infiltration. The posterior tibial slope angle (12.84 ± 2.34° vs 9.58 ± 2.84°) and the rate of medial meniscal posterior root tears (68.4% vs 25.0%) were significantly higher in T-SIFK than OA. Numbers of grade 2 subchondral bone resorption pits in uninvolved areas of the medial tibial plateaus (2.32 ± 1.43 vs 0.72 ± 0.66) and the femoral condyles (5.53 ± 3.73 vs 1.50 ± 2.10) were significantly higher in T-SIFK than OA. Conclusions: Our data demonstrate that T-SIFK is generated by subchondral bone fracture and its repair reaction and suggest that fat necrosis of the bone marrow is involved in BML formation in T-SIFK and OA.