Peri-tunnel bone loss: does it affect early tendon graft to bone tunnel healing after ACL reconstruction?

Abstract

The clinical relevance and mechanisms of local bone loss early post-anterior cruciate ligament (ACL) reconstruction remain unclear. The early spatial and temporal changes of peri-tunnel bone, its molecular mechanisms and its relationships with graft-bone tunnel healing were investigated in a 12-week-old rat model. At various times, the reconstructed ACL complex was harvested for vivaCT imaging, biomechanical test, histology and immunohistochemical staining of CD68+ cells (a monocyte-macrophage lineage marker), MMP1 and MMP13. The peri-tunnel bone resorbed simultaneously with improvement of graft-bone tunnel healing. There were 30.1 ± 17.4, 46.8 ± 10.5 and 81.5 ± 12.3 % loss of peri-tunnel BMD as well as 43.2 ± 21.7, 78.7 ± 8.5 and 92.4 ± 17.7 % loss of peri-tunnel bone volume/total volume (BV/TV) at week 6 at the distal femur, epiphysis and metaphysis of tibia, respectively. MMP1, MMP13 and CD68+ cells were expressed at the graft-bone tunnel interface and peri-tunnel bone and increased with time post-reconstruction at the tibia. The ultimate load and stiffness of the healing complex positively correlated with tibial tunnel bone formation and negatively correlated with tibial peri-tunnel bone. Tunnel BV/TV at the tibial metaphysis and epiphysis showed the highest correlation with ultimate load (ρ = 0.591; p = 0.001) and stiffness (ρ = 0.427; p = 0.026) of the complex, respectively. There was time-dependent loss of peri-tunnel bone early post-reconstruction, with the greatest loss occurring at the tibial metaphysis. This was consistent with high expression of MMP1, MMP13 and CD68+ cells at the graft-bone tunnel interface and the peri-tunnel region. The significant loss of peri-tunnel bone, though not critically affecting early tunnel healing, suggested the need to protect the knee joint early post-reconstruction.