Medial Meniscotibial Ligament Deficiency Increases Medial Meniscus Extrusion and Posterior Root Forces

Background: There is growing evidence that medial meniscotibial ligament (MTL) deficiency and medial meniscus extrusion may precede the development of some medial meniscus posterior root (MMPR) tears. However, no study has investigated the biomechanical consequences of MTL deficiency on the MMPR.

Hypothesis: (1) MTL deficiency leads to increased medial meniscus extrusion, (2) increased medial meniscus extrusion is correlated with increased compression and shear forces at the MMPR, and (3) MTL repair restores medial meniscus extrusion and MMPR forces to native levels.

Study design: Controlled laboratory study.

Methods: Fifteen pairs of fresh-frozen cadaveric knees were tested. Specimens were organized into 3 groups according to a balanced incomplete block design: (1) native, (2) MTL deficiency, and (3) MTL repair. For the MTL deficiency group, a 3-cm deficiency in the MTL was developed under direct arthroscopic visualization. Specimens in the MTL repair group underwent a 2-anchor repair that compressed the joint capsule to the proximal tibia. All specimens were biomechanically tested in full extension with a tensile testing machine. The specimens underwent cyclic loading for 10,000 cycles at 1 Hz and compression of 20 to 500 N, with a 500-N compressive force applied for 30 seconds after the 0th, 100th, 1000th, and 10,000th cycles. Ultrasound was used to measure medial meniscus extrusion. Shear and compressive forces at the MMPR were measured with a 3-axis sensor installed inferior to the MMPR tibial attachment.

Results: Medial meniscus extrusion was significantly increased in the MTL deficiency group compared with the native group (0th: 1.6 ± 0.1 mm vs 1.2 ± 0.1 mm, P < .05; 100th: 2.2 ± 0.2 mm vs 1.5 ± 0.2 mm, P < .05; 1000th: 2.8 ± 0.2 mm vs 1.8 ± 0.2 mm, P < .05; 10,000th: 3.5 ± 0.3 mm vs 2.1 ± 0.2 mm, P < .05). Compression root force was significantly increased in the MTL deficiency group compared with the native group at all cyclic loading points (0th: 21.7 ± 12.8 N vs 13.6 ± 2.4 N, P < .05; 100th: 18.9 ± 11.0 N vs 12.1 ± 7.5 N, P < .05; 1000th: 16.5 ± 9.9 N vs 11.2 ± 7.5 N, P < .05; 10,000th: 12.6 ± 8.6 N vs 9.0 ± 6.9 N, P < .05). Root shear force was significantly increased in the MTL deficiency group compared with the native group at the 0th (17.5 ± 2.5 N vs 13.6 ± 2.4 N, P < .001) and 100th (16.2 ± 2.6 N vs 12.1 ± 2.2 N, P < .001) cycles. Medial meniscus extrusion, root shear force, and compression root force of the MTL repair group were not significantly different from the native group for all cyclic loading points.

Conclusion: Medial MTL deficiency led to increased medial meniscus extrusion as well as greater compression and shear forces at the MMPR compared with the intact and repaired MTL states, suggesting that MTL deficiency may predispose the MMPR to injury in a cadaveric model.

Clinical relevance: MTL deficiency predisposes one to medial meniscus extrusion and MMPR tears. Subsequently, MTL repair can potentially correct medial meniscus extrusion and normalize forces at the MMPR.