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Research Papers

# Does Graft Construct Lengthening at the Fixations Cause an Increase in Anterior Laxity Following Anterior Cruciate Ligament Reconstruction in vivo?

[+] Author and Article Information
Conrad K. Smith

Biomedical Engineering Program, One Shields Avenue, University of California, Davis, CA 95616

M. L. Hull1

Department of Biomedical Engineering, One Shields Avenue, University of California, Davis, CA 95616; Department of Mechanical Engineering, One Shields Avenue, University of California, Davis, CA 95616mlhull@ucdavis.edu

S. M. Howell

Department of Mechanical Engineering, One Shields Avenue, University of California, Davis, CA 95616

1

Corresponding author.

J Biomech Eng 132(8), 081001 (Jun 15, 2010) (8 pages) doi:10.1115/1.4001027 History: Received July 13, 2009; Revised January 05, 2010; Posted January 18, 2010; Published June 15, 2010; Online June 15, 2010

## Abstract

A millimeter-for-millimeter relation between an increase in length of an anterior cruciate ligament graft construct and an increase in anterior laxity has been demonstrated in multiple in vitro studies. Based on this relation, a 3 mm increase in length of the graft construct following surgery could manifest as a 3 mm increase in anterior laxity in vivo, which is considered clinically unstable. Hence, the two primary objectives were to determine whether the millimeter-for-millimeter relation exists in vivo for slippage-resistant fixation of a soft-tissue graft and, if it does not exist, then to what extent the increase in stiffness caused by biologic healing of the graft to the bone tunnel offsets the potential increase in anterior laxity resulting from lengthening at the sites of fixation. Sixteen subjects were treated with a fresh-frozen, nonirradiated, nonchemically processed tibialis allograft. Tantalum markers were injected into the graft, fixation devices, and bones. On the day of surgery and at 1, 2, 3, and 4 months, Roentgen stereophotogrammetric analysis was used to compute anterior laxity at 150 N of anterior force and the total slippage from both sites of fixation. A simple linear regression was performed to determine whether the millimeter-for-millimeter relation existed and a springs-in-series model of the graft construct was used to determine the extent to which the increase in stiffness caused by biological healing of the graft to the bone tunnel offset the increase in anterior laxity resulting from lengthening at the sites of fixation. There was no correlation between lengthening at the sites of fixation and the increase in anterior laxity at 1 month ($R2=0.0$, $slope=0.2$). Also, the increase in stiffness of the graft construct caused by biologic healing of the graft to the bone tunnel offset 0.7 mm of the 1.5 mm potential increase in anterior laxity resulting from lengthening at the sites of fixation. This relatively large offset of nearly 50% occurred because lengthening at the sites of fixation was small.

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## Figures

Figure 6

Graph showing the average total lengthening at the sites of femoral and tibial fixations together with the average increase in anterior laxity over the 4-month time period of the study. At 1 month, there was no one-to-one correspondence between the total lengthening at the sites of fixation and the increase in anterior laxity. After 1 month, the total lengthening did not increase appreciably, which is a consequence of biologic healing of the graft in the bone tunnels, whereas the increase in anterior laxity continued to increase until 3 months presumably as a result of a decrease in the stiffness of the graft due to remodeling.

Figure 1

Schematic of the anterior-posterior view of the knee showing the locations of the 26 tantalum markers inserted in the femur (F1-F6), tibia (T1-T6), graft (G1-G8), femoral fixation device (EL1-EL3), and tibial fixation device (WL1-WL3). Markers with a diameter of 1.0 mm were injected into one strand (G1-G4) and markers with a diameter of 0.8 mm were injected into the other strand (G5-G8). All the markers in the allograft were inside the bone tunnels with markers G1, G4, G5, and G8 inserted 5 mm from the fixation device, and markers G2, G3, G6, and G7 inserted 5 mm inside the tunnel. The different diameters allowed the markers in each strand to be identified unambiguously.

Figure 2

The locations of the 1.0-mm in diameter tantalum markers (arrows) are shown in the multispiked tibial fixation device (left) and the femoral fixation device (right). Three markers were press-fit into milled holes made with a 0.94-mm diameter ball end mill.

Figure 3

Photograph of the limb in the loading apparatus with the knee in 25 deg of flexion centered in the calibration cage, the ankle and thigh secured in supports, and a pneumatic actuator affixed to the proximal tibia. The pneumatic actuator applied posterior and anterior forces to the tibia, while the thigh and ankle were fixed. Load cells were used to measure the applied force and the reaction force at the ankle joint. The force transmitted at the knee was standardized (i.e., 150-N anterior force, 90-N posterior force) using a previously described technique.

Figure 4

Sample biplanar radiographs of a right knee showing the anterior-posterior view (left image) and the medial-lateral view (right image). The 26 tantalum markers fixed to the femur (F1-F6), tibia (T1-T6), graft (G1-G8), femoral fixation device (EL1-EL3), and tibial fixation device (WL1-WL3) are indicated. The tantalum markers fixed to the fixation devices can be distinguished because the devices are made from less radio-opaque metals.

Figure 5

Springs-in-series model of the knee. Kf represents the stiffness of the femoral fixation, Kg represents the stiffness of the graft, and Kt represents the stiffness of the tibial fixation. The stiffness of the graft construct (Kgc) is determined from Kgc=(KfKgKt)/(KfKg+KfKt+KgKt).

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