Elsevier

The Knee

Volume 9, Issue 3, September 2002, Pages 209-214
The Knee

A potential animal model for creating a controlled and reversible anterior cruciate ligament insufficiency

https://doi.org/10.1016/S0968-0160(02)00037-6Get rights and content

Abstract

We developed and tested a device to manipulate the axial position of the tibial anterior cruciate ligament (ACL) insertion in vitro to create a potential animal model that could simulate both ACL insufficiency and ‘optimal’ ACL reconstruction. This model is based on the concept that controlled incremental proximal displacement of the tibial ACL insertion simulates ACL insufficiency. Replacing the insertion at the joint level and then adjusting its position until the forces recorded equaled those in the ACL-intact knee can simulate ‘optimal’ ACL reconstruction. Anterior tibial translation (ATT) was quantified in vitro in 24 sheep cadaver knees with the ACL intact and after the ACL was cut or detached (ACL insufficiency). In 8 knees, a bone plug including the tibial ACL insertion was detached, mounted in a specially designed device, and adjusted to reproduce ATT of the ACL-intact knee. ATT was then measured after proximal displacement of the tibial ACL insertion in calibrated 1 mm increments. The results revealed that detaching the ACL increased ATT by 132–700%. Controlled 3 mm proximal displacement of the insertion using this device increased ATT by more than 100%. Comparing the increase in ATT due to controlled displacement of the ACL insertion to that due to detaching the ACL, in only one case was the same magnitude of ACL insufficiency reproduced. Despite the variability between knees, the device was able to reproduce ATT of the ACL-intact knee and to substantially increase ATT with controlled proximal displacement of the tibial ACL insertion. Use of this device, if successful in an in vivo ACL reconstruction model, could help define any quantitative association between altered joint kinematics and degenerative changes in the joint.

Introduction

Anterior cruciate ligament (ACL) injuries most often involve young patients [1] and can cause joint instability that may lead to meniscus tears and osteoarthritis [2], [3]. ACL reconstruction can subjectively restore joint stability, but whether ACL reconstruction retards the progression of osteoarthritis has not been definitively established [4], [5]. This issue has not been addressed in animal studies. In ACL transection models of osteoarthrosis, ACL reconstruction is not performed [6], and in animal models for optimizing ACL reconstruction, joints without osteoarthritis are used [7]. Yet, examination of the early degenerative changes of osteoarthrosis necessitates animal models [8]. Current techniques for ACL reconstruction do not normalize knee stability or kinematics in animal models [7], [9], [10]. This may be due to the smaller joint size and a more pronounced double bundle anatomy in most animals compared to humans. Anterior tibial translation (ATT) was still increased after ACL reconstruction, whether measured statically [7], [9] or dynamically (during gait [10]). As a consequence, animal studies currently cannot differentiate between effects purely from abnormal kinematics, or effects from accumulated damage of menisci, cartilage and subchondral bone. Such differentiation could clarify the relationship between ACL insufficiency, early osteoarthritis, and ACL reconstruction. Such an approach could validate the current emphasis on mechanical (kinematic) factors, or may suggest alternative or additional treatment strategies; for example, pharmacological modification of cartilage and bone metabolism.

With the long-term goal to create an animal model that can simulate both ACL insufficiency and ‘optimal’ ACL reconstruction, we have developed a device to manipulate the axial position of the tibial ACL insertion. This technique preserves double bundle anatomy and femoral insertion of the ACL. We hypothesized that positioning the tibial ACL insertion to reproduce joint forces measured in the ACL-intact knee would simulate ‘optimal’ ACL reconstruction. In addition, controlled incremental proximal displacement of the tibial ACL insertion would simulate ACL insufficiency. As a first step in validation of this model, we measured the effectiveness of the device to simulate ACL insufficiency and ‘optimal’ ACL reconstruction in sheep cadaver knees in vitro.

Section snippets

Material and methods

ATT was measured in a total of 24 cadaver sheep knees. These same knees were made ACL insufficient by cutting the ACL (n=10) or by freely detaching a bone plug including the tibial ACL insertion (n=14). Eight knees had the device for displacement of the tibial ACL insertion implanted and ATT was assessed at different increments of proximal displacement. Six knees had the device implanted and were tested for fixation strength. In the 10 remaining knees that had the ACL cut, the effect of

Results

In 24 knees, mean ATT under 50 N of anterior load was 1.18±0.4 mm (range 0.70–2.56 mm). Cutting the ACL or detaching the tibial ACL insertion increased the mean ATT by 4.23 mm (360%) to 5.41±2.29 mm (range 1.91–9.03 mm or 132–700%).

In 8 knees that had the device implanted, ATT was similar to that of the ACL-intact knee when the device was placed in the ‘optimal’ reconstruction position (Fig. 3). Precise reproduction of this translation was achieved by adjusting the set-screw of the device so

Discussion

We measured ATT in sheep cadaver knees and used a custom-designed device to simulate ACL insufficiency and ‘optimal’ ACL reconstruction. In 8 sheep cadaver knees, the device could reproduce ATT of the ACL-intact knee, suggesting that this device was able to simulate an ‘optimal’ ACL reconstruction evaluated by an anterior drawer test. Controlled 3 mm proximal displacement of the device increased the ATT by more than 100%, suggesting that this device can create some degree of ACL insufficiency.

Acknowledgements

The authors recognize the technical support of Gunther Hehr and the financial support of Canadian Arthritis Society, GEOIDE, Canadian Institute for Health Research (CIHR), Netherlands Organisation for Scientific Research (NWO), and Stichting Annafonds.

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