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