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Technical Briefs

Development of a Traumatic Anterior Cruciate Ligament and Meniscal Rupture Model With a Pilot In Vivo Study

[+] Author and Article Information
Daniel I. Isaac, Eric G. Meyer, Roger C. Haut

Orthopaedic Biomechanics Laboratories, College of Osteopathic Medicine, Michigan State University, East Lansing, MI 48824

J Biomech Eng 132(6), 064501 (Apr 23, 2010) (4 pages) doi:10.1115/1.4001111 History: Received June 01, 2009; Revised January 08, 2010; Posted January 27, 2010; Published April 23, 2010; Online April 23, 2010

The current study describes the development of a small animal, closed-joint model of traumatic anterior cruciate ligament (ACL) and meniscal rupture. This model can be used in future studies to investigate the roles of these acute damages on the long-term health of an injured knee joint. Forty-two Flemish Giant rabbits received an insult to the left tibiofemoral joint ex vivo in order to document optimal energy and joint orientation needed to generate ACL and meniscal rupture, without gross fracture of bone. Impact energies ranged from 10 J to 22 J, and joint flexion angle ranged from 60 deg to 90 deg. Three in vivo animals were impacted at 13 J with the knee flexed at 90 deg, as this was determined to be the optimal load and joint orientation for ACL and meniscal ruptures, and sacrificed at 12 weeks. Impact data from the ex vivo group revealed that 13 J of dropped-mass energy, generating approximately 1100 N of load on the knee, would cause ACL and meniscal ruptures, without gross bone fracture. Acute damage to the lateral and medial menisci was documented in numerous ex vivo specimens, with isolated lateral meniscal tears being more frequent than isolated medial tears in other cases. The in vivo animals showed no signs of ill health or other physical complications. At 12 week post-trauma these animals displayed marked degeneration of the traumatized joint including synovitis, cartilage erosion, and the formation of peripheral osteophytes. Histological microcracks at the calcified cartilage-subchondral bone interface were also evident in histological sections of these animals. A closed-joint model of traumatic ACL and meniscal rupture was produced, without gross bone fracture, and a pilot, in vivo study showed progressive joint degeneration without any other noticeable physical impairments of the animals over 12 weeks. This closed-joint, traumatic injury model may be useful in future experimental studies of joint disease and various intervention strategies.

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Copyright © 2010 by American Society of Mechanical Engineers
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Figures

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Figure 4

A representative photograph showing a lateral meniscal tear. Isolated lateral meniscal tears were more prominent than isolated medial tears. Radial and longitudinal tears in the posterior regions were typically noted in the menisci.

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Figure 5

Representative photographs showing the appearance of joints from the in vivo animals. (a) Severe erosion of cartilage was noted on the femoral trochlear ridges. The arrows denote joint osteophytes. (b) India ink staining of the medial femoral condyles showed full thickness ulceration of articular cartilage. (c) The medial tibial plateau also showed erosion of cartilage in the posterior aspect of the compartment.

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Figure 6

Histological sections were prepared from the (a) femoral condyles and (b) tibial plateau. Horizontal and vertical microcracks were noted at the articular cartilage/subchondral bone interface in both types of sections.

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Figure 3

Representative photograph showing traumatic ACL rupture. ACL ruptures were documented primarily at the femoral insertion.

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Figure 2

Radiograph showing the flexion angle of the rabbit lower extremity. Note the posterior slope of the tibial plateau that created anterior subluxation of the tibia causing ACL rupture and meniscal injury.

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Figure 1

Impact experiments were performed by dropping a gravity-accelerated mass onto the flexed tibial-femoral joint. The rabbit was oriented with a 90 deg flexed hind limb and a deformable interface struck the femoral condyle with impact forces oriented axially in the tibia.

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