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Analysis of Tibiofemoral Cartilage Deformation in the Posterior Cruciate Ligament-Deficient Knee

¹ Bioengineering Laboratory, Department of Orthopaedic Surgery, Massachusetts General Hospital/Harvard Medical School, 55 Fruit Street, GRJ 1215, Boston, MA 02114. E-mail address for G. Li: gli1{at}partners.org

Investigation performed at the Bioengineering Laboratory, Department of Orthopaedic Surgery, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts

Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from the National Institutes of Health (Grant R01 AR052408-02), the National Football League Charities Foundation, and the Belgian American Educational Foundation. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

Methods: Fourteen patients with a posterior cruciate ligament injury in one knee and the contralateral side intact participated in the study. First, both knees were imaged with use of a specific magnetic resonance imaging sequence to create three-dimensional knee models of the surfaces of the bone and cartilage. Next, each patient performed a single leg lunge as images were recorded with a dual fluoroscopic system at 0°, 30°, 60°, 75°, 90°, 105°, and 120° of knee flexion. Finally, the three-dimensional knee models and fluoroscopic images were used to reproduce the in vivo knee position at each flexion angle with use of a previously described image-matching method. With use of these series of knee models, the location and magnitude of peak tibiofemoral cartilage deformation at each flexion angle were compared between the intact contralateral and posterior cruciate ligament-deficient knees.

Results: In the medial compartment of the posterior cruciate ligament-deficient knees, the location and magnitude of peak cartilage deformation were significantly changed, compared with those in the intact contralateral knees, between 75° and 120° of flexion, with a more anterior and medial location of peak cartilage deformation on the tibial plateau as well as increased deformation of the cartilage. In the lateral compartment, no significant differences in the location or magnitude of peak cartilage deformation were found between the intact and posterior cruciate ligament-deficient knees.

Conclusions: The altered kinematics associated with posterior cruciate ligament deficiency resulted in a shift of the tibiofemoral contact location and an increase in cartilage deformation in the medial compartment beyond 75° of knee flexion. The magnitude of the medial contact shift in the posterior cruciate ligament-deficient knee was on the same order as that of the anterior contact shift.

Clinical Relevance: The observed changes in the location and magnitude of cartilage deformation in the tibiofemoral joint provide insight about the development of degeneration of the tibiofemoral joint cartilage in patients with posterior cruciate ligament deficiency. Our data also suggest that recreating mediolateral stability of posterior cruciate ligament-deficient knees might be of importance in addition to surgically improving anteroposterior translation.

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