Arthritis Rheum. Author manuscript; available in PMC 2010 December 1.
Published in final edited form as: Arthritis Rheum. 2009 December ; 60(12): 3693–3702. doi:10.1002/art.24965.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
Increased in-vivo tibiofemoral cartilage contact deformation in anterior cruciateligament-deficiency
Samuel K. Van de Velde, MD, Jeffrey T. Bingham, MS, Ali Hosseini, MS, Michal Kozanek, MD, Louis E. DeFrate, ScD, Thomas J. Gill, MD, and Guoan Li, PhD Samuel K. Van de Velde, Jeffrey T. Bingham, Ali Hosseini, Michal Kozanek, Thomas J. Gill, and Guoan Li: Bioengineering Laboratory, Massachusetts General Hospital/Harvard Medical School, Boston, MA. Louis E. DeFrate: Orthopaedic ResearchLaboratories, Duke University Medical Center, Durham, NC.
Objective—To investigate the in-vivo cartilage contact biomechanics of the tibiofemoral joint following anterior cruciate ligament (ACL) injury. Methods—Eight patients with an isolated ACL injury in one knee and the contralateral side intact participated in the study. Both knees were imaged using a specific MR sequence to createthree-dimensional knee models of bone and cartilage. Next, each patient performed a lunge as images were recorded with a dual fluoroscopic system from 0° to 90° of flexion. The threedimensional knee models and fluoroscopic images were used to reproduce the in-vivo knee position at each flexion angle. With these series of knee models, the location of tibiofemoral cartilage contact, size of contact area,cartilage thickness at the contact area, and magnitude of cartilage contact deformation were compared between the intact and ACL-deficient knees. Results—Rupture of the ACL changed the cartilage contact biomechanics from 0° to 60° of flexion in the medial knee compartment. The location of peak cartilage contact deformation on the tibial plateaus was more posterior and lateral; the contact area wassmaller; the average cartilage thickness at the tibial cartilage contact area was thinner; and the resultant magnitude of cartilage contact deformation was increased, compared with the contralateral knee. Similar changes were observed in the lateral compartment, with increased cartilage contact deformation from 0° to 30° of knee flexion in ACL deficiency. Conclusion—ACL deficiency alters thein-vivo cartilage contact biomechanics, by shifting the contact location to smaller regions of thinner cartilage, and increasing the magnitude of cartilage contact deformation.
Many experts have abandoned the long-held belief that knee osteoarthritis is a straightforward “wear and tear” disease of cartilage (1). Instead, the metabolic and structural changes of osteoarthritis arecurrently viewed as the adaptive response of synovial joints to a variety of genetic, constitutional, or biomechanical insults (2). Nevertheless, it remains widely accepted that knee joint instability is an important risk factor in the aetiopathogenesis of the disease (3–5). The assumption that abnormal kinematics and consequent abnormal loading within the joint initiate knee osteoarthritis underliesmuch of current osteoarthritis research and orthopaedic practice: transection of the anterior cruciate ligament (ACL) is a
Correspondence to: Guoan Li, PhD, Bioengineering Laboratory, Massachusetts General Hospital/Harvard Medical School, 55 Fruit Street - GRJ 1215, Boston, MA 02114 (email@example.com), Tel: (617) 726-6472, fax: (617) 724-4392.
Van de Velde et al.
Page 2well-established animal model to induce osteoarthritis (6,7); reconstruction of the ruptured ACL has become one of the most frequent orthopaedic procedures in an attempt to restore normal joint motion and prevent long-term complications (3); and a number of alignmentmodifying therapeutic options, including bracing and osteotomy, might be used to alter the rate of osteoarthritis progression (8). However, even...