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Letter to the Editor |
1 Salt Lake City, Utah
Dear Editor:
In reading the August 2006 issue of The American Journal of Sports Medicine, I noticed a striking similarity between Defrate et al’s article, "The 6 Degrees of Freedom Kinematics of the Knee After Anterior Cruciate Ligament Deficiency: An In Vivo Imaging Analysis" (August 2006, pp 1240–1246), and an article by the same group of authors that was not referenced but appeared in The Journal of Bone and Joint Surgery (American Volume) the same month, "Anterior Cruciate Ligament Deficiency Alters the In Vivo Motion of the Tibiofemoral Cartilage Contact Points in both Antero-posterior and Mediolateral Directions" (August 2006, pp 1826–1834). Since the methods and conclusions of these articles seem to be similar, I was wondering if the authors would be willing to explain why they decided to publish them as two separate studies.
2 Boston, Massachusetts
3 Durham, North Carolina
Thank you very much for your interest in our studies on the effects of anterior cruciate ligament (ACL) injury on in vivo knee joint function that were published in The American Journal of Sports Medicine1 and The Journal of Bone and Joint Surgery.5 These 2 papers investigated 2 distinct aspects of the effects of ACL injury on knee joint biomechanics. The paper published in The American Journal of Sports Medicine described the effects of ACL injury on the 6 degrees of freedom (6DOF) knee joint kinematics, and the paper published in The Journal of Bone and Joint Surgery described the effects of ACL injury on tibiofemoral articular cartilage contact patterns. In the paper published in The Journal of Bone and Joint Surgery, we indicated that the altered cartilage contact patterns in ACL-deficient knees were likely the result of altered kinematics and cited our study published in The American Journal of Sports Medicine. During the review of both papers, we discussed with the referees the relationship between 6DOF joint kinematics and cartilage contact. These 2 data sets are different physical variables and each is important to the understanding of the effects of ACL deficiency on in vivo knee joint function.
A major goal of our research was to investigate mechanisms that might contribute to osteoarthritis after ACL deficiency. Numerous studies in the literature have investigated the abnormal kinematics after ACL deficiency, but few have been able to establish a link between the altered kinematics, altered loading of the cartilage, and long-term osteoarthritis in patients. Several recent studies, including our own work,1,7 have made predictions regarding the effects of altered kinematics on cartilage contact.
Although previous studies in the literature have hypothesized that altered kinematics alter cartilage contact patterns and predispose the joint to osteoarthritis, it is important to note that 6DOF kinematics and articular cartilage contact are 2 different physical variables. The 6DOF kinematics data, as presented in the paper in The American Journal of Sports Medicine, represent the relative motion between the tibial coordinate system and the femoral coordinate system. The effects of injury on joint motion have been measured using a variety of methods, including magnetic tracking devices, videographic gait analyses, and radiostereographic analyses. However, these data alone cannot directly be used to predict what is happening inside the knee joint (eg, articular cartilage contact).
To accurately quantify articular cartilage contact, information regarding the cartilage surfaces in contact must be known. Previous studies in the literature have used CT to create models of the knee joint and approximated cartilage contact by measuring the shortest distance between the bony surfaces of the femur and tibia. However, a recent study from our laboratory reported that the ability of using the bony geometry alone to predict contact is limited because of the complex geometry of the cartilage of the knee joint.2 In our model of joint contact, we specifically measured the geometry of the tibiofemoral cartilage surfaces using MRI, and quantified the intersection of the tibial and femoral cartilage layers.2,3,7 These data were then used to measure the locations of the cartilage contact points. The cartilage contact points represent what is occurring inside the knee joint and may provide insight into how load is transferred between the tibia and femur.
In the paper on knee kinematics after ACL deficiency published in The American Journal of Sports Medicine,1 we reported the 6DOF kinematics of patients with ACL deficiency. Although many previous studies have investigated kinematics after ACL deficiency, most focused on anterior-posterior translation. More recently, a few studies have reported that abnormal internal-external rotation occurs after ACL deficiency. However, from these variables, it was not clear to us why ACL deficiency often caused osteoarthritis. In our study, we measured kinematics in all 6DOF. The data indicated that antero-posterior translation, internal-external rotation, and mediolateral translation were altered in patients with ACL injuries. The finding of increased medial tibial translation agreed with our previous thoughts that the ACL has a laterally oriented force component that may constrain medial-lateral translation of the knee.4,6 Based on the geometry of the tibiofemoral joint, we speculated in the discussion that the increased medial translation of the tibia after ACL deficiency might shift the tibiofemoral contact points toward the medial tibial spine and might be a mechanism contributing to osteoarthritis.
In the article published in the The Journal of Bone and Joint Surgery,5 we specifically analyzed the articular cartilage contact patterns in patients with ACL injuries in 1 knee with the other knee intact. The geometry of the cartilage was reconstructed using MRI and used to measure the contact patterns inside the knee joint. This paper was the first to our knowledge of the literature to present the 3-dimensional in vivo articular cartilage contact patterns in ACL-deficient knees. The contact data supported our hypothesis based on the results of the kinematics study1—that the cartilage contact location shifted toward the medial tibial spine after ACL deficiency. This change in cartilage contact cannot be detected from the evaluation of knee kinematics alone. The geometry of the joint (including the cartilage layers) must be quantified to examine changes in contact patterns. In this manuscript, we cited our kinematics data published in The American Journal of Sports Medicine in the Discussion section, and noted that the altered tibiofemoral contact patterns could be a result of the increased medial tibial translation after ACL injury.
In summary, the 2 articles1,5 discussed different physical variables in patients with ACL deficiency. The paper published in The American Journal of Sports Medicine1 presents the 6DOF in vivo knee joint kinematics, while The Journal of Bone and Joint Surgery article5 presents the cartilage contact patterns occurring inside the knee. Because of the complex geometry of the articulating surfaces of the knee joint, it is difficult to accurately predict cartilage contact from kinematics data without quantifying the geometry of the tibial and femoral cartilage layers.2 We believe these 2 articles provide our readers with 2 different aspects of the biomechanical effects of ACL deficiency on joint biomechanics.
We once again thank you for your interest in our 2 manuscripts and for giving us the opportunity to again explain the important effects of ACL deficiency on the in vivo biomechanics of the knee.
REFERENCES
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