For this invited talk, we will focus on two different studies in our research group that have elucidated 1) the role of the healthy meniscus in cartilage load distribution and 2) changes in tibiofemoral cartilage strain in patients with meniscus tears and the relationship of cartilage strain to catabolic biomarkers in the synovial fluid of these joints.
There is currently limited in vivo data in human subjects characterizing the role of the meniscus in load distribution. Therefore, the purpose of this study was to compare the strains experienced in regions of articular cartilage covered by the meniscus to regions of cartilage not covered by the meniscus1. We hypothesized that in response to walking, tibial cartilage covered by the meniscus would experience lower strains than uncovered tibial cartilage. Magnetic resonance imaging (MRI) of the knee joints of 8 healthy subjects was performed before and after walking on a treadmill. Using MRI-generated 3-dimensional models, cartilage thickness was measured in 4 different regions based on meniscal coverage and compartment: uncovered medial, covered medial, uncovered lateral, and covered lateral. In each compartment, covered cartilage was significantly thinner than uncovered cartilage. After 20 minutes of walking, all regions experienced significant decreases in cartilage thickness. The uncovered medial region experienced significantly more strain than the covered medial region. There was no detectable difference in strain between the covered and uncovered regions in the lateral compartment. In the medial compartment in response to walking, cartilage that is covered by the meniscus experiences lower strains than uncovered cartilage. These findings provide important information on the relationship between in vivo tibial compressive strain responses and meniscal coverage that is critical to understanding normal meniscal function.
Meniscal tears are common injuries and meniscus loss is a risk factor for the development of osteoarthritis. Therefore, the goal of this study was to measure the in vivo tibiofemoral cartilage strain in patients with meniscus tears in relation to catabolic biomarkers in the synovial fluid of these joints2. MRI and biplanar fluoroscopy were used to determine the in vivo motion and cartilage contact mechanics of the knee. While performing a quasi-static lunge, subjects with isolated medial meniscus tears were analyzed. The contralateral uninjured knee was used as a control. At the time of surgery, synovial fluid was collected from the injured knee and matrix metalloproteinase (MMP) activity, sulfated glycosaminoglycan, cartilage oligomeric matrix protein, prostaglandin E2, and the collagen type II cleavage biomarker C2C were measured. In the medial compartment, contact strain increased significantly in the injured knees compared to contralateral control knees. In the lateral compartment, the contact strain in the injured knee was significantly increased at 105 degrees of flexion. The average cartilage strain at maximum flexion positively correlated with total MMP activity in the synovial fluid. Our findings reveal that meniscal injury leads to loss of normal joint function and increased strain of the articular cartilage, which correlated to elevated total MMP activity in the synovial fluid. The increased strain and total MMP activity may reflect, or potentially contribute to, the early development of post-traumatic osteoarthritis following meniscal injury.
1. Liu, B., Lad, N.K., Collins, A.T., Ganapathy, P.K., Utturkar, G.M., McNulty, A.L., Spritzer, C.E., Moorman, C.T. 3rd, Sutter, E.G., Garrett, W.E., DeFrate, L.E. In Vivo Tibial Cartilage Strains in Regions of Cartilage-to-Cartilage Contact and Cartilage-to-Meniscus Contact in Response to Walking. American Journal of Sports Medicine, 45(12): 2817-2823, 2017.
2. Carter, T.E., Taylor, K.A., Spritzer, C.E., Utturkar, G.M., Taylor, D.C., Moorman III, C.T., Garrett, W.E., Guilak, F., McNulty, A.L., DeFrate, L.E. In vivo Cartilage Strain Increases Following Medial Meniscal Tear and Correlates with Synovial Fluid Matrix Metalloproteinase Activity. Journal of Biomechanics, 48(8):1461-1468, 2015.
This work was supported in part by funding from the National Institutes of Health.