Explore whether high tibial osteotomy (HTO) changes knee contact forces and to explore the relationship between the external knee adduction moment (EKAM) pre and 12 months post HTO. Three-dimensional gait analysis was performed on 17 patients pre and 12-months post HTO using a modified Cleveland marker-set. Tibiofemoral contact forces were calculated in SIMM. The scaled musculoskeletal model integrated an extended knee model allowing for 6 degrees of freedom in the tibiofemoral and patellofemoral joint. Joint angles were calculated using inverse kinematics then muscle and contact forces and secondary knee kinematics were estimated using the COMAC algorithm. Paired samples t-test were performed using SPSS version 25 (SPSS Inc., USA). Testing for normality was undertaken with Shapiro-Wilk. Pearson correlations established the relationships between EKAM1 to medial KCF1, and EKAM2 to medial KCF2, pre and post HTO.Abstract
Objective
Methods
In knee osteoarthritis (OA) patients, a focal cartilage defect is commonly found, especially in the medial compartment. In addition, cartilage softening is often observed at the defect rim. Both factors may alter the loading distribution and thereby the contact pressures, previously related to cartilage degeneration. To determine contact pressure
Healthy cartilage is essential for optimal joint function. Although, articular cartilage defects are highly prevalent in the active population and might hamper joint function, the effect of articular cartilage defects on knee contact forces and pressures is not yet documented. Therefore, the present study compared knee contact forces and pressures between patients with a tibiofemoral cartilage defect and healthy controls. This might provide additional insights in movement adaptations and the role of altered loading in the progression from defect to OA. Experimental gait data was collected in 15 patients with isolated articular cartilage defects (8 medial-affected, 7 lateral-affected) and 19 healthy asymptomatic controls and was processed using a musculoskeletal model to calculate contact forces and pressures. Differences between medial-affected, lateral-affected and controls were evaluated using Kruskal-Wallis tests and individually compared using Mann-Whitney-U tests (alpha <0.05). The lateral-affected group walked significantly slower compared to the healthy controls. No adaptations in the movement pattern that resulted in decreased loading on the injured condyle were observed. Additionally, the location of loading was not significantly affected. The current results suggest that isolated cartilage defects do not induce changes in the knee joint loading pattern. Consequently, the involved condyle will be equally loaded, indicating that a similar amount of force should be distributed over the remaining cartilage surrounding the articular cartilage defect and may cause local degenerative changes in the cartilage. This in combination with inflammatory responses might play a key role in the progression from articular cartilage defect to a more severe OA phenotype.