Subjects with medial and lateral tibiofemoral articular cartilage defects do not alter compartmental loading during walking

Van Rossom, Sam, Khatib, Nidal, Holt, Cathy ORCID: https://orcid.org/0000-0002-0428-8078, Van Assche, Dieter and Jonkers, Ilse 2018. Subjects with medial and lateral tibiofemoral articular cartilage defects do not alter compartmental loading during walking. Clinical Biomechanics 60 , pp. 149-156. 10.1016/j.clinbiomech.2018.10.015

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Abstract

Background Healthy cartilage is essential for optimal joint function. Although, articular cartilage defects are highly prevalent in the active population and hamper joint function, the effect of articular cartilage defects on knee loading is not yet documented. Therefore, the present study compared knee contact forces and pressures between patients with tibiofemoral cartilage defects and healthy controls. Potentially this provides additional insights in movement adaptations and the role of altered loading in the progression from defect towards OA. Methods Experimental gait data collected in 15 patients with isolated cartilage defects (8 medial involvement, 7 lateral-involvement) and 19 healthy asymptomatic controls was processed using a musculoskeletal model to calculate contact forces and pressures. Differences between two patient groups and controls were evaluated using Kruskal-Wallis tests and individually compared using Mann-Whitney-U tests (alpha <0.05). Findings The patients with lateral involvement walked significantly slower compared to the healthy controls. No movement adaptations to decrease the loading on the injured condyle were observed. Additionally, the location of loading was not significantly affected. Interpretation The current results suggest that isolated cartilage defects do not induce significant changes in the knee joint loading distribution. Consequently, the involved condyle will capture a physiological loading magnitude that should however be distributed over the cartilage surrounding the defect. This may cause local degenerative changes in the cartilage and in combination with inflammatory responses, might play a key role in the progression from articular cartilage defect to a more severe OA phenotype.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Engineering
Publisher:	Elsevier
ISSN:	0268-0033
Date of First Compliant Deposit:	19 October 2018
Date of Acceptance:	11 October 2018
Last Modified:	18 Nov 2024 08:30
URI:	https://orca.cardiff.ac.uk/id/eprint/116008

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