header advert
Orthopaedic Proceedings Logo

Receive monthly Table of Contents alerts from Orthopaedic Proceedings

Comprehensive article alerts can be set up and managed through your account settings

View my account settings

Visit Orthopaedic Proceedings at:



Full Access



8th Combined Meeting Of Orthopaedic Research Societies (CORS)


Summary Statement

Simulated increases in body weight led to increased displacement, von Mises stress, and contact pressure in finite element models of the extended and flexed knee. Contact shifted to locations of typical medial osteoarthritis lesions in the extended knee models.


Obesity is commonly associated with increased risk of osteoarthritis (OA). The effects of increases in body weight and other loads on the stresses and strains within a joint can be calculated using finite element (FE) models. The specific effects for different individuals can be calculated using subject-specific FE models which take individual geometry and forces into account. Model results can then be used to propose mechanisms by which damage within the joint may initiate.

Patients & Methods

Twelve subject-specific FE models (Abaqus 6.11) of three normal healthy subjects were created by combining geometry (3T T1-weighted MRI scans processed using Mimics 13.0, Geomagic Studio 11, and SolidWorks 2010) and load cases (Vicon and AMTI motion analysis data processed within AnyBody Technology Version 3.0 and Matlab R2007a). Model geometry included the femur and tibia (rigid bodies), tibial cartilage and femoral cartilage (E = 12 MPa, ν = 0.45), and menisci (Ecircumferential = 120 MPa, νcircumferential = 0.2; Eaxial/radial = 20 MPa, νaxial/radial = 0.3). The tibia was held fixed while loads were applied to the centre of mass of the femur. Frictional contact (µ = 0.02) was modelled between soft tissues. Of the twelve models, six were of extended knees and six were of mid-range flexed (∼50°) knees. Each of these six models represented a paired set: a “normal” model and an “increased-load” model. In the flexed knee “increased-load” models, loads were doubled; in the extended knee “increased-load” models, loads were increased to a standard 2000 N compressive load across the joint (approximately three to four times larger than the original loads). Maximum displacements, von Mises stresses, and contact pressures on the articulating tibial cartilage and femoral cartilage surfaces were calculated; results of the “normal” and “increased-load” models were compared.


Increasing the applied loads increased the maximum displacements, von Mises stresses, and contact pressures. Contact shifted anteriorly in the extended knee models to typical locations of medial OA cartilage lesions. No contact shift occurred in the flexed knee models; contact remained in typical locations of lateral OA cartilage lesions, but the contact area extended in all directions, and displacements, stresses, and pressures increased.


Comparing the “normal” and “increased-load” results suggested two potential mechanical mechanisms involved in osteoarthritic cartilage lesion development. Contact shifted to areas of previously-unloaded cartilage in the extended knee “increased-load” models. Cartilage has regional material properties, with stiffer cartilage in areas of frequent contact and loading; shifting contact to areas of less-stiff cartilage could damage the cartilage and lead to degenerative diseases such as OA. Contact did not shift in the flexed knee “increased-load” models. Instead, the displacements, stresses, and pressures increased while the centres of contact remained relatively stationary. If these contact variables increase beyond a threshold magnitude, the cartilage could be damaged, potentially leading to OA.