Medial osteoarthritis (OA) and lateral OA have distinct characteristic cartilage lesion locations and knee flexion angles associated with lesion development. These types of OA are suggested to be caused by loading when the knee is in extension and mid-range flexion, respectively. This project used subject-specific finite element (FE) models to investigate contact conditions within the extended and flexed knee. A method of creating subject-specific FE models by combining geometry (derived from magnetic resonance imaging scans) and load cases (calculated from motion analysis data) collected from the same subject was developed. This model creation method was validated by comparing experimentally-measured pressure data to contact data calculated by FE models. Models of normal knees in three subjects were created first. Models with larger subject-specific loads had larger displacements and higher stresses and contact pressures. Contact occurred over most of the articulating cartilage surfaces, both in areas of typical cartilage lesions and outside areas of typical cartilage lesions. Parameters in the normal models were then altered to reflect three mechanical changes hypothesized to lead to OA: increased loading, globally decreased cartilage stiffness, and locally decreased cartilage stiffness. Increased loading led to increased displacements, stresses, and contact pressures. Contact shifted anteriorly in the extended knee models to locations of typical medial OA cartilage lesions; contact remained stationary with elevated stress magnitudes in the flexed knee models. Globally decreasing cartilage stiffness had limited effects on contact results. Locally decreased cartilage stiffness led to locally increased displacement and strain and locally decreased stress and contact pressure. Contact again shifted anteriorly in the extended knee models. Potential mechanisms of OA initiation were then proposed. Increased weight or locally decreased cartilage stiffness increased strains within the cartilage. High strains can damage the cartilage matrix fibres, further decreasing cartilage stiffness and eventually leading to cartilage lesions and OA.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:581320 |
| Date | January 2013 |
| Creators | Boyd, Jennifer Leigh |
| Contributors | Zavatsky, Amy B.; Gill, Harinderjit S. |
| Publisher | University of Oxford |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://ora.ox.ac.uk/objects/uuid:c643e82b-d0e5-41dd-a7d0-543223550c19 |
Page generated in 0.0091 seconds