Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Medical Biophysics

Supervisor

Dr. David W. Holdsworth

Abstract

Osteoarthritis (OA) is degenerative disease caused by a mechanical failure of bone and cartilage. Common risk factors for developing OA include: being over-weight, female, having joint malalignment, or a history of prior joint injury. Post-traumatic OA is extremely common in the knee as individuals frequently suffer injuries to structures that provide stability to the joint. To enhance our understanding about OA, animal models are employed where the injury can be and monitored in a controlled environment. When used in conjunction with pre-clinical imaging techniques the longitudinal degradation of bone and cartilage can be quantitatively monitored in vivo. Recent evidence has identified cystic lesions within the subchondral bone as the possible source of painful symptoms and accelerated disease progression, but little is known about their etiology.

The purpose of this thesis was to improve knowledge regarding the mechanism that causes subchondral cysts. OA was induced in the rodent knee via surgery, and the pathological changes were quantified with micro-CT and MRI. The composition of the cysts was correlated with end-stage histology. Thus, an accurate definition of OA bone cysts was achieved. To assess the effect of cysts in human bone, a study was conducted using a patient data set restrospectively. Using finite element (FE) analysis, higher stress values were found within bone surrounding cysts. Therefore, the probable mechanism of cyst expansion, stress induced resorption, was identified. Finally, the FE models of the bones were combined with soft tissue structures – from a co-registered MRI – to produce comprehensive patient-specific models of the knee.


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