Finite element analysis of an in-vitro traumatic joint loading model.

摘要

Osteoarthritis (OA) is characterized by the degeneration of articular cartilage resulting in eventual bone on bone contact causing pain and inflammation to musculoskeletal joints. Even though the mechanisms linking joint trauma with post-traumatic OA are poorly understood, joint overloading has been shown to decrease cartilage matrix integrity and is associated with chondrocyte necrosis and apoptosis which are early signs of OA.;An in vitro impact injury model that incorporated tangential loading was developed in our lab using intact porcine patellae to produce quantifiable degradation similar to that seen in early stage osteoarthritis. We carried out two separate sets of in vitro impact experiments: (1) axial impactions: an impact insult normal to the cartilage surface at a high load and relatively fast loading rate and (2) shear impactions: a compressive preload normal to the surface subsequently followed by a tangentially applied displacement generating a shear load. The first impact injury model (axial impaction) had been extensively investigated in the literature and incorporated loads known to cause cartilage damage and cell death. The second model incorporated greater shear forces along with the axial forces and was believed to give a better representation of physiological loading.;A finite element model was created to determine the resulting mechanical stresses and strains in the underlying cartilage tissues. An Ogden hyperelastic constitutive model was used as the input material model for the finite element analysis. Cartilage in our model was broken into three homogeneous tissue zones: surface, mid, and deep and separate hyperelastic material models were developed for each of these primary layers. The output variables examined from the model were location and magnitude of compressive, tensile, and shear stresses and strains.;Intact patellae were maintained in organ culture up to two weeks to investigate the time course of cellular and matrix events post-injury. Cell death and matrix proteoglycan loss were quantified. After validation of the finite element model and collection of histological data, statistical analysis was used to correlate type, location and magnitude of stress and strain with cell death and proteoglycan loss. The overall hypothesis was that shear forces arising from traumatic impact injuries are more detrimental to cartilage matrix and chondrocytes than axial forces normally seen in most impact injury models. The long term goal of this project is to gain a better understanding of the effects normal and tangential loading have on the chondrocyte response and determine how this influences cartilage degeneration.