Computational analysis applied to the study of post-traumatic osteoarthritis

Abstract

Post-traumatic osteoarthritis (PTOA) is a debilitating joint disease in which cartilage degenerates following joint trauma, including intra-articular fracture or ligament rupture. Acute damage and chronically altered joint loading have both been implicated in the development of PTOA, but the precise pathway leading from injury to cartilage degeneration is not yet known. A series of computational analyses were performed to gain insight into the initiation and progression of cartilage degeneration. Finite element models of in vitro drop-tower impacts were created to evaluate the local stress and strain distributions that cartilage experiences during such experiments. These distributions were compared with confocal imaging of cell viability and histologically apparent matrix damage. Shear strain and tensile strain both appear to correlate with the non-uniform percentage of cell death seen in the impact region. In order to objectively evaluate structural damage to the cartilage matrix, an automated image processing program was written to quantify morphologic characteristics of cartilage cracks, as seen in histology slides. This algorithm was used to compare the damage caused by different rabbit models of PTOA and to investigate the progression of matrix damage over time. Osteochondral defect insults resulted in more numerous and more severe cracks than ACL transection. Interestingly, no progression of structural damage was identified between 8 weeks and 16 weeks in these rabbit PTOA models. A finite element based optimization algorithm was developed to determine cartilage material properties based on the relaxation behavior of an indentation test. This was then used to evaluate the spatial and temporal progression of cartilage degeneration after impact. Impacting cartilage with 2.18 J/cm 2 through a metal impactor caused an immediate increase in permeability and decrease in modulus, both of which recover to nearly pre-impact levels within two weeks. Biologic testing suggests that the modulus changes were due to collagen fibril damage that is then repaired. Impacting with higher To my wife Jess, for her patient and caring support and my daughter Anna, who quickly became my favorite distraction from thesis writing iii ACKNOWLEDGMENTS I gratefully acknowledge and thank my colleagues and my friends at the Orthopaedic Biomechanics Laboratory for their assistance during the course of my studies. I would especially like to thank Dr. Thomas Brown for giving me the opportunity to become part of orthopaedic biomechanics at Iowa and for his continued support of my professional development. I am also greatly indebted to Julie Mock for her patient and friendly help with all manner of travel and organizational details. The students I have worked with at the biomechanics lab have been a pleasure to work and travel with, and I wish you all the best. Virtually every member of the OBRL staff has assisted me in some phase of this project and I appreciate the efforts this involved. In addition, I would like to thank Dr. Jim Martin, for ...