UVM Theses and Dissertations
Format:
Print
Author:
Michalek, Arthur James
Dept./Program:
Mechanical Engineering
Year:
2009
Degree:
PhD
Abstract:
This dissertation aims to deepen our understanding of the underlying mechanisms through which mechanical signals are carried through multiple size scales in the anulus fibrosus (AF) of the intervertebral disc (IVD), in both the healthy and disrupted states. These mechanisms were investigated through three studies.
The first two studies utilized combined mechanical loading and confocal microscopy to measure micro-scale tissue strains under the application of tissue level deformation. They hypothesized that; A. Transverse shear deformation results from intralamellar skewing in healthy tissue and that elastase digestion will also allow interlamellar sliding. B. Circumferential shear results from independent mechanisms of stretch and rotation of collagen fiber bundles and that disruption. of interlamellar connectivity through elastase digestion will reduce fiber strain and increase fiber rotation. C.A. puncture injury will alter the distribution of strains within AF tissue under shear deformation in the proximity of a needle puncture injury. D. Within physiological levels of cyclic shear, a puncture injury will not propagate through the tissue. These hypotheses were tested using simultaneous dynamic shear loading and confocal microscopy followed by digital image analyses to measure microscale deformations.
The third study set out to investigate the role of the AF in containing disc fluid pressure in both the healthy and injured states. It hypothesizes that; A. Needle puncture injuries alter intervertebral disc compressive properties by introducing a new mechanism by which fluid may enter and exit the disc, Le., a "pressure vent". B. There is a critical size at which this injury offers negligible resistance to fluid flow and the puncture becomes effeotively infinite for a given loading condition. Rat caudal IVDs were tested in axial compression experiments in displacement control under overloading and recovery conditions to assess how needle puncture injuries influenced axial stiffness, and relative energy dissipation. A theoretical model was also utilized to provide a conceptual and quantitative understanding of how needle puncture affects IVD stiffness, relative energy dissipation, and fluid transport patterns under different puncture sizes and loading conditions.
The investigations of microscale deformations of AF tissue under applied strain have provided a unique insight into how this structure behaves mechanically. In particular, it was shown for the first time that the lamellae of the AF are not capable of sliding relative to one another on a macroscopic scale. Additionally, this hierarchical connectivity lends remarkable robustness to the tissue following acute injury. It was seen for the first time that physiological levels of tissue strain result in finite propagation of a puncture type injury. While breakage of the collagen fiber bundle structures results in a disruption in the local strain field, it is the connectivity between fibers that allows this disruption to be effectively arrested. At the organ scale, needle puncture experiments on rat IVDs took a large step towards quantifying the role of penetrating injury in altering disc pressurization and fluid flow pathways. For the first time it was explicitly suggested that a needle puncture produces a pressure vent which alters disc mechanics by acting as a low resistance pathway which re-routes water flow from other boundary paths.
The first two studies utilized combined mechanical loading and confocal microscopy to measure micro-scale tissue strains under the application of tissue level deformation. They hypothesized that; A. Transverse shear deformation results from intralamellar skewing in healthy tissue and that elastase digestion will also allow interlamellar sliding. B. Circumferential shear results from independent mechanisms of stretch and rotation of collagen fiber bundles and that disruption. of interlamellar connectivity through elastase digestion will reduce fiber strain and increase fiber rotation. C.A. puncture injury will alter the distribution of strains within AF tissue under shear deformation in the proximity of a needle puncture injury. D. Within physiological levels of cyclic shear, a puncture injury will not propagate through the tissue. These hypotheses were tested using simultaneous dynamic shear loading and confocal microscopy followed by digital image analyses to measure microscale deformations.
The third study set out to investigate the role of the AF in containing disc fluid pressure in both the healthy and injured states. It hypothesizes that; A. Needle puncture injuries alter intervertebral disc compressive properties by introducing a new mechanism by which fluid may enter and exit the disc, Le., a "pressure vent". B. There is a critical size at which this injury offers negligible resistance to fluid flow and the puncture becomes effeotively infinite for a given loading condition. Rat caudal IVDs were tested in axial compression experiments in displacement control under overloading and recovery conditions to assess how needle puncture injuries influenced axial stiffness, and relative energy dissipation. A theoretical model was also utilized to provide a conceptual and quantitative understanding of how needle puncture affects IVD stiffness, relative energy dissipation, and fluid transport patterns under different puncture sizes and loading conditions.
The investigations of microscale deformations of AF tissue under applied strain have provided a unique insight into how this structure behaves mechanically. In particular, it was shown for the first time that the lamellae of the AF are not capable of sliding relative to one another on a macroscopic scale. Additionally, this hierarchical connectivity lends remarkable robustness to the tissue following acute injury. It was seen for the first time that physiological levels of tissue strain result in finite propagation of a puncture type injury. While breakage of the collagen fiber bundle structures results in a disruption in the local strain field, it is the connectivity between fibers that allows this disruption to be effectively arrested. At the organ scale, needle puncture experiments on rat IVDs took a large step towards quantifying the role of penetrating injury in altering disc pressurization and fluid flow pathways. For the first time it was explicitly suggested that a needle puncture produces a pressure vent which alters disc mechanics by acting as a low resistance pathway which re-routes water flow from other boundary paths.