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Biomechanics of Articular Cartilage: Osteoarthritis and Tissue Engineering
- Jafari, Somaye
- Advisor(s): Cai, Shengqiang;
- Sah, Robert L.
Abstract
In the normal adult synovial articular joint, articular cartilage (AC) as an avascular tissue, is attached to the calcified cartilage (CC). Calcified cartilage is a thin tissue layer, separated from AC by tidemark (TM), and subchondral bone (ScB) by cement line (CL). Calcified cartilage and subchondral bone plate together form subchondral plate (ScP). ScP merges into a porous network called trabecular bone (TB). Cartilage degeneration and loss may be caused by different diseases such as osteoarthritis (OA) or trauma. There are many vascular canals embedded within subchondral plate which carry various types of cells and blood vessels. In OA, the structure of the cartilage and subchondral plate underneath, the geometry of the canals as well as the spacing between them may change. The effect of ScP changes on the biomechanics of articular cartilage is unclear. Furthermore, after cartilage is lost due to OA or trauma, current efforts are underway to resurface the joint. While methods for bending cartilage have been introduced, the mechanics of such bending are unclear. Thus, this dissertation aims to (1) analyze images of normal (NL) and OA samples in order to clarify the structure of the ScP vascular canals, (2) investigate the effect of such vascular canals on the biomechanics of the deep zone of cartilage and (3) evaluate the mechanics of articular cartilage sheet as a poroelastic material under pure bending.
In (1) Digital Volumetric Images were used to obtain 2-D cross sections of cartilage and subchondral plate of 5 OA and 6 NL samples. Vascular canal were found as 12 different types associated with the presence/absence of a cap and the degree of canal penetration of the ScP and AC. In NL samples, there were no invaded open canal through tidemark, while from 37 open canals were found in OA samples, 11 of which penetrated the tidemark. The diameter of canals was smaller (27 μm) in NL samples than (67 μm) in OA samples. The spacing between the open canals was smaller (135 μm) in OA samples than (809 μm) in NL.
In (2), using three small, mean and large diameters and spacing, a confined compression test was analyzed with ABAQUS software to analyze the effect of change of size and spacing of those canals on the spatial and temporal distribution of fluid pressure as well as strain-stress through articular cartilage. With the increase of the diameters of the canals and decrease of the spacing between them, fluid pressure (pore pressure) within cartilage, especially at the deep zone, decays. Furthermore, with the increase of the spacing between canals, the mechanical response of the sample becomes close to that of NL sample
In (3), poroelastic theory was applied to evaluate the biomechanics of cartilage under pure bending. Under pure bending, axial strain varies linearly between compression and tension (concave to convex). In the bent state, the bending moment relaxes as strain redistributes axially, and fluid is exuded from the compressed region and imbibed in the stretched region. At equilibrium, the bending moment and strain stabilize as fluid ceases to flow. After the bending is suddenly released, creep recovery occurs as fluid flow into and out of the sheet reverses and also redistributes within the sheet.
These studies developed models to describe the biomechanics of articular cartilage as a poroelastic material when subjected to various loading and boundary conditions. The prediction of loading effects on the deep zone of OA cartilage may be involved in progressive cartilage degeneration. The understanding of time-dependent mechanical behavior of poroelastic sheet under bending may help develop loading strategies to achieve an appropriately contoured shape before implantation
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