Deleterious changes in the mechanical properties of soft and hard tissues are at the heart of arthritis and musculoskeletal disease. Central to these changes in mechanical properties is matrix degradation or damage. Damage is defined as a permanent change in tissue structure (e.g. crack) that results in material property degradation. Overload, trauma, and repetitive loading lead to degenerative changes in the joint cartilage and underlying subchondral bone in osteoarthritis. It is believed that sclerosis of the subchondral bone may play an important role in cartilage degradation. However, the stimulus for the increased bone formation is not well understood. Based on previous work in cortical bone which suggested that damage acts as a stimulus for the remodeling process, we postulate that the sclerotic changes associated with osteoarthritis represent a repair response to altered damage accumulation mechanisms in the subchondral bone. In the current study, we propose to test whether damage accumulation mechanisms in cortical and subchondral bone are altered with age. We will address these issues in a hierarchical manner by conducting tests at both the tissue (mm scale) and matrix (micron scale) structural levels. Specifically, we propose to accomplish the following: 1. To determine whether tissue-level damage accumulation mechanisms in cortical bone are significantly altered with age. 2. To develop a micro-mechanical testing system which is capable of quantifying alterations in matrix-level damage mechanisms in cortical and subchondral bone. This proposal will provide the opportunity to develop relevant data which is fundamental to studies of the disease process as well as to develop the micro-level mechanical testing tools needed to address these matrix levy changes in subchondral bone.
NIH ExPorter
NIH ExPorter