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The Effect of Cytoprotective Agents on the Metabolic Activity of Articular Cartilage Exposed to Defined Levels of Thermal and Mechanical StressFunding:NFL Charities Principal Investigator:Lab Website:Project Summary:Partial thickness articular cartilage lesions are a common pathology in the field of sports medicine. Biological treatment options for full thickness articular lesions continue to evolve. However, options are limited for partial thickness lesions. Current treatment options include benign neglect, marrow stimulation and debridement utilizing mechanical and thermal instruments. Neither mechanical nor thermal chondroplasty is a benign procedure. Despite clinical and histological evidence of articular surface smoothing, residual collateral damage occurs. The remaining articular cartilage damage has been one of the primary concerns, especially with thermal chondroplasty. Cytoprotective agents such as Insulin-like Growth Factor 1 (IGF-1) and c-Jun N-terminal Kinase (JNK) inhibitor have been shown to enhance metabolic activity following defined levels of thermal stress. The purpose of this study is to evaluate whether these and other selected cytoprotective agents will enhance articular metabolic activity and decrease collateral damage following mechanical and defined thermal stress. In prior work, we have established the thermal stress (defined as temperature and time exposure) required to alter the morphology of fibrillated articular cartilage. This data will establish the thermal stress exposure for this study. Additionally, we have shown that articular cartilage does display an enhanced recovery from thermal exposure with cytoprotective agents. Mechanical chondroplasty has a reported 250 um area of articular damage following utilization. This project will utilize the prior data to establish whether these specific cytoprotective agents will enhance articular cartilage metabolism following mechanical and thermal stress. Results from this study may advance our knowledge about partial thickness cartilage injuries. The biological enhancement of currently utilized treatment options may enable a combination of techniques to potentiate articular cartilage viability and prevent or delay the propagation of partial thickness articular lesions.
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