In vivo cartilage strain increases following medial meniscal tear and correlates with synovial fluid matrix metalloproteinase activity

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Citation

Published Version (Please cite this version)

10.1016/j.jbiomech.2015.02.030

Publication Info

Carter, Teralyn E, Kevin A Taylor, Charles E Spritzer, Gangadhar M Utturkar, Dean C Taylor, Claude T Moorman, William E Garrett, Farshid Guilak, et al. (2015). In vivo cartilage strain increases following medial meniscal tear and correlates with synovial fluid matrix metalloproteinase activity. JOURNAL OF BIOMECHANICS, 48(8). pp. 1461–1468. 10.1016/j.jbiomech.2015.02.030 Retrieved from https://hdl.handle.net/10161/10277.

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Scholars@Duke

Spritzer

Charles Edward Spritzer

Professor of Radiology
  1. Musculoskeletal Imaging, with an emphasis on MR
  2. Imaging of MSK Infection
  3. MR imaging of vascular malformations
  4. MSK Biomechanics
Taylor

Dean Curtis Taylor

Professor of Orthopaedic Surgery

Dr. Dean Taylor is a Sports Medicine Orthopaedic Surgeon whose practice and research interests include shoulder instability, shoulder arthroscopy, knee ligament injuries, meniscus injuries, knee cartilage injuries, and ACL injuries in adults and children. He attended the United States Military Academy at West Point and completed his medical training and residency at Duke University. Dr. Taylor went on to be a part of the John Feagin West Point Sports Medicine Fellowship, retired from the United States Army at the rank of Colonel, and returned to Duke in 2006.

McNulty

Amy Lynn McNulty

Associate Professor in Orthopaedic Surgery

The McNulty Lab is working to develop strategies to prevent osteoarthritis and to promote tissue repair and regeneration following joint injury. In order to accomplish this, we are working in three main areas.  1) We are working to understand the pathways that are activated by normal and injurious mechanical loading of cartilage and meniscus and how these mechanotransduction pathways are altered during aging, injury, and tissue degeneration. A greater understanding of alterations in mechanosensitive signaling mechanisms with aging and injury will likely reveal potential targets to promote tissue repair and prevent tissue degeneration and osteoarthritis development. 2) We are developing meniscus tissue engineered constructs that will be utilized to repair and replace meniscus tissue lost due to injury and surgical resection.  3)  We are focusing on the biological and biomechanical changes that occur in the joint following meniscus injury and how these may contribute to osteoarthritis development.   


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