Meniscus-Derived Matrix Bioscaffolds: Effects of Concentration and Cross-Linking on Meniscus Cellular Responses and Tissue Repair.

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Meniscal injuries, particularly in the avascular zone, have a low propensity for healing and are associated with the development of osteoarthritis. Current meniscal repair techniques are limited to specific tear types and have significant risk for failure. In previous work, we demonstrated the ability of meniscus-derived matrix (MDM) scaffolds to augment the integration and repair of an in vitro meniscus defect. The objective of this study was to determine the effects of percent composition and dehydrothermal (DHT) or genipin cross-linking of MDM bioscaffolds on primary meniscus cellular responses and integrative meniscus repair. In all scaffolds, the porous microenvironment allowed for exogenous cell infiltration and proliferation, as well as endogenous meniscus cell migration. The genipin cross-linked scaffolds promoted extracellular matrix (ECM) deposition and/or retention. The shear strength of integrative meniscus repair was improved with increasing percentages of MDM and genipin cross-linking. Overall, the 16% genipin cross-linked scaffolds were most effective at enhancing integrative meniscus repair. The ability of the genipin cross-linked scaffolds to attract endogenous meniscus cells, promote glycosaminoglycan and collagen deposition, and enhance integrative meniscus repair reveals that these MDM scaffolds are promising tools to augment meniscus healing.





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Lyons, Lucas P, Sofia Hidalgo Perea, J Brice Weinberg, Jocelyn R Wittstein and Amy L McNulty (2019). Meniscus-Derived Matrix Bioscaffolds: Effects of Concentration and Cross-Linking on Meniscus Cellular Responses and Tissue Repair. International journal of molecular sciences, 21(1). pp. 44–44. 10.3390/ijms21010044 Retrieved from

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Jocelyn Ross Wittstein

Associate Professor of Orthopaedic Surgery

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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