Improved Meniscus Integration via Controlled Degradation of the Wound Interface

Introduction Meniscal tears are prevalent and poor intrinsic healing (especially in avascular zones) directs clinical treatment towards partial removal rather than repair. However, removal alters joint biomechanics and can lead to early osteoarthritis. As there are limited restorative strategies (e.g. replacement using allografts), methods to foster repair by promoting cell growth, extracellular matrix (ECM) production, and integration would represent a marked clinical advance. Previously, we showed that fetal and juvenile menisci have greater intrinsic healing capacity compared to adult meniscus, and hypothesized that the high ECM density and low local cell density in adult meniscus may present physical and biologic barriers to endogenous healing. Such considerations have also arisen in cartilage-tocartilage integration, where decreasing the local ECM density improves tissue repair. To test this hypothesis in the context of the meniscus, we explored how controlled degradation of the local ECM at the wound interface might expedite healing by facilitating cell migration and division at the wound site and subsequent tissue remodeling. Furthermore, we used enzyme-releasing scaffolds to demonstrate how this technology might be applied clinically to promote meniscal repair.