Riccardo Gottardi, PhD, University of Pennsylvania and the Children’s Hospital of Philadelphia

In the continuum cycle of renewal, the meniscus, once just the silent guardian of the knee, finds new purpose as a scaffold for airway and tympanic membrane repair. This talk explores the transformation of decellularized meniscal fibrocartilage (MEND), repurposed to restore both voice and hearing through tissue engineering and structural regeneration.

The meniscus, with its unique biomechanical properties, offers a foundation for reimagining airway reconstruction. Pressed by the stringent requirements of translation in children, we have re-imagined the creation of scaffolds based on decellularized extracellular matrix. We have developed MEND as a hyaline cartilage substitute, combining it with cartilage-resident progenitor cells to create a minimally invasive and regenerative alternative to autologous grafts. I will be sharing the success of this approach providing a structural and biological framework that integrates and remodels over time in medium and large animal models of the pediatric airway, as well as our findings in using cartilage-resident progenitor cells as an exciting, minimally invasive cell source for repair.

In the auditory realm, MEND undergoes another transformation. Where tympanic membrane perforations fail to heal, MEND serves as an engineered fibrocartilage graft that mimics the native structure, providing superior integration compared to traditional cartilage grafts. Its microchannel network supports cell migration, allowing it to become part of the living tissue rather than remaining as a static implant.

In this talk, I will depict the strategies of biomaterial repurposing, where a discarded product from the food industry such as porcine meniscus, can find new life as an instrument of healing, restoring breath and sound in a new dimension of function.

Jay Rubenstein, PhD, University of Washington

Dr. Rubinstein will review the concept of the cochlear amplifier and describe behavioral studies of human subjects with STRC mutations which disable the cochlear amplifier.

Jennifer Stone, PhD, University of Washington

Jing Zheng, PhD, Northwestern University Feinberg School of Medicine

Mammalian hearing relies on the mechanical sound amplification provided by outer hair cells (OHCs), which enhance sensitivity and improve frequency selectivity. Unfortunately, OHCs are among the most vulnerable components in the cochlea and can be easily damaged by various stressors. To investigate the relationship between OHC function and vulnerability, we focus on several proteins essential for their function. These include Prestin, the motor protein responsible for OHC electromotility, and Oncomodulin, a cytosolic calcium-binding protein critical for the survival of OHCs. The knockout of these proteins in OHCs results in OHC loss. In this presentation, I will discuss our findings related to these OHC proteins and identify potential biomarkers for cochlear stress.

Anna Lysakowski, PhD, University of Illinois at Chicago