J. Patel (Decature, US)

Emory University Orthopaedics
Dr. Jay Patel is currently an Assistant Professor in the Department of Orthopaedics at Emory University. Previously; he was a postdoctoral researcher at the University of Pennsylvania and the Philadelphia VA Medical Center. Dr. Patel obtained a BS in Bioengineering from Rice University in 2011. He then completed in doctoral work at Rutgers University/Robert Wood Johnson Medical School in Biomedical Engineering; focusing on the translation of a fiber-reinforced scaffold for total meniscus reconstruction. This work received the 2018 Excellence in Research Award from the American Orthopaedic Society of Sports Medicine and received a 2018 New Investigator Recognition Award (NIRA) from the Orthopaedic Research Society (ORS). Dr. Patel joined the laboratory of Dr. Robert Mauck for his postdoctoral studies in 2017; and became involved in numerous cartilage repair studies. Through his work at the Mauck lab; Dr. Patel has presented at the World Congress of Biomechanics and recently received a Career Development Award through the Department of Veterans Affairs. Dr. Patel’s current research interests utilize cell-material interactions and mechanobiology principles to inform and guide cell-based translational therapeutics for orthopaedic soft tissue injuries.

Presenter Of 1 Presentation

Poster Biomaterials and Scaffolds

P043 - Cartilage-Penetrating Hydrogel Mitigates Tissue Degeneration and Chondrocyte Catabolism

Presentation Topic
Biomaterials and Scaffolds
Date
13.04.2022
Lecture Time
09:30 - 09:30
Room
Exhibition Foyer
Session Name
7.3 - Poster Viewing / Coffee Break / Exhibition
Session Type
Poster Session
Disclosure
J. Patel, NovoPedics Inc, Consultant J. Patel, Forsagen LLC, Co-Founder

Abstract

Purpose

Cartilage injuries often result in progressive tissue degeneration, characterized by mechanical and biochemical loss. The purpose of this study was to determine the protective effects of a tissue-reinforcing hydrogel in slowing this deteriorative process.

Methods and Materials

figure1.pngCartilage explants (bovine trochlea) were trimmed to remove the superficial and calcified zones to simulate defected tissue. Plugs were kept in basal (control) or degenerative media (10ng/mL IL-1β), with hydrogel application at 0 and 1 weeks (Fig 1A/B). Methacrylated hyaluronic acid (MeHA; 4% w/v) with LAP photo-initiator (0.05% w/v) was applied to the explant surface, allowed 5 minutes to diffuse, and photo-crosslinked for 3 minutes. Four conditions were tested: Control, IL-1, Reinforced (MeHA at t=1w) and Pre-Reinforced (MeHA at t=0w). At two weeks, a biphasic creep test was performed to obtain biphasic mechanical properties. Samples were then subject to s-GAG quantification (DMMB), staining for proteoglycan content (Safranin-O/Fast Green) and breakdown (NITEGE - aggrecan neoepitope), and measurement of catabolic gene expression (MMP-13).

Results

figure2.pngCartilage fortification provided a protection of macroscale tissue mechanics in a degenerative culture (Fig 1C). s-GAG content of entire cartilage plugs showed no significant differences (Fig 1D). However, histological staining highlighted localized s-GAG depletion at the explant surface in degenerative media, while MeHA application led to enhanced s-GAG retention (Fig 2A/B). NITEGE exhibited a greater presence in the IL-1 group and mitigation in the MeHA-treated explants (Fig 2A/C). MMP-13 expression of IL-1 treated explants exhibited a 20+ fold increase, whereas reinforcement reduced these increases by more than half (Fig 2D).

Conclusion

Our MeHA hydrogel system, in a degenerative environment, provides protection from mechanical loss, improves s-GAG retention, and reduces matrix breakdown. This strategy could provide a simple yet effective treatment to halt the cartilage degenerative process. Future studies will explore these changes at the cellular level and translate this approach to an animal model.

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Presenter Of 1 Presentation

Biomaterials and Scaffolds

P043 - Cartilage-Penetrating Hydrogel Mitigates Tissue Degeneration and Chondrocyte Catabolism

Abstract

Purpose

Cartilage injuries often result in progressive tissue degeneration, characterized by mechanical and biochemical loss. The purpose of this study was to determine the protective effects of a tissue-reinforcing hydrogel in slowing this deteriorative process.

Methods and Materials

figure1.pngCartilage explants (bovine trochlea) were trimmed to remove the superficial and calcified zones to simulate defected tissue. Plugs were kept in basal (control) or degenerative media (10ng/mL IL-1β), with hydrogel application at 0 and 1 weeks (Fig 1A/B). Methacrylated hyaluronic acid (MeHA; 4% w/v) with LAP photo-initiator (0.05% w/v) was applied to the explant surface, allowed 5 minutes to diffuse, and photo-crosslinked for 3 minutes. Four conditions were tested: Control, IL-1, Reinforced (MeHA at t=1w) and Pre-Reinforced (MeHA at t=0w). At two weeks, a biphasic creep test was performed to obtain biphasic mechanical properties. Samples were then subject to s-GAG quantification (DMMB), staining for proteoglycan content (Safranin-O/Fast Green) and breakdown (NITEGE - aggrecan neoepitope), and measurement of catabolic gene expression (MMP-13).

Results

figure2.pngCartilage fortification provided a protection of macroscale tissue mechanics in a degenerative culture (Fig 1C). s-GAG content of entire cartilage plugs showed no significant differences (Fig 1D). However, histological staining highlighted localized s-GAG depletion at the explant surface in degenerative media, while MeHA application led to enhanced s-GAG retention (Fig 2A/B). NITEGE exhibited a greater presence in the IL-1 group and mitigation in the MeHA-treated explants (Fig 2A/C). MMP-13 expression of IL-1 treated explants exhibited a 20+ fold increase, whereas reinforcement reduced these increases by more than half (Fig 2D).

Conclusion

Our MeHA hydrogel system, in a degenerative environment, provides protection from mechanical loss, improves s-GAG retention, and reduces matrix breakdown. This strategy could provide a simple yet effective treatment to halt the cartilage degenerative process. Future studies will explore these changes at the cellular level and translate this approach to an animal model.

Collapse