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Orthopaedic Proceedings
Vol. 100-B, Issue SUPP_14 | Pages 73 - 73
1 Nov 2018
Chubinskaya S
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In least 12% of patients with symptomatic OA, the cause is joint injury that progressed over time to post-traumatic OA. Human adult articular cartilage has a limited innate ability to regenerate. Available treatment options are unable to restore native structure and function of hyaline cartilage. Agili-C (CartiHeal, Israel) is a first-in-class acellular scaffold consisted of two layers corresponding to cartilage and bone that is capable of attracting stem cells and guide a regenerative process in both tissues. Agili-C has been extensively tested in vitro in our laboratory using human normal cartilage and in vivo in preclinical and currently clinical studies. This scaffold consists of a natural crystalline aragonite, derived from corals, to which hyaluronic acid is added. It showed a great ability to induce regeneration of chondral and osteochondral lesions and attract chondrocytes and stems cells to fill the defect area. Cells remained viable over the course of the study (up to 2 months). Signs of the extracellular matrix formation were evident inside 3D structure of the scaffold. PG synthesis and gene expression of collagen type II and aggrecan were elevated by more than 2.5-fold in cartilage with the scaffold vs corresponding controls. Agili-C scaffold displays a potential in the treatment of focal chondral and osteochondral defects.


Orthopaedic Proceedings
Vol. 96-B, Issue SUPP_11 | Pages 330 - 330
1 Jul 2014
Olewinski R Gupta M Wimmer M Hakimiyan A Margulis A Rappoport L Pacione C Chubinskaya S
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Summary

The ideal therapy for post-traumatic osteoarthritis (PTOA) must be mechanism-based and target multiple anabolic and catabolic pathways. Our results suggest an innovative combination of known pro-anabolic and anti-catabolic biologics to treat post-traumatic cartilage degeneration.

Introduction

Untreated joint injuries can result in cartilage wear and the development of PTOA. Previous studies identified the mechanisms that may govern the progression to PTOA. Here we hypothesised that targeted biologic interventions combined based on the type/time of cellular responses may constitute an effective novel treatment algorithm to arrest PTOA.