Research

  • 4/13 Master's Thesis Defense of Sandro D. Cloiseau

    WEBEX link - https://uconn-cmr.webex.com/uconn-cmr/j.php?MTID=ma670358e2f44d184198342d9a6cfde50

    This event will be held on April 13th from 11:00am to 1:00pm

    Title - A GROWTH FACTOR-BASED APPROACH FOR CARTILAGE REPAIR

    Statement of the Problem and Background - The response of human articular cartilage to injury is currently one of the most complex challenges in our attempt to stimulate cartilage regeneration. Degeneration of this connective tissue presents patients with the onset of Osteoarthritis (OA), a progressive degradation of joint articular cartilage that impairs shock absorption qualities, and smoothness of the articulating surface in addition to a multifaceted inflammatory response. Currently incurable, one can only imagine the severity of pain patients diagnosed with such an unforgiving disease. This disease may proceed into a more aggressive condition via a lifetime's worth of microtrauma to the joint resulting in focal damage to chondroprogenitors in the superficial zone (SZ). Studies in mice show that signals from the Epidermal Growth Factor Receptor (EGFR/HER) family are required for Superficial Zone maintenance and can potentially be utilized to deliver future therapeutic treatment to patients.

    Research Question and Hypothesis - Current clinical evidence shows that in order to delay disease onset, injured athletes typically undergo a surgical procedure known as Osteochondral Allografting (OCA), where the damaged cartilage is excised and replaced by healthy donor cartilage. The challenge with the procedure is the absence of complete integration between the graft and host cartilage. The graft-host integration failure results in a temporary rather than a permanent treatment which may compel patients to require subsequent surgeries. The clinical challenge of articular cartilage is its limited capacity for self-healing. This is surprising because articular cartilage contains cells (chondroprogenitors) with latent regenerative capacity. Our prior studies showed that signals from the EGFR family stimulate chondroprogenitor proliferation and matrix synthesis in the articular cartilage of mice, suggesting EGFR family factors might be useful in promoting chondroprogenitor responses in human articular cartilage. We used an in vitro model to test the hypothesis that exogenous EGFR factor stimulates chondroprogenitor activity accompanied by seamless self-healing in explants of injured human articular cartilage. 

    For more information, contact: Sandro Cloiseau at cloiseau@uchc.edu