Amy Silverstein Defends Her Thesis!

Thesis committee members included (left to right): Dr. Roshan Shah, Dr. Clark Hung, Dr. Gerard Ateshian, and Dr. Helen Lu. Dr. Bulinski not pictured.

CEL lab members celebrating Amy's defense (left to right): Clark Hung, Charlie Cai, Colden Lyons, Lance Murphy, Amy Silverstein, Evie Sobczak, Rob Stefani, Andrea Tan, Will Yu, Eben Estell, Saiti Holder, Krista Durney, Gerard Ateshian

Amy successfully defended her PhD thesis "Development of Biofidelic Culture Models of Osteoarthritis." Congratulations Dr. Silverstein!

Thesis Abstract: Osteoarthritis (OA) is a debilitating degenerative joint disease affecting 27 million Americans over the age of 25. Whereas OA is a disease of the entire joint organ, the contribution of the synovium, a specialized lining that envelops the knee joint, to cartilage degeneration and disease progression has been underappreciated. Synovial inflammation often precedes the development of cartilage damage and is observed in early and late stage OA. The onset of synovitis is driven by both elevated concentrations of pro-inflammatory cytokines and tissue debris in the joint space.  Accordingly, surgeons have observed cartilaginous debris embedded within the synovium of OA patients presenting with severe synovial hyperplasia.  It has been hypothesized that the fibrotic shortening of the synovial capsule results in OA pain and joint stiffness and contributes to further joint destruction through the release of degradative enzymes.  Current strategies to treat synovial inflammation and joint pain, such as intra-articular injections and synovectomy, have had limited and variable success.  

To this end, cell and tissue engineering culture models provide a versatile platform to study the tissues and cells involved in OA.  Our lab has typically employed mechanical overload or cytokine insult of chondrocytes and cartilage explants to study cartilage degradation.   Similarly, to isolate the role of synovium in OA, synovial explants or fibroblast-like synoviocytes (FLS) can be exposed to chemical or physical OA stimuli.  Although often overlooked as an instigator of OA, cartilage wear particles have been reported to induce synovial inflammation and OA-like joint changes in various animal models.  As opposed to non-biologic (metal or plastic) wear particles, small (sub-10mm) cartilage wear particles are comprised of extracellular matrix constituents that are degradable and may interact with cells beyond phagocytosis. Using cells derived from the pathologic joint provides the opportunity to study inherent changes to OA cells (both FLS and chondrocytes) within their own de novo extracellular matrix. The work presented in this dissertation aims to combine knowledge from basic science and pre-clinical culture models of OA to develop a clinically relevant disease model using cells derived from clinical samples. 

Dr. Hung Presents Recent Work at Invited Seminars in London, UK

Clark Hung (center) with Martin Knight (left) and David Lee (right)

Clark Hung (center) with Martin Knight (left) and David Lee (right)

Dr. Clark Hung was invited to speak at Queen Mary University of London and Imperial College London. Hosted by Drs. Martin Knight (Professor of Mechanobiology) and David Lee (Professor of Cell and Tissue Engineering and Dean for Research) at Queen Mary University of London, Dr. Hung shared recent findings in engineering cartilage using cells from expired human donor grafts. He also discussed new strategies for cartilage repair including the use of a novel dexamethasone delivery system and electrotherapeutics. Furthermore, as osteoarthritis is believed to be a disease of the entire joint, additional focus was spent on in vitro disease models involving engineered synovium and parameters that modulate the injury response.

Gerard Ateshian wins 2017 H.R. Lissner Medal

Gerard Ateshian with MBL alum Alex Cigan

Gerard Ateshian with MBL alum Alex Cigan

Congratulations to Dr. Ateshian (director of Musculoskeletal Biomechanics Laboratory, MBL) on winning a top honor from the American Society of Mechanical Engineers (ASME). Dr. Ateshian was awarded the Lissner Medal for his "outstanding contributions to theoretical formulations and experimental investigations of cartilage mechanics and tissue engineering, and for pivotal contributions to the implementation and dissemination of open-source finite element computational tools for the biomechanical analysis of living tissues.” His research is focused on developing better modalities for the treatment of osteoarthritis, such as stronger engineered cartilage for resurfacing knee, hip, and shoulder joints.

Dr. Ateshian will be recognized at the 2017 Summer Biomechanics, Bioengineering, and Biotransport Conference in Tucson, Arizona in June. Congratulations Gerard!

Brendan Roach Successfully Defends PhD Thesis!

Thesis committee members included (left to right): Dr. Kacey Marra, Dr. Clark Hung (advisor), Dr. Roshan Shah, and Dr. Gerard Ateshian (chair).

Thesis committee members included (left to right): Dr. Kacey Marra, Dr. Clark Hung (advisor), Dr. Roshan Shah, and Dr. Gerard Ateshian (chair).

CEL lab members (left to right): Eben Estell, Clark Hung, Brendan Roach, Andrea Tan, Amy Silverstein, Charlie Cai, Rob Stefani

CEL lab members (left to right): Eben Estell, Clark Hung, Brendan Roach, Andrea Tan, Amy Silverstein, Charlie Cai, Rob Stefani

Brendan successfully defended his PhD thesis "Modulation of the in vitro mechanical and chemical environment for the optimization of tissue-engineered articular cartilage." Congratulations Dr. Roach!

Thesis Abstract: Articular cartilage is the connective tissue lining the ends of long bones, providing a dynamic surface that bears load while providing a smooth surface for articulation. When damaged, however, this tissue exhibits a poor capacity for repair, lacking the lymphatics and vasculature necessary for remodeling. Osteoarthritis (OA), a growing health and economic burden, is the most common disease afflicting the knee joint. Impacting nearly thirty million Americans and responsible for approximately $90 billion in total annual costs, this disease is characterized by a progressive loss of cartilage accompanied by joint pain and dysfunction. Moreover, while generally considered to be a disease of the elderly (65 years and up), evidence suggests the disease may be traced to joint injuries in young, active individuals, of whom nearly 50% will develop signs of OA within 20 years of the injury. For these reasons, significant research efforts are directed at developing tissue-engineered cartilage as a cell-based approach to articular cartilage repair. Clinical success, however, will depend on the ability of tissue-engineered cartilage to survive and thrive in a milieu of harsh mechanical and chemical agents.

 

To this end, previous work in our laboratory has focused on growing tissues appropriate for repair of focal defects and entire articular surfaces, thereby investigating the role of mechanical and chemical stimuli in tissue development. While we have had success at producing replacement tissues with certain qualities appropriate for clinical functionality, engineered cartilage capable of withstanding the full range of insults in vivo has yet to be developed. For this reason, and in an effort to address this shortcoming, the work described in this dissertation aims to (1) further characterize and (2) optimize the response of tissue-engineered cartilage to physical loading and the concomitant chemical insult found in the injured or diseased diarthrodial joint, as well as (3) provide a clinically relevant strategy for joint resurfacing. Together, this holistic approach maximizes the chances for in vivo success of tissue-engineered cartilage.

Cuban official delegation of Higher Education comes to visit CEL!

The Cuban official delegation from the Ministry of Higher Education visited CEL on October 27, 2016. Led by the deputy minister, Aurora Fernandez, the rector of the Technological University of Havana (Cujae), Alicia Alonso Becerra, and Luis Javier Baro, First Secretary at Permanent Mission of Cuba to the UN, the island educators met with leaders and members of various universities and government entities in the sector to explore areas of bilateral cooperation.

We shared our lab's efforts in cartilage tissue engineering, further fostering biomedical engineering across our two universities.

 

 

 

 

William Yu Presents Undergrad Research at BMES 2016

William T. Yu, SEAS '17, was invited to present his summer research in the undergraduate session at the BMES 2016 Annual Meeting in Minneapolis, Minnesota. Will presented on our ongoing work looking at strategies for increasing collagen content in engineered cartilage and is mentored by Andrea Tan. Congratulations Will!

Columbia Engineering Celebrates CEL Lab Renovation

The BME Department and Columbia Engineering celebrated the completion of four new laboratory spaces, including our own, on May 9, 2016. Be sure to stop by to check out our new lab in 366 Engineering Terrace!

Dr. Hung Wins ORS Marshall R. Urist, MD Award

clark_award.jpg

Congratulations to Dr. Clark Hung on winning the ORS Marshall R. Urist, MD Award. The Marshall R. Urist, MD Award was created in 1996 and is sponsored by the Journal or Orthopaedic Surgery (JOR) with a grant from Wiley Blackwell. This prestigious award honors an investigator who has established himself as a cutting-edge researcher in tissue regeneration research and has done so with a sustained ongoing body of focused research in the area of tissue regeneration as it relates to the musculoskeletal system. Dr. Hung will be recognized at the 2016 ORS Awards Gala on March 6, 2016 in Orlando, FL.

About Marshall R. Urist, MD

Born on June 11, 1914, in Chicago, and reared in a small farm community near Glen, Mich., Marshall R. Urist received his B.S. in chemistry from the University of Michigan, earned his M.S. from the University of Chicago and obtained his medical degree from Johns Hopkins University in 1941. He completed his surgical residency at Johns Hopkins and at Massachusetts General Hospital.Dr. Urist joined the U.S. Army Medical Corps in 1943. In 1946 he was assigned to the Pentagon, Headquarters of the Surgeon General, to write with co-author Mather Cleveland their book Orthopaedic Surgery in World War II, In the European Theatre of Operations. After leaving the Army, Dr. Urist taught physiology and research at the University of Chicago before joining the UCLA School of Medicine faculty in 1954, a tenure that was to last for 46 years.

Dr. Urist’s pioneering studies on bone induction and the identification of bone morphogenetic protein, or BMP, revolutionized orthopaedic medicine by helping to establish the newly emerging field of orthopaedic growth factor research. The practical implication of this discovery is to allow more rapid bone healing and even replacement of portions of lost bone tissue. With severe fractures and even loss of limited amounts of bone, BMP has the potential of replacing and bridging the defect.

Dr. Urist served as president of several major national orthopaedic associations and societies including the Association of Bone and Joint Surgeons, the Society of International Research in Orthopaedic Surgery and Traumatology, and The Hip Society. For 27 years was editor-in-chief of the journal Clinical Orthopaedics and Related Research. His academic accomplishments and research efforts, supported by numerous grants, resulted in a bibliography of more than 415 publications.

Dr. Urist was a distinguished leader in the field of orthopaedics nationally and internationally for several decades, and as a clinician, scientist, surgeon, writer and editor, his contributions are legendary. Dr. Urist won numerous academic honors, including two Kappa Delta awards, the Claude Bernard Medal, a Simon Guggenheim Fellowship, and the Sir Henry Wellcome Award. In 1977 Urist was named Doctor Medicin, Honoris Causa from the University of Lund, Sweden. His 1965 Science Magazine article on autoinduction was selected by the National Institute of Health Research as a Landmark Contribution to science in 1997. Dr. Urist passed away on February 4, 2001, at the age of 86 years.