Professor Jeffrey Lotz, has been the Director of the Orthopaedic Bioengineering Laboratory at UCSF since 1992. Dr. Lotz earned a doctorate degree in Medical Engineering from the Harvard/MIT Division of Health Sciences and Technology, a Masters Degree in Mechanical Engineering Design from Stanford University, and Bachelors of Science in Mechanical Engineering from UC Berkeley. Prior work experience includes medical device design (Stanford Research Institute) and medical device failure evaluation (Failure Analysis Associates). Dr. Lotz is a Member of the NIH Peer Review Committee for Tissue Engineering Grants.
As a principal investigator, Dr. Lotz has procured over $8M in extramural funding for spine-related projects. He has earned several awards for spine research, including the ISSLS Prize (2007), Volvo Award (1998), and the North American Spine Society Award (1993). He serves as a Deputy Editor for the journal Spine, and an Associate Editor for The Spine Journal. He has expertise in spine biomechanics and intervertebral disc biology and has published 100 peer-reviewed journal articles. His laboratory work focuses on identifying mechanisms of intervertebral disc degeneration, exploring tissue engineering approaches for treating low back pain, and the biomechanics of spinal instrumentation.
Approximately 1.5 million Americans currently have chronic back pain that hasn’t responded to conservative therapy. For a significant portion of these patients, the pain generator is suspected to be a degenerated intervertebral disc. Unfortunately, no reliable treatments are currently available beyond traditional fusion or, more recently, spinal arthroplasty, both of which are complex procedures with significant patient risk, cost, and uncertain outcomes. This presentation will overview research efforts at UCSF that focus on: identifying factors that distinguish painful from non-painful discs; developing improved methods to identify discs that would benefit from surgery; and novel minimally-invasive procedures to treat back pain and/or restore disc function.
