Differential Carbonyl Stress Expression in the Intervertebral Disc between Singular- and Persistent-Mechanical Injuries.

Abstract

Low back pain is a significant public health problem worldwide. Intervertebral disc degeneration is most significant known risk factor for low back pain. Yet the mechanisms of degeneration remain relatively unknown. Carbonyl stress and oxidation have been implicated in cartilage and fibrocartilage degeneration. Here we investigate the role of oxidative stress and carbonyl production in the intervertebral disc after mechanical injury using an in vitro organ model of the mouse functional spine unit. We use a single-stab insult to model mild injury, and the three-stab insult to model severe trauma. Our results indicate that mild injury increases the carbonyl response that may be required for tissue repair, while severe trauma tempers this response and rapidly accelerates degeneration.