188 MORPHOLOGICAL DESCRIPTION OF THE ANATOMY OF CERVICAL SPINE FACET JOINTS BY FACET ORIENTATION

Abstract

Results: Impact injuries to osteochondral explants cause chondrocyte death and a localized production of superoxide radicals. Previously, a time-course for post-impact chondrocyte viability was determined for two different energy levels (2.5 and 5 J) and treatment with NAC within 4 hours of impact injury spared significant numbers of chondrocytes (Figure 1). DHE staining revealed a dramatic accumulation of ethidium in chondrocytes within 30 minutes of impact injury, indicating increased superoxide production (Figure 2). Apocynin, an inhibitor of NADPH-oxidase (NOX) reduced chondrocyte death induced by impact (Figure 3). Conclusions: Our data support the hypothesis that superoxide production is initiated by chondrocytes after mechanical trauma and suggest chondrocyte death results from superoxide release. The observation that apocynin blocked impact induced death suggests that NOX is a source of superoxide production post-injury. The next step in these studies will be to test various inhibitors of NADPH oxidase and other potential sources of ROS for effects on free radical production and chondrocyte death. Such inhibitors may be used to augment the cell-sparing effects of NAC, a strategy that has the potential to forestall the onset of PTOA.