Intervertebral Disc Cell Death in the Porcine and Human Injured Cervical Spine After Trauma : A Histological and Ultrastructural Study

Histologic and ultrastructural study of disc cell death after traumatic injury to the human cervical spine and postmortem (p-m) in the porcine cervical spine. To determine the changes in disc cell morphology, viability, and manner of cell death after trauma in human discs and p-m in porcine discs. Similarities in the morphology of human and porcine spine have been shown in many histologic and biomechanical investigations. It is known that compressive or traumatic injuries to cartilage and intervertebral discs can result in cell death by necrosis or apoptosis. An additional form of apoptosis, chondroptosis, has been reported in articular cartilage, but not to date in the disc. The anterior portion of intervertebral discs and endplates of 30 patients with traumatic injuries to the cervical spine were studied histologically (including trypan blue exclusion and TUNEL staining) and ultrastructurally. Fractures were classified according to Magerl and degeneration of the intervertebral disc according to Thompson and Benneker. Similar studies of disc and endplate were undertaken on porcine cervical spine 0 to 24 hours p-m. Electron and light microscopy showed up to 75% of human disc cells die within the first 24 hours of trauma, mainly by necrosis, similar to that seen in pig discs p-m. This study reports on 2 morphologies, chondroptosis and balloon cells, previously not described in the disc. Chondroptosis had been significantly higher and ballooned cells were exclusively seen in discs from fractures with compression, where apoptosis was also most common. Porcine samples revealed comparable rates of apoptosis and chondroptosis as fractures with less compression. Glycogen was commonly found in disc cells after trauma. Traumatic injuries of the human cervical spine lead to rapid changes in disc cell morphology and cell death, particularly via necrosis. The type of fracture and load seems to influence cell death.