The vertebral end plate is a thin layer of hyaline cartilage (approximately 0.6-1 mm thick) covering the superior and inferior surfaces of each vertebral body at its junction with the intervertebral disc. The end plate provides nutrition to the avascular disc by diffusion from the subchondral bone, and acts as a mechanical interface distributing compressive load between the disc and the vertebral body.
Vertebral end plate failure is central to multiple spinal pathologies. Schmorl nodes are end plate herniations of nucleus pulposus into the vertebral body, visible as focal depressions on MRI and CT. Modic changes (Types I-III) reflect progressive end plate and adjacent vertebral body signal changes from acute inflammation to fatty degeneration that correlate with discogenic low back pain. Spondylodiscitis (disc space infection) destroys both adjacent end plates symmetrically, a key feature distinguishing infection from disc degeneration. Scheuermann disease produces irregular end plate ossification at the thoracic level.
Inflammatory (Modic I, T1 low/T2 high) or fatty (Modic II, T1 high/T2 high) end plate changes adjacent to degenerated discs on MRI correlate with chronic discogenic low back pain; Modic I changes may represent active inflammatory end plate pathology that responds to antibiotic treatment in selected patients with positive bacterial cultures from disc aspiration.
Axial loading fractures the end plate before the annulus fails, allowing nuclear material to herniate into the vertebral body (Schmorl node) or producing a superior end plate fracture pattern in thoracolumbar burst fractures that requires posterior instrumented reduction.
