퇴행성 디스크 질환 II: 병태생리학

As intervertebral discs lose height and elasticity during degeneration, the nucleus pulposus becomes more likely to herniate. This herniation can compress adjacent nerve roots, causing radicular pain. Additional factors like ligamentum flavum hypertrophy and facet joint osteoarthritis further narrow the spinal canal, contributing to spinal stenosis and nerve compression.

Intervertebral discs are avascular and rely on nutrient diffusion through endplates from adjacent vertebral bodies. Degenerative changes like endplate sclerosis reduce this nutrient exchange, leading to disc cell death and progressive degeneration. This vascular compromise appears as Modic changes on MRI and is associated with discogenic pain.

Herniated disc material triggers an immune response that releases cytokines, nitric oxide, and matrix-degrading enzymes. These inflammatory mediators recruit macrophages and sensitize nerve roots, producing chemical radiculitis even without significant mechanical compression. Growth factors like nerve growth factor promote abnormal nerve ingrowth, contributing to chronic discogenic pain.

Disc protrusion occurs when the nucleus pulposus bulges with the annulus remaining intact. Extrusion happens when the nucleus extends beyond the disc but stays connected. Sequestration involves a free fragment in the spinal canal that may regress through macrophage clearance. Each type produces different degrees of nerve compression and pain.

Nerve root compression first impairs venous outflow, causing congestion and edema. Continued compression restricts arterial flow, leading to ischemia and nerve dysfunction. This vascular compromise can trigger increased intracranial pressure and secondary neural injury, similar to mechanisms seen in spinal cord injury pathophysiology.

Symptoms result from combined mechanical compression, ischemia, inflammation, and neural sensitization. Many individuals with radiographic disc degeneration remain asymptomatic because they lack sufficient inflammatory response or neural sensitization. Genetic polymorphisms in collagens, aggrecan, and enzymes like ADAMTS-4/5 influence degeneration severity and symptom development.

Obesity and adipokines such as leptin, TNF-alpha, and IL-6 accelerate disc degeneration. Genetic polymorphisms affecting collagen, aggrecan, and matrix-degrading enzymes also increase susceptibility. These systemic factors combine with local mechanical and inflammatory processes to drive progressive degeneration and variable clinical presentations.