Mechanical Basis of Lumbar Intervertebral Disk Degeneration

Abstract

Abstract The etiology of degenerative disk disease (DDD) is multifactorial. Among the various factors, mechanical processes contributing to endplate or discal injuries have been discussed as the initiating events in the degenerative cascade. DDD encompasses the multitudinous changes undergone by the different structures of the spinal segment, namely intervertebral disk (IVD), facet joints, vertebral end plate (VEP), adjoining marrow (Modic changes), and vertebral body. It has been etiologically linked to a complex interplay of diverse mechanisms. Mechanically, two different mechanisms have been proposed for intervertebral disk degeneration (IVDD): endplate-driven, especially in upper lumbar levels, and annulus-driven degeneration. VEP is the weakest link of the lumbar spine, and fatigue damage can be inflicted upon them under physiological loads, leading to the initiation of DDD. Disk calcification has been put forth as another initiator of inflammation, stiffening, and abnormal stresses across the IVD. The initial mechanical disruption leads to secondary IVDD through unfavorable loading of the nucleus pulposus and annulus fibrosis. The final degenerative cascade is then propagated through a combination of biological, inflammatory, autoimmune, or metabolic pathways (impaired transport of metabolites or nutrients). Abnormal spinopelvic alignment, especially pelvic incidence, also significantly impacts the degenerative process. Hence, the etiology of DDD is multifactorial. Mechanical pathways, including VEP injuries, increased disk stiffness, and abnormal spinopelvic alignment, play a significant role in the initiation of IVDD.