Intervertebral disc degeneration and vertebral end plate damage in acute lumbar disc herniation

Abstract

Background: Although microtrauma, gene polymorphisms, or subclinical infection could initiate lumbar disc herniation (LDH), the final pathway culminating in herniation can involve two possible trajectories—degeneration of nucleus pulposus or vertebral end plate (EP) damage. We performed a retrospective case–control study to understand the relative role played by disc degeneration (DD) and EP changes in acute LDH. Materials and Methods: MRI of 300 consecutive patients with acute LDH (<6 weeks) was evaluated for the type of LDH, severity of DD by Pfirrmann’s grading, and EP Modic changes (MC) for its type, distribution, and location in EPs. Among the1500 discs evaluated in 300 patients, 308 had disc herniation (cases) and 1192 acted as controls. Results: 98.8% of LDH had grade ≥3 DD (P < 0.001). The mean DD was higher in herniated discs (P < 0.05). From a mean 1.98 in normal discs, it increased to 3.31 in disc bulges, 3.73 in disc protrusions/extrusions, and 3.83 in sequestrations. Herniated discs had more MCs than normal discs (38.3%, 118/308) (P < 0.001). Although in normal discs, only 7.7% had MC, herniated disc subtypes showed a progressive increase in the incidence of MC (26.2% in disc bulges, 37.5% in disc protrusion/extrusions, and 58.3% in sequestrations). MC on both EP was strongly associated with LDH (odds ratio = 9.76). Posterior corner MC had a significant association with LDH (72.72%, P < 0.001). Conclusion: DD seems to be a common thread in all patients (98.8%) with LDH, whereas EP damage seems to be specific pathway in a subset (38.3%). The study showed a significant degeneration of nucleus pulposus in most (98.8%) herniated discs. Compared with nonherniated discs, vertebral MC had a higher incidence in herniated discs (38%), and interestingly these were of subacute fatty type 2.