Disc herniations often include hyaline cartilage pulled from the vertebral endplates. Cartilage fragments show little swelling or proteoglycan loss, and may be slow to resorb, increasing the risk of persisting sciatica. Loss of cartilage will increase endplate permeability, facilitating endplate inflammation and disc infection.

This review suggests why some discs degenerate rather than age normally. Intervertebral discs are avascular pads of fibrocartilage that allow movement between vertebral bodies. Human discs have a low cell density and a limited ability to adapt to mechanical demands. With increasing age, the matrix becomes yellowed, fibrous, and brittle, but if disc structure remains intact, there is little impairment in function, and minimal ingrowth of blood vessels or nerves. Approximately half of old lumbar discs degenerate in the sense of becoming physically disrupted. The posterior annulus and lower lumbar discs are most affected, presumably because they are most heavily loaded. Age and genetic inheritance can weaken discs to such an extent that they are physically disrupted during everyday activities. Damage to the endplate or annulus typically decompresses the nucleus, concentrates stress within the annulus, and allows ingrowth of nerves and blood vessels. Matrix disruption progresses by mechanical and biological means. The site of initial damage leads to two disc degeneration "phenotypes": endplate-driven degeneration is common in the upper lumbar and thoracic spine, and annulus-driven degeneration is common at L4-S1. Discogenic back pain can be initiated by tissue disruption, and amplified by inflammation and infection. Healing is possible in the outer annulus only, where cell density is highest. We conclude that some discs degenerate because they are disrupted by excessive mechanical loading. This can occur without trauma if tissues are weakened by age and genetic inheritance. Moderate mechanical loading, in contrast, strengthens all spinal tissues, including discs.

The aim of the current study was to investigate the multi-dimensional characteristics of lumbar endplate defects in humans in relation to disc degeneration and other MRI phenotypes as well as their role with pain and disability. A total of 108 subjects were recruited and underwent 3T MRI of the lumbar spine. Structural endplate defects were identified and their dimensions were measured in terms of maximum width and depth, and were then standardized to the actual width of the endplate and depth of the vertebral body, respectively. Both width and depth of all endplate defects in each subject were added separately and scores were assigned on the basis of size from 1 to 3. Combining both scores provided "cumulative endplate defect scores." Disc degeneration scores, Modic changes, disc displacement, HIZ, and facet joint changes were assessed. Subject demographics, pain profile, and Oswestry Disability Index (ODI) were also obtained. Endplate defects were observed in 67.5% of the subjects and in 13.5% of the endplates. All dimensions of endplate defects showed significance with disc degenerative scores, Modic changes, and posterior disc displacement (p < 0.05). Maximum width (p ¼ 0.009) and its standardized value (p ¼ 0.02), and cumulative endplate defect scores (p ¼ 0.004) increased with narrow facet joints. Cumulative endplate defect scores showed a strong positive association with ODI (p < 0.05) compared to disc degenerative scores. Large size endplate defects were strongly associated with degenerative spine changes and more back-related disability. Findings from this study stress the need to assess endplate findings from a multi-dimensional perspective, whose role may have clinical utility. ß 2019 Orthopaedic Research

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