Lumbar Degenerative Disc Disease

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Degenerative disc disease does not correlate strongly with back pain. Internal disc disruption on the other hand, is a separate concept to disc degeneration, and does correlate (imperfectly) with pain. While there are many similar processes and features, internal disc disruption is a response to injury that occurs either through single or repetitive compressive loads.[1]

Association Studies

Degenerative disc disease on plain films does not correlate strongly with back pain, unlike internal disc disruption. A great many studies have examined the association between disc degeneration and back pain. Amongst the high quality studies, there is no clinically significant association (sensitivity 56%, specificity 58%, +LR 1.33, -LR 0.76), and if low quality studies are included to there is an even worse correlation.[2] Statistically for a given patient with low back pain and degenerative changes, there is a 75% chance that the degenerative changes are not relevant to their pain. With such overwhelming odds, it is not possible to identify the 25% where the degenerative change might be relevant.[3]

Similar studies have been done with MRI, and generally these have only found weak to moderate associations between degenerative changes and pain. This is in contrast to high-intensity zones and Modic changes which correlate with the disc being painful (although imperfectly so).[3]

Pathology

Degenerative changes by in large appear to reflect normal age changes.[4]

Degenerative changes are an expression of metabolic stress, not a disease. There are no known mechanisms whereby degenerative changes can be painful. There are lots of different triggers with a final common pathway. Degenerative joint disease is a disturbing label that patients associate with a poor prognosis. Genetic factors predispose to degenerative changes, but age is the strongest correlate. Specific metabolic causes are rare, and limited to diabetes mellitus and ochronosis. Impaired nutrition is promoted but the evidence is lacking. Smoking is a weak correlate. Low grade infection has been explored but the evidence is not conclusive.

In the lumbar spine degenerative changes are chemical in nature, expressed as changes in proteoglycan content and hydration. This is seen on MRI with changes in signal intensity.

Chondrocytes maintain the balance between synthesis and degradation of the extracellular matrix. Synthesis is promoted by growth factors. Degradation is achieved by the activation of various enzymes such as the MMP family, whose expression is controlled by various cytokines (see Fibrous Connective Tissues, and Synovial Joints). Osteophytes are simply adaptive modelling, where there is an attempt to increase surface area to reduce load. This can be be a normal joint with excessive load, or joint where the capacity to bear loads is compromised by degradation of the matrix.

With aging, chondrocytes might be subject to innate senescence. They may have genetic abnormalities that affect matrix quality. Normal cells may become impaired with the accumulation of toxins and mechanical stresses. Zygapophysial joints have not been explicitly studied with regards to ageing changes, but come under the umbrella of synovial joints - i.e. the changes are likely a combination of genetics and abnormal biomechanics. For lumbar disc degeneration the evidence is more explicit from twin studies. Environmental influences play a role, but larger proportions are explained by genetic factors.[5] Smoking has a small effect across all disc levels, but hard physical work did not show a significant effect.[5]

See Also

Key Reading

Bogduk on degenerative joint disease of the spine (closed source)[4]

References

  1. โ†‘ Bogduk N, Aprill C, Derby R. Lumbar discogenic pain: state-of-the-art review. Pain Med. 2013 Jun;14(6):813-36. doi: 10.1111/pme.12082. Epub 2013 Apr 8. PMID: 23566298.
  2. โ†‘ van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine (Phila Pa 1976). 1997 Feb 15;22(4):427-34. doi: 10.1097/00007632-199702150-00015. PMID: 9055372.
  3. โ†‘ 3.0 3.1 Bogduk N. Degenerative joint disease of the spine. Radiol Clin North Am. 2012 Jul;50(4):613-28. doi: 10.1016/j.rcl.2012.04.012. PMID: 22643388.
  4. โ†‘ 4.0 4.1 Bogduk N. Degenerative joint disease of the spine. Radiol Clin North Am. 2012 Jul;50(4):613-28. doi: 10.1016/j.rcl.2012.04.012. PMID: 22643388.
  5. โ†‘ 5.0 5.1 Battiรฉ MC, Videman T, Kaprio J, Gibbons LE, Gill K, Manninen H, Saarela J, Peltonen L. The Twin Spine Study: contributions to a changing view of disc degeneration. Spine J. 2009 Jan-Feb;9(1):47-59. doi: 10.1016/j.spinee.2008.11.011. PMID: 19111259.