As we age a number of biochemical and morphologic degenerative changes occur in the spine, with lumbar disc degeneration particularly common due to the mobility of that area of the back. However, the cervical spine is even more mobile and the lack of circulation to the spinal discs means that when they are damaged it can take a considerable time for them to heal, if at all, due to a lack of direct blood supply bringing nutrients and hydration to the tissues.
Spinal Disc Degeneration – How it Happens
The tissue inside our spinal discs is rich in proteoglycans, which play a significant role in keeping the discs hydrated so as to help them act as shock absorbers in the spine. Proteoglycan synthesis decreases with age, leading to a loss of such substance and a reduction in the discs’ height.
What’s more, the annulus fibrosus (the collagenous exterior of the disc) is also subject to the challenges of age. Collagen production declines quite sharply after the age of thirty or so and is also affected by such things as smoking, dehydration, lack of nutrients like vitamin C and zinc, and a range of other factors, including the use of some painkillers.
This decline in collagen production can leave the shell of our discs brittle and more liable to rupture, leaking the inflammatory contents of the discs out onto nearby tissues, including spinal nerves. Degenerative discs are often asymptomatic, though, with signs of tissue degradation visible on imaging such as MRIs often proving to be a surprise to those undergoing screening for an unrelated condition. Degenerated discs do not always cause neck pain or back pain, some remain silent for years.
Conversely, for some patients even the slightest degree of degeneration in the spinal discs can trigger profound, severe, chronic neck pain. What is it, then, that causes some to feel no pain and others to be left bedridden and in agony?
How Damaged Discs Cause Neck Pain
One key factor appears to be the increased production of inflammatory mediators by damaged discs. A range of such molecules and substances have been implicated in disc degeneration, including nitric oxide (NO), interleukins, matrix metalloproteinases (MMP), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha) and a group of cytokines. MMPs, PGE2, and various cytokines have been shown to mediate articular cartilage degradation, and nitric oxide ha been found at elevated levels in the cerebrospinal fluid of patients with degenerative lumbar disease.
We do not, yet, however, fully understand how NO and other inflammatory mediators contribute to spinal disc degeneration and the occurrence of neck pain and back pain. Additionally, we are not, yet, fully able to explain the nociceptive experience of pain – pain produced by mechanical, thermal or noxious stimuli of pain receptors as opposed to neuropathic pain which arises due to nerve damage. In all likelihood, the high incidence of neck pain and back pain connected to degenerative disc disease is attributable to a gradual decline in the spine’s structural integrity and a loss of normal motion and function.
The Inflammatory Cascade and Discogenic Pain
In recent years, scientists have discovered more about the inflammatory processes that contribute to spinal disc degeneration, including the involvement of the proinflammatory cytokines TNF, IL-1a, IL-1ß, IL-6 and IL-17 secreted by cells in the discs themselves. These cytokines actually promote the degradation of the extracellular matrix (the scaffold that holds tissues together). In addition, these cytokines also increase chemokine production and prompt changes in the phenotype of the discs’ cells, altering their catabolic and anabolic activity (i.e. changing the way that tissue is broken down and rebuilt as a normal part of cellular turnover).
These changes are what then lead to further disc degeneration, herniation, and radicular pain. Chemokine release from damaged discs encourages immune system cells to flock to the area and this itself increases the inflammatory processes. The immune system cells called leukocytes (white blood cells) are also linked to the development of blood vessels and nerve fibers in the disc, which is abnormal. The discs themselves do not contain nerve fibers as the constant shock to the discs would result in persistent pain. This new, abnormal nerve growth contributes, in part, to discogenic pain and neck pain.
In addition to the processes mentioned above, both the discs and the immune cells alter the activity of pain channels in the dorsal root ganglion, meaning that pain signals are more likely to get transmitted to the spinal cord and brain. In turn, this encourages more cytokines to be released in the area of pain and the cascade continues.
Relieving Neck Pain from Disc Inflammation
The field of neck pain treatment for discogenic pain is increasingly focused on halting this inflammatory cascade and encouraging the body to heal damaged tissues without releasing further inflammatory substances, including cytokines. As well as looking at lifestyle and dietary interventions to reduce inflammation, such as lowering the intake of simple sugars, controlling blood glucose, and increasing the intake of anti-inflammatory plant-based foods, many medications are being developed for pain associated with inflammation and tissue degeneration. Although these may become useful in relieving neck pain from inflammatory degenerative disc disease, it may be that such drugs require refinement so as to improve their delivery to the avascular tissues of the spine.
Podichetty VK. (2007) The aging spine: the role of inflammatory mediators in intervertebral disc degeneration. Cell Mol Biol (Noisy-le-grand). May 30;53(5):4-18.
Risbud MV, Shapiro IM. (2013). Role of cytokines in intervertebral disc degeneration: pain and disc content. Nat Rev Rheumatol. 2013 Oct 29. doi: 10.1038/nrrheum.2013.160.