A review investigating the role of inflammatory mediators in the degeneration of intervertebral discs (IVD) found that in-vitro disc cells exposed to inflammatory conditions can release cytokines and other neurogenic and angiogenic factors and that these, along with the development of nerve and vessel roots within the fissured annular fibrosis (AF), can contribute to the development of discogenic lower back pain (LBP) in patients suffering from disc degeneration (DD).
The Role of the AF and Nucleus Pulposus (NP)
The collagen-rich AF of an adult intervertebral disc has roughly 25 lamellae with parallel fibers that help to support the spine during bending and twisting. Randomly aligned collagen fibers in the NP help to capture anionic proteoglycan fluids and allows for swelling that will resist forces of compression in the disc during loading. The pressure created by the high fluid content in the NP inhibits the ingrowth of nerves and blood vessels in the AF. A healthy disc should not contain nerves or vessels, but degeneration creates fissures that allow for the escape of fluids and infiltration of nerves and blood vessels into the AF and decrease disc height and weight bearing potential. In extreme cases of degeneration, the NP may extrude through the lamellar walls and create pain when the in-grown nerves become compressed. Better understanding of how inflammatory mediators assist in the development of DD and LBP may help practitioners better target therapies and preventative interventions.
While it appears that greater degeneration is associated with the presence of greater IVD inflammatory mediators, other factors also may contribute to inflammation. These factors include heredity, mechanical loading, extant inflammation, oxygenation, and other types of cells infiltrating the AF of the disc. The introduction of cytokines into IVD cells, for example, create an upregulation of several types of inflammatory mediators, and certain loading configurations can increase or decrease inflammation within the disc, depending upon the loading conditions and location of the IVD being stressed when mechanical loads are applied. The health of the surrounding IVD tissues may also play a role in determining the effect of potential inflammatory mediators, as well as levels of oxygenation within the IVD. The exposure of a DD to macrophage or notochordal cells may also affect levels of prostaglandin and other cerebrospinal fluids, and studies have shown higher levels of these fluids exuded from dissected herniated lumbar and cervical discs in cultured biopsies from LBP patients.
Conclusion
Disc degeneration is a common malady that is associated with pain and social and economic costs worldwide. Despite the prevalence of DD, there are still few ways to diagnose and effectively treat the early stages of DD. A review of the available medical studies data suggests that a biochemical matrix within the degenerating disc may cause a release of fluids that serve to pressurize the IVD environment and prevent the in-growth of nerves and vessels that can activate pain. Further study of this biochemical matrix may lead to more effective therapies in treating the underlying cause and symptoms of DD and LBP.
KEYWORDS: the role of inflammatory mediators in the degeneration of intervertebral discs, in-vitro disc cells exposed to inflammatory conditions can release cytokines and other neurogenic and angiogenic factors, development of discogenic lower back pain, disc degeneration, heredity, mechanical loading, extant inflammation, oxygenation, exposure of a DD to macrophage or notochordal cells may also affect levels of prostaglandin and other cerebrospinal fluids
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