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      Regulatory Effect of Inflammatory Mediators in Intervertebral Disc Degeneration

      review-article
      Author(s): , , ,
      Publication date (Electronic):
      Journal: Mediators of Inflammation
      Publisher: Hindawi

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          Abstract

          Intervertebral disc degeneration (IDD) is a major contributor to back, neck, and radicular pain. It is related to changes in tissue structure and function, including the breakdown of the extracellular matrix (ECM), aging, apoptosis of the nucleus pulposus, and biomechanical tissue impairment. Recently, an increasing number of studies have demonstrated that inflammatory mediators play a crucial role in IDD, and they are being explored as potential treatment targets for IDD and associated disorders. For example, interleukins (IL), tumour necrosis factor- α (TNF- α), chemokines, and inflammasomes have all been linked to the pathophysiology of IDD. These inflammatory mediators are found in high concentrations in intervertebral disc (IVD) tissues and cells and are associated with the severity of LBP and IDD. It is feasible to reduce the production of these proinflammatory mediators and develop a novel therapy for IDD, which will be a hotspot of future research. In this review, the effects of inflammatory mediators in IDD were described.

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          A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17.

          Heon Park, Zhaoxia Li, Xuexian O. Yang … (2005)
          Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-gamma negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
          Article 0 comments Cited 1027 times – based on 0 reviews     Review now
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            Role of cytokines in intervertebral disc degeneration: pain and disc content.

            Makarand Risbud, Irving Shapiro (2014)
            Degeneration of the intervertebral discs (IVDs) is a major contributor to back, neck and radicular pain. IVD degeneration is characterized by increases in levels of the proinflammatory cytokines TNF, IL-1α, IL-1β, IL-6 and IL-17 secreted by the IVD cells; these cytokines promote extracellular matrix degradation, chemokine production and changes in IVD cell phenotype. The resulting imbalance in catabolic and anabolic responses leads to the degeneration of IVD tissues, as well as disc herniation and radicular pain. The release of chemokines from degenerating discs promotes the infiltration and activation of immune cells, further amplifying the inflammatory cascade. Leukocyte migration into the IVD is accompanied by the appearance of microvasculature tissue and nerve fibres. Furthermore, neurogenic factors, generated by both disc and immune cells, induce expression of pain-associated cation channels in the dorsal root ganglion. Depolarization of these ion channels is likely to promote discogenic and radicular pain, and reinforce the cytokine-mediated degenerative cascade. Taken together, an enhanced understanding of the contribution of cytokines and immune cells to these catabolic, angiogenic and nociceptive processes could provide new targets for the treatment of symptomatic disc disease. In this Review, the role of key inflammatory cytokines during each of the individual phases of degenerative disc disease, as well as the outcomes of major clinical studies aimed at blocking cytokine function, are discussed.
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              Magnetic resonance classification of lumbar intervertebral disc degeneration.

              C Pfirrmann, A Metzdorf, M. Zanetti … (2001)
              A reliability study was conducted. To develop a classification system for lumbar disc degeneration based on routine magnetic resonance imaging, to investigate the applicability of a simple algorithm, and to assess the reliability of this classification system. A standardized nomenclature in the assessment of disc abnormalities is a prerequisite for a comparison of data from different investigations. The reliability of the assessment has a crucial influence on the validity of the data. Grading systems of disc degeneration based on state of the art magnetic resonance imaging and corresponding reproducibility studies currently are sparse. A grading system for lumbar disc degeneration was developed on the basis of the literature. An algorithm to assess the grading was developed and optimized by reviewing lumbar magnetic resonance examinations. The reliability of the algorithm in depicting intervertebral disc alterations was tested on the magnetic resonance images of 300 lumbar intervertebral discs in 60 patients (33 men and 27 women) with a mean age of 40 years (range, 10-83 years). All scans were analyzed independently by three observers. Intra- and interobserver reliabilities were assessed by calculating kappa statistics. There were 14 Grade I, 82 Grade II, 72 Grade III, 68 Grade IV, and 64 Grade V discs. The kappa coefficients for intra- and interobserver agreement were substantial to excellent: intraobserver (kappa range, 0.84-0.90) and interobserver (kappa range, 0.69-0.81). Complete agreement was obtained, on the average, in 83.8% of all the discs. A difference of one grade occurred in 15.9% and a difference of two or more grades in 1.3% of all the cases. Disc degeneration can be graded reliably on routine T2-weighted magnetic resonance images using the grading system and algorithm presented in this investigation.
              Article 0 comments Cited 640 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yong Hai:
                ORCID: https://orcid.org/0000-0002-7206-325X
                Yunzhong Cheng:
                ORCID: https://orcid.org/0000-0001-5553-5211
                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): mi
                Title: Mediators of Inflammation
                Publisher: Hindawi
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date Collection: 2023
                Publication date (Electronic): 17 April 2023
                Volume: 2023
                Electronic Location Identifier: 6210885
                Affiliations
                Department of Orthopedic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China
                Author notes

                Academic Editor: Sidong Yang

                Author information
                https://orcid.org/0000-0002-0112-1678
                https://orcid.org/0000-0001-5300-1283
                https://orcid.org/0000-0002-7206-325X
                https://orcid.org/0000-0001-5553-5211
                Article
                DOI: 10.1155/2023/6210885
                PMC ID: 10125773
                PubMed ID: 37101594
                SO-VID: 82e6d1f1-a62f-4289-b366-96e388415419
                Copyright © Copyright © 2023 Zhangfu Li et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 September 2022
                Date revision received : 11 November 2022
                Date accepted : 18 March 2023
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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