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New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes

Within the last 5 years, international research collaborations including those of several research groups skilled in microbiology, immunology and pathophysiology, have identified a low-virulent intradiscal infection with the ability to provoke gradual and progressive disc degeneration, end-plate dis...

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Autores principales: Manniche, Claus, O'Neill, Søren
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Future Science Ltd 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6554696/
https://www.ncbi.nlm.nih.gov/pubmed/31245043
http://dx.doi.org/10.2144/fsoa-2019-0022
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author Manniche, Claus
O'Neill, Søren
author_facet Manniche, Claus
O'Neill, Søren
author_sort Manniche, Claus
collection PubMed
description Within the last 5 years, international research collaborations including those of several research groups skilled in microbiology, immunology and pathophysiology, have identified a low-virulent intradiscal infection with the ability to provoke gradual and progressive disc degeneration, end-plate disruption, Modic changes and persistent clinical lower-back pain. Certain strains of the Propionibacterium acne bacterium seem able to invade, colonize and develop a protective biofilm inside the disc. The interaction of P. acne, disc tissues and mononuclear cells of the bone marrow are shown to trigger a relevant immunological response and an ensuing destructive inflammation of the disc and adjacent vertebrae. This process presents on MRI as Modic changes. Recent proof-of-concept data provide compelling evidence for this bacterial disc infection hypothesis.
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spelling pubmed-65546962019-06-26 New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes Manniche, Claus O'Neill, Søren Future Sci OA Perspective Within the last 5 years, international research collaborations including those of several research groups skilled in microbiology, immunology and pathophysiology, have identified a low-virulent intradiscal infection with the ability to provoke gradual and progressive disc degeneration, end-plate disruption, Modic changes and persistent clinical lower-back pain. Certain strains of the Propionibacterium acne bacterium seem able to invade, colonize and develop a protective biofilm inside the disc. The interaction of P. acne, disc tissues and mononuclear cells of the bone marrow are shown to trigger a relevant immunological response and an ensuing destructive inflammation of the disc and adjacent vertebrae. This process presents on MRI as Modic changes. Recent proof-of-concept data provide compelling evidence for this bacterial disc infection hypothesis. Future Science Ltd 2019-03-18 /pmc/articles/PMC6554696/ /pubmed/31245043 http://dx.doi.org/10.2144/fsoa-2019-0022 Text en © 2019 Claus Manniche This work is licensed under a Creative Commons Attribution 4.0 License (http://creativecommons.org/licenses/by/4.0/)
spellingShingle Perspective
Manniche, Claus
O'Neill, Søren
New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title_full New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title_fullStr New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title_full_unstemmed New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title_short New insights link low-virulent disc infections to the etiology of severe disc degeneration and Modic changes
title_sort new insights link low-virulent disc infections to the etiology of severe disc degeneration and modic changes
topic Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6554696/
https://www.ncbi.nlm.nih.gov/pubmed/31245043
http://dx.doi.org/10.2144/fsoa-2019-0022
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