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Anticytokine therapy for periodontal diseases: Where are we now?

Periodontal destruction is initiated by bacteria that stimulate host responses leading to excess production of cytokines. Anticytokine therapy for periodontal diseases especially targets proinflammatory cytokines, that is, TNF-α, IL-1, and IL-6, because these are essential for the initiation of the...

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Detalles Bibliográficos
Autores principales: Waykole, Yogesh Prakash, Doiphode, S. S., Rakhewar, P. S., Mhaske, Maya
Formato: Texto
Lenguaje:English
Publicado: Medknow Publications 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847126/
https://www.ncbi.nlm.nih.gov/pubmed/20407652
http://dx.doi.org/10.4103/0972-124X.55837
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author Waykole, Yogesh Prakash
Doiphode, S. S.
Rakhewar, P. S.
Mhaske, Maya
author_facet Waykole, Yogesh Prakash
Doiphode, S. S.
Rakhewar, P. S.
Mhaske, Maya
author_sort Waykole, Yogesh Prakash
collection PubMed
description Periodontal destruction is initiated by bacteria that stimulate host responses leading to excess production of cytokines. Anticytokine therapy for periodontal diseases especially targets proinflammatory cytokines, that is, TNF-α, IL-1, and IL-6, because these are essential for the initiation of the inflammatory immune reaction and are produced for prolonged periods in periodontitis. This therapy aims to bind the cytokines with the receptors present on target cells such as the fibroblasts. The three basic treatment strategies are: (1) neutralization of cytokines, (2) blockage of cytokine receptors, and (3) activation of anti-inflammatory pathways, such as, immune-suppressive pathways. This new therapy can act as a host response modulator in the control of inflammatory diseases of gums and may provide the basis for new molecular therapeutic approaches to the treatment of periodontitis.
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spelling pubmed-28471262010-04-20 Anticytokine therapy for periodontal diseases: Where are we now? Waykole, Yogesh Prakash Doiphode, S. S. Rakhewar, P. S. Mhaske, Maya J Indian Soc Periodontol Review Article Periodontal destruction is initiated by bacteria that stimulate host responses leading to excess production of cytokines. Anticytokine therapy for periodontal diseases especially targets proinflammatory cytokines, that is, TNF-α, IL-1, and IL-6, because these are essential for the initiation of the inflammatory immune reaction and are produced for prolonged periods in periodontitis. This therapy aims to bind the cytokines with the receptors present on target cells such as the fibroblasts. The three basic treatment strategies are: (1) neutralization of cytokines, (2) blockage of cytokine receptors, and (3) activation of anti-inflammatory pathways, such as, immune-suppressive pathways. This new therapy can act as a host response modulator in the control of inflammatory diseases of gums and may provide the basis for new molecular therapeutic approaches to the treatment of periodontitis. Medknow Publications 2009 /pmc/articles/PMC2847126/ /pubmed/20407652 http://dx.doi.org/10.4103/0972-124X.55837 Text en © Journal of Indian Society of Periodontology http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Waykole, Yogesh Prakash
Doiphode, S. S.
Rakhewar, P. S.
Mhaske, Maya
Anticytokine therapy for periodontal diseases: Where are we now?
title Anticytokine therapy for periodontal diseases: Where are we now?
title_full Anticytokine therapy for periodontal diseases: Where are we now?
title_fullStr Anticytokine therapy for periodontal diseases: Where are we now?
title_full_unstemmed Anticytokine therapy for periodontal diseases: Where are we now?
title_short Anticytokine therapy for periodontal diseases: Where are we now?
title_sort anticytokine therapy for periodontal diseases: where are we now?
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847126/
https://www.ncbi.nlm.nih.gov/pubmed/20407652
http://dx.doi.org/10.4103/0972-124X.55837
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