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Article: Mechanical force modulates inflammation and immunomodulation in periodontal ligament cells

TitleMechanical force modulates inflammation and immunomodulation in periodontal ligament cells
Authors
Keywordsimmunomodulation
inflammation
mechanical stimuli
periodontal ligament
periodontal ligament stem cell
Issue Date13-Aug-2024
PublisherDe Gruyter
Citation
Medical Review, 2024, v. 4, n. 6, p. 544-548 How to Cite?
Abstract

Mechanical forces control a multitude of biological responses in various cells and tissues. The periodontal ligament, located between the tooth’s root and alveolar bone, is a major tissue compartment that is incessantly subjected to such mechanical stimulation through either normal or abnormal oral functionality. It is now known that mechanical stimulation activates periodontal ligament stem cells (PDLSCs) to modulate periodontal immunity and regulate inflammation – a basic feature of periodontal disease that affects virtually every human during their lifetime. For instance, shear stress induces the expression of immunomodulatory-related gene, indoleamine 2,3-dioxygenase (IDO). IDO cleaves l-tryptophan, resulting in increased l-kynurenine levels that, in turn, further promote regulatory T-cell differentiation and inhibit T cell proliferation. These and other related data reinforce the notion that mechanical stimulation plays a crucial role in controlling inflammation and immunomodulation of periodontal tissues. Further investigations, however, are warranted to evaluate the immunomodulatory features of PDLSCs so as to understand the pathological basis of periodontal disease and translate these into clinical interventions.


Persistent Identifierhttp://hdl.handle.net/10722/366397

 

DC FieldValueLanguage
dc.contributor.authorChansaenroj, Jira-
dc.contributor.authorSuwittayarak, Ravipha-
dc.contributor.authorEgusa, Hiroshi-
dc.contributor.authorSamaranayake, Lakshman P-
dc.contributor.authorOsathanon, Thanaphum-
dc.date.accessioned2025-11-25T04:19:12Z-
dc.date.available2025-11-25T04:19:12Z-
dc.date.issued2024-08-13-
dc.identifier.citationMedical Review, 2024, v. 4, n. 6, p. 544-548-
dc.identifier.urihttp://hdl.handle.net/10722/366397-
dc.description.abstract<p>Mechanical forces control a multitude of biological responses in various cells and tissues. The periodontal ligament, located between the tooth’s root and alveolar bone, is a major tissue compartment that is incessantly subjected to such mechanical stimulation through either normal or abnormal oral functionality. It is now known that mechanical stimulation activates periodontal ligament stem cells (PDLSCs) to modulate periodontal immunity and regulate inflammation – a basic feature of periodontal disease that affects virtually every human during their lifetime. For instance, shear stress induces the expression of immunomodulatory-related gene, indoleamine 2,3-dioxygenase (IDO). IDO cleaves l-tryptophan, resulting in increased l-kynurenine levels that, in turn, further promote regulatory T-cell differentiation and inhibit T cell proliferation. These and other related data reinforce the notion that mechanical stimulation plays a crucial role in controlling inflammation and immunomodulation of periodontal tissues. Further investigations, however, are warranted to evaluate the immunomodulatory features of PDLSCs so as to understand the pathological basis of periodontal disease and translate these into clinical interventions.</p>-
dc.languageeng-
dc.publisherDe Gruyter-
dc.relation.ispartofMedical Review-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectimmunomodulation-
dc.subjectinflammation-
dc.subjectmechanical stimuli-
dc.subjectperiodontal ligament-
dc.subjectperiodontal ligament stem cell-
dc.titleMechanical force modulates inflammation and immunomodulation in periodontal ligament cells-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1515/mr-2024-0034-
dc.identifier.scopuseid_2-s2.0-85201205912-
dc.identifier.volume4-
dc.identifier.issue6-
dc.identifier.spage544-
dc.identifier.epage548-
dc.identifier.eissn2749-9642-

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