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dc.creatorJakovljević, Aleksandar
dc.creatorMiletić, Maja
dc.creatorNikolić, Nadja
dc.creatorBeljić-Ivanović, Katarina
dc.creatorAndrić, Miroslav
dc.creatorMilašin, Jelena
dc.date.accessioned2020-07-02T13:26:11Z
dc.date.available2020-07-02T13:26:11Z
dc.date.issued2019
dc.identifier.issn0306-9877
dc.identifier.urihttps://smile.stomf.bg.ac.rs/handle/123456789/2455
dc.description.abstractApical periodontitis represents a chronic inflammatory process within periapical tissues, mostly caused by etiological agents of endodontic origin. Progressive bone resorption in the periapical region represents the hallmark of apical periodontitis and occurs as the consequence of interplay between polymicrobial infections and host response. The Notch signaling pathway is an evolutionary conserved cell-signaling system that plays an important role in a variety of cell functions including proliferation, differentiation and apoptosis. In recent years its involvement in bone homeostasis has attracted a significant consideration. We hypothesized that Notch signaling pathway, which has a complex interplay with proinflammatory cytokines and bone resorption regulators, contributes to alveolar bone resorption via increased Notch receptors on immune cell surface and stimulates Notch receptor intracellular domain (NICD) translocation into the nucleus. The potential benefit of medications aimed to down-regulate these pathways in apical periodontitis treatment remains to be assessed.en
dc.publisherChurchill Livingstone, Edinburgh
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175075/RS//
dc.rightsrestrictedAccess
dc.sourceMedical Hypotheses
dc.titleNotch signaling pathway mediates alveolar bone resorption in apical periodontitisen
dc.typearticle
dc.rights.licenseARR
dcterms.abstractНиколић, Нађа; Бељић-Ивановић, Катарина; Милетић, Маја; Јаковљевић, Aлександар; Милашин, Јелена; Aндрић, Мирослав;
dc.citation.volume124
dc.citation.spage87
dc.citation.epage90
dc.citation.other124: 87-90
dc.citation.rankM23
dc.identifier.wos000461407900020
dc.identifier.doi10.1016/j.mehy.2019.02.018
dc.identifier.pmid30798925
dc.identifier.scopus2-s2.0-85061062852
dc.type.versionpublishedVersion


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