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Cited by 472

The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Inflammatory mediators in the pathogenesis of periodontitis

Open access
Yucel-Lindberg, Tülay, Båge, Tove·2013·Expert Reviews in Molecular Medicine

Abstract

Periodontitis is a chronic inflammatory condition of the periodontium involving interactions between bacterial products, numerous cell populations and inflammatory mediators. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. dental plaque. Substances released from this biofilm such as lipopolysaccharides, antigens and other virulence factors, gain access to the gingival tissue and initiate an inflammatory and immune response, leading to the activation of host defence cells. As a result of cellular activation, inflammatory mediators, including cytokines, chemokines, arachidonic acid metabolites and proteolytic enzymes collectively contribute to tissue destruction and bone resorption. This review summarises recent studies on the pathogenesis of periodontitis, with the main focus on inflammatory mediators and their role in periodontal disease.

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Metadata

Authors
Yucel-Lindberg, T., & Båge, T.
Venue
Expert Reviews in Molecular Medicine
Published
2013
Volume
15
Pages
e7-e7
ISSN
1462-3994 (ISSN-L)
OpenAlex
W2110043964
Cited by
472
References
12
FWCI
28.02
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Inflammatory mediators in the pathogenesis of periodontitis. https://app.cochat.ai/papers/10.1017/erm.2013.8
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Yucel-Lindberg, T., & Båge, T. (2013). Inflammatory mediators in the pathogenesis of periodontitis. Expert Reviews in Molecular Medicine. https://doi.org/10.1017/erm.2013.8

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.