Mechanisms of bone resorption in periodontitis

Hienz, Stefan A., Paliwal, Sweta and Ivanovski, Saso (2015) Mechanisms of bone resorption in periodontitis. Journal of Immunology Research, 2015 615486. doi:10.1155/2015/615486


Author Hienz, Stefan A.
Paliwal, Sweta
Ivanovski, Saso
Title Mechanisms of bone resorption in periodontitis
Journal name Journal of Immunology Research   Check publisher's open access policy
ISSN 2314-7156
2314-8861
Publication date 2015-01-01
Sub-type Article (original research)
DOI 10.1155/2015/615486
Open Access Status DOI
Volume 2015
Start page 615486
Total pages 7
Place of publication New York, NY United States
Publisher Hindawi Publishing Corporation
Language eng
Abstract Alveolar bone loss is a hallmark of periodontitis progression and its prevention is a key clinical challenge in periodontal disease treatment. Bone destruction is mediated by the host immune and inflammatory response to the microbial challenge. However, the mechanisms by which the local immune response against periodontopathic bacteria disturbs the homeostatic balance of bone formation and resorption in favour of bone loss remain to be established. The osteoclast, the principal bone resorptive cell, differentiates from monocyte/macrophage precursors under the regulation of the critical cytokines macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin. TNF-α, IL-1, and PGE2 also promote osteoclast activity, particularly in states of inflammatory osteolysis such as those found in periodontitis. The pathogenic processes of destructive inflammatory periodontal diseases are instigated by subgingival plaque microflora and factors such as lipopolysaccharides derived from specific pathogens. These are propagated by host inflammatory and immune cell influences, and the activation of T and B cells initiates the adaptive immune response via regulation of the Th1-Th2-Th17 regulatory axis. In summary, Th1-type T lymphocytes, B cell macrophages, and neutrophils promote bone loss through upregulated production of proinflammatory mediators and activation of the RANK-L expression pathways.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Dentistry Publications
 
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