Mechanisms of Bone Resorption in Periodontitis
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 respo...
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Wiley
2015-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2015/615486 |
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| author | Stefan A. Hienz Sweta Paliwal Saso Ivanovski |
| author_facet | Stefan A. Hienz Sweta Paliwal Saso Ivanovski |
| author_sort | Stefan A. Hienz |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-8a669b126f974b778751bbf8066d3dde |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
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| series | Journal of Immunology Research |
| spelling | doaj-art-8a669b126f974b778751bbf8066d3dde2025-02-03T01:24:23ZengWileyJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/615486615486Mechanisms of Bone Resorption in PeriodontitisStefan A. Hienz0Sweta Paliwal1Saso Ivanovski2School of Dentistry and Oral Health, Griffith Health Institute, Griffith University, Gold Coast, QLD 4222, AustraliaSchool of Dentistry and Oral Health, Griffith Health Institute, Griffith University, Gold Coast, QLD 4222, AustraliaSchool of Dentistry and Oral Health, Griffith Health Institute, Griffith University, Gold Coast, QLD 4222, AustraliaAlveolar 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.http://dx.doi.org/10.1155/2015/615486 |
| spellingShingle | Stefan A. Hienz Sweta Paliwal Saso Ivanovski Mechanisms of Bone Resorption in Periodontitis Journal of Immunology Research |
| title | Mechanisms of Bone Resorption in Periodontitis |
| title_full | Mechanisms of Bone Resorption in Periodontitis |
| title_fullStr | Mechanisms of Bone Resorption in Periodontitis |
| title_full_unstemmed | Mechanisms of Bone Resorption in Periodontitis |
| title_short | Mechanisms of Bone Resorption in Periodontitis |
| title_sort | mechanisms of bone resorption in periodontitis |
| url | http://dx.doi.org/10.1155/2015/615486 |
| work_keys_str_mv | AT stefanahienz mechanismsofboneresorptioninperiodontitis AT swetapaliwal mechanismsofboneresorptioninperiodontitis AT sasoivanovski mechanismsofboneresorptioninperiodontitis |