The effects of tumour necrosis factor-α on bone cells involved in periodontal alveolar bone loss; osteoclasts, osteoblasts and osteocytes
Periodontitis is the most common bone loss pathology in adults and if left untreated is responsible for premature tooth loss. Cytokines, such as tumour necrosis factor‐α (TNFα), involved in the chronic inflammatory response within the periodontal gingiva, significantly influence the normal bone remo...
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Published in | Journal of periodontal research Vol. 51; no. 5; pp. 549 - 566 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.10.2016
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Subjects | |
Online Access | Get full text |
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Summary: | Periodontitis is the most common bone loss pathology in adults and if left untreated is responsible for premature tooth loss. Cytokines, such as tumour necrosis factor‐α (TNFα), involved in the chronic inflammatory response within the periodontal gingiva, significantly influence the normal bone remodelling processes. In this review, the effects of TNFα on bone metabolism in periodontitis are evaluated in relation to its direct and indirect actions on bone cells including osteoclasts, osteoblasts and osteocytes. Evidence published to date suggests a potent catabolic role for TNFα through the stimulation of osteoclastic bone resorption as well as the suppression of osteoblastic bone formation and osteocytic survival. However, the extent and timing of TNFα exposure in vitro and in vivo greatly influences its effect on skeletal cells, with contradictory anabolic activity observed with TNFα in a number of studies. None the less, it is evident that managing the chronic inflammatory response in addition to the deregulated bone metabolism is required to improve periodontal and inflammatory bone loss treatments. |
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Bibliography: | ark:/67375/WNG-7NH9J9ZX-Z ArticleID:JRE12339 istex:396D6AF0E871A07C56A724B768356C007B07FC9D Australian Postgraduate Award (APA) National Health and Medical Research Council (NHMRC) ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-3484 1600-0765 |
DOI: | 10.1111/jre.12339 |