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RANKL and osteoimmunology in periodontitis

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Abstract

Periodontitis, one of the most common infectious diseases in humans, is characterized by inflammation of the periodontal tissue and subsequent destruction of the alveolar bone, which ultimately leads to tooth loss. Recently, it was revealed that the osteoclastic bone damage that occurs during periodontitis is dependent on the receptor activator of NF-kB ligand (RANKL) produced by osteoblastic cells and periodontal ligament cells. Immune cells provide essential cues for the RANKL induction that takes place during periodontal inflammation. The knowledge accumulated and experimental tools established in the field of “osteoimmunology” have made crucial contributions to a better understanding of periodontitis pathogenesis and, reciprocally, the investigation of periodontitis has provided important insights into the field. This review discusses the molecular mechanisms underlying periodontal bone loss by focusing on the osteoimmune interactions and RANKL.

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Acknowledgements

I thank H.Takayanagi, N.Komatsu, K.Nagashima, T.Nitta, W.Pluemsakunthai, C.Shukunami, Y.Iwakura, T.Nakashima and K.Okamoto for their great contribution to the publications, on which this work is based. This work was supported in part by a grant for the Young Scientists (19K18943) and JSPS fellows (18J00744) from the Japan Society for the Promotion of Science (JSPS).

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Tsukasaki, M. RANKL and osteoimmunology in periodontitis. J Bone Miner Metab 39, 82–90 (2021). https://doi.org/10.1007/s00774-020-01165-3

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