RANKL and osteoimmunology in periodontitis
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INVITED REVIEW
RANKL and osteoimmunology in periodontitis Masayuki Tsukasaki1 Received: 26 June 2020 / Accepted: 1 October 2020 © The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020
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. Keywords Periodontitis · RANKL · Osteoimmunology · Mucosal immunology · Osteoclasts · Immune cells
Introduction Epithelial barrier function is essential for the maintenance of host-microbe homeostasis. The human body surface is mostly covered by an epithelial layer, a physical barrier functioning as the first line of defense against the invasion of pathogens as well as commensal microbes. The human oral barrier, which harbors around 700 bacterial species, is a unique exception as the integrity of the epithelium is physically breached by the teeth, and thus is susceptible to the infectious disease caused by oral bacteria, periodontitis [1, 2]. In severe periodontitis, oral bacteria and their components flow into the bloodstream via the inflamed gingiva and translocate to other organs [1, 2]. Thus, periodontitis may not only cause tooth loss, but also can affect systemic health. Epidemiological studies have suggested that periodontitis is associated with various systemic conditions, such as diabetes, cardiovascular diseases, adverse pregnancy outcomes, Alzheimer’s disease and rheumatoid arthritis [1, 2]. RANKL (encoded by the Tnfsf11 gene) is the master regulator of osteoclast differentiation and function [1]. The * Masayuki Tsukasaki tsuka‑[email protected]‑tokyo.ac.jp 1
Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7‑3‑1, Hongo, Bunkyo‑ku, Tokyo 113‑0033, Japan
indispensable role of RANKL in osteoclastogenesis was demonstrated by the finding that RANKL-deficient mice as well as RANKL-mutated patients exhibit osteopetrosis due to a complete lack of osteoclasts [3, 4]. It was also shown that RANKL-deficient mice were protected from bone erosion during arthritis, indicating that osteoclast formation under inflammatory conditions is also dependent on RANKL [5–7]. Thus, an understanding
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