11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Mechanism of alveolar bone destruction in periodontitis — Periodontal bacteria and inflammation

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Periodontal disease is an inflammatory disease caused by periodontopathogenic bacteria, which eventually leads to bone tissue (alveolar bone) destruction as inflammation persists. Periodontal tissues have an immune system against the invasion of these bacteria, however, due to the persistent infection by periodontopathogenic bacteria, the host innate and acquired immunity is impaired, and tissue destruction, including bone tissue destruction, occurs. Osteoclasts are essential for bone destruction. Osteoclast progenitor cells derived from hematopoietic stem cells differentiate into osteoclasts. In addition, bone loss occurs when bone resorption by osteoclasts exceeds bone formation by osteoblasts. In inflammatory bone disease, inflammatory cytokines act on osteoblasts and receptor activator of nuclear factor-κB ligand (RANKL)-producing cells, resulting in osteoclast differentiation and activation. In addition to this mechanism, pathogenic factors of periodontal bacteria and mechanical stress activate osteoclasts and destruct alveolar bone in periodontitis. In this review, we focused on the mechanism of osteoclast activation in periodontitis and provide an overview based on the latest findings.

          Related collections

          Most cited references109

          • Record: found
          • Abstract: found
          • Article: not found

          Periodontitis: from microbial immune subversion to systemic inflammation.

          Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities that can mediate inflammatory pathology at local as well as distant sites. This Review discusses the mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Functions of RANKL/RANK/OPG in bone modeling and remodeling.

            The discovery of the RANKL/RANK/OPG system in the mid 1990s for the regulation of bone resorption has led to major advances in our understanding of how bone modeling and remodeling are regulated. It had been known for many years before this discovery that osteoblastic stromal cells regulated osteoclast formation, but it had not been anticipated that they would do this through expression of members of the TNF superfamily: receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG), or that these cytokines and signaling through receptor activator of NF-kappaB (RANK) would have extensive functions beyond regulation of bone remodeling. RANKL/RANK signaling regulates osteoclast formation, activation and survival in normal bone modeling and remodeling and in a variety of pathologic conditions characterized by increased bone turnover. OPG protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK. Thus, the relative concentration of RANKL and OPG in bone is a major determinant of bone mass and strength. Here, we review our current understanding of the role of the RANKL/RANK/OPG system in bone modeling and remodeling.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The keystone-pathogen hypothesis.

              Recent studies have highlighted the importance of the human microbiome in health and disease. However, for the most part the mechanisms by which the microbiome mediates disease, or protection from it, remain poorly understood. The keystone-pathogen hypothesis holds that certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one. In this Opinion article, we critically assess the available literature that supports this hypothesis, which may provide a novel conceptual basis for the development of targeted diagnostics and treatments for complex dysbiotic diseases.
                Bookmark

                Author and article information

                Contributors
                Journal
                Jpn Dent Sci Rev
                Jpn Dent Sci Rev
                The Japanese Dental Science Review
                Elsevier
                1882-7616
                2213-6851
                13 October 2021
                November 2021
                13 October 2021
                : 57
                : 201-208
                Affiliations
                [a ]Division of Periodontology, Department of Oral Function, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan
                [b ]Department of Oral and Maxillofacial Surgery, Saitama Medical University, 38 Moro-hongou, Moroyama-machi, Iruma-gun, Saitama 350-0495, Japan
                [c ]Division of Molecular Signaling and Biochemistry, Department of Health Promotion, Kyushu Dental University, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan
                [d ]Division of Infection and Molecular Biology, Department of Health Improvement, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan
                Author notes
                [* ]Corresponding author. r12usui@ 123456fa.kyu-dent.ac.jp
                Article
                S1882-7616(21)00027-2
                10.1016/j.jdsr.2021.09.005
                8524191
                34703508
                0bb019a2-740f-430c-a7c7-5b5f593ee6b7
                © 2021 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 2 July 2021
                : 23 September 2021
                : 29 September 2021
                Categories
                Review Article

                periodontitis,osteoclast,periodontal bacteria,inflammation,rankl,keystone pathogen hypothesis

                Comments

                Comment on this article