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      Association of salivary RANKL and osteoprotegerin levels with periodontal health

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          Abstract

          The aim of this study is to determine the association of salivary levels of the bone remodelling regulators (RANKL) and osteoprotegerin (OPG) with periodontal clinical status. One‐hundred fifty‐eight participants selected from a pool of adult patients via systematic random sampling were included in this descriptive cross‐sectional study carried out at the University of Nairobi Dental Hospital. About 5 ml of unstimulated whole saliva was collected from each participant followed by periodontal clinical examination. Salivary levels of RANKL and OPG were determined using human RANKL and OPG ELISA kits from R&D systems, UK. The mean salivary level of RANKL was 14.65pg/ml ( +18.72 SD) with strong association to periodontal disease severity ( F = 64.82, p < .001). Mean OPG levels was 139.03 pg/ml ( +51.19 SD) with significantly high levels in cases without periodontitis ( F = 19.031, p < .001). Consequently, a relative RANKL/OPG ratio was established with a strong positive correlation to disease severity ( r s  = .759, p < .001). Statistically significant area under curve value of .932 was reported (.1613 cutoff ratio, 95% sensitivity, 6.2% specificity). The levels of RANKL and OPG in saliva and their relative ratio have strong association with the severity of periodontal disease, hence a potential adjunctive diagnostic in evaluating periodontal disease.

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          Case definitions for use in population-based surveillance of periodontitis.

          Paul Eke, Robert C Page (2007)
          Many definitions of periodontitis have been used in the literature for population-based studies, but there is no accepted standard. In early epidemiologic studies, the two major periodontal diseases, gingivitis and periodontitis, were combined and considered to be a continuum. National United States surveys were conducted in 1960 to 1962, 1971 to 1974, 1981, 1985 to 1986, 1988 to 1994, and 1999 to 2000. The case definitions and protocols used in the six national surveys reflect a continuing evolution and improvement over time. Generally, the clinical diagnosis of periodontitis is based on measures of probing depth (PD), clinical attachment level (CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bleeding on probing, or a combination of these measures. Several other patient characteristics are considered, and several factors, such as age, can affect measurements of PD and CAL. Accuracy and reproducibility of measurements of PD and CAL are important because case definitions for periodontitis are based largely on either or both measurements, and relatively small changes in these values can result in large changes in disease prevalence. The classification currently accepted by the American Academy of Periodontology (AAP) was devised by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. However, in 2003 the Centers for Disease Control and Prevention and the AAP appointed a working group to develop further standardized clinical case definitions for population-based studies of periodontitis. This classification defines severe periodontitis and moderate periodontitis in terms of PD and CAL to enhance case definitions and further demonstrates the importance of thresholds of PD and CAL and the number of affected sites when determining prevalence.
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            B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease.

            Seicho Makihira, Cory Ernst, Takashi Matsuyama … (2006)
            Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.
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              Mapping the pathogenesis of periodontitis: a new look.

              Kenneth S Kornman (2008)
              Chronic adult periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissue and bone that support teeth. Concepts of the specific mechanisms involved in the disease have evolved with new technologies and knowledge. Histopathologic observations of diseased human tissues were used previously to speculate on the causes of periodontitis and to describe models of pathogenesis. Experimental evidence later emerged to implicate bacterial plaque deposits as the primary factor initiating periodontitis. At the same time, specific bacteria and immunoinflammatory mechanisms were differentially implicated in the disease. In the mid-1990s, early insights about complex diseases, such as periodontitis, led to new conceptual models of the pathogenesis of periodontitis. Those models included the bacterial activation of immunoinflammatory mechanisms, some of which targeted control of the bacterial challenge and others that had adverse effects on bone and connective tissue remodeling. Such models also acknowledged that different environmental and genetic factors modified the clinical phenotype of periodontal disease. However, the models did not capture the dynamic nature of the biochemical processes, i.e., that innate differences among individuals and changes in environmental factors may accelerate biochemical changes or dampen that shift. With emerging genomic, proteomic, and metabolomic data and systems biology tools for interpreting data, it is now possible to begin describing the basic elements of a new model of pathogenesis. Such a model incorporates gene, protein, and metabolite data into dynamic biologic networks that include disease-initiating and -resolving mechanisms. This type of model has a multilevel framework in which the biochemical networks that are regulated by innate and environmental factors can be described and the interrelatedness of networks can be captured. New models in the next few years will be merely frameworks for integrating key knowledge as it becomes available from the "-omics" technologies. However, it is possible to describe some of the key elements of the new models and discuss distinctions between the new and older models. It is hoped that improved conceptual models of pathogenesis will assist in focusing new research and speed the translation of new data into practical applications.
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                Author and article information

                Contributors
                A. A. Ochanji: ochanji100@gmail.com
                Journal
                Journal ID (nlm-ta): Clin Exp Dent Res
                Journal ID (iso-abbrev): Clin Exp Dent Res
                Journal ID (doi): 10.1002/(ISSN)2057-4347
                Journal ID (publisher-id): CRE2
                Title: Clinical and Experimental Dental Research
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2057-4347
                Publication date (Electronic): 12 April 2017
                Publication date Collection: April 2017
                Volume: 3
                Issue: 2 ( doiID: 10.1002/cre2.v3.2 )
                Pages: 45-50
                Affiliations
                [ 1 ] University of Nairobi Kenya
                Author notes
                [*] [* ] Correspondence

                Ochanji AA, University of Nairobi, P.O. BOX 9344‐00200, Nairobi, Kenya.

                Email: ochanji100@ 123456gmail.com

                Article
                Publisher ID: CRE249 Other ID: CRE2.20160041.R1
                DOI: 10.1002/cre2.49
                PMC ID: 5719813
                PubMed ID: 29744178
                SO-VID: 439032f3-7b2d-4a71-9797-497ecd43685c
                Copyright © ©2017 The Authors. Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 July 2016
                Date revision received : 14 October 2016
                Date accepted : 17 October 2016
                Page count
                Figures: 4, Tables: 2, Pages: 6, Words: 3484
                Funding
                Funded by: Bio‐Techne Corporation
                Funded by: R&D Systems UK
                Funded by: Kenya AIDS Vaccine Initiative (KAVI) Institute of Clinical Research Lab
                Funded by: University of Nairobi Dental Hospital
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id cre249
                cover-date April 2017
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.5 mode:remove_FC converted:17.11.2017

                Keywords: elisa,osteoprotegerin,periodontal disease,rankl
                Data availability:
                Keywords: elisa, osteoprotegerin, periodontal disease, rankl

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