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      Comparative evaluation of the levels of nod-like receptor family pyrin domain-containing protein (NLRP) 3 in saliva of subjects with chronic periodontitis and healthy controls

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          Abstract

          Context:

          Periodontitis is an inflammatory disease which is ubiquitous. When there is an onset of infection, the innate immunity gets activated followed by the adaptive immune system. Inflammasomes identify the pathogen-associated molecular patterns or danger-associated molecular patterns and initiate inflammation. Nod- like receptor family pyrin domain-containing protein 3 (NLRP 3) is a protein belonging to the intracellular innate immune sensors that act against bacteria. The inflammasome acts along with the toll-like receptor pathways to initiate an action against pathogens. NLRP3 (also known as PYPAF-1 or cryopyrin) acts via apoptosis-associated speck-like protein (ASC).

          Aims:

          The study aimed at finding out the relation between levels of NLRP3 in chronic periodontitis and healthy subjects via the enzyme-linked immunosorbent assay (ELISA).

          Settings and Design:

          This was a Cross-sectional study.

          Materials and Methods:

          Clinical examination and saliva sampling of the study population was done. Reagents were prepared and NLRP3 levels were estimated using ELISA analysis.

          Statistical Analysis:

          Intergroup comparison was initiated using the unpaired t-test and for within the group (intragroup), the two-way analysis of variance was used. The Pearson correlation coefficient helped to determine the strength of linear association.

          Results:

          Increased levels of NLRP3 were seen in subjects suffering from chronic periodontitis. NLRP3 was also seen to be positively correlated to probing pocket depth, clinical attachment loss, gingival index, and plaque index.

          Conclusions:

          A positive correlation exists between NLRP3 and chronic periodontitis, and hence, NLRP3 can be a potential biomarker.

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          Most cited references28

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          The NLRP3 inflammasome: molecular activation and regulation to therapeutics

          NLRP3 (NACHT, LRR and PYD domains-containing protein 3) is an intracellular sensor that detects a broad range of microbial motifs, endogenous danger signals and environmental irritants, resulting in the formation and activation of the NLRP3 inflammasome. Assembly of the NLRP3 inflammasome leads to caspase-1-dependent release of the proinflammatory cytokines, IL-1β and IL-18, as well as to gasdermin D-mediated pyroptotic cell death. Recent studies have revealed new regulators of the NLRP3 inflammasome, including new interacting or regulatory proteins, metabolic pathways and a regulatory mitochondrial hub. In this Review, we present the molecular, cell biological and biochemical basis of NLRP3 activation and regulation, and describe how this mechanistic understanding is leading to potential therapeutics that target the NLRP3 inflammasome.
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            PERIODONTAL DISEASE IN PREGNANCY. II. CORRELATION BETWEEN ORAL HYGIENE AND PERIODONTAL CONDTION.

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              Is Open Access

              Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity

              The inflammasome generates caspase-1 p20/p10, presumed to be the active protease. Boucher et al. demonstrate that the inflammasome contains an active caspase-1 species, p33/p10, and functions as a holoenzyme. Further caspase-1 self-processing generates and releases p20/p10 to terminate protease activity.
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                Author and article information

                Journal
                J Indian Soc Periodontol
                J Indian Soc Periodontol
                JISP
                Journal of Indian Society of Periodontology
                Wolters Kluwer - Medknow (India )
                0972-124X
                0975-1580
                May-Jun 2022
                02 May 2022
                : 26
                : 3
                : 230-235
                Affiliations
                [1] Department of Periodontology, Terna Dental College, Navi Mumbai, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Shazneen Adil Kandawalla, Department of Periodontology, Terna Dental College, Plot No. 12, Sector 22, Nerul, Navi Mumbai - 400 706, Maharashtra, India. E-mail: shazneen.kandawalla@ 123456gmail.com

                The work belongs to the Department of Periodontology, Terna Dental College, Nerul, Navi Mumbai, Maharashtra, India

                Article
                JISP-26-230
                10.4103/jisp.jisp_5_21
                9118941
                35602535
                5dcbda7e-22a3-4e02-8ed2-9c2d026d3016
                Copyright: © 2022 Indian Society of Periodontology

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 15 March 2021
                : 19 May 2021
                : 05 September 2021
                Categories
                Original Article

                Dentistry
                interleukin-1 beta,nlrp3 protein,periodontal diseases,saliva
                Dentistry
                interleukin-1 beta, nlrp3 protein, periodontal diseases, saliva

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