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NLRP3 Regulates Alveolar Bone Loss in Ligature-induced Periodontitis by Promoting Osteoclastic Differentiation

Overview
Journal Cell Prolif
Date 2020 Dec 31
PMID 33382502
Citations 56
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Abstract

Objectives: NLRP3 inflammasome is a critical part of the innate immune system and plays an important role in a variety of inflammatory diseases. However, the effects of NLRP3 inflammasome on periodontitis have not been fully studied.

Materials And Methods: We used ligature-induced periodontitis models of NLRP3 knockout mice (NLRP3 ) and their wildtype (WT) littermates to compare their alveolar bone phenotypes. We further used Lysm-Cre/Rosa mouse to trace the changes of Lysm-Cre osteoclast precursors in ligature-induced periodontitis with or without MCC950 treatment. At last, we explored MCC950 as a potential drug for the treatment of periodontitis in vivo and in vitro.

Results: Here, we showed that the number of osteoclast precursors, osteoclast differentiation and alveolar bone loss were reduced in NLRP3 mice compared with WT littermates, by using ligature-induced periodontitis model. Next, MCC950, a specific inhibitor of the NLRP3 inflammasome, was used to inhibit osteoclast precursors differentiation into osteoclast. Further, we used Lysm-Cre/Rosa mice to demonstrate that MCC950 decreases the number of Lysm-Cre osteoclast precursors in ligature-induced periodontitis. At last, treatment with MCC950 significantly suppressed alveolar bone loss with reduced IL-1β activation and osteoclast differentiation in ligature-induced periodontitis.

Conclusion: Our findings reveal that NLRP3 regulates alveolar bone loss in ligature-induced periodontitis by promoting osteoclastic differentiation.

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