Leucine‐rich alpha‐2‐glycoprotein 1 affects bone destruction via IL‐6 in mouse periodontitis model

Author:

Ouhara Kazuhisa1ORCID,Takemura Tasuku1,Taniguchi Yuri1,Fujimori Ryousuke1,Tamura Tetsuya1,Akane Yuki1,Matsuda Shinji1,Hamamoto Yuta1,Shintani Tomoaki2ORCID,Kajiya Mikihito2,Munenaga Syuichi1,Iwata Tomoyuki1,Fujita Tsuyoshi1,Mizuno Noriyoshi1

Affiliation:

1. Department of Periodontal Medicine, Graduate School of Biomedical and Health Sciences Hiroshima University Hiroshima Japan

2. Department of Innovation and Precision Dentistry Hiroshima University Hospital Hiroshima Japan

Abstract

AbstractObjectiveTo investigate the production of leucine‐rich α‐2‐glycoprotein‐1 (LRG1) in periodontitis patients and its effectiveness as a new diagnostic marker for periodontitis.Subjects and MethodsIn vitro experiments were conducted to analyze LRG1 mRNA expression in human gingival epithelial cells and fibroblasts via quantitative real‐time PCR. In vivo experiments were conducted to analyze LRG1 localization in periodontitis patients. The correlation between the serum LRG1 levels and alveolar bone resorption in the mouse periodontitis model was also investigated.ResultsA positive correlation existed between the periodontal inflamed surface area and serum LRG1 levels (Spearman's rank correlation coefficient: 0.60). LRG1 mRNA expression in human gingival epithelial cells and fibroblasts was upregulated by Porphyromonas gingivalis stimulation or tumor necrosis factor‐α stimulation. Interleukin‐6 in human gingival epithelial cells and fibroblasts induced the production of LRG1 and transforming growth factor‐β. LRG1 levels in the periodontal tissue and serum in the periodontitis model were higher than those in control mice. LRG1 local administration resulted in alveolar bone resorption, whereas the administration of interleukin‐6R antibody inhibited bone resorption.ConclusionsLRG1 levels in serum and periodontal tissue are upregulated in periodontitis and are implicated in periodontal tissue destruction through interleukin‐6 production.

Funder

Japan Society for the Promotion of Science

Publisher

Wiley

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