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ORIGINAL RESEARCH article

Front. Pharmacol.

Sec. Experimental Pharmacology and Drug Discovery

Volume 16 - 2025 | doi: 10.3389/fphar.2025.1533468

Exogenous Galectin-9 Prevents Peri-implantitis in Rats by Regulating Macrophage Polarization

Provisionally accepted
Lujin Cheng Lujin Cheng 1,2Xiaowei Ji Xiaowei Ji 1,2Huerxidai Yilihamujiang Huerxidai Yilihamujiang 1Shuya Dong Shuya Dong 1Long Mei Long Mei 1Guo Lin Guo Lin 3Qihan Tang Qihan Tang 3Zhongcheng Gong Zhongcheng Gong 4*
  • 1 Department of Prosthodontics and Dental Implant, The First Affiliated Hospital of Xinjiang Medical University (Affiliated Stomatology Hospital), Urumqi, China
  • 2 Stomatological Research Institute of Xinjiang Uygur Autonomous Region, Urumqi, China
  • 3 Xinjiang Medical University, Ürümqi, Xinjiang Uyghur Region, China
  • 4 Department of Oral and Maxillofacial Tumor Surgery, The First Affiliated Hospital of Xinjiang Medical University (Affiliated Stomatology Hospital), Urumqi, China

The final, formatted version of the article will be published soon.

    Background: Peri-implantitis (PI) is a common complication of oral implants with no definitive treatment strategy. Lipopolysaccharides (LPS) are involved in PI by activating macrophages and influencing osteoclasts and osteoblasts. Galactin-9 (Gal-9) is known for its immunomodulatory properties and interactions with macrophage polarization receptors. This study investigated the mechanism of prophylactic exogenous Gal-9 in the prevention and treatment of PI in rats.Methods: Male SD rats with titanium implants were divided into the Control, Saline, and Gal-9 groups. Rats in the Saline group and Gal-9 group were prophylactically administered Gal-9 and Saline, respectively, before inducing PI. Periodontal examinations, X-ray imaging, flow cytometry analyses, and micro-CT evaluations were conducted to assess clinical, imaging, and immunological parameters.Results: After inducing PI, the implant loss rate in the Gal-9 group was lower than that in the Saline group. The gingival index was higher in the Saline group and Gal-9 group compared to the Control group. The bleeding on probing positivity rate was higher in the Saline group than in the other two groups. X-ray and micro-CT images both showed lower alveolar bone resorption in the Gal-9 group than in the Saline group. Flow cytometry showed that the proportions of M1-type macrophages and M2-type macrophages, and M1/M2 ratio were lower in the Gal-9 group than those in the Saline group. Multivariate linear regression indicated that Tb.Th had the greatest impact on the gingival index and Tb.Sp had the greatest impact on the M1/M2 ratio. Conclusion: Exogenous Gal-9 administration demonstrated promising effects in mitigating inflammation associated with PI in rat models by promoting M2 macrophage polarization and enhancing alveolar bone stability.

    Keywords: Peri-Implantitis, rat, galectin-9, Macrophage polarization, Alveolar bone resorption

    Received: 24 Nov 2024; Accepted: 10 Feb 2025.

    Copyright: © 2025 Cheng, Ji, Yilihamujiang, Dong, Mei, Lin, Tang and Gong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Zhongcheng Gong, Department of Oral and Maxillofacial Tumor Surgery, The First Affiliated Hospital of Xinjiang Medical University (Affiliated Stomatology Hospital), Urumqi, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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