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Background <p>Oral ulcer (OU) is among the most common oral mucosal disease, and immune factors are generally considered to play crucial roles in OU. Photobiomodulation (PBM) therapy can promote healing and alleviate pain; however, the effect and mechanism of early ulceration remain unclear.</p> Objective <p>This study aimed to establish a model of early persistent aggravation, assess the impact of PBM on early persistent aggravation, and map the involvement of different immune cells.</p> Methods <p>In this study, an OU model was established in C57BL/6 mice, and the mice were subsequently treated with PBM. Haematoxylin and eosin staining, stem cell immunofluorescence, and collagen III immunohistochemical staining were used to evaluate the wound healing process. Flow cytometry and immunohistochemistry were used to assess changes in various immune cells, including neutrophils, macrophages, T cells, and B cells.</p> Results <p>PBM effectively inhibited the aggravation of early ulcers and inflammation by decreasing the number of neutrophils and Th1 cells while promoting the polarization of macrophages towards the M2 phenotype and the generation of regulatory T cells (Tregs).</p> Conclusion <p>Our study investigated the PBM-induced patterns of changes in various immune cells during the development of OU, thereby facilitating understanding of the disease and providing a theoretical basis for the clinical application of PBM.</p>

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Photobiomodulation limits oral ulcer development by regulating the immune response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月12日

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  • Siying Zhu,
  • Jingfei Fu,
  • Xiaoyan Li,
  • Juan Du,
  • Yi Liu

摘要

Background

Oral ulcer (OU) is among the most common oral mucosal disease, and immune factors are generally considered to play crucial roles in OU. Photobiomodulation (PBM) therapy can promote healing and alleviate pain; however, the effect and mechanism of early ulceration remain unclear.

Objective

This study aimed to establish a model of early persistent aggravation, assess the impact of PBM on early persistent aggravation, and map the involvement of different immune cells.

Methods

In this study, an OU model was established in C57BL/6 mice, and the mice were subsequently treated with PBM. Haematoxylin and eosin staining, stem cell immunofluorescence, and collagen III immunohistochemical staining were used to evaluate the wound healing process. Flow cytometry and immunohistochemistry were used to assess changes in various immune cells, including neutrophils, macrophages, T cells, and B cells.

Results

PBM effectively inhibited the aggravation of early ulcers and inflammation by decreasing the number of neutrophils and Th1 cells while promoting the polarization of macrophages towards the M2 phenotype and the generation of regulatory T cells (Tregs).

Conclusion

Our study investigated the PBM-induced patterns of changes in various immune cells during the development of OU, thereby facilitating understanding of the disease and providing a theoretical basis for the clinical application of PBM.