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<p>Diabetes mellitus disrupts macrophage function and immune homoeostasis, thereby increasing susceptibility toward periodontitis. PBMT shows emerging potential in oral rehabilitation. However, it remains underexplored for targeting diabetes-associated periodontal complications. This study aimed to investigate the biomodulatory effects of PBMT on hyperglycaemia-associated macrophage dysfunction, metabolic disorders, and periodontal tissue impairment.&#xa0;Immortalized bone marrow-derived macrophages undergoing glucose transition and streptozotocin-induced diabetic mice received PBMT (980&#xa0;nm, 3&#xa0;J/cm²), insulin, or combined therapy. Pharmacological inhibition using specific inhibitors targeting FOXO1, AKT, and ERK was employed to elucidate signaling mechanisms. Cellular functions were assessed through Transwell migration, phagocytosis, and senescence-associated β-galactosidase staining. Metabolic parameters were evaluated via western blotting, ATP/LDH assays, and immunostaining. Tissue morphology was analyzed using micro-CT and H&amp;E staining.&#xa0;PBMT enhanced macrophage phagocytosis, migration, and anti-inflammatory phenotype. The combined PBMT-insulin therapy demonstrated superior efficacy in restoring periodontal architecture compared to monotherapy. Mechanistically, PBMT attenuated FOXO1 hyperactivation primarily through MEK/ERK signaling.&#xa0;PBMT effectively counteracted hyperglycemia-induced metabolic dysregulation, restored macrophage function and phenotype, and mitigated subsequent periodontal tissue damage. The MEK/ERK/FOXO1 signalling pathway may represent a novel mechanism underlying the benefits of PBMT.</p>

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Photobiomodulation therapy reduces diabetic periodontal damage through modulation of macrophage metabolism and functions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月2日

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  • Pawuziya Abulizi,
  • Hao Dong,
  • Aimin Cui,
  • Haonan Zou,
  • Yuezhang Sun,
  • Lulinxiao Nie,
  • Bomiao Cui,
  • Shimeng Xiao,
  • Yi Ding,
  • Wai Keung Leung,
  • Qi Wang

摘要

Diabetes mellitus disrupts macrophage function and immune homoeostasis, thereby increasing susceptibility toward periodontitis. PBMT shows emerging potential in oral rehabilitation. However, it remains underexplored for targeting diabetes-associated periodontal complications. This study aimed to investigate the biomodulatory effects of PBMT on hyperglycaemia-associated macrophage dysfunction, metabolic disorders, and periodontal tissue impairment. Immortalized bone marrow-derived macrophages undergoing glucose transition and streptozotocin-induced diabetic mice received PBMT (980 nm, 3 J/cm²), insulin, or combined therapy. Pharmacological inhibition using specific inhibitors targeting FOXO1, AKT, and ERK was employed to elucidate signaling mechanisms. Cellular functions were assessed through Transwell migration, phagocytosis, and senescence-associated β-galactosidase staining. Metabolic parameters were evaluated via western blotting, ATP/LDH assays, and immunostaining. Tissue morphology was analyzed using micro-CT and H&E staining. PBMT enhanced macrophage phagocytosis, migration, and anti-inflammatory phenotype. The combined PBMT-insulin therapy demonstrated superior efficacy in restoring periodontal architecture compared to monotherapy. Mechanistically, PBMT attenuated FOXO1 hyperactivation primarily through MEK/ERK signaling. PBMT effectively counteracted hyperglycemia-induced metabolic dysregulation, restored macrophage function and phenotype, and mitigated subsequent periodontal tissue damage. The MEK/ERK/FOXO1 signalling pathway may represent a novel mechanism underlying the benefits of PBMT.