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<p>This study investigated the role of interleukin-17 (IL-17) and the oral microbiome in peri-implant inflammation and bone loss under hyperglycemic and normoglycemic conditions. Wild-type (WT) and diabetic (db/db) mice with maxillary implants underwent ligature placement with or without IL-17A neutralization. Bone loss, osteoclast activity, inflammatory cytokines, Th17/Treg balance, and expression of IL-17Family members were analyzed. The oral microbiota was profiled by 16S rRNA sequencing, and its inflammatory potential was evaluated by co-culture with immune cells. Diabetic db/db mice exhibited greater peri-implant bone loss, osteoclast numbers, and RANKL/OPG ratios than WT, accompanied by elevated Il17a expression, reduced anti-inflammatory cytokines, enhanced Th17-associated inflammatory features, and altered FOXP3⁺ cell profiles. IL-17A neutralization significantly attenuated, but did not fully normalize, heightened inflammatory responses in db/db mice, whereas ligature-induced <i>Il17f</i> upregulation was observed only in db/db mice. Microbial alterations were partially shifted toward control profiles by IL-17A inhibition in WT mice, while diabetes-associated changes persisted regardless of ligation or anti-IL-17A. In vitro, peri-implant microbiota induced pro-inflammatory cytokine responses in splenocytes, with residual inflammatory responses remaining more evident in DB-derived microbiota after IL-17A inhibition. These findings suggest that peri-implantitis in diabetes is exacerbated by heightened IL-17-mediated inflammation and persistent microbial alterations, underscoring the need for more comprehensive therapeutic approaches to address the disease under diabetic conditions.</p>

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Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月29日

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  • Takumi Memida,
  • Jacques Christopher Jaar,
  • Tsute Chen,
  • Guoqin Cao,
  • Nanako Kuriki,
  • Elaheh Dalir Abdolahinia,
  • Satoru Shindo,
  • Shohei Yamashita,
  • Sunniva Ruiz,
  • Avissasadat Meraji,
  • Alex Albu,
  • Motoki Okamoto,
  • Xuesong He,
  • Saynur Vardar,
  • Maiko Suzuki,
  • Jiang Lin,
  • Toshihisa Kawai,
  • Xiaozhe Han

摘要

This study investigated the role of interleukin-17 (IL-17) and the oral microbiome in peri-implant inflammation and bone loss under hyperglycemic and normoglycemic conditions. Wild-type (WT) and diabetic (db/db) mice with maxillary implants underwent ligature placement with or without IL-17A neutralization. Bone loss, osteoclast activity, inflammatory cytokines, Th17/Treg balance, and expression of IL-17Family members were analyzed. The oral microbiota was profiled by 16S rRNA sequencing, and its inflammatory potential was evaluated by co-culture with immune cells. Diabetic db/db mice exhibited greater peri-implant bone loss, osteoclast numbers, and RANKL/OPG ratios than WT, accompanied by elevated Il17a expression, reduced anti-inflammatory cytokines, enhanced Th17-associated inflammatory features, and altered FOXP3⁺ cell profiles. IL-17A neutralization significantly attenuated, but did not fully normalize, heightened inflammatory responses in db/db mice, whereas ligature-induced Il17f upregulation was observed only in db/db mice. Microbial alterations were partially shifted toward control profiles by IL-17A inhibition in WT mice, while diabetes-associated changes persisted regardless of ligation or anti-IL-17A. In vitro, peri-implant microbiota induced pro-inflammatory cytokine responses in splenocytes, with residual inflammatory responses remaining more evident in DB-derived microbiota after IL-17A inhibition. These findings suggest that peri-implantitis in diabetes is exacerbated by heightened IL-17-mediated inflammation and persistent microbial alterations, underscoring the need for more comprehensive therapeutic approaches to address the disease under diabetic conditions.