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

Authors

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

Published in

Scientific reports. Jun 29, 2026. Epub Jun 29, 2026.

Abstract

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.

PMID:
42374093
Bibliographic data and abstract were imported from PubMed on 30 Jun 2026.

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