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The oral mucosa is a key barrier and entry point for microorganisms into the gastrointestinal tract. Interleukin-17 (IL-17) and T helper 17 (Th17) cells contribute to mucosal defense against bacterial and fungal pathogens. Gingival fibroblasts recruit neutrophils, construct a mechanical barrier of gingival tissue, and produce osteoprotegerin, which prevents bone resorption. In periodontitis, inflammatory cytokines induce RANKL expression by osteoblasts and periodontal ligament fibroblasts, resulting in alveolar bone resorption. In diabetes mellitus, excessive IL-17 activity increases the risk of periodontal tissue destruction and fungal infections. In patients with diabetes, periodontitis worsens insulin resistance and glycemic control while introducing periodontopathic bacteria and Th17 cells to the gut, exacerbating intestinal inflammation. Infection with periodontopathic bacteria sharing homology with β2 glycoprotein I (β2GPI) may induce antibodies against β2GPI, increasing blood clot risk. Thus, in patients with diabetes and periodontitis, symptoms vary due to localized and systemic immune responses to bacteria and fungi, necessitating a comprehensive understanding for accurate diagnosis and treatment. The biopsychosocial model aids in addressing these complexities, while the common risk approach and cognitive-behavioral therapy address social and psychological challenges. Therefore, comprehensive treatment strategies are necessary for managing periodontitis in patients with diabetes, considering both microbial factors and immune responses.

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Immunological Diagnosis and Treatments of Periodontitis in Patients with Type 2 Diabetes Mellitus

  • 章节

  • 发表日期：

    2026年

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  • Koki Yoshida,
  • Kengo Iwasaki,
  • Osamu Uehara,
  • Satsuki Kato,
  • Shintaro Shimizu,
  • Kohei Sato,
  • Nodoka Sugiyama,
  • Yukichi Okada,
  • Yoshiki Fujimoto,
  • Sho Hirose,
  • Norihiro Nakamoto,
  • Yuko Matsuki,
  • Takashi Kado,
  • Yukie Murata,
  • Katsuya Kawanishi,
  • Hirofumi Matsuoka,
  • Hiroko Miura,
  • Keiji Nagano,
  • Yoshihiro Abiko,
  • Yasushi Furuichi,
  • Toshiyuki Nagasawa

摘要

The oral mucosa is a key barrier and entry point for microorganisms into the gastrointestinal tract. Interleukin-17 (IL-17) and T helper 17 (Th17) cells contribute to mucosal defense against bacterial and fungal pathogens. Gingival fibroblasts recruit neutrophils, construct a mechanical barrier of gingival tissue, and produce osteoprotegerin, which prevents bone resorption. In periodontitis, inflammatory cytokines induce RANKL expression by osteoblasts and periodontal ligament fibroblasts, resulting in alveolar bone resorption. In diabetes mellitus, excessive IL-17 activity increases the risk of periodontal tissue destruction and fungal infections. In patients with diabetes, periodontitis worsens insulin resistance and glycemic control while introducing periodontopathic bacteria and Th17 cells to the gut, exacerbating intestinal inflammation. Infection with periodontopathic bacteria sharing homology with β2 glycoprotein I (β2GPI) may induce antibodies against β2GPI, increasing blood clot risk. Thus, in patients with diabetes and periodontitis, symptoms vary due to localized and systemic immune responses to bacteria and fungi, necessitating a comprehensive understanding for accurate diagnosis and treatment. The biopsychosocial model aids in addressing these complexities, while the common risk approach and cognitive-behavioral therapy address social and psychological challenges. Therefore, comprehensive treatment strategies are necessary for managing periodontitis in patients with diabetes, considering both microbial factors and immune responses.