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The Interrelationship Between Diabetes, IL-17 and Bone Loss.
Zhen Huang1,2, Xiyan Pei2,3, Dana T Graves4
1Department of Periodontology, Peking University School and Hospital of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology & Beijing Key Laboratory of Digital Stomatology, 22 Zhongguancun South Avenue, Haidian District, Beijing, 100081, China.
Diabetes worsens periodontitis by increasing inflammation and altering oral bacteria. Interleukin-17 (IL-17) drives this destructive process, promoting bone loss in diabetic individuals.
Area of Science:
- Immunology
- Endocrinology
- Periodontology
Background:
- Diabetes mellitus is associated with increased fracture risk and osteolytic bone lesions.
- Diabetic complications often stem from heightened inflammatory responses.
- Periodontitis, an inflammatory gum disease, is exacerbated by diabetes.
Purpose of the Study:
- To review the mechanisms linking Interleukin-17 (IL-17) to diabetes-enhanced periodontitis.
- To examine the role of IL-17 in other diabetes-related bone pathologies.
Main Methods:
- Literature review focusing on IL-17's role in inflammation and bone metabolism.
- Analysis of studies investigating the interplay between diabetes, IL-17, and periodontal disease.
Main Results:
- IL-17 enhances anti-bacterial defenses but also promotes destructive host responses in the periodontium.
- Diabetes-induced IL-17 increases gingival inflammation and alters oral microbiota pathogenicity.
- IL-17 induces osteoclastogenesis via TNF and RANKL, affecting osteoblasts and promoting bone resorption.
Conclusions:
- Increased IL-17 production in diabetes contributes to periodontal bone loss.
- IL-17 plays a significant role in the detrimental effects of diabetes on bone health.
- Targeting IL-17 may offer therapeutic strategies for diabetic periodontitis.
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