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The Interrelationship Between Diabetes, IL-17 and Bone Loss

  • Osteoimmunology (M Nakamura and J Lorenzo, Section Editors)
  • Published:
Current Osteoporosis Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

Diabetes has a detrimental effect on bone, increasing the risk of fracture and formation of osteolytic lesions such as those seen in periodontitis. Several diabetic complications are caused by diabetes-enhanced inflammation. This review examines mechanisms by which IL-17 contributes to diabetes-enhanced periodontitis and other effects of IL-17 on bone.

Recent Findings

IL-17 upregulates anti-bacterial defenses, yet its expression is also linked to a destructive host response in the periodontium. Periodontal disease is caused by bacteria that stimulate an inflammatory response. Diabetes-enhanced IL-17 increases gingival inflammation, which alters the composition of the oral microbiota to increase its pathogenicity. In addition, IL-17 can induce osteoclastogenesis by upregulation of TNF and RANKL in a number of cell types, and IL-17 has differential effects on osteoblasts and their progenitors.

Summary

Increased IL-17 production caused by diabetes alters the pathogenicity of the oral microbiota and can promote periodontal bone resorption.

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Huang, Z., Pei, X. & Graves, D.T. The Interrelationship Between Diabetes, IL-17 and Bone Loss. Curr Osteoporos Rep 18, 23–31 (2020). https://doi.org/10.1007/s11914-020-00559-6

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