Zhen Huang1,2, Xiyan Pei2,3, Dana T Graves4. 1. Department 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. 2. Department of Periodontics, School of Dental Medicine, University of Pennsylvania, 240 S 40th St, Philadelphia, PA, 19104, USA. 3. First Clinical Division, 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, 37 Xishiku Avenue, Xicheng District, Beijing, 100034, China. 4. Department of Periodontics, School of Dental Medicine, University of Pennsylvania, 240 S 40th St, Philadelphia, PA, 19104, USA. dtgraves@dental.upenn.edu.
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. Increased IL-17 production caused by diabetes alters the pathogenicity of the oral microbiota and can promote periodontal bone resorption.
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. Increased IL-17 production caused by diabetes alters the pathogenicity of the oral microbiota and can promote periodontal bone resorption.
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