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1
1] State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China [2] School of Dental Medicine, University of Pennsylvania, Philadelphia, USA.
2
1] School of Dental Medicine, University of Pennsylvania, Philadelphia, USA [2] Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing, China.
3
School of Dental Medicine, University of Pennsylvania, Philadelphia, USA.
1
1] State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China [2] School of Dental Medicine, University of Pennsylvania, Philadelphia, USA.
2
1] School of Dental Medicine, University of Pennsylvania, Philadelphia, USA [2] Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing, China.
3
School of Dental Medicine, University of Pennsylvania, Philadelphia, USA.
Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide. Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus. Alveolar bone loss is one of the main outcomes of periodontitis, and diabetes is among the primary risk factors for periodontal disease. In this review, we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects, focusing on alveolar bone loss. Bone remodelling begins with osteoclasts resorbing bone, followed by new bone formation by osteoblasts in the resorption lacunae. Therefore, we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts.
A potential mechanism of diabetes-related alveolar bone loss in periodontal disease.
Diabetes increases the RANKL/OPG ratios and enhances the expression level of AGEs, ROS and inflammatory mediators, which induce osteoblast apoptosis and osteoclastogenesis. This cascade of events contributes to both increased bone resorption and reduced reparative bone formation leading to greater alveolar bone loss in periodontal disease that is caused by bacterial pathogens. AGE, advanced glycation end product; IL, interleukin; OPG, osteoprotegerin; PDL, periodontal ligament; RANKL, receptor activator of nuclear factor kappa-B ligand; ROS, reactive oxygen species; TNF, tumor necrosis factor.
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