The impact of diabetes on periodontal diseases

Abstract

The susceptibility and severity of periodontal diseases is made more severe by diabetes, with the impact on the disease process inversely proportional to the level of glycemic control. Although type 1 diabetes mellitus and type 2 diabetes mellitus have different etiologies, and their impact on bone is not identical, they share many of the same complications. Studies in animals and humans agree that both forms of diabetes increase inflammatory events in periodontal tissue, impair new bone formation, and increase expression of RANKL in response to bacterial challenge. High levels of glucose, reactive oxygen species, and advanced glycation end‐products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor‐kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin‐1. Studies in animals, moreover, suggest that there are multiple cell types in periodontal tissues that are affected by diabetes, including leukocytes, vascular cells, mesenchymal stem cells, periodontal ligament fibroblasts, osteoblasts, and osteocytes. The etiology of periodontal disease involves the host response to bacterial challenge that is affected by diabetes, which increases the expression of RANKL and reduces coupled bone formation. In addition, the inflammatory response also modifies the oral microbiota to render it more pathogenic, as demonstrated by increased inflammation and bone loss in animals where bacteria are transferred from diabetic donors to germ‐free hosts compared with transfer from normoglycemic donors. This approach has the advantage of not relying upon limited knowledge of the specific bacterial taxa to determine pathogenicity, and examines the overall impact of the microbiota rather than the presumed pathogenicity of a few bacterial groups. Thus, animal studies have provided new insights into pathogenic mechanisms that identify cause‐and‐effect relationships that are difficult to perform in human studies.

Histone Methylation: Achilles Heel and Powerful Mediator of Periodontal Homeostasis

“…Periodontal ligament degradation and alveolar bone loss indicate that the periodontium has lost its homeostasis capacity under inflammation (Graves et al 2019). Several studies have shown that PDL stem cells from patients with periodontitis display changes in proliferation and differentiation potential and cell migration capacity (Zhang et al 2012).…”

SETD1 and NF-κB Regulate Periodontal Inflammation through H3K4 Trimethylation

“…Confirming the role of SETD1 in p65-mediated periodontal inflammation, the IKK2 inhibitor BOT-64 reduced the number of SETD1-positive cells in inflamed periodontal tissues, restored periodontal tissue integrity, and enhanced osteogenesis in a periodontal inflammation model in vivo. Based on the inhibitory effect of inflammation on osteogenic potential of mesenchymal stem cells (Lacey et al 2009, Graves et al 2019), we expect that NF-κB signaling inhibitors such as BOT-64 display similar effects on SETD1 function in terms of gene regulation. In the present study, we successfully introduced the IKK2/NF-κB activation inhibitor BOT-64 to enhance osteogenic differentiation of PDL cells in the subcutaneously implanted collagen sponges and to facilitate alveolar bone regeneration.…”

Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues

“…Diabetes affected bacteria-host interactions to promote inflammation and periodontal disease. 23 The inflammatory response modified oral microbiota to render it more pathogenic. Complement system may also be involved in the process.…”