One potential mechanism could be the excessive accumulation of AGEs, which are formed through non-enzymatic glycosylation of various proteins in the serum of individuals with diabetes mellitus.51 The elevated levels of AGEs further stimulate the production of receptors for AGEs.27 This interaction ultimately gives rise to the generation of various types of detrimental proinflammatory cytokines, including IL-6 and collagenases (matrix metalloproteinase), which are synthesised by periodontal and peri-implant gingival fibroblasts. This evidence concerns the gene IL6 and diabetes mellitus.