Periodontal disease has been identified as a major complication of diabetes mellitus. Diabetics experience increased destruction of periodontal tissues as a result of an abnormal immune response, altered fibroblast function and levels of collagen, as well as the microvascular effects of advanced glycosylation end products (AGE). The accumulation of AGE in the periodontium is correlated with an increase in the level of inflammatory mediators, which are associated with tissue destruction. These inflammatory mediators may contribute to the severity of tissue destruction in diabetics with periodontal disease. The increased prevalence of periodontal disease in diabetics is an example of an oral/systemic relationship. There is evidence that this relationship may be two-dimensional as well, as diabetics with active periodontitis tend to have poor glycemic control when compared to patients without periodontitis.
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