Diabetes involves the under-expression or intolerance to insulin which can result in impaired inflammatory and immune responses. Periodontitis is the combined result of microbial dysbiosis and a host immune-inflammatory response in susceptible individuals, resulting in substantive attachment loss and alveolar bone resorption. We often describe the notable connection as bidirectional - wherein diabetes heightens susceptibility to periodontitis and vice versa. It is thought these conditions intersect primarily through inflammation.
Plausible mechanisms by which diabetes is a risk factor for periodontal disease involve: increased expression of pro-inflammatory cytokines; the irreversible creation of advanced glycation end products (AGEs) (sugars react with proteins or lipids) which amplify pro-inflammatory and pro-oxidant influences on cells; and alveolar bone loss via receptor activator of nuclear factor-kappa B ligand (RANKL) and its receptor, RANK (expressed on pre-osteoclasts and osteoclasts – bone resorbing cells) with evidence revealing higher RANKL levels in poorly controlled diabetes patients, correlating with increased bone loss (1). Heightened systemic inflammation observed in individuals with periodontitis is thought to play a role in fostering insulin resistance, potentially exacerbating glycaemic control and diabetes-associated complications (2).