Improving metabolic and inflammatory balance prevents periodontal complications in diabetes

Figure 1 Proposed mechanisms linking metabolic-inflammatory imbalance and periodontal complications in type 2 diabetes. Chronic hyperglycaemia, insulin resistance, and oxidative stress in type 2 diabetes promote systemic inflammation via increased production of pro-inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6) and activation of nuclear factor kappa B signaling. These processes impair host-microbiome homeostasis, leading to gingival inflammation, alveolar bone resorption, and dysbiotic microbial changes. Conversely, periodontitis aggravates systemic inflammation and insulin resistance, forming a bidirectional pathogenic loop. Improved metabolic and inflammatory balance may disrupt this cycle and protect oral health. TNF-α: Tumor necrosis factor-alpha; IL-6: Interleukin-6; NF-κB: Nuclear factor kappa B.