Periodontitis and type 1 diabetes mellitus (T1DM) are chronic inflammatory diseases that interact bidirectionally, with periodontal inflammation worsening glycemic control and hyperglycemia aggravating periodontal inflammation. This interaction is mediated by synergistic and non-synergistic mechanisms associated with the innate and adaptive immune response, including pattern recognition receptors, cytokines, advanced glycation end products (AGEs), mediators of the RANKL/OPG axis, oxidative stress, impaired immune regulation, and the oral biofilm. Periodontitis is driven by dysbiosis and a dysregulated host response, leading to alveolar bone loss through RANKL/OPG imbalance, whereas T1DM is characterized by chronic hyperglycemia and disrupted homeostasis. AGEs accumulate as a consequence of hyperglycemia and aging, promoting oxidative stress and inflammatory signaling while potentially contributing to dysregulation of the RANKL/OPG axis and subsequent bone resorption. By investigating AGEs and RANKL/OPG axis biomarkers, the study aims to improve understanding of the biological mechanisms underlying the bidirectional relationship between periodontitis and diabetes.