Background: Diabetes mellitus and periodontitis are two prevalent inflammatory diseases affecting 9.3% and 46% of the US adult population, so it is essential to understand their pathophysiologic relation to each other. Type 2 Diabetes Mellitus (T2D) is a known risk factor for periodontal disease due to an overactive inflammatory response and an impaired wound healing response. Additionally, inflammatory mediators present in periodontitis increase systemic inflammation and contribute to decreased insulin sensitivity, indicating the bidirectional relationship between periodontal disease and T2D. Non-surgical periodontal therapy (NSPT) may contribute to improved glycemic control, which in turn promotes improved healing mechanisms and enhanced resolution of periodontitis. A better understanding of these relationships provides practitioners the opportunity to further improve their patients’ quality of life. Purpose: The purpose of this study was to analyze changes in host immune biomarkers present in gingival crevicular fluid (GCF) in patients with T2D and periodontitis, before and after NSPT, in correlation with local treatment outcomes. Patients were further categorized based on their level of glycemic control to evaluate its effect on the host response.
Materials and Methods: Patients with T2D and periodontitis were tested for their HbA1c levels, then GCF was collected from 4 diseased and 2 non-diseased sites prior to initiating NSPT. Four months after NSPT, a second sample collection and HbA1c test were performed. Control patients with periodontitis and no T2D underwent the same sample collection protocol. Cytokines levels were determined through a 38-plex cytokine panel.
Results: Overall, T2D and ND patients had favorable changes in PD after the treatment. T2D patients had a significantly greater number of sites with more attachment loss following NSPT, compared to ND patients. Changes in BOP were similar amongst T2D and ND patients, but there were more initially healthy sites in T2D patients that presented with BOP at the four month visit. In diseased sites, T2D patients had increased levels of cytokines that affect neutrophil activation such as granulocyte-colony stimulating factor (GCSF) and interleukin (IL)-8, before and after NSPT. Interferon Alpha 2 (IFN-a2) increased in resolved sites in the T2D group, while IL-1b was increased in healthy sites of the T2D group. Compared to ND patients, T2D patients had higher levels of monocyte chemoattractant protein-1(MCP-1) in healthy sites, an increase in monokine induced gamma interferon (MIG) in all sites, and higher levels of macrophage inflammatory protein 1-beta (MIP-1b) in all sites after NSPT.
Conclusions: The higher concentrations of chemoattractant molecules involved in the recruitment of neutrophils, macrophages, and T cells present in T2D patients even after NSPT indicate a prolonged period of inflammation. An IL-1 increase has been linked to periodontitis and T2D which is also observed in our study. Overall, the results indicate that patients with T2D maintain exacerbated inflammatory responses and limited clinical improvement after NSPT.