Salivary Biomarkers and Pseudomonas aeruginosa Levels in Type 1 Diabetes with Periodontitis: An Uncontrolled State May Exacerbate Oral Inflammation

Periodontitis is a chronic inflammatory disease known to be more severe in individuals with diabetes. However, the specific impact of glycemic control in Type 1 Diabetes (T1D) on a comprehensive panel of oral inflammatory and stress biomarkers, alongside opportunistic pathogens like Pseudomonas aeruginosa, requires further elucidation. This study aimed to investigate the associations between glycemic control status in T1D patients with periodontitis and levels of salivary stress (cortisol, Chromogranin A [CgA], Salivary Alpha-Amylase [sAA]) and inflammatory (C-reactive protein [CRP], albumin) biomarkers, subgingival P. aeruginosa counts, and clinical periodontal parameters.

This cross-sectional study enrolled 116 adults who were divided into four equal groups (n=29 each): Uncontrolled T1D with Periodontitis (UC-T1D; HbA1c ≥ 6.5%), controlled T1D with Periodontitis (C-T1D; HbA1c < 6.5%), Non-Diabetics with Periodontitis (NP), and Non-Diabetics with Healthy Periodontium (NH). Salivary biomarkers were quantified using commercial ELISA kits. Subgingival P. aeruginosa bacterial loads were determined by real-time Polymerase Chain Reaction (PCR) targeting the oprL gene. Clinical periodontal parameters (PPD, CAL, PI, BOP) were recorded by a single calibrated examiner. Non-parametric tests (Kruskal-Wallis, Mann-Whitney U) were used for group comparisons, and Spearman's correlation was used to assess relationships.

The UC-T1D group exhibited significantly higher salivary cortisol, CgA, sAA, CRP, and albumin levels, along with greater subgingival P. aeruginosa counts, compared to all other groups (all p<0.001). This group also presented with the most severe periodontal parameters (highest mean PPD, CAL, PI, and BOP%; p<0.001). Subgingival P. aeruginosa counts were significantly and positively correlated with salivary cortisol (r=0.52, p<0.01), CgA (r=0.48, p<0.01), CRP (r=0.67, p<0.001), and albumin (r=0.62, p<0.001).

The findings indicated that an uncontrolled glycemic state in T1D is strongly associated with a heightened oral inflammatory and stress environment. The elevation of both HPA and SAM axis markers (cortisol, CgA, sAA) suggests that systemic physiological stress in uncontrolled T1D may contribute to oral inflammation. The parallel increase in salivary CRP and albumin confirms a state of local and systemic inflammation with compromised gingival vascular integrity. The higher burden of the opportunistic pathogen P. aeruginosa in the UC-T1D group suggests that poor glycemic control may create a favorable niche for its colonization, potentially exacerbating periodontal destruction. Study limitations include the cross-sectional design and focus on a single opportunistic pathogen.

Uncontrolled T1D is associated with significantly elevated salivary stress and inflammatory biomarkers, increased subgingival P. aeruginosa colonization, and more severe periodontitis. These findings underscore the critical importance of diligent glycemic management in T1D patients to mitigate oral inflammation and alter microbial profiles that contribute to the development of periodontal disease. Longitudinal studies are warranted to confirm these associations and explore causality.