Oxidative stress and inflammatory status in type 2 diabetes with periodontitis

Research Topic:

Background + Aims

Periodontitis is a chronic inflammatory disease affecting tooth-supporting tissues, driven by pathogenic plaque biofilm and a hyper-inflammatory host response. It leads to periodontal pocket formation, tissue destruction, and potential tooth loss. Individuals with Type 2 diabetes face an increased risk and severity of periodontitis due to their predisposition to oxidative stress and inflammation.
Oxidative stress in periodontitis arises from hyperactive neutrophils, producing reactive oxygen species (ROS) that cause direct tissue damage and trigger pro-inflammatory cascades via redox-sensitive pathways. This localized oxidative burden extends systemically, with increased inflammatory markers like C-reactive protein (CRP) and reduced antioxidant capacity linked to heightened cardiovascular and metabolic risks.
Conversely, periodontitis may negatively affect glycaemic control in diabetes, with evidence suggesting periodontal therapy improves HbA1c levels and lipid profiles. Type 2 diabetes amplifies oxidative stress through hyperglycaemia-driven ROS production, AGE/RAGE interactions, and mitochondrial dysfunction, further exacerbating inflammation and insulin resistance.
This study hypothesizes that oxidative stress acts as a central link between periodontitis and Type 2 diabetes, potentially worsening both conditions when coexisting.
This study aimed to elucidate the oxidative and inflammatory interplay between diabetes and periodontitis, evaluating systemic and local impacts on glycaemic and lipid control.

Materials + Methods

This comparative study recruited 60 patients, divided into three groups of 20: Type 2 diabetes with periodontitis (DP), Type 2 diabetes without periodontitis (DNP), and non-diabetes with periodontitis (NDP). The study aimed to examine the relationship between periodontal inflammation and diabetes (DP vs. DNP) and the impact of diabetes on periodontitis (DP vs. NDP). Participants were individually matched for age and gender.
Type 2 diabetes patients were diagnosed per WHO criteria and managed via dietary interventions or oral hypoglycaemic agents.
Recruitment included diabetes outpatients and periodontal patients referred to Cork University Dental Hospital. Inclusion criteria required participants aged 30–70, non-smokers, and periodontitis patients with at least 16 teeth and ≥6 sites with pocket depths (PD) ≥4mm. Exclusion criteria ruled out significant systemic diseases, recent myocardial infarction, cancer, immunosuppression, or recent periodontal therapy.
Clinical assessments included PD, bleeding on probing (BOP), radiographic evaluation, and fasting blood samples.
Blood analyses measured HbA1c, lipid profiles, inflammatory markers (CRP), and oxidative stress markers, including protein carbonyls and plasma small molecule antioxidant capacity (pSMAC).
The study used SPSS for statistical analysis, with significance set at p < 0.05.

Results

BMI was significantly higher in both diabetes groups compared to the non-diabetes group (p < 0.024).
Periodontal parameters, such as PPD and plaque levels, were similar across periodontitis groups, BOP was significantly higher in diabetes patients with periodontitis compared to non-diabetes patients (p = 0.03).
Oxidative status showed lower pSMAC in diabetes patients with periodontitis than those without periodontitis (p = 0.03), and higher protein oxidation levels compared to both groups (p = 0.007).
Inflammatory marker CRP was elevated in diabetes patients with periodontitis compared to non-diabetes patients (p = 0.004), though fibrinogen and leukocyte counts showed no significant differences.
Glycaemic control markers were worse in diabetes patients with periodontitis, with significantly higher HbA1c (p = 0.002) and fasting glucose levels compared to other groups.
β-cell function was notably impaired in diabetes patients with periodontitis (p = 0.01), though insulin resistance was unaffected.
Lipid profiles showed no significant differences between groups, except for lower HDL cholesterol (p = 0.006) and trends toward higher triglycerides and VLDL in diabetes patients with periodontitis compared to non-diabetes patients.
These findings highlight the interplay between periodontitis, oxidative stress, and diabetes outcomes.

Limitations

The study’s small sample size (20 participants per group) reduced its statistical power, as shown by low post hoc power for several outcome measures. This was due to strict inclusion criteria and matching requirements. The recruitment process, requiring a large pool of screened candidates (949 diabetes patients), may have introduced selection bias, as only those meeting strict criteria were included.
The exclusion of smokers and the tight matching for gender, age, and periodontal status aimed to control confounding factors but limited the diversity of the study population, reducing the generalisability of the findings.
Although BMI, medications (e.g., statins), fruit/vegetable intake, and diabetes duration were analysed post-recruitment, residual confounding cannot be entirely ruled out. For instance, statin use and diet could influence oxidative status and were not fully controlled.
The study’s design limits the ability to establish causality between periodontitis, oxidative stress, and metabolic outcomes.
The absence of randomisation in group selection might have introduced unmeasured biases affecting the results.
The study focused primarily on oxidative stress and metabolic parameters but did not explore other potential systemic effects of periodontitis or long-term outcomes.
The predominantly Caucasian sample lacks ethnic diversity, which might limit the applicability of results to broader populations.
The uniformity of medication regimens among diabetes groups may have masked subtle differences in the effects of periodontitis on metabolic status.

Conclusion

This study demonstrates that periodontitis exacerbates oxidative stress and metabolic dysfunction in Type 2 diabetes patients, with higher protein oxidation, lower antioxidant capacity, and worse glycaemic control compared to those without periodontitis. These findings suggest that periodontitis may play a role in the systemic inflammatory burden and metabolic imbalance in diabetes.
The research underscores the importance of oral health in managing metabolic and cardiovascular risks in Type 2 diabetes patients. It highlights the need for integrated periodontal and diabetes care, encouraging further investigation through larger cohort studies and randomized trials to strengthen the evidence and guide clinical recommendations.

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