Is there a connection between insulin resistance and periodontitis in a non-diabetic population?

Research Topic:

Background + Aims

Insulin resistance, a condition where cells fail to respond effectively to insulin, is central to metabolic disorders like type 2 diabetes and cardiovascular disease. It often leads to systemic low-grade inflammation, a feature shared with periodontal disease, suggesting a potential biological link between these conditions.
Periodontitis, a chronic inflammatory disease affecting the supporting structures of teeth, is triggered by bacterial infection and modulated by host immune responses. Elevated levels of inflammatory mediators such as cytokines and acute-phase reactants are key in both insulin resistance and periodontal disease. These shared pathways highlight the potential bidirectional relationship, where systemic inflammation may exacerbate periodontal disease, and periodontal inflammation could impair insulin sensitivity.
Previous research has found associations between insulin resistance and periodontitis. However, confounding factors, including smoking, diabetes, and age, have limited the clarity of these findings. This study focuses on a non-smoking, non-diabetic population to investigate whether insulin resistance independently contributes to periodontal diseases.
Periodontal disease’s high prevalence and systemic health implications make understanding its links with metabolic health critical. By examining these associations in a well-characterised cohort, this study aims to provide insights that could help clinicians integrate metabolic and periodontal care, improving outcomes for both systemic and oral health.
This study aimed to explore the association between insulin sensitivity, measured using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) index, and periodontal infection, in a non-diabetic, non-smoking adult population using data from the nationally representative Health 2000 Survey.

Materials + Methods

Data was derived from the Health 2000 Survey, which included 2050 dentate, non-smoking, and non-diabetic adults aged 30–64 years. Diabetes status was confirmed through laboratory testing and clinical examination. Ethical approval and informed consent were obtained.
Periodontitis was assessed by measuring the number of teeth with pocket depths (PD) ≥4 mm and ≥6 mm. PD was recorded on four surfaces per tooth (excluding third molars), with the deepest site per tooth documented. Examiners were calibrated, achieving high reliability (kappa = 0.83).
Insulin sensitivity was assessed using the HOMA-IR index, calculated from fasting glucose and insulin levels using the formula: (fasting insulin × fasting glucose)/22.5. HOMA-IR values were categorised into quintiles, with the highest quintile split into 5a and 5b due to data skewness.
Key covariates included age, gender, education level, BMI, dental plaque, toothbrushing frequency, dental attendance, alcohol use, and lipid-lowering medication. BMI was included to explore its potential confounding or mediating role.
Poisson regression models were used to estimate relative risks (RR) and 95% confidence intervals (CI) for associations between HOMA-IR and periodontal infection. Models accounted for potential confounders, with additional stratified analyses by age (30–49 and 50–64 years) and BMI categories (normal, overweight, obese). Two-stage cluster sampling weights were applied to adjust for the survey design.

Results

In the total population (30–64 years), a weak association was observed between the HOMA-IR index and teeth with PD ≥6 mm, but not with PD ≥4 mm.
Higher mean HOMA-IR values correlated with an increased number of teeth with deep PD (e.g., 2.46 for seven or more PD ≥6 mm vs. 1.81 for no pockets).
In younger individuals (30–49 years), HOMA-IR showed a stronger association with periodontal pockets:
- Quintile 5b (highest HOMA-IR) had a relative risk (RR) of 1.4 (95% CI: 1.0–1.8) for PD ≥4 mm compared to the lowest quintile.
- For PD ≥6 mm, RR reached 2.3 (95% CI: 0.9–5.7), though smaller sample sizes reduced consistency.
No significant associations were observed in the older group (50–64 years), indicating a possible age-related effect.
Adjusting for BMI negated the HOMA-IR and periodontal relationship, highlighting BMI as a significant confounder.
Among normal weight and overweight participants, no clear association was found.
BMI and HOMA-IR were moderately correlated (r = 0.52).
Adjustments for other factors, including oral hygiene and alcohol use, further attenuated the association.

Limitations

This study’s cross-sectional design limits its ability to establish causation between insulin sensitivity and periodontal diseases. While associations were observed, the directionality of the relationship remains unclear—reduced insulin sensitivity may contribute to periodontal infection, or conversely, periodontal inflammation may impair insulin sensitivity.
Residual confounding is possible despite adjustments for key factors such as BMI, oral hygiene behaviours, and alcohol use. BMI, in particular, both confounds and potentially mediates the relationship, complicating interpretation.
The reliance on the HOMA-IR index, while suitable for large-scale studies, provides only an indirect estimate of insulin sensitivity and may not fully capture its complexity.
The limited sample size for participants with severe periodontal disease (PD ≥6 mm) reduces the robustness of findings in this subgroup. Stratified analyses by age and BMI further subdivided the dataset, potentially amplifying statistical variability. These limitations highlight the need for longitudinal studies to explore causal pathways and clarify the role of obesity in this relationship.

Conclusion

This study underscores the complex interplay between insulin resistance, body weight, and periodontal diseases. While associations between HOMA-IR and periodontal pockets were observed in younger adults (30–49 years), BMI adjustments largely attenuated these links. The findings suggest that body weight may mediate the relationship or act as a confounder.
The study reinforces the importance of managing obesity and systemic inflammation in preserving periodontal health. Clinicians should consider systemic metabolic markers in periodontal disease assessment and tailor interventions to address overlapping metabolic and oral health challenges.
Further research is essential for integrating periodontal care within holistic patient management. Although intriguing, these results emphasise the need for longitudinal studies to clarify causality and explore potential pathways connecting insulin resistance with periodontal health.

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