Mechanisms linking periodontitis and diabetes

Background + Aims

• Impaired glucose regulation, an intermediate metabolic state between normal glucose homeostasis and diabetes, arises from factors such as obesity and genetics. It is associated with increased inflammation, hyperlipidemia, cardiovascular diseases, and periodontitis.
• Studies have linked impaired glucose metabolism (including elevated serum glucose, impaired fasting glucose, and insulin resistance) with periodontal conditions like alveolar bone loss, increased probing pocket depth (PPD), and chronic periodontitis. However, findings remain inconsistent, with some studies showing no such associations.
• Obesity, a common risk factor for both conditions, complicates these relationships. Research suggests that reduced insulin sensitivity may not independently cause periodontitis but could mediate the effects of obesity.
• Many studies lack rigorous control for obesity or genetic factors, highlighting the need for more robust analyses. Furthermore, most research has been cross-sectional, and longitudinal studies are limited.
• This study aimed to examine the relationship between insulin resistance, beta cell function, and PPD formation in a non-diabetic, non-smoking adult population.

Materials + Methods

• This study analysed data from the Health 2000 Survey and its follow-up (2004–2005) conducted in Finland.
• The nationally representative baseline sample included 8,028 adults aged 30 years or older, with 79% undergoing health and oral examinations. After exclusions for edentulism, periodontal pockets at baseline, or missing data, 157 non-diabetic, non-smoking participants aged 30–64 were included.
• Assessments included:
  • PPD at 4 surfaces per tooth (excluding third molars).
  • Dental plaque was assessed on 3 index teeth.
  • Toothbrushing and dental attendance patterns were categorised.
  • Fasting glucose and insulin levels were measured, and insulin sensitivity (HOMA-IR) and beta cell function (HOMA-B) were calculated.
  • CRP levels and physical activity were also measured.
  • Covariates included age, gender, BMI, educational level, dental plaque, toothbrushing frequency, dental attendance, and systemic conditions (e.g., asthma, rheumatoid arthritis).
• The outcome variable was the presence of PPD ≥4 mm at follow-up.
• Statistical analysis used Poisson regression to estimate incidence rate ratios (IRR) with 95% confidence intervals, adjusting for confounders. Analyses were conducted on the entire cohort and separately for participants with normal BMI (<25).

Results

• Participants in the highest HOMA-IR tertile had an annual incidence of 1.1 teeth with deepened pockets, compared to 0.65 in the lowest tertile.
• Those in the highest HOMA-B tertile had an annual incidence of 1.0, compared to 0.6 in the lowest tertile.
• After adjusting for confounders, the incidence rate ratio (IRR) for developing deepened pockets was 1.7 (95% CI 1.1–2.7) for the highest HOMA-IR tertile and 1.6 (95% CI 1.0–2.6) for the highest HOMA-B tertile, compared to their respective lowest tertiles.
• These associations were less pronounced among participants with normal BMI, particularly for HOMA-IR, indicating that body weight influenced the relationship between glucose metabolism and periodontal disease.
• Further adjustment for BMI among normal-weight participants did not substantially change the risk estimates, suggesting that while body weight plays a role, HOMA-IR and HOMA-B independently contribute to the risk of developing periodontal pockets.

Limitations