Mechanisms linking periodontitis and diabetes

Background + Aims

• Type 1 diabetes mellitus (T1DM) is closely associated with systemic inflammation, increasing the risk of conditions such as periodontitis. Elevated markers such as interleukin-6 (IL-6) are implicated in this link.
• Periodontitis, a chronic condition that damages tooth-supporting apparatus, is prevalent in people living with diabetes. This is likely to be exacerbated by elevated systemic inflammation.
• IL-6, a key inflammatory cytokine, has dual roles in modulating immune responses and exacerbating inflammation, potentially hindering periodontal healing post-treatment.
• This study explored the connection between serum IL-6 levels and periodontal health in people living with type 1 diabetes, investigating its impact on treatment outcomes and recovery.

Materials + Methods

• 80 T1DM patients were recruited and examined by a periodontal specialist.
• Exclusions included recent antibiotic use or immunosuppressive therapy.
• After anti-infective periodontal therapy, 65 participants were re-examined, with 58 completing follow-up analyses.
• Data collected included clinical periodontal parameters (probing pocket depth (PPD), bleeding on probing (BOP)), glycosylated haemoglobin (HbA1c), high-density lipoprotein (HDL), low-density lipoprotein (LDL), IL-6, and ultrasensitive C-reactive protein (usCRP) levels.
• Therapy included oral hygiene education, scaling, root planing, and periodontal surgery when needed.
• Venous blood samples were taken at baseline and follow-up, and serum IL-6 levels were measured using enzyme-linked immunosorbent assay (ELISA).
• usCRP, LDL, and HDL cholesterol were analysed with advanced enzymatic methods.
• Changes in IL-6 were categorized as increase, decrease, or stable.
• Periodontal healing was evaluated using the reduction in bleeding sites and PPD ≥ 4 mm.
• Statistical analyses assessed associations between periodontal parameters and inflammatory markers, and were adjusted for BMI and smoking. Stratified analyses controlled for confounders such as BMI ≥ 26 kg/m² and smoking status.

Results

• The study group characteristics were consistent across treated and total subjects in terms of age, gender, smoking, BMI, diabetes duration, and number of teeth.
• Despite effective periodontal therapy, no significant changes in the mean serum inflammatory markers, including IL-6, were observed between baseline and follow-up.
• Unadjusted analyses showed significant associations between periodontal inflammation markers (BOP and bleeding with PPD ≥ 4 mm) and serum IL-6. Multiple regression analyses confirmed this association at baseline and after therapy. However, interactions between IL-6, smoking, and BMI were not statistically significant.
• IL-6 changes varied:
  • 7% showed a decrease
  • 0% remained stable
  • 3% increased
• These changes did not correlate with reductions in bleeding and PPD ≥ 4 mm.
• Higher post-therapy IL-6 levels were significantly linked to poorer periodontal healing, even after controlling for confounders. Subjects with higher residual inflammation had elevated IL-6 levels, highlighting its potential role in impaired healing.
• Smoking did not significantly affect outcomes post-therapy.

Limitations