Impact of diabetes management on periodontitis

Background + Aims

• Periodontal disease and type 2 diabetes mellitus (T2DM) are interrelated, with evidence suggesting that periodontal disease worsens diabetic control and, conversely, that managing periodontal disease can improve glycaemic control. The host inflammatory response plays a key role in increasing susceptibility to periodontal disease, particularly in individuals with systemic conditions like T2DM. Studies show that individuals with severe periodontitis experience more diabetes-related complications and have poorer HbA1c levels over time.
• The Gullah population of coastal South Carolina and Georgia, descendants of enslaved Africans, has a high burden of T2DM, alongside distinctive population ancestry and longstanding geographical and social circumstances. The Gullah have a higher prevalence of chronic diseases, including obesity and hypertension, compared to other populations.
• Notably, periodontal disease is more prevalent among Gullah individuals with T2DM (70.6%) compared to national estimates for African Americans with diabetes (31.3%).
• This study aimed to explore the relationship between glycaemic control and periodontal disease progression in Gullah individuals with T2DM.

Materials + Methods

• This longitudinal observational study analysed 88 Gullah African American adults with T2DM. Of 98 participants from an earlier cross-sectional study who enrolled in a subsequent clinical trial, 88 had complete HbA1c and covariate data.
• Trial enrolment between December 2007 and March 2009 provided the follow-up assessment, before trial treatment. The interval from the earlier baseline examination averaged 2.99 years (range 1.93–4.08 years).
• Eligibility required at least three natural teeth, excluding third molars, and no periodontal treatment during the six months before trial enrolment.
• Trial exclusions included finger-prick glucose below 70 or above 350 mg/dL, fasting C-peptide below 1 ng/mL, serum creatinine ≥1.6 mg/dL, abnormal liver function, haemoglobinopathy affecting HbA1c assessment, and other conditions preventing adherence. Pregnancy, a requirement for antibiotic prophylaxis, periodontal disease requiring full-mouth extraction, and antibiotic use within the preceding six months were also exclusions.
• Medical history, anthropometric measurements, blood pressure and laboratory markers were recorded. Glycated haemoglobin (HbA1c) was measured at baseline and follow-up using liquid chromatography. Glycaemic control was classified using follow-up HbA1c: below 7% versus ≥7%.
• Calibrated examiners measured probing pocket depth (PPD), clinical attachment level and bleeding on probing (BOP) at six sites per tooth, excluding third molars.
• Progression was defined separately at each tooth site as an increase of ≥2 mm in PPD, ≥2 mm worsening of clinical attachment loss (CAL), or a change from no bleeding to bleeding on probing.
• Analyses included sites measured at both visits: 9,648 for PPD and attachment loss, and 9,599 for BOP. Sites missing at either visit, including those lost through tooth extraction, were excluded.
• Multivariable logistic regression with generalised estimating equations accounted for clustering of sites within participants. Candidate covariates included baseline PPD, age, sex, smoking, BMI, tooth type and jaw location. Final models retained different covariates and relevant interactions; adjusted odds ratios (ORs) describe site-level progression.

Results

• At baseline, mean age was 55.57 years and mean diabetes duration was 10.65 years. Most participants were women (78.41%), obese (71.59%) and never-smokers (76.14%). Mean PPD was 1.85 mm and mean attachment level was 1.86 mm.
• Mean HbA1c was 8.09% at baseline (range 5.10–15.10%) and 8.13% at follow-up (range 4.70–12.80%). At follow-up, 60 participants (68.18%) had HbA1c ≥7% and 28 (31.82%) had HbA1c below 7%.
• The mean proportion of sites per participant showing progression was 9% for PPD, 12% for attachment loss and 24% for new bleeding.
• Poor glycaemic control was associated with higher odds of site-level PPD and attachment-loss progression. The association was stronger at sites with deeper baseline pockets.
• Adjusted ORs for PPD progression, comparing HbA1c ≥7% with below 7%, were:
  • Baseline PPD 3 mm: 1.98 (95% CI 1.22–3.21).
  • Baseline PPD 5 mm: 2.76 (95% CI 1.52–5.01).
  • Baseline PPD 7 mm: 3.84 (95% CI 1.74–8.49).
• Corresponding adjusted ORs for attachment-loss progression were:
  • Baseline PPD 3 mm: 1.93 (95% CI 1.20–3.10).
  • Baseline PPD 5 mm: 2.64 (95% CI 1.36–5.14).
  • Baseline PPD 7 mm: 3.62 (95% CI 1.45–9.05).
• Compared with sites in participants with normal BMI, sites in participants with obesity had higher odds of PPD progression (OR 2.64; 95% CI 1.26–5.55) and attachment-loss progression (OR 6.09; 95% CI 3.04–12.19). These are odds of progression at tooth sites, not a person’s overall risk.
• Molar sites had higher odds of both outcomes. Older age, past smoking and overweight were also associated with attachment-loss progression. The absence of a significant association for current smoking should be interpreted cautiously because only six participants were current smokers.
• Poor glycaemic control was not significantly associated with new bleeding on probing (OR 1.23; 95% CI 0.81–1.86; p = 0.327).

Limitations

• The small, selected cohort consisted exclusively of Gullah African Americans with T2DM, limiting generalisability. Only five participants had normal BMI, making the obesity comparisons particularly sensitive to the small reference group.
• Participants were predominantly of lower socioeconomic status with limited dental care access. Residual confounding by social, behavioural and other factors remains possible.
• Although periodontal changes were followed over time, the study was observational. It cannot establish causation or determine which condition—obesity, diabetes or periodontitis—first developed before baseline.
• Glycaemic-control groups were defined using follow-up HbA1c. This does not capture glucose control throughout the observation period and limits interpretation as a baseline predictor of future progression.
• The study did not test whether improving glycaemic control or providing periodontal treatment prevents progression. Some participants may have received emergency dental care, mainly extractions, between examinations; excluded sites could influence the findings.

Conclusion

• Among these adults with T2DM, poor glycaemic control was associated with greater odds of periodontal attachment-loss and pocket-depth progression at individual tooth sites, particularly where pockets were initially deeper. Obesity was also associated with progression. The findings support attention to periodontal health in diabetes care, but do not demonstrate that improving glycaemic control prevents periodontal deterioration.