AbstractObjective: To monitor clinical and microbiological changes during experimental gingivitis in type 1 diabetics and non‐diabetics.Materials and Methods: Nine type 1 diabetics with good/moderate metabolic control and nine age‐gender matched non‐diabetics were recruited. Probing pocket depths in all subjects did not exceed 4 mm and none were affected by attachment loss. According to the original model, an experimental 3‐week plaque accumulation resulting in experimental gingivitis development and a subsequent 2‐week period of optimal plaque control were staged. Subgingival plaque samples were collected at days 0, 21 and 35 from one site per quadrant, pooled and analysed using checkerboard DNA–DNA hybridization.Results: Diabetics (mean age 25.6±5.8 standard deviation (SD), range 16–35 years) had a mean HbA1c level of 8.1±0.7% (SD), while non‐diabetics (mean age 24.8±5.7 (SD), range 15–36 years) were metabolically controlled (HbA1c6.5%). Between Days 0, 21 and 35, no statistically significant differences in mean plaque and gingival index scores were observed between diabetics and non‐diabetics. At days 7 and 21, however, diabetics showed statistically significantly higher percentages of sites with gingival index scores 2 compared with non‐diabetics. Mean DNA probe counts of the red and orange complex species increased significantly (p<0.05) between days 0 and 21 and decreased significantly (p<0.05) between days 21 and 35 in both groups.Conclusion: Both diabetics and non‐diabetics react to experimental plaque accumulation with gingival inflammation. Type 1 diabetics, however, develop an earlier and higher inflammatory response to a comparable bacterial challenge.