OBJECTIVE: 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 (HbA1c< or =6.5%). 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 > or =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.
OBJECTIVE: 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 (HbA1c< or =6.5%). 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 > or =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.
Authors: Douglas C Hardy; Jonathan H Ross; Corinne A Schuyler; Renata S Leite; Elizabeth H Slate; Yan Huang Journal: J Clin Periodontol Date: 2011-10-20 Impact factor: 8.728