| 1783 Quantitative Detection of Porphyromonas gingivalis in Diabetes Mellitus | |||||||||
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N. HAMMAN1, J.A. KATANCIK1, and K. LAMAR2, 1University of Tennessee, College of Dentistry, Memphis, USA, 2University of Tennessee, Memphis, USA Objective: The increased prevalence and severity of periodontitis (PD) observed in diabetes mellitus (DM) has been partially attributed to an exaggerated immune response to putative periodontal pathogens such as Porphyromonas gingivalis (Pg). The purpose of this study was to determine the association among a diagnosis of DM, a diagnosis of PD, and the levels of Pg. Methods: 6 subgingival sites were sampled for each subject with 376 samples analyzed in duplicate. DNA was isolated from each sample and Pg counts were derived by RT-PCR with Pg specific primers and known Pg DNA standards. A mean Pg count was derived for each subject and an independent sample t-test was conducted to compare the groups. Results: The study cohort: 38 subjects (27 female, 11 male, 28 African-Americans, 9 Caucasians, and 1 other), with a mean age of 44 ± 12. DM subjects had a mean HbA1c of 7.8 and the HbA1c of non-DM subjects was 5.4.
There was not a statistically significant difference in Pg bacterial cell counts between diabetics (42±119) and non-diabetics (655±2712; p=0.345), between subjects with (916±3239) or without (43±142) periodontal disease (p=0.191), or between diabetic subjects with (94±187) or without (426±2181) periodontal disease (p=0.694). We next tested the hypothesis that periodontal disease subjects with diabetes demonstrate lower bacteria counts compared to periodontal subjects without diabetes. Periodontal disease subjects with diabetes had lower bacteria counts (94±188) compared with periodontal disease subjects without diabetes (1738±4596); however, given the high variability this did not reach significance (p=0.097). Conclusion: There was a tendency for periodontitis subjects with a diagnosis of DM to have a lower bacterial load, consistent with a lesser bacterial insult required to elicit a destructive immune response in DM. NIH K23 RR-16106-03 and GCRC M01-RR00211. | |||||||||
| Seq #207 - Clinical Science 2:00 PM-3:00 PM, Saturday, 11 March 2006 Dolphin Hotel Pacific Hall | |||||||||
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